Biomedical subjects
Publications and source records attributed to S Narayan.
Lupus Anticoagulant, first discovered in patients of SLE, is now known to be associated with a wide spectrum of diseases. The presence of LA is associated with adverse fetal outcome in an obstetric population. In the present series the incidence of LA was found to be 16.6% and 80% of LA positive subgroup had an unsuccessful outcome.
Acute Lymphoblastic Leukaemia (ALL) with intracytoplasmic inclusions is a rare and unusual subtype of acute leukaemia. Here we describe a case of ALL with intracytoplasmic inclusions in an adult female. These inclusions stained negative for Myeloperoxidase (MPO), Sudan Black E (SBB) and alpha-naphthyl acetate estarase (ANAE) and positive for Periodic Acid Schiff (PAS). This case is being presented for its unusual occurrence and to recognise the characteristics of this subtype of ALL to avoid a misdiagnosis of AML.
[formula: see text] TMS-OTf- or TBS-OTf-promoted glycosidation reactions of 2-deoxy-2-iodo-alpha-mannopyranosyl acetates 8-10 and the 2-deoxy-2-iodo-alpha-talopyranosyl acetate 11 provide the corresponding 2-deoxy-2-iodo-alpha-pyranosides, precursors to 2-deoxy-alpha-glycosides, as the only observed reaction products.
[formula: see text] The reactions of glycals with ceric(IV) ammonium nitrate and sodium iodide in the presence of acetic acid provides 2-deoxy-2-iodo-alpha-mannopyranosyl acetates with good stereoselectivity. In the majority of the cases examined, the selectivity was considerably better than that from reactions using N-iodosuccinimide and HOAc.
The purpose of this study was to evaluate the probability and extent of response to radiation therapy in patients with chemotherapy-resistant intermediate grade non-Hodgkin's lymphoma. Thirty-five patients with chemotherapy-resistant non-Hodgkin's lymphoma received local radiation therapy after initial treatment with at least six cycles of systemic chemotherapy. There were 17 men and 18 women in our study. Ages ranged from 15 to 68 years, median age was 42 years. Chemotherapy resistance was defined as relapse after initial chemotherapy (11 patients) or failure to achieve complete remission (partial response in 18 patients, stable disease in 1 patient, and disease progression in 5 patients). Radiation doses were between 1,980-5,040 cGy (median dose of 3,200 cGy). Treatment outcome was evaluated with respect to any subsequent relapse either within or outside the irradiated region. The 2-year actuarial survival was 65%. The cumulative incidence of isolated local failure and any local failure at 2 years were 33% and 54%, respectively. Tumors that responded to initial chemotherapy had a better local control probability than tumors that did not respond. The 2-year actuarial local failure rates for these two groups were 51% and 83%, respectively (P = 0.01). There was a trend for improved local control with radiation doses > or = 3,960 cGy, suggesting the presence of a dose-control relationship. The rate of disease progression within an irradiated region in patients with intermediate grade non-Hodgkin's lymphoma that relapsed after or failed to respond completely to full course chemotherapy was substantially higher than the historical in-field failure rates when radiation therapy was used as the sole modality of treatment. Prior response to initial chemotherapy was a predicting factor for local control following radiation therapy.
We examined the effect of a protein synthesis inhibitor, cycloheximide (CHX) on the adenomatous polyposis coli (APC) mRNA levels in HCT-116 colon cancer cell line. The HCT-116 cells were treated with different concentrations of CHX for 15 h. APC, p53 and beta-actin mRNA levels were determined by Northern blotting. Results showed that APC and beta-actin mRNA levels were significantly increased in a dose-dependent manner after CHX treatment. The p53 mRNA levels were moderately increased. The increase in APC mRNA levels after CHX treatment was due to increase in its stability instead of transcription. These results provide a model for CHX-induced APC mRNA stabilization and its implication in cell cycle arrest and cell survival studies.
When family caregivers are faced with making daily decisions, they may feel burdened, frustrated, and even in conflict with other family members. The OOVL Guide is a tool to help people think about the various aspects of a decision situation and combine them to make a decision. The OOVL Guide supports nurses in their advocacy role because it affirms the importance of the clients' values and preferences. The OOVL Guide provides decision-makers, both professionals and lay people, with a structure and procedure for making choices for themselves or others.
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Recent experiments on permeabilized anterior byssus retractor muscle (ABRM) of Mytilus edulis have shown that phosphorylation of twitchin releases catch force at pCa > 8 and decreases force at suprabasal but submaximum [Ca2+]. Twitchin phosphorylation decreases force with no detectable change in ATPase activity, and thus increases the energy cost of force maintenance at subsaturating [Ca2+]. Similarly, twitchin phosphorylation causes no change in unloaded shortening velocity (Vo) at any [Ca2+], but when compared at equal submaximum forces, there is a higher Vo when twitchin is phosphorylated. During calcium activation, the force-maintaining structure controlled by twitchin phosphorylation adjusts to a 30% Lo release to maintain force at the shorter length. The data suggest that during both catch and calcium-mediated submaximum contractions, twitchin phosphorylation removes a structure that maintains force with a very low ATPase, but which can slowly cycle during submaximum calcium activation. A quantitative cross-bridge model of catch is presented that is based on modifications of the Hai and Murphy (1988. Am. J. Physiol. 254:C99-C106) latch bridge model for regulation of mammalian smooth muscle.
Reactive perforating collagenosis is characterised by trans-epidermal elimination of collagen and is hypothesized to be both autosomally dominant and recessive. We report a family in which two brothers and a sister had lesions of reactive perforating collagenosis.
In the present study, we show that treatment of wild-type (p53+/+) mouse embryonic fibroblast (MEF) cells with a DNA-alkylating agent, N-methyl-N'-nitro-N-nitro-soguanidine (MNNG), resulted in increased levels of adenomatous polyposis coli (APC) mRNA compared to p53 gene-knocked out (p53-/-) MEF cells, indicating that p53 is required for APC expression after alkylation damage. By using HCT-116 colon cancer cells (containing wild-type p53 gene) or p53-/- MEF cells transfected with a pCMV-p53 overexpression plasmid [p53-/-(CMV-p53)], we show that p53 is a labile factor for APC gene expression, and that pretreating HCT-116 cells with a protein synthesis inhibitor, cycloheximide (CHX), inhibited MNNG-induced APC mRNA levels by inhibiting p53 protein synthesis. The effect of CHX on p53 protein synthesis was reversible, as the withdrawal of CHX permitted p53 protein synthesis to resume with a concomitant increase in APC mRNA levels after MNNG treatment. To examine whether p53 regulates APC gene expression at the transcriptional level, we treated HCT-116 or p53-/-(CMV-p53) MEF cells with 5,6-dichloro-1-beta-D-ribofuranosylbenzamidazole (DRB; a transcriptional inhibitor), before the MNNG treatment. Although treatment of cells with DRB resulted in increased p53 protein levels, that the APC mRNA levels were decreased suggests that p53 may enhance APC gene expression upstream of the transcriptional machinery where DRB interacts. That the withdrawal of DRB, and subsequent MNNG treatment, increased the level of APC mRNA indicated that the binding of DRB to the transcriptional machinery was reversible.
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Abnormalities in coagulation profile were correlated with clinical outcome in neonates (n = 30) of mothers with pregnancy induced hypertension (PIH). Same number of neonates born to normotensive mothers was taken as control. Significant correlation was observed between decreasing gestational age and alterations in all coagulation parameters. Higher incidence of prematurity, hyperbilirubinaemia and significant prolongation in partial thromboplastin time with kaolin (PTTK) and thrombin time (TT) values were observed with increasing severity of PIH. Incidence of disseminated intravascular coagulation (DIC) was higher in preterm neonates than in term neonates.
Development of colon cancer is a multistep process frequently involving mutations in both the APC and p53 tumor suppressor genes. In this study we treated the HCT-116 colon cancer cell line with alkylating agents including N-methyl-N'-nitro-N-nitrosoguanidine (MNNG),which is known to cause colon cancer in animals, and examined the expression of both APC and p53 genes. Exposure of cells with MNNG caused an 8-12-fold increase in the level of APC mRNA and protein. APC induction was shown to result from increased nuclear transcription of the APC gene and correlated with a concomitant increase in the p53 protein level after MNNG treatment. A necessary role for p53 in APC gene regulation is supported by the failure of MNNG to induce APC expression in cell lines either expressing very low levels of p53 (HeLa cells) or no p53 (K562 erythroleukemia cells). The overexpression of wild-type p53 gene into HCT-116 cells mimicked the effect of MNNG-induced expression of APC mRNA. A direct causal role for p53 in APC gene regulation was further evaluated by transfecting the wild-type p53 gene into K562 cells and observing a 5-fold increase in the APC gene expression. These results support a model featuring a direct link between p53 and APC in response to alkylation-induced DNA damage and suggest a novel role for p53 in a stress-response pathway involving APC.