Anii fara ani

...pentru cei carora le place sa scrie

Mesajde jl_rona » Mar Iun 10, 2008 9:14 pm

cat despre asta:

http://bp1.blogger.com/_1ymr9DLlsXw/SDxi_r3lZnI/AAAAAAAABwk/NVVfP4xdARA/s1600-h/IMG_1471_1.jpg

acum realizez ca e o combinatie intre reveneagu si piskeshu: parul lui reveneagu si ciocu lu piskeshu. Oribil!
“Love, work and knowledge are the wellsprings of our lives, they should also govern it.â€Â
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Mesajde jl_rona » Mar Oct 28, 2008 12:13 am

Dimineata cu nor

Ma desfac de visul cu clesti;
Cruste de iubire las in urma, batand, ca un gat de pasare pierdut in iarba.
Rasaritul s-a lasat peste zvacnirile noptii
Ca un nor intins ce-mi netezeste mintile cu care tocmai trudisem din nou,
Neavand ce face,
Si-mi spune cald, din pata rosie de senin,
Pe nume,
Buna dimineata!

~lui Vicentiu
“Love, work and knowledge are the wellsprings of our lives, they should also govern it.â€Â
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Mesajde jl_rona » Vin Noi 21, 2008 9:55 pm

Pal

Vii de departe...
Privindu-ma, prin piele-ti intinzi radacini
Si, fara cunostinta, ma prinzi
Pe sub ritualuri, tresarire si valuri,
In linistea ce palpaie atat de placut
A moarte,
Desprins parca dintr-o carte
Vii...

Sculptat in oase si ierni,
Parfumuri calde si reci imi asterni
Pe obrajii care nu mai stiu de mine,
Pe inima care nu ma mai tine
Cand iti vorbesc...

Nori si soare ma trec,
Orizontul se rastoarna si incordarea ma toarna,
Obrajii ca tortele
Mi se aprind,
Fiori
Mai presus, ma cuprind,
Venele topite ei mi le intind
Scurgandu-mi in pamant fortele...

Pal,
Dulce-amarui ca un migdal
Cu gust slab de ceara-
Un impuls ramas din visul de-aseara-
Nevazut,
Privindu-te scurt
Si luminandu-te mut
Sunt...

~lui Valeriu Stefan (Vicentiu)
“Love, work and knowledge are the wellsprings of our lives, they should also govern it.â€Â
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Mesajde jl_rona » Mie Mai 06, 2009 9:15 pm

Thyle, am crezut ca esti mai destupat, dar esti un papagal, mai! Multinationala la care lucrezi ti se potriveste manusa!

Mitzi, Ayala si alte fete dragute. Daca vreti sa vorbiti cu mine, oricand pe mess, nici o problema. Id-ul e cel din stanga.

Piskeshule, tu esti destept ma, din nou, pentru a 1000-a oara iti spun, ca ma repet ca Vadim Tudor: e pacat sa te scalzi in mocirla. Tu ai timp, nu esti ca mine, citeste ceva, studiaza ceva, netul e mare, daca vorbesti numai despre biciclete si fete de la OTV o sa-ti moara nu numai memoria, dar si pula. E pacat, zau.

In ce priveste cacatul de forum, thyl e mai gutufan decat credeam, cu banul lui. Eu am crezut ca ma relaxez acolo, dar n-am timp sa ascult cretinitatile lui si ale altor snobi cu pretentii de intelectuali si macelarimea ordinara la care sunt supusa zilnic pentru ca am o boala autoimuna. Mai toti ati dat dovada de cretinism pur in ce priveste subiectul asta, asa ca m-as fi retras incet sau brusc, dar m-as fi retras. Era clar ca eu eram ca o raza laser intr-un morman de melci acolo, asa ca erati pierdere de vreme cel putin.

Sincer, va doresc si voua sa aveti exact acelasi lucru (o boala autoimuna), cu toate ca blestemele mele nu prea se implinesc, dar tare v-as dori si voua si oricui a ras de mine sau de un alt om bolnav in viata lui sa aiba exact boala de care a ras.

Oricum de boala in general nu scapati, si cine rade la urma, cine stie, poate rade mai mult si mai bine.

Va doresc multa sanatate, exact asa cum imi doriti si voi mie. Sa dea Dumnezeu sa se faca dreptate pe lumea asta. Abia cand o sa fiti bolnavi o sa vedeti cata stiinta va trebuie, cata strofocare de creier ca sa invingeti sau macar sa pacaliti boala.

=========================================================

Intre timp am descoperit o metoda de a ma fute cat de cat. Prezervativele scaldate in nonoxynol 9 care provoaca candida:

http://en.wikipedia.org/wiki/Nonoxynol-9

trebuie combinate cu o crema antimicotica, pentru a crea macar un fel de mediu neutru.

Some studies have noted a possible link between the use of spermacides containing nonoxynol-9 with vaginal yeast infection. The likely mechanism is that the spermacide kills off friendly bacteria in the vagina thus allowing a rapid growth of other micro-organisms including yeast. Many condoms and lubricants contain nonoxynol-9.

http://www.home-remedies-yeast-infection.com/yeast-infection-causes.html

Crema Meclon e amara ca chinina si nu mai poate nimeni sa te linga-n pizda, da nu-i mare pierdere. Mai este crema cu terbinafine pe care am folosit-o o data cu succes, dar este pentru unghii, nu e crema vaginala si s-ar putea in timp sa cauzeze cine stie ce altceva. Aia n-are nici un gust, asa ca prostu nu se prinde. Poti sa-l otravesti linistita. A-)

Deocamdata cu cremele astea a mers. Sper sa mearga in continuare, dar nu trebuie folosite on a daily basis pentru ca se-nvata ciuperca cu ele. Sunt doar pentru ocazii festive. :)

Cat despre prezervative, cu cat sunt mai scumpe, cu atat au mai multe substante nocive pe ele, provocatoare de micoze si alergii, sunt mai subtiri si se rup mai repede.

Prezervativele LOVE sunt foarte bune! Astia de la Durex poa sa unga o franghie cu nonoxynol 9 si sa si-o lege de gat! Ar fi cel mai bun lucru pe care l-au facut vreodata.
“Love, work and knowledge are the wellsprings of our lives, they should also govern it.â€Â
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Mesajde jl_rona » Vin Mai 08, 2009 1:26 am

jl_rona: ce e cu tilica
jl_rona: a innebunit baiatu?
mary: aha
mary: da nu acu
jl_rona: da cand
mary: mai demult cred
jl_rona: e cretin
jl_rona: l-a innebunit piskeshu
jl_rona: ;)
jl_rona: e mai tare
jl_rona: cel mai tare
mary: toti sunt tari
jl_rona: nope
jl_rona: io numai pe el il iubesc
mary: pe cine ?
jl_rona: pe piskeshu
jl_rona: restu-s slabuti
mary: ah
mary: k
jl_rona: si el ma iubeste
mary: f frumos
jl_rona: ai vazut ca i-a zis lu tilica sa ia pula-n gura?
jl_rona: sau ceva asa
jl_rona: ca m-a banat cretinelu
-----------------------------------------
jl_rona: auzi? da de ce ma iubesti tu asa?
mary: nu stiu
mary: ca mi place de tine
jl_rona: jesus!
jl_rona: pai sa-l invit pe piskeshu sa ne vada impreuna
jl_rona: tilica e banat :)
mary: =))
jl_rona: poti sa trimiti asta pe forum
jl_rona: copy + paste
jl_rona: fara misto
“Love, work and knowledge are the wellsprings of our lives, they should also govern it.â€Â
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Mesajde jl_rona » Vin Mai 08, 2009 12:12 pm

Sleep and the Immune System. Is Good Health Mediated by Brain-Mind States?
by J. Allan Hobson


Invaders are assaulting our body's portals at all times, not just during winter, when we tend to get sick more, and not just during local outbreaks of viruses. This means that the margin of safety of our health - the degree to which we are resistant to infection, and perhaps even cancer - may be determined by how well our sleep state enhances our immune system. The daily sequencing of normal brain-mind states, therefore, mediates our health.

None of the declarations of folk psychology is more widely believed than that linking good sleep and good health. Mothers have exhorted their children to "get a good night's sleep" since time began, it seems. In the early 1970s, studies conducted at the California Human Population Laboratory identified several behaviors that were positively correlated with length of life. Sleep headed the list, followed by exercise (which is known to promote sleep), eating breakfast (commuters take note), and not snacking (icebox raiders beware). Weight watching, not smoking, and moderating alcohol intake were also positive predictors of good health.

To make a long and fascinating story short, it turns out that when animals are sleep deprived, a protein known as di-muramyl peptide accumulates in their spinal fluid. The peptides do not originate in the brain. Instead, they come from bacteria in the body, suggesting that sleep deprivation may enable bacterial growth and that sufficient sleep impedes bacterial growth.

What's even more interesting is that these di-muramyl peptides enhance non-REM sleep (but not REM sleep). [REM=rapid eye movements] The peptides also cause fever. The two effects are dissociable, however; the sleep effect is independent of the fever. More interesting still is the fact that the peptides stimulate cells in the brain and the body to produce interleukin-1, a powerful immune-system molecule that promotes the destruction of both bacteria and tumor cells.

Highly significant and desirable health effects are mediated by interleukin's ability to encourage the B lymphocytes to produce antibodies, which kill viruses, and to trigger the proliferation of T lymphocytes, which attack microbial invaders. The net effect is to mobilize the body's defensive forces.

By depriving his animals of sleep, Krueger made them more vulnerable to infection.

J. Allan Hobson, M.D., is professor of psychiatry at Harvard Medical School, director of the Laboratory of Neurophysiology at the Massachusetts Mental Health Center, and a member of the MacArthur Foundation Mind-Body Network who lectures regularly around the world. The author of The Dreaming Brain and Sleep, he lives in Brookline, Massachusetts.

Reprinted with permission. "Sleep and the Immune System" is an excerpt from The Chemistry of Conscious States: How The Brain Changes Its Mind by J. Allan Hobson. Copyright © 1994. Published by Little, Brown (a Time Warner Co.), Time & Life Bldg., 1271 Avenue of the Americas, New York, NY 10020. ISBN 0-316-36754-0, 300pp; hardback $22.95.


http://www.truthseekerjournal.com/1995archive/122_2/ts222e.html
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Mesajde jl_rona » Vin Mai 08, 2009 8:54 pm

BY AMERICAN NATIONAL SPACE BIOMEDICAL RESEARCH INSTITUTE

National Space Biomedical Research Institute
One Baylor Plaza, NA-425, Houston, TX 77030



Research Area: Musculoskeletal Alterations
[color="red"]Human Performance Factors, Sleep and Chronobiology[/color]
Radiation Effects

Synergy Project
Principal Investigator: Janet M. Mullington, Ph.D.
Organization: Harvard Medical School
Project Title: Sustained Partial Sleep Deprivation: Effects on Immune Modulation and Growth Factors
Funding Period: 1997-1999


The vulnerability to medical emergencies is greatest in space where there are real limits to the availability or effectiveness of ground based assistance.

Moreover, astronaut safety and health maintenance will be of increasing importance as we venture out into space for extended periods of time.

It is therefore critical to understand the mechanisms of the regulatory physiology of homeostatic systems (sleep, circadian, neuroendocrine, fluid and nutritional balance) and the key roles played in adaptation.

This synergy project has combined aims of the Human Performance Factors, Sleep and Chronobiology Team; the Immunology, Infection and Hematology Team; and the Muscle Alterations and Atrophy Team, to broadly address the effects of long-term sleep reduction, as is frequently encountered in space exploration, on neuroendocrine, neuroimmune and circulating growth factors.

Astronaut sleep is frequently curtailed to averages of between 4-6.5 hours per night. There is evidence that this amount of sleep is inadequate for maintaining optimal daytime functioning.

However, there is a lack of information concerning the effects of chronic sleep restriction, or reduction, on regulatory physiology in general, and there have been no controlled studies of the cumulative effects of chronic sleep reduction on neuroendocrine and neuroimmune parameters.

This synergy project represents a pilot study designed to characterize the effects of chronic partial sleep deprivation (PSD) on neuroendocrine, neuroimmune and growth factors.

This project draws its subjects from two (of 18) conditions of the larger NSBRI project, Countermeasures to Neurobehavioral Deficits from Cumulative Partial Sleep Deprivation During Space Flight (PI: David Dinges), one of the projects on the Human Performance Factors, Sleep and Chronobiology Team.

For the purposes of this study, to investigate the effects of chronic sleep loss on neuroendocrine and neuroimmune function, we have focused on the two extreme sleep conditions from this larger study: a 4.2 hour per night condition, and an 8.2 hour per night condition.

During space flight, muscle mass and bone density are reduced, apparently due to loss of GH and IGF-I, associated with microgravity.

Since greater than 70 percent of growth hormone (GH) is secreted at night in normal adults, we hypothesized that the chronic sleep restriction to four hours per night would reduce GH levels as measured in the periphery. In this project, in collaboration with the Muscle Alterations and Atrophy Team, we have measured insulin-like growth factor-I (IGF-I) in peripheral circulation to test the prediction that it will be reduced by chronic sleep restriction.

In addition to stress, recent research suggests that sleep is also involved in modulation of immune function.

While we all have the common experience of being sleepy when suffering from infection, and being susceptible to infection when not getting enough sleep, the mechanisms involved in this process are not understood and until recently have gone largely overlooked.

We believe that the immune function changes seen in spaceflight may also be related to the cumulative effects of sleep loss.

Moreover, in space flight, the possibility of compromised immune function or of the reactivation of latent viruses is serious potential hazards for the success of long-term missions.

Confined living conditions, reduced sleep, altered diet and stress are all factors that may compromise immune function, thereby increasing the risks of developing and transmitting disease.

Medical complications, which would not pose serious problems on Earth, may be disastrous if they emerged in space.

Understanding the long-term consequences of sleep curtailment on general health and physiological functioning is critical to the success of any space mission where astronauts will be away from critical care facilities for extended periods of time.

http://www.nsbri.org/Research/Projects/viewsummary.epl?pid=94



==============

[color="Red"]Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.[/color]

D F Dinges, S D Douglas, L Zaugg, D E Campbell, J M McMann, W G Whitehouse, E C Orne, S C Kapoor, E Icaza, and M T Orne
Unit for Experimental Psychiatry, Institute of Pennsylvania Hospital, Philadelphia, Pennsylvania 19139.


Our data indicate that acute loss of sleep to the point of impairment of neurobehavioral function in humans is associated with leokocytosis and increased NK cell counts and activity and that these outcomes are reveresed by recovery sleep.

===================


[color="red"]Differential Effects of Rapid Eye Movement Sleep Deprivation and Immobilization Stress on Blood Lymphocyte Subsets in Rats[/color]

Javier Velazquez-Moctezumaa, Emilio Dominguez-Salazara, Edith Cortes-Barberenab, Oralia Najera-Medinab, Socorro Retana-Marqueza, Ernesto Rodriguez-Aguilerab, Anabel Jiménez-Anguianoa, Leticia Cortes-Martinezb, Rocio Ortiz-Muñizb

aDepartment of Reproductive Biology, and
bDepartment of Health Sciences, Universidad Autónoma Metropolitana-Iztapalapa, Mexico City, Mexico


Abstract

Objectives: There is growing evidence of the relationship between sleep and the immune response.

Studies aimed at elucidating the function of rapid eye movement (REM) sleep have found it difficult to separate the effects due to REM sleep deprivation and the effects due to the stress produced by the deprivation procedure.

It has been claimed that immobilization is the main stressor that the animals have to face during the deprivation process.

In this study, we analyzed the effects of short-term (24 h) and long-term (240 h) REM sleep deprivation on the distribution of lymphocyte subsets in the peripheral blood of rats.

In addition, these effects were compared with those obtained after both short- and long-term stress by immobilization.

Methods: Lymphocyte population bearing surface markers such as CD5 (T cells), CD45RA (B cells), CD4 (T helper/inducer cells), CD8 (T suppressor/cytotoxic cells) and CD161 (NK cells) were analyzed using monoclonal antibodies.

Lymphocyte subsets were assessed by flow cytometry.

Results: Both short- and long-term REM sleep deprivation decreased the percentage of T lymphocytes and induced a significant increase in NK cells.

Short-term immobilization induced only a significant increase in the percentage of B lymphocytes and a decrease in the percentage of T lymphocytes, while long-term immobilization did not elicit any change.

Conclusion: The present results support the notion that REM sleep deprivation and immobilization stress each exert particular effects on the immune system.

These data suggest that the characteristics of the immune response will depend on the nature of the behavioral manipulation.

Copyright © 2004 S. Karger AG, Basel


Author Contacts

Dr. Javier Velazquez Moctezuma
Departamento de Biologí­a de la Reproducción
Universidad Autónoma Metropolitana-Iztapalapa
09340 Mexico City (Mexico)


http://content.karger.com/produktedb/produkte.asp?typ=fulltext&file=NIM2004011004261
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Mesajde jl_rona » Vin Mai 08, 2009 8:55 pm

The FASEB Journal, Vol 3, 1972-1977, Copyright © 1989 by The Federation of American Societies for Experimental Biology

RESEARCH COMMUNICATIONS


[color="red"]Effects of sleep deprivation on human immune functions[/color]

H Moldofsky, FA Lue, JR Davidson and R Gorczynski
Toronto Western Division, Toronto Hospital, Ontario, Canada.


The effect of 40 h of wakefulness on a variety of immunological parameters in the peripheral blood from 10 normal male subjects was studied.


Sleep deprivation led to enhanced nocturnal plasma interleukin 1-like and interleukin 2-like activities.

The rise in nocturnal response of lymphocytes to pokeweed mitogen stimulation during a normal 24 h sleep-wake cycle was delayed by sleep deprivation, but the response to the phytohemagglutinin mitogen was unaffected.

With resumed nocturnal sleep, there was a prolonged decline in natural killer cell activity (measured as spontaneous cytolytic activity for human tumor cells) and return of an increased response to pokeweed mitogen.

The altered patterns in immune functions occurred independently of the cortisol circadian rhythm, which remained unchanged.

http://www.fasebj.org/cgi/content/abstract/3/8/1972

The FASEB Journal, Vol 10, 643-653, Copyright © 1996 by The Federation of American Societies for Experimental Biology

RESEARCH COMMUNICATIONS


[color="red"]Partial night sleep deprivation reduces natural killer and cellular immune responses in humans[/color]

M Irwin, J McClintick, C Costlow, M Fortner, J White and JC Gillin
Department of Psychiatry, University of California, San Diego, USA.

Prolonged and severe sleep deprivation is associated with alterations of natural and cellular immune function.

To determine whether alterations of immune function also occur after even a modest loss of sleep, the effects of early-night partial sleep deprivation on circulating numbers of white blood cells, natural killer (NK) cell number and cytotoxicity, lymphokine-activated killer (LAK) cell number and activity, and stimulated interleukin-2 (IL-2) production were studied in 42 medically and psychiatrically healthy male volunteers.

After a night of sleep deprivation between 10 P.M. and 3 A.M., a reduction of natural immune responses as measured by NK cell activity, NK activity per number of NK cells, LAK activity, and LAK activity per number of LAK precursors (CD16,56, CD25) was found.

In addition, concanavalin A-stimulated IL-2 production was suppressed after sleep deprivation due to changes in both adherent and nonadherent cell populations.

After a night of recovery sleep, NK activity returned to baseline levels and IL-2 production remained suppressed.

These data implicate sleep in the modulation of immunity and demonstrate that even a modest disturbance of sleep produces a reduction of natural immune responses and T cell cytokine production.

http://www.fasebj.org/cgi/content/abstract/10/5/643

The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 10 3597-3603
Copyright © 2000 by The Endocrine Society


Original Studies

[color="red"]Effects of Sleep and Sleep Deprivation on Interleukin-6, Growth Hormone, Cortisol, and Melatonin Levels in Humans1 [/color]

Laura Redwine, Richard L. Hauger, J. Christian Gillin and Michael Irwin
Department of Psychiatry, University of California and San Diego Veterans Healthcare System, San Diego, California 92161


The objective of this study was to evaluate the effects of nocturnal sleep, partial night sleep deprivation, and sleep stages on circulating concentrations of interleukin-6 (IL-6) in relation to the secretory profiles of GH, cortisol, and melatonin.

In 31 healthy male volunteers, blood samples were obtained every 30 min during 2 nights: uninterrupted, baseline sleep and partial sleep deprivation-early night (awake until 0300 h). Sleep was measured by electroencephalogram polysomnography.

Sleep onset was associated with an increase in serum levels of IL-6 (P < 0.05) during baseline sleep. During PSD-E, the nocturnal increase in IL-6 was delayed until sleep at 0300 h.

Sleep stage analyses indicated that the nocturnal increase in IL-6 occurred in association with stage 1–2 sleep and rapid eye movement sleep, but levels during slow wave sleep were not different from those while awake. The profile of GH across the 2 nights was similar to that of IL-6, whereas the circadian-driven hormones cortisol and melatonin showed no concordance with sleep.

Loss of sleep may serve to decrease nocturnal IL-6 levels, with effects on the integrity of immune system functioning.

Alternatively, given the association between sleep stages and IL-6 levels, depressed or aged populations who show increased amounts of REM sleep and a relative loss of slow wave sleep may have elevated nocturnal concentrations of IL-6 with implications for inflammatory disease risk.

http://jcem.endojournals.org/cgi/content/abstract/85/10/3597

See more at this link:

http://jcem.endojournals.org/cgi/content/full/85/10/3597
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Mesajde jl_rona » Vin Mai 08, 2009 8:56 pm

Stanley Medical College, Chennai-600001, India

[color="red"]Innate immunity during rem sleep deprivation [/color]

Biomedicine. 2001; 21(1): 41-5

ABSTRACT:

Change in innate immune parameters were observed after 48 and 72 hours of Rapid Eye Movement (REM)sleep deprivation in albino rats.

There was a significant fall in total white blood cell count, decrease in lymphocyte and eosinophil counts associated with an increase in polymorphs in the peripheral blood.

The phagocytic and avidity indices of the neutrophils were also elevated after 48 and 72 hours of REM deprivation.

However the nitro blue tetrazolium(NBT)reduction by neutrophil and plasma corticosteroid were elevated only in 48 hours REM sleep deprived animals.

there was a significant fall in spleen weight/body weight ratio with a concomitant increase in lymph node/body weight ratio, while the thymus weight/body weight ratio remained unaltered.

These findings indicate that REM sleep deprivation mediated changes, were not mediated through corticosterone alone (as stress induced elevated corticosterone levels are known to cause thymic involution) as shown by the unaltered thymus weight/body weight ratio in these animals.

http://medind.nic.in/imvw/imvw1963.html


[color="red"]4 days of REM sleep deprivation contributes to a reduction of cell proliferation in rats[/color]

WESTCHESTER, Ill. Four days exposure to a REM sleep deprivation procedure reduces cell proliferation in the part of the forebrain that contributes to long-term memory of rats, according to a study published in the February 1 issue of the journal SLEEP.

The study, authored by Dennis McGinty, PhD, of the V.A. Greater Los Angeles Healthcare System, focused on male Sprague-Dawley rats. REM sleep deprivation was achieved by a brief treadmill movement initiated by automatic online detection of REM sleep. A yoked-control (YC) rat was placed in the same treadmill and experienced the identical movement regardless of the stage of the sleep-wake cycle.

According to the results, REM sleep was reduced by 85 percent in REM sleep deprived rats and by 43 percent in YC rats. Cell proliferation was reduced by 63 percent in REM sleep deprived rats compared with YC rats. Across all animals, cell proliferation exhibited a positive correlation with the percentage of REM sleep.

Several studies have shown that sleep contributes to brain plasticity in general, and to adult neurogenesis, in particular, said Dr. McGinty.

Neurogenesis is a concrete example of brain plasticity, suppression of adult neurogenesis is thought to be important in pathologies such as depression.

One current question has to do with the relative contribution of the two sleep states, non-REM and REM, which have very different, even opposite, physiological properties.

This study showed that REM sleep has a critical role in facilitating brain plasticity.

The study does not exclude an equally important role for non-REM sleep. In other recent work, we have shown that sleep fragmentation can also suppress adult neurogenesis.
How sleep affects the molecular mechanisms underlying neurogenesis remains to be explored.

It is recommended that older adults get between seven and eight hours of nightly sleep.


The American Academy of Sleep Medicine (AASM)


http://www.bio-medicine.org/biology-news-1/4-days-of-REM-sleep-deprivation-contributes-to-a-reduction-of-cell-proliferation-in-rats-2090-1/

=======================
[color="red"]
REM sleep deprivation effects on NK-cell cytotoxicity and lymphocyte subpopulations from peripheral blood in male rats[/color]


LANDIS C, TSUJI J, LENTZ M, SHAVER J, POLLACK S
Sleep Research 1996; 25: 470.
Department of Biobehavioral Nursing, Box 357266, The University of Washington, Seattle, WA 98195-7266.


Abstract:

Sleep deprivation has complex multiple effects on neural, hormonal, and immune systems.

Emerging evidence suggests that immune function is compromised by sleep deprivation, but studies both in rodents and humans show equivocal results (reviewed in1,2).

The degree of stress imposed by methods used to keep subjects awake and subsequent activation of the HPA and sympathetic nervous systems may explain, in part, the lack of consistent evidence for immunosuppression in sleep deprivation studies.

REM sleep deprivation by the standard single platform technique is considered stressful, although rats housed alone on both small and large platforms (used as a control) or housed with other rats and with multiple platforms show increased levels of corticosterone.3

[color="red"]Given the well documented immunosuppressive effect of adrenal steroids4 and the recent finding that corticosterone plasma levels are inversely related to peripheral lymphocyte numbers,5 we hypothesized that cytotoxic activity of Natural Killer (NK) cells and subpopulations of other peripheral lymphocytes would be reduced in rats subjected to REM sleep deprivation procedures for 72 hours. [/color]

Methods. Twenty-four male, pathogen free Sprague-Dawley rats 80 days old upon arrival to the laboratory were housed in individual 25 liter buckets containing an inverted flower pot with a round plexiglas top (8cm). Rats were maintained in constant light (80 lux) for 3 weeks to reduce their diurnal rhythms prior to being sleep deprived.6 During sleep deprivation water to a depth of 2.5 cm replaced wood shavings in the buckets of 12 randomly selected rats. Food and water were delivered ad libitum from a feeder and spout on each side of the bucket within easy reach when the rat was on the platform.

Under deep anesthesia, peripheral blood was drawn from control and sleep deprived rats by direct cardiac puncture into heparinzed syringes. Mononuclear cells were obtained after centrifugation on Histopaque (Sigma). Aliquots were used in a standard NK-cell cytotoxicity assay and stained for flow cytometric analysis using monoclonal antibodies for NK-cells (3.2.37), monocytes (CD11b), and T-cell subpopulations (CD3, CD4, and CD8). FITC-conjugated antibodies and their isotype controls (Pharmingen) were used at an optimal dilution of 1:1000, based on preliminary titrations. Cytotoxicity was measured in a standard 4-h 51Cr release assay with NK-cell sensitive YAC-1 cell line maintained in our laboratory.

Results. There was a modest but significant decrease in CD4+T-helper cells in REM sleep deprived compared to control rats, but no change in CD8+T-cells or CD11b+monocytes. There was an increase in 3.2.3+NK cells that was not statistically significant (Table 1).


Table 1. Peripheral Lymphocyte Subpopulations. FITC-labeled Antibodies CD3 CD4** CD8 CD11b 3.2.3***
Sleep Deprived* 58.9 ± 7.2 46.3 ± 4.6 18.9 ± 3.8 9.7 ± 5 9.2 ± 4.2
Control* 62.8 ± 9.6 52.1 ± 8.4 19.5 ± 3.9 9.7 ± 6.5 6.8 ± 1.8
*n = 8, x ± SD; ** p< 0.05, Z = 1.99; *** p< 0.08, Z = 1.8, Mann-Whitney U Test.

Interestingly, there was a large significant increase in mean NK-cell spontaneous cytotoxicity at each effector:target ratio in REM sleep deprived (n = 8) compared to control (n = 6) rats (Table 2.) When NK-cell activity was represented as lytic units (LUs), mean LUs were 5 fold higher in REM sleep deprived (5.1 ± 1.9) vs control (0.83 ± 0.25) rats (Z=2.5, p<0.02).


Table 2. NK-Cell Spontaneous Cytotoxicity Effector:Target Ratio 100:1* 50:1** 25:1** 12.5:1
Sleep Deprived 19.19 ± 7.3 16.07 ± 11.7 11.28 ± 9.28 6.39 ± 7.97
Control 7.65 ± 4.0 5.1 ± 4.4 1.94 ± 3.8 -1.1 ± 3.7
x ± SD, * p< 0.01, Z = 2.8; ** p< 0.04, Z = 2.1, Mann-Whitney U Test.

Conclusion.

REM sleep deprivation is associated with greatly enhanced spontaneous cytotoxicity of peripheral NK cells with only a small increase in the percentage of 3.2.3+NK-cells, suggesting that individual NK-cells possess greater killing effectiveness.

The modest decrease in peripheral T-helper cells might be attributable to high corticosterone levels in REM sleep deprived rats, as hypothesized.

[color="red"]These differential effects of REM sleep deprivation on immune parameters support the hypothesis that short term sleep deprivation dysregulates the immune system.2[/color]

The classic platform method of sleep deprivation is a useful model to study alterations in the neuroendocrine control of immune function.

The findings from such studies could yield clues to the physiological basis for the common experience of altered disease susceptibility with inadequate and disrupted sleep.

http://74.125.77.132/search?q=cache:EVQC6VNsMGkJ:www.websciences.org/cftemplate/NAPS/archives/indiv.cfm%3FID%3D19960483+rem+immune+system&cd=1&hl=en&ct=clnk&gl=ro
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[color="red"]Leukocytosis and natural killer cell function parallel neurobehavioral fatigue induced by 64 hours of sleep deprivation.[/color]

D F Dinges, S D Douglas, L Zaugg, D E Campbell, J M McMann, W G Whitehouse, E C Orne, S C Kapoor, E Icaza, and M T Orne
Unit for Experimental Psychiatry, Institute of Pennsylvania Hospital, Philadelphia, Pennsylvania 19139.

The hypothesis that sleep deprivation depresses immune function was tested in 20 adults, selected on the basis of their normal blood chemistry, monitored in a laboratory for 7 d, and kept awake for 64 h. At 2200 h each day measurements were taken of total leukocytes (WBC), monocytes, granulocytes, lymphocytes, eosinophils, erythrocytes (RBC), B and T lymphocyte subsets, activated T cells, and natural killer (NK) subpopulations (CD56/CD8 dual-positive cells, CD16-positive cells, CD57-positive cells). Functional tests included NK cytotoxicity, lymphocyte stimulation with mitogens, and DNA analysis of cell cycle. Sleep loss was associated with leukocytosis and increased NK cell activity. At the maximum sleep deprivation, increases were observed in counts of WBC, granulocytes, monocytes, NK activity, and the proportion of lymphocytes in the S phase of the cell cycle. Changes in monocyte counts correlated with changes in other immune parameters. Counts of CD4, CD16, CD56, and CD57 lymphocytes declined after one night without sleep, whereas CD56 and CD57 counts increased after two nights. No changes were observed in other lymphocyte counts, in proliferative responses to mitogens, or in plasma levels of cortisol or adrenocorticotropin hormone. The physiologic leukocytosis and NK activity increases during deprivation were eliminated by recovery sleep in a manner parallel to neurobehavioral function, suggesting that the immune alterations may be associated with biological pressure for sleep.


SEE THE ORIGINAL PDF SCANNED FILES HERE,

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=294300

WHERE IT SAYS:


Limited studies in mice and rats have failed to document consistent alterations of immune responses during sleep loss, although [color="Red"]DEATH OCCURRED IN RATS DEPRIVED OF SLEEP FOR 7-32 DAYS[/color]!

[color="red"]GIVEN THE DISPARITY BETWEEN THE EFFECTS OF ONE VERSUS TWO NIGHTS WITHOUT SLEEP ON IMMUNE PARAMETERS, EVEN MORE SEVERE SLEEP LOSS MAY RESULT IN FAILURE OF IMMUNE FUNCTION, AS HAS BEEN SUGGESTED MAY OCCUR IN THE LETHAL OUTCOME STUDIES OF RATS DEPRIVED OF SLEEP FOR MANY DAYS (44). [/color]
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Mesajde jl_rona » Vin Mai 08, 2009 10:40 pm

[color="Red"]What causes Candida?[/color]

1) Poor immunity is undoubtedly a major factor in allowing Candida to overgrow. A weak immune system appears to be the norm these days, the main reason for which in our opinion is nutrient deficiency.

© The Finchley Clinic 2007 UK

http://www.thefinchleyclinic.co.uk/nojavascript/products/What_Is_Candida.htm
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[color="Red"]Sleep, sleep deprivation and infectious disease: studies in animals.[/color]

TOTH LA.
Adv Neuroimmunol 1995;5(1):79-92.
Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN 38101, USA.

Abstract:

Common perceptions that the desire for sleep is increased during mild infectious diseases like colds and 'the flu' have fostered beliefs that sleep promotes recovery from infectious disease and that lack of sleep increases susceptibility to infections. However, until recently, the relationship between infectious disease and vigilance received relatively little systematic study. At present, several model systems provide evidence that infectious disease is accompanied by alterations in sleep. Indeed, increased sleepiness, like fever and anorexia, may be viewed as a facet of the acute phase response to infectious challenge. Recent studies also suggest that sleep, sleep deprivation and infectious disease may be related via mechanisms of the immune system (Fig. 1). Data are now accumulating to address questions such as whether immune processes alter sleep, whether sleep or sleep deprivation influences immune competence, and whether sleep facilitates recovery from infectious disease.

http://www.websciences.org/cftemplate/NAPS/archives/indiv.cfm?ID=19964581
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Mesajde jl_rona » Sâm Mai 09, 2009 12:43 am

[color="Red"]IMMUNOMODULATORS: The thymus gland, zinc and HIV [/color]

TreatmentUpdate 66, Volume 8, No 2; February 1996
Sean Hosein

Background

Zinc is one of many nutrients needed by the body, particulary by the immune system. Research on non-HIV-infected children who could not absorb enough zinc from their food found that they developed a number of problems, including:

* damaged thymus glands * less-than-normal levels of T cells * reduced ability to effectively fight infections * hair loss

* low levels of zinc in their blood

* damaged lymph nodes

Non-SIV or HIV-infected animals who do not absorb enough zinc develop similar problems and their immune systems do not respond to stimulation with DNCB (dinitrochlorobenzene). The inability of their immune systems to fight certain infections suggest that a critical immune response, CMI (cell-mediated-immunity), is weakened. Both children and animals recover when given supplements of zinc.

The thymus gland

Located in the upper chest, the thymus gland contains T cells and macrophages. In addition to helping T cells mature, the thymus gland also makes hormones (called thymic hormones). Although researchers have found several thymic hormones;

* thymosin

* thymosin fraction 5

* thymopoietin

* thymulin

* thymopentin

* thymic humoral factor

* thymosin alpha1

They do not know the precise function of each hormone. Thymic hormones can enhance the functioning of T cells. Some researchers have used thymic hormones improve the immune response in subjects with cancer, hepatitis B and HIV infection. Reports on some of these products appear in TreatmentUpdate 61, 52, 39 and 17.

Thymulin or Zinc?

Thymulin is one thymic hormone that has been studied for over a decade. To have any effect on T cells, thymulin must be attached or bound to zinc. Once the zinc is bound, thymulin becomes activated. People with some forms of arthritis can have weakened CMI. One research team in the 1980s tested (activated) thymulin in subjects with arthritis and found that it reduced their symptoms. In further studies, another team conducted a double-blind trial on subjects with arthritis, some of whom received thymulin while others received zinc alone. The researchers found that subjects who received zinc alone benefited as much as the subjects who received thymulin. Faced with these results the company conducting the research stopped further studies of thymulin.

Thymic hormones, zinc and HIV

Several groups of researchers have found that, on average, people with HIV/AIDS have less than normal levels of thymic hormones in their blood. This situation may arise because their thymus glands come under attack both by HIV and the immune system. In one study, researchers found that the level of inactive thymulin remained the same while levels of active thymulin fell as symptoms of HIV infection appeared. Thus some researchers think that supplements of zinc may prove useful for people with HIV/AIDS.

Zinc and copper

Issues to consider when testing the effect of zinc include the long-term toxicity of zinc and its relation with copper. In other experiments, researchers found that as the immune system weakens, levels of copper in the blood rise while those of zinc fall. Details from this experiment are reported in TreatmentUpdate 29. Results from other experiments on over 200 non-HIV-infected subjects with lymphoma suggest a trend toward worsening illness in subjects with relatively high levels of copper in their blood. Those subjects who improved had relatively lower levels of copper. These results do not mean that increasing levels of copper in the blood damage the immune system. Rather, during times of infection or cancer, changes in the balance of zinc and copper occur. Under these conditions, zinc is removed from some parts of the body and sent to the liver, bone marrow and thymus gland. Certain monkeys infected with SIV eventually develop AIDS. One of the first nutrients for which they become deficient is zinc. This happens despite eating an adequate diet and probably occurs because their intestines become less efficient at absorbing nutrients and perhaps because their need for zinc increases. Taking all of these factors into account, it should not be surprising that supplements of zinc can provide benefit to humans with HIV infection.

REFERENCES:

1. Hadden JW. The treatment of zinc deficiency is an immunotherapy. International Journal of Immunopharmacology 1995;17(9):697-701.

2. Sarin PS, Sun DK, Thornton AH, et al. Neutralization of HTLV-III/LAV replication by antiserum to thymosin alpha1. Science 1986;232:1135-1137.

3. Dardenne M, Savino W, Berrih S and Bach JF. A zinc-dependent epitope on the molecule of thymulin, a thymic hormone. Proceedings of the National Academy of Sciences USA 1985;82:7035-7038.

4. Fabris N, Mocchegiani E, Galli M, et al. AIDS, zinc deficiency, and thymic hormone failure. Journal of the American Medical Association 1988;259(6):839-840.

5. Graham NMH, Sorenson D, Odaka N, et al. Relationship of serum copper and zinc levels to HIV-1 seropositivity and progression to AIDS. Journal of Acquired Immune Deficiency Syndrome 1991;4(10):976-980.

6. Hrgovic M, Tessmer CF, Thomas FB, et al. Serum copper observations in patients with malignant lymphoma. Cancer 1973;32:1512-1524.

7. Cousins RJ and Leinart AS. Tissue specific regulation of zinc metabolism and metallothionein genes by interleukin 1. Federation of the American Societies for Experimental Biology Journal 1988;2:2884-2890.


960201
CATE6606


--------------------------------------------------------------------------------
Always watch for outdated information. This article first appeard in 1996. This material is designed to support, not replace, the relationship that exists between you and your doctor.
Copyright © 1996 - TreatmentUpdate. Reproduced with permission. Reproduction of this article (other than one copy for personal reference) must be cleared through the Editor, The Canadian AIDS Treatment Information Exchange, 555 Richmond St. West, Suite 505, Box 1104, Toronto
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Mesajde jl_rona » Sâm Mai 09, 2009 12:45 am

[color="Red"]Zinc status in women with recurrent vulvovaginal candidiasis.[/color]

Edman J, Sobel JD, Taylor ML

Zinc status has been shown to influence various cell-mediated immunologic mechanisms. These cell-mediated mechanisms are important in preventing mucocutaneous infections caused by Candida albicans. This study evaluated the relationship between zinc status and recurrent vaginal candidiasis by comparing plasma and erythrocyte zinc in 29 patients with recurrent vaginal candidiasis and 20 control subjects matched for age, race, and parity. The results indicated that there was a significantly lower level of plasma zinc in women with recurrent vaginal candidiasis (81 + 11.6 mg/dl) than in the control subjects (91 +/- 14.2 mg/dl) with a significant value of p = 0.015. These differences in plasma zinc levels were even greater when adjusted for dietary zinc and supplemental zinc with the use of analyses of covariance. No differences in erythrocyte zinc measurements were found between the two groups. These results suggest that mild zinc deficiency is associated with recurrent vaginal candidiasis and may play a role in the susceptibility of women to recurrent vaginal candidiasis.

http://www.ithyroid.com/candida.htm
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Mesajde jl_rona » Sâm Mai 09, 2009 12:46 am

[color="Red"]Title: Zinc status in women with recurrent vulvovaginal candidiasis.[/color]

Personal Authors: Edman, J., Sobel, J. D., Taylor, M. L.
Author Affiliation: Dep. Nutrition, Drexel Univ., Philadelphia, PA, USA.
Editors: No editors
Document Title: American Journal of Obstetrics and Gynecology


Abstract:
The relationship between zinc status and recurrent vaginal Candida infection was studied by comparing plasma and erythrocyte zinc levels in 29 patients with recurrent vaginal candidosis and 20 control subjects. The results indicated that there was a significantly lower level of plasma zinc in women with recurrent vaginal candidosis (81 ± 11.6µg/dl) than in the control subjects (91 ± 14.2µg/dl, p=0.015). These differences in plasma zinc levels were even greater when adjusted for dietary zinc and supplemental zinc with the use of analyses of covariance. No differences in erythrocyte zinc measurements were found between the 2 groups. From these results it is suggested that mild zinc deficiency is associated with recurrent vaginal candidosis and may play a role in the susceptibility of women to this disease.

http://www.cababstractsplus.org/abstracts/Abstract.aspx?AcNo=19881385498
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Mesajde jl_rona » Sâm Mai 09, 2009 1:02 am

[color="Red"]The Impact of Sleep Deprivation on Hormones and Metabolism[/color]

Eve Van Cauter, PhD; Kristen Knutson, PhD; Rachel Leproult, PhD; Karine Spiegel, PhD

Authors and Disclosures

Published: 04/28/2005


Introduction
Sleep loss can occur as a result of habitual behavior or due to the presence of a pathological condition that is associated with reduced total sleep time. This column focuses on the impact of behavioral sleep curtailment, an endemic condition in modern society, and provides evidence against the old notion that "sleep is for the mind, and not for the rest of the body."

Prevalence of Sleep Curtailment in Modern Society
Sleep curtailment is a hallmark of modern society, one that is often considered harmless and efficient. The advent of artificial light has permitted the curtailment of sleep to the minimum tolerable and an increase in the time available for work and leisure. In our 24-hour-a-day society, millions work during the night and sleep during the day, a schedule that generally results in substantial sleep loss.

Figure 1 illustrates changes in self-reported sleep duration over the past 50 years. In 1960, a survey of over 1 million people found a modal sleep duration of 8.0-8.9 hours.[1] In 2000, 2001, and 2002, polls conducted by the National Sleep Foundation indicated that the average duration of sleep for Americans had fallen to 6.9-7.0 hours.[2] Overall, sleep duration thus appears to have decreased by 1.5-2 hours during the second half of the 20th century. Today, many people are in bed only 5-6 hours per night on a regular basis.


(Enlarge Image) Figure 1.
Self-reported sleep duration, 1960-2002.



[ CLOSE WINDOW ]

Figure 1.
Self-reported sleep duration, 1960-2002.
The 2 major pathways by which sleep affects the release of hormones are the hypothalamic-pituitary axes and the autonomous nervous system.

The release of hormones by the pituitary — the "master" endocrine organ that controls the secretion of other hormones from the peripheral endocrine glands — is markedly influenced by sleep. Modulation of pituitary-dependent hormonal release is partly mediated by the modulation of the activity of hypothalamic-releasing and/or hypothalamic-inhibiting factors controlling pituitary function. During sleep, these hypothalamic factors may be activated — as in the case of growth hormone (GH)-releasing hormone — or inhibited, as is the case for corticotropin-releasing hormone.

The other pathway by which sleep affects peripheral endocrine regulation is via the modulation of autonomic nervous system activity. During deep sleep, sympathetic nervous system activity is generally decreased and parasympathetic nervous system activity is increased. Sleep loss is associated with an elevation of sympathovagal balance, with higher sympathetic but lower parasympathetic tone. Most endocrine organs are sensitive to changes in sympathovagal balance. Well-documented examples are pancreatic insulin secretion and release by the fat cells of leptin, an appetite-suppressing hormone.

A profound and generalized impact of sleep loss on the endocrine system should therefore be expected. Until recently, however, it was considered unlikely that the adverse effects of sleep deprivation on endocrine function would be long-term. The studies from which this notion was drawn examined the effects of only 1 or 2 nights of acute total sleep deprivation. In general, the data suggested that endocrine alterations that occurred during the sleepless night(s) were completely reversed during recovery sleep.

More recently, a few studies have examined the impact on hormones, metabolism, and immune function of the much more common, real-life situation — chronic partial sleep deprivation.[3-5] The earliest study measured hormonal and metabolic parameters in subjects studied after 6 days of sleep restriction (4-hour bedtime) and after full sleep recovery (6 days of 12-hour bedtime).[3] Subsequent studies examined the impact of less severe sleep restriction (6.5 hours per night) over 1 week[4] as well as the effects of short-term sleep curtailment (2 days with 4-hour vs 12-hour bedtime).[5]
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Alterations of Pituitary-Dependent Hormones During Sleep Loss
The first effect of partial sleep loss on circulating levels of pituitary-dependent hormones to be documented under various study conditions is an increase in the early evening levels of the stress hormone cortisol.[3,6] Normally at that time of day, cortisol concentrations are rapidly decreasing to attain minimal levels shortly before habitual bedtime. The rate of decrease of cortisol concentrations in the early evening was approximately 6-fold slower in subjects who had undergone 6 days of sleep restriction than in subjects who were fully rested.[3] Elevations of evening cortisol levels in chronic sleep loss are likely to promote the development of insulin resistance, a risk factor for obesity and diabetes.

The upper and middle panels of Figure 2 illustrate the impact of sleep restriction on the thyroid axis.[3] After 6 days of 4-hour sleep time, the normal nocturnal thyroid-stimulating hormone (TSH) rise was strikingly decreased, and the overall mean TSH levels were reduced by more than 30%.[3] A normal pattern of TSH release reappeared when the subjects had fully recovered. Differences in TSH profiles between the 2 bedtime conditions were probably related to changes in thyroid hormone concentrations via a negative-feedback regulation, because the free thyroxine index (FT4I) was higher in the sleep-restriction condition than in the fully rested condition (middle panels of Figure 2). Thyroid axis function was thus markedly altered by partial recurrent sleep restriction.


(Enlarge Image) Figure 2.
Levels of thyroid-stimulating hormone (TSH), free thyroxine index, and leptin in sleep-deprived vs well-rested subjects. From top to bottom, 24-hour (+SEM) profiles of TSH, free thyroxine indexes, and leptin in healthy young subjects when submitted to partial sleep restriction for 6 days (4-hour sleep times; mean total sleep time during previous 2 nights, 3 hours 49 minutes; left panels) and after full sleep recovery (12-hour sleep times for 6 nights; mean total sleep time during previous 2 nights, 9 hours 3 minutes; right panels). The black bars represent the sleep periods.[3,10]



[ CLOSE WINDOW ]

Figure 2.
Levels of thyroid-stimulating hormone (TSH), free thyroxine index, and leptin in sleep-deprived vs well-rested subjects. From top to bottom, 24-hour (+SEM) profiles of TSH, free thyroxine indexes, and leptin in healthy young subjects when submitted to partial sleep restriction for 6 days (4-hour sleep times; mean total sleep time during previous 2 nights, 3 hours 49 minutes; left panels) and after full sleep recovery (12-hour sleep times for 6 nights; mean total sleep time during previous 2 nights, 9 hours 3 minutes; right panels). The black bars represent the sleep periods.[3,10]
The temporal organization of GH secretion is also altered by chronic partial sleep loss.[7] The normal single GH pulse occurring shortly after sleep onset splits into 2 smaller pulses, 1 before sleep and 1 after sleep; as a result, the peripheral tissues are exposed to high GH levels for an extended period of time, which, because GH has anti-insulin-like effects, could also have an adverse impact on glucose tolerance.

Impact of Sleep Loss on Hormones Controlling Appetite
Sleeping and feeding are intricately related. Animals faced with food shortage or starvation sleep less;[8] conversely, animals subjected to total sleep deprivation for prolonged periods of time increase their food intake markedly.[9] Recent studies in humans have shown that the levels of hormones that regulate appetite are profoundly influenced by sleep duration. Sleep loss is associated with an increase in appetite that is excessive in relation to the caloric demands of extended wakefulness.

The regulation of leptin, a hormone released by the fat cells that signals satiety to the brain and thus suppresses appetite, is markedly dependent on sleep duration. After 6 days of bedtime restriction to 4 hours per night, the plasma concentration of leptin was markedly decreased, particularly during the nighttime.[10] The magnitude of this decrease was comparable to that occurring after 3 days of restricting caloric intake by approximately 900 kcal/day. But the subjects in the sleep-restriction condition received identical amounts of caloric intake and had similar levels of physical activity as when they were fully rested. Thus, leptin levels were signaling a state of famine in the midst of plenty.

In a later study, the levels of ghrelin, a peptide that is secreted by the stomach and stimulates appetite, were measured with the levels of leptin after 2 days of sleep restriction (4 hours of sleep) or sleep extension (10 hours of bedtime).[5] The subjects also assessed their levels of hunger and appetite at regular intervals. Sleep restriction was associated with reductions in leptin (the appetite suppressant) and elevations in ghrelin (the appetite stimulant) and increased hunger and appetite, especially an appetite for foods with high-carbohydrate contents. Similar findings were obtained simultaneously in a large epidemiologic study in which sleep duration and morning levels of leptin and ghrelin were measured in over 1,000 subjects.[11] The Table summarizes the remarkable concordance between the results of the 2 studies. Despite the differences in study design, both studies found a decrease in the satiety hormone leptin and an increase in appetite-stimulating ghrelin with short sleep.

Sleep loss therefore seems to alter the ability of leptin and ghrelin to accurately signal caloric need and could lead to excessive caloric intake when food is freely available. The findings also suggest that compliance with a weight-loss diet involving caloric restriction may be adversely affected by sleep restriction.

During the second half of the 20th century, the incidence of obesity has nearly doubled, and this trend is a mirror image of the decrease in self-reported sleep duration illustrated in Figure 1. The discovery of a profound alteration in the neuroendocrine control of appetite in conditions of sleep loss is consistent with the conclusions of several epidemiologic studies that revealed a negative association between self-reported sleep duration and body mass index. Taken together, the current evidence suggests a possible role for chronic sleep loss in the current epidemic of obesity.

Metabolic Implications of Recurrent Sleep Curtailment
Recent work also indicates that sleep loss may adversely affect glucose tolerance and involve an increased risk of type 2 diabetes.

In young, healthy subjects who were studied after 6 days of sleep restriction (4 hours in bed) and after full sleep recovery, the levels of blood glucose after breakfast were higher in the state of sleep debt despite normal or even slightly elevated insulin responses.[3] The difference in peak glucose levels in response to breakfast averaged ±15 mg/dL, a difference large enough to suggest a clinically significant impairment of glucose tolerance.

These findings were confirmed by the results of intravenous glucose tolerance testing.[3] Indeed, the rate of disappearance of glucose post injection — a quantitative measure of glucose tolerance — was nearly 40% slower in the sleep-debt condition than after recovery, and the acute insulin response to glucose was reduced by 30%. Glucose tolerance measured at the end of the recovery period was similar to that reported in an independent study[12] in young, healthy men, but glucose tolerance in the state of sleep debt was comparable to that reported for older adults with impaired glucose tolerance.[13] Thus, less than 1 week of sleep restriction can result in a prediabetic state in young, healthy subjects. Of note, the adverse impact of sleep deprivation on glucose tolerance demonstrated in laboratory studies is consistent with the finding of an increased risk of symptomatic diabetes with short sleep in a cohort study of women.[14]

Multiple mechanisms are likely to mediate the adverse effects of sleep curtailment on parameters of glucose tolerance, including decreased cerebral glucose utilization, increases in sympathetic nervous system activity, and abnormalities in the pattern of release of the counterregulatory hormones cortisol and GH.

Conclusion
Clearly, sleep is not only for the brain but also for the rest of the body. Recent evidence suggests that sleep loss, a highly prevalent — and often strongly encouraged — condition in modern society could be a risk factor for major chronic diseases, including obesity and diabetes.

Supported by an independent educational grant from Pfizer/Neurocrine.

http://cme.medscape.com/viewarticle/502825
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Mesajde jl_rona » Dum Mai 10, 2009 7:52 am

Reproductive Sciences, Vol. 14, No. 6, 560-567 (2007)
DOI: 10.1177/1933719107307647

[color="Red"]Sleep Disturbances Increase Interleukin-6 Production During Pregnancy: Implications for Pregnancy Complications[/color]'

Michele L. Okun, PhD

University of Pittsburgh Medical Center/Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, University of Colorado at Denver and Health Sciences Center

Martica Hall, PhD

University of Pittsburgh Medical Center/Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, University of Colorado Denver and Health Sciences Center and was supported by a Clinical Training Grant in Psychiatry

Mary E. Coussons-Read, PhD

University of Colorado at Denver and Health Sciences Center,

mary.coussons-read@cudenver.edu

Pregnant women experience disturbed sleep that varies throughout the gestational period.

In clinical studies of nonpregnant cohorts, data link disturbed sleep with increases in inflammatory markers.

Emerging evidence has also found associations between increased inflammation and medical morbidity, including various pregnancy complications.


The authors have previously shown a correlation between sleep disturbances and serum cytokine levels.


They extend this initial observation by evaluating the relationship between sleep during mid and late pregnancy and inflammatory cytokines in both serum and stimulated peripheral blood mononuclear cells.

Subjective sleep during pregnancy, described by the Pittsburgh Sleep Quality Index and sleep diaries, and circulating and stimulated measures of interleukin (IL)—6 and tumor necrosis factor (TNF)— were evaluated in 19 pregnant women.

The authors found that greater sleep complaints in late pregnancy were associated with both increased circulating and stimulated IL-6 levels.

Short sleep duration and poor sleep efficiency in both mid and late pregnancy were associated with higher stimulated levels of IL-6.

No relationships were observed for TNF-.


These preliminary findings indicate that women who experience sleep disturbances as early as mid gestation are likely to have an increase in inflammation.


Key Words: Sleep • cytokines ,pregnancy complications • interleukin-6.

http://rsx.sagepub.com/cgi/content/abstract/14/6/560


[color="red"]Morbidity[/color]

Morbidity (from Latin morbidus: sick, unhealthy) refers to a diseased state, disability, or poor health due to any cause.[12] The term may be used to refer to the existence of any form of disease, or to the degree that the health condition affects the patient. Among severely ill patients, the level of morbidity is often measured by ICU scoring systems.

Comorbidity is the simultaneous presence of two medical conditions, such as a person with schizophrenia and substance abuse.

In epidemiology and actuarial science, the term morbidity rate can refer to either the incidence rate, or the prevalence of a disease or medical condition. This measure of sickness is contrasted with the mortality rate of a condition, which is the proportion of people dying during a given time interval.

http://en.wikipedia.org/wiki/Disease#Morbidity
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Mesajde jl_rona » Dum Mai 10, 2009 7:57 am

Am J Physiol Regul Integr Comp Physiol 265: R1148-R1154, 1993;
0363-6119/93 $5.00

AJP - Regulatory, Integrative and Comparative Physiology, Vol 265, Issue 5 1148-R1154, Copyright © 1993 by American Physiological Society

[color="Red"]
Sustained sleep deprivation impairs host defense[/color]


C. A. Everson
Clinical Psychobiology Branch, National Institute of Mental Health, Bethesda, Maryland 20892.


Prolonged sleep deprivation in rats causes an unexplained hypercatabolic state, secondary malnutrition symptoms, and mortality.


The nature of the vital impairment has long been a mystery.

Its determination would help to elucidate the type of organic dysfunction that sleep prevents.

There are no gross detectable disturbances in intermediary metabolism, clinical chemistry, or hematological indexes that provide substantial clues to the mediation of sleep-deprivation effects.

Furthermore, postmortem examinations reveal no systematic morphological or histopathological findings.

Taken together, the cachexia and the absence of evidence of structural damage or organ dysfunction pointed to involvement of a regulatory system that was diffuse, possibly the immune system.

Blood cultures revealed invasion by opportunistic microbes to which there was no febrile response.

[color="red"]These results suggest that the life-threatening condition of prolonged sleep deprivation is a breakdown of host defense against indigenous and pathogenic microorganisms.[/color]

http://ajpregu.physiology.org/cgi/content/abstract/265/5/R1148
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Mesajde jl_rona » Dum Mai 10, 2009 8:00 am

[color="Red"]Sleep and inflammation.[/color]


Simpson N, Dinges DF.
Division of Sleep and Chronobiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.

Among adults in the United States, sleep durations appear to have decreased in recent years.

Inadequate sleep and sleep deprivation cause numerous neurobehavioral and physiological changes.

A number of recent studies have reported associations between disrupted sleep/sleep deprivation and inflammatory responses, although the physiological mechanisms underlying these relationships remain unclear.


Alterations in sleep due to [color="red"]lifestyle factors[/color], the aging process, and disease states have all been associated with increases in a range of inflammatory markers.

Several of these inflammatory processes have been associated with reduced health status (e.g., C-reactive protein and cardiovascular disease).

Thus, maintaining adequate sleep duration and quality through good sleep habits and treatment of sleep disorders may reduce inflammatory processes associated with aging and increase the wellness phenotype.

PMID: 18240557 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/pubmed/18240557
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Mesajde jl_rona » Dum Mai 10, 2009 8:02 am

[color="Red"]Higher systemic inflammation is associated with poorer sleep quality in stable haemodialysis patients[/color]

Yen-Ling Chiu1,2, Yi-Fang Chuang3, Kai-Chi Fang4, Shih-Kai Liu4, Hung-Yuen Chen1,2, Ju-Yeh Yang1,2, Mei-Fen Pai1, Yu-Sen Peng1, Kwan-Dun Wu2 and Tun-Jun Tsai2

1 Department of Internal Medicine, Far-Eastern Memorial Hospital 2 Department of Medicine, National Taiwan University Hospital 3 Department of Psychiatry, Min-Sheng Hospital 4 Department of Psychiatry, Far-Eastern Memorial Hospital, Taiwan, Republic of China

Yu-Sen Peng, Department of Medicine, Far-Eastern Memorial Hospital, Taiwan, Republic of China. Tel: +886-2-8966-7000, Ext. 1164; Fax: +886-2-8966-7000, Ext. 1162; E-mail: yenling.chiu@gmail.com

Abstract


Background. Increased inflammation has been noted in sleep disorder patients [color="red"]with normal renal function[/color].

However, the relationship between sleep quality and circulating inflammatory markers has not been previously studied in haemodialysis (HD) patients.

Methods.

A total of 114 HD end-stage renal disease patients receiving maintenance HD for >3 months were included in this study.

Pittsburgh Sleep Quality Index (PSQI) was used to measure individual's sleep quality. Based on the global PSQI score, patients were divided into groups of good sleepers (PSQI < 5) and bad sleepers (PSQI 5).

Results.

Twenty-three patients (20.2%) were classified as good sleepers and 91 patients (79.8%) were bad sleepers.

Bad sleepers have significantly higher serum hsCRP level and lower serum phosphate level (all P < 0.05).

The global PSQI score, or worse sleep quality are positively correlated with [B]serum triglyceride level[/B], high-sensitivity C-reactive protein (hsCRP) level, [color="red"]IL-1β level [/color]and negatively correlated with the haemoglobin and phosphate level.

In the multi-variable linear regression model, levels of hsCRP (β = 0.209, P = 0.029) and triglyceride (β = 0.212, P = 0.025) were both significant independent predictors for the global PSQI score.

Conclusion. Our study demonstrated severe impairment of sleep quality in HD patients and corroborated the role of inflammation in the pathogenesis of sleep disturbance.

Keywords: haemodialysis; inflammation; sleep quality; triglyceride

Received for publication: 13. 5.08
Accepted in revised form: 8. 7.08

http://ndt.oxfordjournals.org/cgi/content/abstract/24/1/247
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Mesajde jl_rona » Dum Mai 10, 2009 10:37 am

OMG
L-am visat pe Piskeshu cum ma mangaia pe tate si imi baga degetele-n pizda...

Nu aveam prezervative si m-am dus sa caut, nu stiu, pe niste facalete de lemn cu care ma masturbez eu, dar toate facaletele erau curbate...

Ii spuneam sa mai stea putin sa caut, dar m-am trezit.
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Mesajde jl_rona » Mar Mai 12, 2009 4:59 am

Posted by eyewitness:

"liviu si cr3tz, va rog io terminati cu jicnirile
multumesc"

Se scrie JiGnri, idiotule!

[B]JIGNí
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Mesajde jl_rona » Mar Mai 12, 2009 5:16 am

dar sa trecem din concretul mizerabil in absolutul celestial.

Nu am mai avut timp sa ma ocup de muzica in ultima vreme, drept pentru care abia acum am ascultat noul single al lui Placebo (aka Brian Molko): Battle for the Sun.

E frumos si veridic ca un orgasm. Incepe incet, impingand si iesind din cuvinte, si ajunge la climax cu "Dream brother, my killler, my lover!".

Dumnezeule, cat de high poti fi, Brian!

Zeii sa te binecuvanteze pentru ceea ce reusesti sa ne transmiti si noua din trairile tale inalte!

Probabil ca planeta ar ajunge rapid in prapastie daca toti am fi ca tine! Asta e singura explicatie pe care o am pentru ca nu am fost toti nascuti sa fim atat de HIGH!

I don't know...

EDIT: puteti sa-l download-ati de aici fara probleme de virusi:

http://isohunt.com/torrent_details/71746369/placebo?tab=summary

sau puteti sa-l ascultati aici, though it's not very high sound fidelity:

http://www.youtube.com/watch?v=wu9X0Kg9VEs&feature=related

Si pentru ca oricum nu o sa mai pot sa adorm: Eu il consider pe Brian Molko cel mai mare muzician al timpurilor noastre. Oricat s-a straduit Matt Bellamy (de la Muse) cu versurile sale politice, cu tot, nu o sa reuseasca NICIODATA sa-l egaleze pe Brian!

In timp ce Matt este un chinuit baiat de la tara, destept de altfel, dar ATAT, Brian este natural in tot ce face. E un city specimen veritabil, un englez care-si poata cu inalta demnitate numele. Are calitate data de mama-sa din nastere! Are educatie, are traire, are talent, are frumusete fizica si intelectuala, are TOT ce oricine si-ar putea dori sa aiba!

If his previous album proved HIGHLY depressive, Brian a renascut din propria cenusa cu acest single!

Poate va arde prea repede, la fel cum alti artisti au facut-o, mi-ar pare rau sa se intample asta, dar a dovedit pana acum ca poate fi foarte aproape de suprem.

Daca e vorba de muzica, nu mai e nevoie sa dovedeasca nimic nimanui! A dovedit-o cu prisosinta pana acum si NU REGRET cu nimic COZILE interminabile la care am stat ca sa il vad live, transpirata si intr-o caldura insuportabila!

Multi ar dori sa-i asculte in continuare lumina!

Pentru noi, mai stai, mai traieste, mai compune, mai spune-ne, mai incanta-ne!
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Mesajde jl_rona » Sâm Mai 16, 2009 9:42 am

vad ca incepem sa conversam de pe un forum pe altul. eu sunt banata acolo, dar unii citesc aici si imi raspund acolo. ceea ce se intampla cu banatul asta e o stupiditate fara de margini, dar sa lasam asta.

si sefa mea mi-a lasat un bilet pe masa ieri unde zicea ca se "aranjaza" suportii.

bai eyewitnessica, uite cum sta treaba: ori stii sa scrii, ori nu stii. nu adaptam ortografia la analfabeti, asa cum s-a facut in ziua de azi cu "nicio" si cu "care" in loc de "pe care".

eu cand am dat examen la gramatica in clasa a 8-a, ori stiam sa scriu, ori nu. puteam eu sa fac orice contestatii vreau si sa ma justific in orice fel. Scriam corect, bine, nu, pa!

Dar acuma suntem in democratie. Asa e.

==========================================

Cat despre serviciul meu imputit la multinationala, va rog daca cititi acest post si daca aveti timp, sa-mi dati si mie un sfat.

Eu vreau sa incerc sa-mi schimb serviciul. Criza lu' peste, nu ma intereseaza.

A ramane aici inseamna sa imi semnez cu buna stiinta sentinta la boala si ulterior la moarte prematura.

NU sunt un om bolnav. Mama m-a facut destul de bine. Am stomac, inima si ficat bun, plamani buni, ca sa nu zic de corp care arata chiar bine pentru o femeie de 40 de ani. Pot sa mananc ORICE ca nu ma ingras, iar sportul imi intareste doar muschii, eu nu ma duc acolo sa dau suncile jos. Nu am mai facut aerobic timp de o luna si am tot 49 de kilograme. Asta e foarte misto si ii multumesc MULT lui Dumnezeu pentru ce mi-a dat, cu destule bune si cu putine rele, ca de, nimeni nu e perfect.

Insa NU REZIST LA HIGHEREALA PE TERMEN LUNG.

Sunt sensibila, adorm greu, insa in conditii de viata normale, fara stres excesiv si cu 8 ore jumate de somn pe noapte, sunt ABSOLUT sanatoasa, ma misc si gandesc repede si bine. Sunt peste multe femei de varsta mea ca grad de sanatate si vigoare, ca sa zic asa.

In discoteci sunt o flacara care arde printre breakdanceri de 20 de ani cu care se completeaza facand un dance show veridic si electrizand o lume intreaga.

Sunt vie, sunt energica atat fizic cat si intelectual, dar energia asta de foc trebuie compensata printr-un somn lung. Mi-e drag de mine si imi accept conditia de om sensibil. Nu as schimba mintea si fizicul meu cu ale unui adormit care rezista la multinationala timp de 14 ore pe zi non-stop si vrea bani dar nu stie pentru ce-i vrea. Ala nu traieste, ala e intr-o stare vegetativa non-stop. Daca ii pui tuburi sau nu, el e fix la fel. Momaie!

Nu se valorizeaza, nu se ambitioneaza sa fie mai bun, mai inteligent si mai frumos, mai cult, nu il intereseaza sa isi descopere si sa isi valorifice talentul. Maimuta de multionationala vrea doar BANI ca sa-si inveleasca in ei complexele pe care nu are ambitia si poate ca nici nu e in stare sa si le depaseasca.

Nu sunt vreo stramba sau vreo grasa, nu sunt vreo oligofrena sau vreo tuta. Sunt foarte ok, dar IN CONDITII DE VIATA NORMALE. Eu nu sunt CAL DE POVARA, magar sa pot cara in spate ani de nesomn si stres la multinationala.

Mie-mi prieste mult mai bine un servici unde se MUNCESTE si se GANDESTE pe timp scurt (8 ore pe zi, aproape de casa), decat unul unde se spala bani pe timp lung (12 ore pe zi de simulacru si eventual chiar frecare de menta, stand intepenit in scaun si cu badge magnetic de puscarias).

M-am sculat astazi de dimineata. Cica somnul e un sfetnic bun. Nu eram nervoasa, eram lucida dupa un somn fara pastile.

Eh, dupa somnul asta tot efortul si stresul inadmisibil la care sunt supusa mi se pareau absolut inutile, ba chiar inspaimantator de daunatoare.

De ce daca dorm suficient nu am probleme? De ce in weekend reusesc sa ma cac fara ceaiuri laxative? Acolo ceva NU MERGE!

Ala este un lagar de munca fortata, un cuptor uscat si incins unde niste sobolani care nu sunt in stare sa faca altceva decat sa simuleze (nestiind nici macar sa scrie in limba romana si engleza), se complac, pentru bani multi.

Pe mine NU MA INTERESEAZA banii multi. Nu ma intereseaza decat vreo 15 milioane pe luna (20 ar fi fantastic de bine), cu un program de lucru omenesc in compania unor oameni NORMALI, nu a unor roboti cretini care vorbesc numai despre tevi in exclusivitate. Vreau un mediu de oameni, nu de cloni mutanti, Dumnezeule Mare!

Acolo am facut hemoroizi care nu imi mai trec. Am incercat diverse tratamente, dar nu dau nici un rezultat. Daca mai continui in stilul asta, in aerul ala uscat, stand nemiscata cu curul pe scaun 8-9 ore pe zi, o sa ajung la operatie.

Unghii nu mai am la picioare pentru ca mi le-au mancat ciupercile.

Glandele sexuale, tiroida si, in general, tot organismul mi-e inflamat de nesomn. Racelile sunt din ce in ce mai dese si imi trec extrem de greu, iar infectiile, in special cu caracter genital, ma terorizeaza.

Eu nu mai sunt femeie. Nu mai pot sa fiu din cauza bolii, iar in putinele momente cand infectiile dispar, nu am timp de un barbat.

Ma fut aleatoriu prin discoteci ca o curva mizera de pe centura, contra cronometru. Insa nu eu sunt cea care castiga bani, ci invers.

In conditiile astea, ma intreb CE DREAQ AM DE PIERDUT daca ii bag in pizda masii???!

In Bucuresti n-a murit nimeni de foame, dar daca eu am sa continui sa imi fortez organismul sa lucreze peste capacitatea lui admisibila, daca o sa continui sa ignor toate semnele astea date de la un Dumnezeu care o exista probabil si care ma tot atentioneaza de ANI, am sa fac o boala grava cat de curand. Deja am niste noduli benigni la sani, iar ganglionii inflamati nu pot sa stea asa umflati la nesfarsit fara sa explodeze intr-o zi.

Dumnezeu m-a avertizat. Am un organism bun. Avertismentele astea nu sunt de rau, ci de BUN augur. Altii dau in cancer direct, fara nici o avertizare.

Daca in conditiile in care Dumnezeu insista sa imi spuna ca NU imi este BINE, trebuie sa il ascult si sa fac ceva, trebuie sa plec de acolo.

Dumnezeu si-a facut datoria si m-a avertizat. Acum EU trebuie sa fac ceva, ca el da, dar in sac nu iti pune cu mana. Daca esti cretin si nu intelegi ce tot iti spune El de ani de zile, daca il ignori in mod repetat, atunci iti meriti soarta.



Eu imi dau maxim 5 ani in conditiile astea.

======================================================

Si ca sa dau si un link si de unde relatia stare inflamatorie-cancer:

Macrophages are white blood cells within tissues, produced by the division of monocytes.

[color="Red"]Macrophages provide yet another line of defense against tumor cells and somatic cells infected with fungus or parasites. [/color]

Once a T cell has recognized its particular antigen on the surface of an aberrant cell, the T cell becomes an activated effector cell, chemical mediators known as lymphokines that stimulate macrophages into a more aggressive form. These activated macrophages can then engulf and digest affected cells much more readily.[2]

The macrophage does not generate a response specific for an antigen, but attacks the cells present in the local area in which it was activated.[2]


[color="Red"]AVETI AICI SI O POZA unde aceste macrophages inghit celulele canceroase.
Shown: Macrophages begin to fuse with, and inject its toxins into, the cancer cell. The cell starts rounding up and loses its spikes (3). [/color]


Source: Image and description: Dr. Raowf Guirguis. US National Cancer Institute


http://commons.wikimedia.org/wiki/File:Macs_killing_cancer_cell.jpg

-------------------

INSA CAND ELE DEVIN INEFFECTIVE, produc un efect invers, de promovare a inflamatiei si a cancerului.



Some disorders, mostly rare, of ineffective phagocytosis and macrophage function have been described.[citation needed]

Macrophages are the predominant cells involved in creating the progressive plaque lesions of atherosclerosis.[citation needed][3]

Macrophages also play a role in Human Immunodeficiency Virus (HIV) infection. Like T cells, macrophages can be infected with HIV, and even become a reservoir of ongoing virus replication throughout the body.[citation needed]

[color="Red"]Macrophages are believed to help cancer cells proliferate as well. They are attracted to oxygen-starved (hypoxic) tumour cells and promote chronic inflammation.[/color] Inflammatory compounds such as Tumor necrosis factor (TNF) released by the macrophage activates the gene switch nuclear factor-kappa B. NF-kB then enters the nucleus of a tumour cell and turns on production of proteins that stop apoptosis and promote cell proliferation and inflammation.[4]

Programmed cell death is also called apoptosis.

Aicea e mai complicat, n-am inteles nici eu foarte bine.

Ideea e oricum, ca in cazul unei PROASTE FUNCTIONARI A SISTEMULUI IMUNITAR, CANCERUL TE PASTE.

Poza de mai sus e cea mai relevanta.
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Mesajde jl_rona » Sâm Mai 16, 2009 12:16 pm

Back to Placebo, the crystal boy Brian Molko and his brand new song "Battle for the Sun".

I really love the speech of this guy. No fake modesty, no cheap shit. The guy just speaks his mind:

BRIAN: You know I'm really, really, really, proud of that song. I think it's, it's possibly one of the best songs that Stephan and I have ever written, so we are quite proud of it.

Interviewer: This is another phase in the band this is more commitment really.

BRIAN: Absolutely, yeah, you know, 110 % commitment, you know, and we just kind of really wanted to step up, step everything up, really, this time around, and... you know, more than ever it feels like a new beginning for us.

WATCH THE VIDEO HERE:

http://www.youtube.com/watch?v=CpPKnNwYpLk&feature=related
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Mesajde jl_rona » Sâm Mai 16, 2009 10:52 pm

Night Shift Work, Light at Night, and Risk of Breast Cancer

Scott Davis, Dana K. Mirick, Richard G. Stevens

Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, WA, and Department of Epidemiology, School of Public Health and Community Medicine, University of Washington, Seattle;D. K. Mirick, Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center;R. G. Stevens, Department of Community Medicine, University of Connecticut Health Center, Farmington.

Correspondence to: Scott Davis, Ph.D., Program in Epidemiology, Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave., N., MP-474, P.O. Box 19024, Seattle, WA 98109–1024 (e-mail: sdavis@fhcrc.org).

Background: Exposure to light at night may increase the risk of breast cancer by suppressing the normal nocturnal production of melatonin by the pineal gland, which, in turn, could increase the release of estrogen by the ovaries. This study investigated whether such exposure is associated with an increased risk of breast cancer in women. Methods: Case patients (n = 813), aged 20–74 years, were diagnosed from November 1992 through March 1995; control subjects (n = 793) were identified by random-digit dialing and were frequency matched according to 5-year age groups. An in-person interview was used to gather information on sleep habits and bedroom lighting environment in the 10 years before diagnosis and lifetime occupational history. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by use of conditional logistic regression, with adjustment for other potential risk factors. Results: Breast cancer risk was increased among subjects who frequently did not sleep during the period of the night when melatonin levels are typically at their highest (OR = 1.14 for each night per week; 95% CI = 1.01 to 1.28). Risk did not increase with interrupted sleep accompanied by turning on a light. There was an indication of increased risk among subjects with the brightest bedrooms. Graveyard shiftwork was associated with increased breast cancer risk (OR = 1.6; 95% CI = 1.0 to 2.5), with a trend of increased risk with increasing years and with more hours per week of graveyard shiftwork (P = .02, Wald chi-squared test). Conclusion: The results of this study provide evidence that indicators of exposure to light at night may be associated with the risk of developing breast cancer.
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Mesajde jl_rona » Vin Mai 22, 2009 8:30 pm

O doctorita s-a gasit sa-mi dea melatonina ca sa dorm. De dormit nu ma adoarme ea cine stie ce, dar, curios, mi s-a reglat ciclul care a ajuns sa semene cu ceva normal (26-27 de zile).

In trecut aveam ciclu regulat la 21 de zile, cu dureri si hemoragii mari.

Asta era, se pare, din cauza starii de veghe prelungite (la lumina, evident). Ceasului meu biologic i se parea ca au trecut 28 de zile, cand de fapt trecusera doar 21.

Se pare ca e adevarat ca ciclul este fixat in functie de timpul de expunere la lumina, melatonina fiind intr-o relatie directa cu lumina primita de organism.

Production of melatonin by the pineal gland is under the influence of the suprachiasmatic nuclei (SCN) of the hypothalamus, which receives information from the retina about the daily pattern of light and darkness. Both SCN rhythmicity and melatonin production are affected by non-image-forming light information traveling through the recently-identified retinohypothalamic tract (RHT).

Facand un fals, am si dormit mai mult, dar mai ales am pacalit organismul cu pastile.

Nu e bine, dar e mai mult decat nimic.

In tot cazul, unde dai si unde crapa. Ea mi-a dat pastilele ca sa imi regleze somnul, iar efectul a fost ca mi-a reglat ciclul. Bun si-asea.

In tot cazul gutufanii cu care discut sunt criminal de idioti.

Mi-a zis unu ca mi s-a reglat ciclul de la futai. Pai intre un futai cu un necunoscut cu prezervativ pe el, cu care nici nu ai avut orgasm decat o data din 12 futaiuri si un facalet de asemenea cu prezervativ pe el si cu care ma fut singura, avand orgasm de fiecare data, e vreo diferenta???!!

Cum zicea idolul meu Brian Molko: "It's a loser, a sinner, a cock in a dildo's disguise"...

Insa idiotii care spun asta, nu gandesc, este evident. Pai ar trebui ca toate maicile de la manastire si mai stiu eu ce calugari sihastri sa aiba ciuperci, inflamatii si boli imunologice. Ori n-au!

Mai jos este research-ul meu pe tema ciclului si a somnului.

Am descoperit, cu ajutorul gutufanului care m-a starnit sa fac acest research, ce si cum mi-a reglat ciclul: era melatonina.

Daca nu era cretinul caruia am vrut sa-i demonstrez ca e un bou care baga vrajeala ieftina ca doar-doar i-oi da si lui o bucata de pizda, nu cred ca m-as fi prins de unde vine schimbarea, sau poate m-as fi prins greu, in timp...

Asa, a fost bun si el la ceva.

ASTA spuneam eu cand ziceam ca internetul e INTERACTIV si ca indiferent cu ce bou vorbesti, el fara sa vrea iti da idei, iar tu te apuci de studiu, cauti, inveti, descoperi lucruri noi, in timp ce el ramane tot un bou.

[color="Red"]In ASTA CONSTA MARETIA INTERNETUI! PENTRU CINE STIE SA-L FOLOSEASCA! Este o MAGNIFICA biblioteca INTERACTIVA!

Acuma intelegi tu Ayalo de ce m-apuca pe mine toate frustrarile pamantului ca nu am timp de studiu??? INTELEGI??

[/color]


===============================================

Biological Research For Nursing, Vol. 9, No. 1, 49-69 (2007)
DOI: 10.1177/1099800407303337


[color="Red"]Light Exposure, Melatonin Secretion, and Menstrual Cycle Parameters: An Integrative Review[/color]

Mary Lee Barron, APRN, BC
Saint Louis University, St. Louis, Missouri, barronml@slu.edu

Dysfunction in menstrual physiology has pronounced effects on quality of life, involving mood changes, body image, infertility, and pregnancy complications.

[color="red"]Light exposure may affect menstrual cycles and symptoms through the influence of melatonin secretion.[/color]

The purpose of this systematic review is to determine the current state of knowledge about the effects of light and melatonin secretion on menstrual phase and cycle alterations.

A brief overview of the influence of melatonin on human physiology is included.

[color="red"]There is evidence of a relationship between light exposure and melatonin secretion and irregular menstrual cycles, menstrual cycle symptoms, and disordered ovarian function.[/color]

In women with a psychopathology such as bipolar disorder or an endocrinopathy such as polycystic ovary syndrome, there seems to be greater vulnerability to the influence of light—dark exposure.

Research on the complex role of light—dark exposure in menstrual physiology has implications for treatment of menstrual-associated disorders.

http://brn.sagepub.com/cgi/content/abstract/9/1/49

[color="red"]The Pineal Gland and the Menstrual Cycle[/color]
Author: Reuven Sandyk a

Affiliation: Department of Psychiatry, Albert Einstein College of Medicine/Montefiore Medical Center, Bronx, NY, USA

DOI: 10.3109/00207459208987195

Publication Frequency: 12 issues per year

Published in: International Journal of Neuroscience, Volume 63, Issue 3 & 4 April 1992 , pages 197 - 204

Subject: Neuroscience;

Formats available: PDF (English)

Article Requests: Order Reprints : Request Permissions

Abstract

The menstrual cycle reflects the expression of a cyclical process involving the interaction between the hypothalamic-pituitary axis and the ovaries.

This complex process requires an integrated neural and humoral control mechanism.

It is now well established that a hypothalamic “transducerâ€Â
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Mesajde jl_rona » Vin Mai 22, 2009 8:30 pm

Abstract

Women with ovulatory menstrual cycles have a circadian rhythm superimposed on the menstrual-associated rhythm;

in turn, menstrual events affect the circadian rhythm.

In this paper, we review circadian rhythms in temperature, selected hormone profiles, and sleep–wake behavior in healthy women at different phases of the menstrual cycle.

The effects on menstrual cycle rhythmicity of disrupted circadian rhythms, for example, with shiftwork and altered circadian rhythms in women with menstrual-related mood disturbances, are discussed.

Compared to the follicular phase, in the post-ovulation luteal phase, body temperature is elevated, but the amplitude of the temperature rhythm is reduced.

Evidence indicates that the amplitude of other rhythms, such as melatonin and cortisol, may also be blunted in the luteal phase.

Subjective sleep quality is lowest around menses, but the timing and composition of sleep remains relatively stable across the menstrual cycle in healthy women, apart from an increase in spindle frequency activity and a minor decrease in rapid eye movement (REM) sleep during the luteal phase.

[color="red"]Disruption of circadian rhythms is associated with disturbances in menstrual function. [/color]

Female shiftworkers compared to non-shiftworkers are more likely to report menstrual irregularity and longer menstrual cycles.

There also is accumulating evidence that circadian disruption increases the risk of breast cancer in women, possibly due to altered light exposure and reduced melatonin secretion.

Further investigations into the biological consequences of circadian disruption in women will offer insight into some menstrual-associated disorders, including mood changes, as well as reproductive function and possible links with breast cancer.

http://linkinghub.elsevier.com/retrieve/pii/S1389945706006216

[color="red"]Irregular and long menstrual cycles[/color]

It may be comforting to know that most women don't have consistent 28-day menstrual cycles. A menstrual cycle can be considered regular if it averages between 26 and 35 days. An irregular cycle is frequently shorter or longer than this average, and may also include a missed period.

Concerns with irregular and long cycles

An irregular menstrual pattern may be an indication of ovulation problems and can be a major factor in infertility. [color="red"]Irregular cycles [/color]may also release hormones inconsistently and may add to mood and pain problems. Irregular and long cycles are sometimes also associated with [color="red"]heavy cramping and bleeding[/color].

What makes a regular menstrual cycle?

[color="red"]Menstrual cycles depend heavily on our body clocks to cycle properly. The Suprachiasmatic Nucleus in the brain (SCN or body clock) signals the ovaries to develop the egg sac, and again about 14 days later, the body clock starts the release of the egg. [/color]

The body clock uses bright light signals like sunlight to set its daily sleep/wake rhythm, and it relies on moonlight to regulate the menstrual cycle.

As explained in Dr. Smolensky's book, The Body Clock Guide to Better Health:

"Our words, 'menstruation,' 'moon,' and 'month,' all come from the Greek word for 'measure of time.'

A woman's menstrual cycle runs its course in about twenty-eight days, one lunar cycle. Periods usually start spontaneously in the week of the full moon in women not using birth control pills or hormone replacement therapy, particularly those with ample exposure to natural daylight and dark cues."

What causes a menstrual cycle to change?

[color="red"]Darkness may be one of the biggest reasons menstrual cycles become irregular.[/color]

Women who live near the equator or in sunny regions are more fertile and have stronger and more regular menstrual patterns than women who live in northern regions or spend more time indoors. Also, menstrual cycles during the darker winter months are longer than in the summer.

Irregularity may also be caused by stress, too much exercise, illness or weight problems.

Low body weight can prevent ovulation because the body needs a minimum amount of body fat.

Being overweight is linked to irregular cycles and heavy bleeding. Because of health concerns, you should consult with your doctor if you experience irregular menstrual cycles.

Restoring regular cycles

Knowing that healthy periods are in sync with the lunar cycle, scientists use artificial moonlight to regularize erratic menstrual cycles. Several studies show that using light at night regulates irregular and longer menstrual cycles, even in women whose periods lasted nine weeks or more. Irregular and long menstrual cycles were normalized within a few weeks of treatment. We have participated in many of these studies.

Predictability

Aside from improved health, a main advantage is that regular cycles are much easier to deal with. Women schedule their lives around their cycle; work, vacations, physical activities and social engagements are all affected by a period. Regular periods help you to schedule better and anticipate and minimize pain.

http://www.lighttherapy.com/irregular_menstrual_cycle.html
“Love, work and knowledge are the wellsprings of our lives, they should also govern it.â€Â
jl_rona
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Mesaje: 887
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Mesajde jl_rona » Vin Mai 22, 2009 9:00 pm

OH YES! I found the answer and it's not only official, but also offered by Putin himself!! ==D

Copyright © 2006 Elsevier Ireland Ltd All rights reserved.
Brief report

[color="Red"]Shortening of the menstrual cycle following light therapy in seasonal affective disorder[/color]

References and further reading may be available for this article. To view references and further reading you must purchase this article.


Konstantin V. Danilenko, a,

[color="Red"]Institute of Internal Medicine, Siberian Branch of the Russian Academy of Medical Sciences, Bogatkova 175/1, Novosibirsk 630089, Russia[/color]

Abstract

A significantly earlier onset of menstruation by 1.2 days, on average, was found following light therapy in 38 winter depressives; in two of them it could be classified as a minor side effect. There was no association between this shortening and depression improvement. [color="red"]A direct action of light on the hypothalamic–pituitary–gonadal axis is suggested.[/color]

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TBV-4P2B3X3-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=7c81d1fa24c82719959bbdda98fd997b

=======================

Deci hai sa ma-ngrozesc putzin:

Eu am ciclu la 21 de zile de vreo 7 ani (cam de cand nu dorm suficient a inceput treaba).

Am pierdut deci 7 zile pe luna ==> 84 de zile pe an ==> 588 de zile de viata ==> 1.61 ani de viata si respectiv 49 de ovule.

Am castigat insa vreo 252 de zile de viata in facultate, respectiv 21 de ovule, cand dormeam cate 12 ore pe zi, iar ciclul imi venea la 35 de zile.

Si maturarea spermatozoizilor functioneaza pe acelasi principiu, deci asta ar putea sa explice de ce oamenii de la poli traiesc mai mult decat cei din tarile calde: sunt mai putin expusi la lumina (e cel putin un factor important).
“Love, work and knowledge are the wellsprings of our lives, they should also govern it.â€Â
jl_rona
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Membru din: Mar Mai 29, 2007 9:32 pm
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