Posted by Grant Grunow on May 25th 2008 to
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The Anti-HIV drugs reduce the cause of some forms of the loss of the vision
A therapeutical use new potential for the drugs anti-HIV known as inhibiting of protease was suggested by a team of the investigators of the College of Medicine, the Boston, and the Inserm U848 of Harvard, France, in consequence of its work in a model of the rat of the retinal detachment.
An important cause of the loss of the vision in many illnesses of the eye is the death (for a known process as the apoptosis) of stacks of nerve in the eye (known as photoreceptors) after the retinal detachment. In the study, the inhibitor administration of protease of the HIV of alive voice diminished marked the apoptosis of the photoreceptor in the model of the rat of the retinal detachment. The Mechanistic analysis in cultures of retinal stack of the rat and in the rats that to express diminished amounts of specific proteins established that the inhibitors of protease of the HIV had interrupted two ways moleculars that they cause the stack death apoptotic, ambo affect the known compartments of stack as the mitocndria. Because the same ways deinduo of the stack apoptotic had been shown to be activated in the human retinas after the retinal detachment, the authors suggest that even so the inhibitors of protease of the HIV cannot reattach the retina, can be of the clinical benefit with its ability to hinder the apoptosis it photoreceptor that after has a basic paper in the loss of the vision the retinal detachment.
HEADING: The inhibitors of protease of the HIV supply neuroprotection with the mitochondrial inhibition of apoptosis in the rats
CONTACT OF THE AUTHOR:
Joan W. Miller
College of Medicine of Harvard, Boston, Massachusetts, U.S.A.
Guido Kroemer
INSERM U848, Villejuif (Paris), France.
What identifies to the cancerous cells that cause relapse and metstase? Not CD133
The data new, generated by Shahin Rafii and colleagues, in the medical college of Weill of the University of Cornell, New York, with the analysis of stacks and human rats of the cancer of clon, had shed the doubt in the assignment recently to consider of protein CD133 as a marker of stacks of connecting rod of the cancer of clon - a term given to the small number of stacks inside of a cancer of clon that they can probably cause a new tumor and that they are consequently responsible for the return and metstase of the tumor.
In the study, the rats had been projected such that had expressed a protein of the reporter in all part that CD133 is expressed normally. In contrast with the preceding studies where expression CD133 had been shown to be expressed very by few stacks in colon, this protein of the reporter was detected in many stacks in colon, including stacks of the not-connecting rod. A similarly wide expression of CD133 in colon of both the rats and human beings were observed to use the antibodies that bind CD133. The analysis of preliminary tumors of colon of the human and spontaneous rat it indicated that CD133 estve expressed by the majority of stacks. Inversely, all the stacks human beings of the cancer of clon that they had multiplied for metstese to the liver had not expressed CD133. More, the stacks of CD133+ and CD133- had generated transplantadas tumors when in rats immunocompromised. Some of the reasons for which this preceding study and inquiries such distinct conclusions if or not of CD133 alcangaram is a marker of the cancer of clon the stacks of connecting rod that are written down by the argued authors and in detail in a commentary of accompaniment for Mark LaBarge and Mina Bissell, in the national laboratory of Lawrence Berkeley, Berkeley.
HEADING: Expression CD133 is not restricted to the stacks of connecting rod, and the metastticas stacks of the cancer of clon of CD133+ and CD133- initiated tumors
CONTACT OF THE AUTHOR:
Shahin Rafii
Medical college of Weill of the University of Cornell, New York, New York, U.S.A.
FOLLOWING THE HEADING OF THE COMMENTARY: Is CD133 a marker of metastticas stacks of connecting rod of the cancer of clon?
CONTACT OF THE AUTHOR:
Mine J. Bissell
National laboratory of Lawrence Berkeley, Berkeley, California, U.S.A.
It marks. the LaBarge
National laboratory of Lawrence Berkeley, Berkeley, California, U.S.A.
It is not a AKT: the genetic variation affects the region of the disfuncional brain in the schizophrenia
The new data, generated by Daniel Weinberger and colleagues, in the national justinian codes of the health, Bethesda, had indicated that in healthful individuals, the variation in a known gene as AKT1 affects the structure and the function of the part of the brain that is disfuncional in the individuals with schizophrenia. Specifically, in healthful individuals, a particular variation AKT1 was associated with the damaged cognition (an ability damaged to the process information), something that is affected marked in the individuals with schizophrenia. Beyond, same variation AKT1 was associated with the diminished volume of the gray-substance in the frontostriatal region of the brain, that is disfuncional in the individuals with schizophrenia. A additional analysis indicated that variation AKT1 estve associated with an increased risk of schizophrenia and the therapeutical implications of this, as well as the other results of the study, is argued in a commentary of accompaniment for Alexander Arguello and Joseph Gogos, in the college of the University of Columbia of the doctors and the surgeons, New York.
HEADING: The genetic variation in AKT1 is lig the cortical structure and the function prefrontal dopamine-associates in the human beings
CONTACT OF THE AUTHOR:
Daniel R. Weinberger
National justinian codes of the health, Bethesda, Maryland, U.S.A.
FOLLOWING THE COMMENTARY
HEADING: A AKTing way of the signalling above in the schizophrenia
CONTACT OF THE AUTHOR:
Joseph. the Gogos
College of the University of Columbia of the doctors and the surgeons, New York, New York, U.S.A.
OFTALMOLOGIA: Sight of a new perspective in drugs to correct a cause of the loss of the vision
A frequent complication in the individuals with diabetes in the long run is retinopathy of the diabetic one, an eye condition that is the root cause of the blindness in the adults of the propitious age for the work. A factor that contributes to the loss of the vision is the accumulation of liquid in the retina of the eye because the sanguineous vases in the retina if had become permeveis more. The new data, suggesting that a family of the known drugs as vasoinhibins retinopathy of the diabetic one could supply a new approach to diminish the permeability in the sanguineous vases of the eye of the individuals, had been generated in the rats for Carmen Clapp and colleagues, of the Autonomous National Universidad of Mexico.
Vasoinhibins opposes a known molecule as VEGF, that is an important starter of the increased permeability of the sanguineous vase in the retina of the individuals with retinopathy of the diabetic one. In the study, the injection of vasoinhibins in the eye was found to obstruct increases in the permeability of the sanguineous vase in the eye of rats of the diabetic one and to obstruct increases in the permeability of the sanguineous vase in the eye of the normal rats injected (in the eye) with the VEGF or the liquid of the eye of an individual with retinopathy of the diabetic one. Vasoinhibins had been shown to Mechanistically to the work activating a known protein as PP2A, that, in turn, inactivated a known protein as eNOS.
HEADING: Vasoinhibins hinders vasopermeability retinal associate with retinopathy diabetic it in the rats through the inactivao it eNOS of fosfatase 2A-dependent of the protein
CONTACT OF THE AUTHOR:
Carmen Clapp
Autonomous National Universidad of Mexico, Quertaro, Mexico.
IMUNOLOGIA: A new target for the imunoterapia of the tumor in stacks dendritic?
Many investigators are interested in approaches becoming to induce the antitumorosas immune answers carried through by the known immune stacks as CTLs. In the rats, one-way to make that is to whiten proteins of the tumor to a subgroup of the known immune stacks as the stacks dendritic (DCS) that they express the CD8-alpha protein. That is because the DCS that express CD8-alpha can direct CTLs efficiently to attack all the proteins that will be whitened to them. A new way to whiten proteins of the tumor to the DCS that express CD8-alpha was discovered by Caetano Reis and Sousa and colleagues, in the United kingdom research of the cancer, the United kingdom, that they had identified a molecule whose the expression was restricted in the rats to the DCS that express CD8-alpha and one another subgroup of the known C.C as the DCS of plasmacytoid.
The functional studies had indicated that the molecule, that was nominated the group dendritic receiver-1 of lectin of stack NK (DNGR-1), was a receiver endocytic and that if an antibody that recognized DNGR-1 was lig to one peptide it delivered peptide specifically to the DCS that express CD8-alpha. The CTL answers had directed to peptide had been induced in the rats vacinados with the antibody peptide-lig of DNGR-1-specific and an adjuvant. To direct these answers of CTL for stacks of the melanoma lig the antibody of DNGR-1-specific to peptides of proteins overexpressed for an eradicated melanoma cellular line of the melanoma in a therapeutical model of the rat. More, as the expression of DNGR-1 in the human beings was found to be restricted to a subgroup of the DCS with the similar characteristics to the DCS of the rat that express CD8-alpha, the authors had suggested that this to whiten the DCS through DNGR-1 could supply a new approach to the imunoterapia of the tumor.
HEADING: Therapy of the tumor in the rats through the antigen that it whitens to one lectin new, C.C. - restricted of the C
CONTACT OF THE AUTHOR:
Caetano Reis and Sousa
Research the United kingdom of the cancer, London, the United kingdom.
NEUROBIOLOGIA: To protect of meeting or to promote, that one is the question on the paper of the cellular process autophagy in the illness of Alzheimer
All the clutters neurodegenerative (for example illness of Alzheimer [ANNOUNCEMENT], illness of Parkinson, and illness of Huntington) are characterized by the presence of added of the protein in the death of stack of the brain and the nerve. The recent data had implied a known cellular process as autophagy (by means of that the stacks can degrade proteins and compartments long-lived to remodel its interiors and/or to survive the fatigantes situations) in neurodegeneration, but if it protects of meeting or it promotes neurodegeneration remains controversial. The data new, generated by Tony Wyss-Coray and colleagues, in the University of Stanford, had indicated that one diminished autophagy in stacks of nerve can increase neurodegeneration in a model of the rat of the ANNOUNCEMENT.
In the study, the rats that lack one of its Becn1 genes, that carreg the demanded information to make beclin autophagy key 1 of the protein, had been found to show the diminished stack of nerve autophagy and to this they had been associates with neurodegeneration increased. When a model of the rat of the ANNOUNCEMENT was projected similarly to lack a Becn1 gene, an increased amount of accumulation of neurodegeneration and of the protein in the brain it was observed. Inversely, if the model of the rat of the ANNOUNCEMENT was projected to express amounts increased of beclin 1, the diminished accumulation of the protein in the brain was observed. The authors suggest consequently that one the increasing levels of beclin 1 can be of the benefit to the individuals with ANNOUNCEMENT.
In a accompaniment commentary, Jin-Um Lee and fen-Biao Gao, in the University of California in San Francisco, writes down that even so to modulate levels of beclin 1 it can be a attractive approach to treat individuals with the ANNOUNCEMENT, studies more adds in other animal models is demanded for verific the viability of this strategy.
HEADING: The samples autophagy-related of beclin 1 of the protein had reduced the expression in the illness of advanced Alzheimer and regulate the amyloid-beta accumulation in the rats
CONTACT OF THE AUTHOR:
Tony Wyss-Coray
University of Stanford, Stanford, California, U.S.A.
FOLLOWING THE COMMENTARY
HEADING: Regulation of a-beta pathology for beclin 1: a protective paper for autophagy?
CONTACT OF THE AUTHOR:
Fen-Biao Gao
University of California in San Francisco, San Francisco, California, U.S.A.
INFLAMMATION: Round Redondo and we go: bow of positive answer sheet proinflammatory identified in the intestines of the individuals with illness of Crohn
Although the illness of Crohn (COMPACT DISC) and colitits ulcerosos (UC) are both the types of the illness of viscera inflammatory (IBD), the mechanisms that are the base of these two illnesses are different. The new introspection in the inflammatory riots of the stack in the intestines of the individuals with COMPACT DISC was supplied by Toshifumi Hibi and colleagues, in the College of Medicine of the university of Keio, Japan, who had suggested that these changes could contribute to the development of the illness.
The majority of known immune stacks as the macrophages that live in the intestine does not express molecule CD14 and this characteristic proinflammatory is associates with a lack of the production of known factors as cytokines. In the study, an increased number of macrophages that they express CD14 (as well as other molecules expressed not generally for intestinais macrophages) was detected in the intestines of the individuals with the COMPACT DISC compared with the intestines of healthful individuals and those with UC. These stacks had produced great amounts of cytokines proinflammatory IL-23 and TNF-alpha, that had made with that other immune stacks in the area produced one another one cytokine proinflammatory, IFN-gamma. Because IFN-gamma was found to cause a later increase in the number of macrophages that express CD14 and that they produce IL-23, the authors suggest that IL-23 and IFN-gamma give form to a bow of positive answer sheet that promotes the inflammation in the intestine of the individuals with COMPACT DISC.
HEADING: The original intestinais macrophages of CD14+ contribute to patognese of the illness of Crohn through the central line of IL-23/IFN-gamma
CONTACT OF THE AUTHOR:
Toshifumi Hibi
College of Medicine of the university of Keio, Tokyo, Japan.
VIROLOGY: The stacks of T of CD4+ are really rest candy home for the relative of the monkey of the HIV
Many tensions of the monkey become of course contaminated with viruses that are related to the HIV. These viruses are known collectively because the SIV and the monkeys of course contaminated do not develop the AIDS. One expects that because the monkeys contaminated of course with SIV if do not become the comprehensive AIDS it could teach the investigating lies important on the mechanisms that are the base of the development of the AIDS in the contaminated human beings with HIV and to identify ways to hinder this event. The new introspection in the mechanisms that of course control the particle number of the virus in the blood of mangabeys sooty contaminated with SIVsmm, the tension of the SIV that contaminates mangabeys of course sooty, has been supplied now for a team of the investigators of the University of the Pensilvnia, the Philadelphfia, and the university of Emory, Atlanta.
The HIV and the SIV contaminate the known immune stacks as stacks of T of CD4+. Thus, the authors to display to determine as the stacks of T of CD4+ had of course affected the particle number of the virus in the blood of mangabeys sooty contaminated with SIVsmm - they had supplied the immune control of the particle number of the virus or them they had supplied a place simply to live one replicate. The particle number of SIVsmm in the blood of mangabeys sooty of course contaminated diminished when the monkeys had been depleted of stacks of T of CD4+ and had increased then another time while the number of proliferating stacks of T of CD4+ repercutiriu. Thus, a little of what was concluded that the availability of proliferating stacks of T of CD4+ is a determinative cause key how many particles of SIVsmm could be detected in the blood of mangabeys sooty of course contaminated, of the stacks of T of CD4+ that supply the immune control of the virus.
HEADING: The availability of stacks of T activated of said CD4+ the level of viremia in mangabeys sooty of course SIV-contaminated
CONTACT OF THE AUTHOR:
Guido Silvestri
College of Medicine of the University of the Pensilvnia, Philadelphfia, Pensilvnia, U.S.A.
Aftab. the Ansari
College of Medicine of the university of Emory, Atlanta, Gergia, U.S.A.
METABOLIC ILLNESS: The FoxO1 protein of the liver can lig overindulgence with the type - diabetes 2
The high levels of blood of known fats as triglycerides and triglyceride-rich molecule VLDL are factors of risk for the cardiac illness and diabetes. The VLDL production is dependent of the regulator of insulin of the levels of blood sugar (works to lower levels of blood sugar) and of protein MTP of the liver, these interactions are even so not understood well. In a new study, dong of Henry and its colleagues in the university of the College of Medicine of Pittsburgh had disclosed a relationship enters the FoxO1 protein of the liver and the superproduction of VLDL.
Using cellular line cultivated human beings of the liver, the investigators had shown that the FoxO1 limit and the stimulated expression of MTP and secretion inhibited of insulin. Consistent with this, overexpression of FoxO1 increased, and prostrao diminished FoxO1, levels of MTP and VLDL in the rats. Moreover, the rats with deficiencies in damage of triglycerides had equally had high levels of FoxO1 and VLDL. The authors conclude consequently that this relationship between FoxO1, insulin, and VLDL could explain, in the part, the simultaneous increases in the blood sugar and triglyceride is even at risk seen in the patients for the type - diabetes 2. A commentary of accompaniment for sparks of Janet and Charles in the university of the College of Medicine of Rochester concludes more than this study it establishes a linking between overindulgence dietary and the multiple clutters that for an individual in the increased risk to develop the type - diabetes 2, including the hipertenso, the obesidade, the high neses of the cholesterol, and the resistance to the effect of insulin.
HEADING: FoxO1 negotiates the regulation insulin-dependent of the production hepatic of VLDL in the rats
CONTACT OF THE AUTHOR:
Dong of the H. Henry
University of the College of Medicine of Pittsburgh, Pittsburgh, Pensilvnia, U.S.A.
FOLLOWING THE COMMENTARY
HEADING: Overindulgence and metabolic syndrome: is FoxO1 a missing linking?
CONTACT OF THE AUTHOR:
Sparks of Janet D.
University of the medical center of Rochester, Rochester, New York, U.S.A.
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The article was adaptou today for the medical notice of the release of the original press.
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Source: Honey of Karen
Periodical of the clinical inquiry