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Pathogen research abs 1 || Pathogen research abs 2 || Pathogen research abs 3 || Pathogen research abs 4 || Pathogen research abs 5 || Hormone and endocrine research abs 1 || Hormone and endocrine research abs 2 || Hormone and endocrine research abs 3 || Hormone and endocrine research abs 4 || Hormone and endocrine research abs 5 || Follicle and follicular cells research abs 1 || Interferon research abs 1







Gynecol Oncol. 1999 Mar;72(3):392-401.
Interferon-gamma and tumor necrosis factor-alpha induce synergistic cytolytic effects in ovarian cancer cell lines-roles of the TR60 and TR80 tumor necrosis factor receptors.

Kost ER, Mutch DG, Herzog TJ.

Division of Gynecologic Oncology, Brooke Army Medical Center, Ft. Sam, Houston, Texas, 78234-6200, USA.

OBJECTIVE: Utilizing ovarian cancer cell lines, we examined the effect of IFN-gamma on each type of TNF receptor. Additionally, we sought to determine the effect of receptor modulation on TNF-alpha-mediated cytolysis. METHODS: Ovarian cancer cell lines Caov-3, A2780, and SK-OV-3 were employed. The number of TNF receptors was determined by a TNF-alpha binding assay utilizing 125I-labeled TNF-alpha. Monoclonal antibodies specific for the 55- to 60-kDa (TR60) and the 75- to 80-kDa (TR80) TNF receptors were used to determine the relative density of each receptor type. Northern blot analyses were performed employing cDNA probes for the TR60 and TR80 mRNAs. To elucidate which receptor(s) was responsible for mediating the signal for cytolysis, 24-h MTT cytolytic assays were performed in the presence of receptor-specific monoclonal antibodies. RESULTS: IFN-gamma treatment resulted in an increase in TNF receptors in the cell lines A2780 and Caov-3 (P < 0.001), but not SK-OV-3. Northern blot analyses suggested distinct regulatory mechanisms for the two receptors. In Caov-3 and SK-OV-3 cells a synergistic increase in TNF-alpha-mediated cytolysis was seen when cells were pretreated with IFN-gamma. In both cell lines, pretreatment with IFN-gamma markedly enhanced the ability of the TR60 receptor to mediate cell lysis. Conversely, under similar treatment conditions, the TR80 receptor did not appear capable of generating a cytolytic signal. CONCLUSIONS: TNF receptor modulation by IFN-gamma appears to be unique to individual cell lines. The TR60 TNF receptor plays a central role in the synergistic cytolytic effects of IFN-gamma and TNF-alpha. Sequential therapy with IFN-gamma and TNF-alpha and specific TNF receptor activation may provide novel translational strategies for the use of cytokines in the treatment of ovarian cancer. 1999 Academic Press.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10053112&dopt=Abstract



J Hepatol. 1999 Feb;30(2):185-91.
Soluble tumor necrosis factor receptors in chronic hepatitis C: a correlation with histological fibrosis and activity.

Zylberberg H, Rimaniol AC, Pol S, Masson A, De Groote D, Berthelot P, Bach JF, Brechot C, Zavala F.

Unite d'Hepatologie, Hopital Necker, Paris, France.

BACKGROUND/AIMS: Tumor necrosis factor-alpha (TNF) is a mediator of inflammation and cellular immune response. Soluble TNF receptors (sTNFR) sTNF-R55 and sTNF-R75, which compete with cellular receptors for the binding of TNF, have been detected at high levels in infectious diseases including human immunodeficiency virus and HBV infection. In order to investigate the activation of the TNF system in HCV infection, we have analyzed the balance between TNF and sTNF-R in 60 HCV-infected subjects according to their clinical, biological, virological and histological characteristics. METHODS: Serum TNF, sTNF-R55 and sTNF-R75 levels were determined by ELISA before any therapy and were compared to a control group of 60 healthy subjects and a group of 34 HBV-infected patients. RESULTS: Mean TNF levels were 50.5+/-4.5 pg/ml in HCV patients, and undetectable (<5 pg/ml) in the control subjects. sTNF-R55 and sTNF-R75 levels were significantly higher in HCV-infected patients than in the controls: 2.88+/-0.14 ng/ml vs. 1.30+/-0.05, (p = 0.0001), and 9.54+/-0.58 ng/ml vs. 4.19+/-016, (p = 0.0001), respectively. sTNF-R55 and TNF-alpha levels in HCV patients were not significantly different from levels in HBV patients. sTNF-R75 levels were slightly lower than in HBV patients (9.54+/-0.58 vs. 11.4+/-0.79 ng/ml, p = 0.03). In contrast to other infectious diseases, there was no correlation between levels of sTNF-R and TNF. sTNF-R75 but not TNF levels were correlated with aminotransferases levels (p = 0.0001 and p = 0.0015 for aspartate and alanine aminotransferase, respectively), while sTNF-R55 levels were significantly correlated only with aspartate aminotransferase levels (p = 0.003). sTNF-R75 levels were significantly correlated with the Metavir activity index (p = 0.01), and sTNF-R55 and sTNF-R75 levels were significantly higher in patients with vs. without cirrhosis (3.22+/-0.21 vs. 2.54+/-0.17 ng/ml (p<0.02) and 11.6+/-0.86 vs. 7.5+/-0.53 ng/ml (p<0.001), respectively). sTNF-R55, sTNF-R75 and TNF levels were not correlated with viral load, genotype or response to interferon therapy. CONCLUSIONS: Levels of soluble TNF receptors, and particularly sTNF-R75, are significantly correlated with the severity of the disease but not with virological parameters such as quantitative viremia and genotype. High TNF-R production could thus suggest that HCV-related liver disease involves immunological mechanisms, including activation of the TNF system.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10068094&dopt=Abstract



Hepatology. 1999 Mar;29(3):777-84.
Peroxynitrite formation during rat hepatic allograft rejection.

Yamaguchi Y, Okabe K, Matsumura F, Akizuki E, Matsuda T, Ohshiro H, Liang J, Yamada S, Mori K, Ogawa M.

Department of Surgery II, Kumamoto University Medical School, Kumamoto, Japan.

The role of nitric oxide (NO) on tissue injury of hepatic allografts during rejection remains controversial. We investigated inducible nitric oxide synthase (iNOS) expression and formation of peroxynitrite in ACI rat liver grafts implanted in recipients. Animals were divided into four experimental groups: group I, isografts; group II, untreated hepatic allografts; group III, allografts treated with FK506; and group IV, allografts pretreated with donor-specific blood transfusion (DST). Serum nitrite/nitrate, interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) concentrations increased significantly in group II rats after transplantation but were significantly lower in groups I, III, and IV. The numbers of macrophages that reacted with an antimacrophage iNOS monoclonal antibody as well as iNOS messenger RNA (mRNA) levels in liver specimens were also much lower in groups I, III, and IV as compared with group II. Immunostaining and Western blot analysis showed prominent tissue nitrotyrosine expression in untreated hepatic allografts, but not in allografts treated with FK506 or donor-specific blood. These results suggest that one of the mechanisms by which production of NO results in injury in rat hepatic allografts may be because of its reaction with superoxide to form peroxynitrite.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10051479&dopt=Abstract



J Endod. 2003 Feb;29(2):95-9.
In vitro evaluation of the cytotoxicity of two root canal sealers on macrophage activity.

de Oliveira Mendes ST, Ribeiro Sobrinho AP, de Carvalho AT, de Souza Cortes MI, Vieira LQ.

Departamento de Odontologia Restauradora, Faculdade de Odontologia, Universidade Federal de Minas Gerais, MG, Brazil.

Although some studies have been concerned with the cytotoxicity of endodontic sealers and their components, few have approached the effects of endodontic sealers on macrophage viability and activity. In this study the effect of two zinc oxide-eugenol-based sealers, freshly prepared or after setting for 24 h, was determined on macrophage activity in vitro. Sealers were placed inside a glass capillary tube and added to mouse-elicited macrophage cultures. Sealers did not affect macrophage viability; however, adherence to glass and phagocytosis were impaired. Moreover, nitric oxide production in response to activation with interferon-gamma was diminished, but interleukin-12 production in response to Listeria monocytogenes was not altered. Interestingly, freshly mixed and solid test samples had similar inhibitory activities. In conclusion, the tested sealers did not affect a pro-inflammatory response (interleukin-12 production) but had an inhibitory effect on the effector responses measured (phagocytosis and nitric oxide production).


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12597705&dopt=Abstract



Nature. 1999 Feb 25;397(6721):710-3.
Inhibition of transforming growth factor-beta/SMAD signalling by the interferon-gamma/STAT pathway.

Ulloa L, Doody J, Massague J.

Cell Biology Program and Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

Transforming growth factor-beta (TGF-beta) and interferon-gamma (IFN-gamma) have opposite effects on diverse cellular functions, but the basis for this antagonism is not known. TGF-beta signals through a receptor serine kinase that phosphorylates and activates the transcription factors Smads 2 and 3, whereas the IFN-gamma receptor and its associated protein tyrosine kinase Jak1 mediate phosphorylation and activation of the transcription factor Stat1. Here we present a basis for the integration of TGF-beta and IFN-gamma signals. IFN-gamma inhibits the TGF beta-induced phosphorylation of Smad3 and its attendant events, namely, the association of Smad3 with Smad4, the accumulation of Smad3 in the nucleus, and the activation of TGFbeta-responsive genes. Acting through Jak1 and Stat1, IFN-gamma induces the expression of Smad7, an antagonistic SMAD, which prevents the interaction of Smad3 with the TGF-beta receptor. The results indicate a mechanism of transmodulation between the STAT and SMAD signal-transduction pathways.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10067896&dopt=Abstract








The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer an essential part of our body, just like appendix. What little hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

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