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Biomedical subjects

R Banerjee

Publications and source records attributed to R Banerjee.

At least 91 records · Page 5Linked to original sources
PubMed1998

Coagulopathy secondary to vitamin K deficiency in hyperemesis gravidarum.

BACKGROUND: Hyperemesis gravidarum is a condition of pregnancy characterized by excessive nausea and vomiting, which can be associated with malnutrition. Vitamin K deficiency is a known complication of malnutrition as well as a known cause of coagulopathy. To date, there is no reported case in the literature of vitamin K deficiency in hyperemesis gravidarum. CASE: A woman at 15 weeks' gestation presented with hyperemesis gravidarum complicated by an episode of severe epistaxis. Investigation revealed coagulopathy secondary to vitamin K deficiency. The coagulopathy resolved after vitamin K replacement, with complete correction of all clotting factors. CONCLUSION: Vitamin K deficiency and coagulopathy should be considered in women with hyperemesis gravidarum who present with a bleeding diathesis. Prophylactic vitamin K replacement should be considered in cases in which hyperemesis is severe and protracted.

Adult↗
PubMed1998

Amino-terminal region of poliovirus 2C protein is sufficient for membrane binding.

The poliovirus-encoded, membrane associated polypeptide 2C is required for viral replication. We have previously established that, while the 2C protein lacks a defined membrane binding domain, the N-terminal region containing a putative amphipathic helix plays an important role in membrane binding both in vivo and in vitro. In order to determine whether the N-terminal region is sufficient for membrane binding, we have made fusion constructs between this region of 2C (amino acids 1-72 and 1-88) and a soluble protein, chloramphenicol acetyltransferase (CAT). The ability of CAT and the fusion polypeptides to bind to membranes was examined by in vitro translation in the presence of microsomal membrane. While CAT was found in the soluble fraction, both 2C/CAT fusion constructs (1-72/CAT and 1-88/CAT) were membrane associated, suggesting that the N-terminal region of 2C was sufficient to impart membrane binding. To confirm these results in vivo, CAT, 1-72/CAT, and 1-88/CAT were expressed in HeLa cells and their localization was examined using indirect immunofluorescence. Results presented here demonstrate that, while CAT is expressed throughout the cell, 1-72/CAT and 1-88/CAT constructs are capable of localizing to the endoplasmic reticulum (ER) area in transfected cells in the absence of other poliovirus proteins. These results suggest that the first 72 amino acids of 2C contain a membrane binding domain that is capable of targeting soluble proteins to the ER region of the cell.

Binding Sites↗
PubMed1998

Reproductive disorders associated with pelvic pain.

Pelvic pain is common in adolescents and can result from a number of physiological and pathological etiologies, both gynecologic and nongynecologic in origin. The evaluation, diagnosis, and management of these conditions involve both medical and surgical approaches. In this review, the authors present a comprehensive approach to the care of adolescents with pelvic pain associated with dysmenorrhea, endometriosis, and obstruction of the genital tract.

Adolescent↗
PubMed1998

Renal transplantation in a patient with methylmalonic acidaemia.

Renal insufficiency is frequently reported in mutase-deficient methylmalonic acidaemia. We present a case report of a patient with mut- methylmalonic acidaemia who developed chronic tubulointerstitial nephropathy during adolescence. At 24 years of age, she developed end-stage renal failure and underwent renal transplantation. Both plasma and urine methylmalonic acid levels decreased significantly with improved renal function following transplantation. Complications included cyclosporin toxicity and development of diabetes. Renal, metabolic, and clinical status remained improved at 3 years after the kidney transplant.

Adult↗
PubMed1998

Children's understanding of extended identity.

As adults, we appreciate that judgments of us may reflect our associations with other people. This article examines the development of "extended identity" (G.R. Semin & K. Papadopoulou, 1989) in children between 5 and 11 years. In Experiment 1, children were presented with hypothetical scenarios in which they imagined a close associate had committed a rule violation in a highly public context. Only the older children judged that they would be evaluated negatively through their association with the wrongdoer and that they themselves would feel embarrassment. Given the late appearance of extended identity, Experiment 2 addressed contexts in which the child was responsible for a younger child, so that accountability for the other was explicitly demanded. In such contexts, an appreciation of extended identity appeared earlier than it did in Experiment 1, in which no responsibility for the other was involved.

Child↗
PubMed1998

Studies of the interaction between Rad52 protein and the yeast single-stranded DNA binding protein RPA.

The RFA1 gene encodes the large subunit of the yeast trimeric single-stranded DNA binding protein replication protein A (RPA), which is known to play a critical role in DNA replication. A Saccharomyces cerevisiae strain carrying the rfa1-44 allele displays a number of impaired recombination and repair phenotypes, all of which are suppressible by overexpression of RAD52. We demonstrate that a rad52 mutation is epistatic to the rfa1-44 mutation, placing RFA1 and RAD52 in the same genetic pathway. Furthermore, two-hybrid analysis indicates the existence of interactions between Rad52 and all three subunits of RPA. The nature of this Rad52-RPA interaction was further explored by using two different mutant alleles of rad52. Both mutations lie in the amino terminus of Rad52, a region previously defined as being responsible for its DNA binding ability (U. H. Mortenson, C. Beudixen, I. Sunjeuaric, and R. Rothstein, Proc. Natl. Acad. Sci. USA 93:10729-10734, 1996). The yeast two-hybrid system was used to monitor the protein-protein interactions of the mutant Rad52 proteins. Both of the mutant proteins are capable of self-interaction but are unable to interact with Rad51. The mutant proteins also lack the ability to interact with the large subunit of RPA, Rfa1. Interestingly, they retain their ability to interact with the medium-sized subunit, Rfa2. Given the location of the mutations in the DNA binding domain of Rad52, a model incorporating the role of DNA in the protein-protein interactions involved in the repair of DNA double-strand breaks is presented.

Alleles↗
PubMed1998

Hemorheological parameters for biocompatibility evaluation.

Biomaterials have been extensively used for various clinical applications. Since blood is very sensitive to the presence of any foreign substances, testing for hemocompatibility is a major part of biocompatibility evaluation. At present, blood viscosity parameters are being used as screening tests for biomaterial compatibility. Successful use of these parameters will help eliminate many incompatible materials from being subjected to extensive testing. In this study, we evaluated the blood viscosity parameters (n = 10)--whole blood viscosity, plasma viscosity, red cell rigidity, hematocrit, and biochemical parameters (total proteins and albumin). A significant increase in hemorheological parameters after incubation with material was found to be an indicator of incompatibility.

Adult↗
PubMed1998

Hemorheological changes in blood transfusion-treated beta thalassemia major patients.

Beta thalassemia major is an inherited impairment of haemoglobin structure, in which there is partial or complete failure to synthesize a specific type of globin chain. The study was undertaken to assess the hemorheological changes in beta thalassemic major patients. We studied hemorheological parameters in thalassemic patients (n = 37) immediately after blood transfusion. The parameters studied were whole blood viscosity (WBV), plasma viscosity (PV), red cell rigidity (RCR) and hematocrit (Hct). Blood samples from age-and sex-matched normal controls were also analysed for comparison. Statistical analysis was done using Student's t-test and p values were recorded. The results showed a significant decrease in level of WBV and Hct in patients when compared to normal controls. However, the red cell rigidity was higher when compared to normal controls. Increase in RCR should show an increase in WBV. But in our study cases there was a significant decrease in WBV which was probably due to the significant decrease in level of hematocrit.

Blood Transfusion↗
PubMed1998

Hemorheological changes in nephrotic syndrome.

Hemorheological parameters of childhood nephrotic syndrome cases, in relapse and remission (n = 60 in each group), were studied and their results were compared with those of an equal number of age and sex matched normal children free from any renal disease. During relapse, it was noticed that the viscosity parameters, viz. plasma viscosity, red cell rigidity and whole blood viscosity, were deranged when compared to the values obtained in the remission period. These observations were statistically analyzed using t-test with the level of significance p = 0.05. It was also noted that serum/plasma biochemistry played an important role with regards to the fluidity of blood. During relapse period, fibrinogen level was significantly high, which persisted at a high level even during remission when compared to normal controls. The high cholesterol and triglyceride levels during relapse were responsible for a high plasma viscosity, increased red cell rigidity and thereby contributed directly to a marked increase in whole blood viscosity. Total protein and albumin levels were significantly decreased during relapse when compared to remission period. Hence, hemorheological parameters can be used for early detection of cases prone to relapse and could be of prognostic significance.

Blood Viscosity↗
PubMed1998

The diagnostic relevance of red cell rigidity.

Red cell rigidity is an important hemorheological parameter determining the passage of erythrocyte through narrow capillaries and the reduction of blood viscosity under high shear rates. The changes in red cell rigidity in various diseases of altered blood flow - hypertension (HT), diabetes mellitus (DM), myocardial infarction (MI) and cerebrovascular accidents (CVA), using equal sample sizes of 25 each, have been analysed in this paper. One of the essential elements of red cell rigidity is the structural and functional properties of erythrocyte membrane which, in turn, is determined by the membrane biochemistry. Since cholesterol-rich erythrocytes have increased rigidity, the serum cholesterol and triglycerides levels have been monitored in order to detect the extent to which they affect red cell rigidity. No significant change in red cell rigidity have been found in CVA. RBC rigidity is found to be significantly increased in the other diseases. Significant increase in triglyceride levels have been found in all the diseases studied. Cholesterol levels were significantly increased in all diseases except CVA. Hence, increased cholesterol levels have been found to consistently cause a simultaneous increase in RBC rigidity. Triglycerides levels, on the other hand, have not shown a consistent change with changes in RBC rigidity, but have been shown to be a more sensitive marker for early detection of diseased status.

Blood Viscosity↗
PubMed1997

Defects in auxiliary redox proteins lead to functional methionine synthase deficiency.

Methionine synthase catalyzes a methyl transfer reaction from methyltetrahydrofolate to homocysteine to form methionine and tetrahydrofolate and is dependent on methylcobalamin, a derivative of vitamin B12, for activity. Due to the lability of the intermediate, cob(I)alamin, the activity of methionine synthase is additionally dependent on a redox activation system. In bacteria, two flavoproteins, NADPH-flavodoxin reductase and flavodoxin, shuttle electrons from NADPH to methionine synthase. Their mammalian counterparts are unknown, and a putative intrinsic thiol oxidase activity of the mammalian methionine synthase has been proposed to be involved. We demonstrate that the mammalian methionine synthase can be activated in an NADPH-dependent reaction and requires a minimum of two redox proteins. This model is consistent with our results from biochemical complementation studies between cblG and cblE cell lines and mutation detection analysis in cblG cell lines. These demonstrate that the cblG cell line has defects affecting methionine synthase directly, whereas the cblE cell line has defects in the redox proteins. We have also identified a P1173L mutation in the activation domain of methionine synthase in the cblG cell line WG1505.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1997

Biosynthesis and maturation of the malaria aspartic hemoglobinases plasmepsins I and II.

During the intraerythrocytic stage of infection, the malaria parasite Plasmodium falciparum digests most of the host cell hemoglobin. Hemoglobin degradation occurs in the acidic digestive vacuole and is essential for the survival of the parasite. Two aspartic proteases, plasmepsins I and II, have been isolated from the vacuole and shown to make the initial cleavages in the hemoglobin molecule. We have studied the biosynthesis of these two enzymes. Plasmepsin I is synthesized and processed to the mature form soon after the parasite invades the red blood cell, while plasmepsin II synthesis is delayed until later in development. Otherwise, biosynthesis of the plasmepsins is identical. The proplasmepsins are type II integral membrane proteins that are transported through the secretory pathway before cleavage to the soluble form. They are not glycosylated in vivo, despite the presence of several potential glycosylation sites. Proplasmepsin maturation appears to require acidic conditions and is reversibly inhibited by the tripeptide aldehydes N-acetyl-L-leucyl-L-leucyl-norleucinal and N-acetyl-L-leucyl-L-leucyl-methional. These compounds are known to inhibit cysteine proteases and the chymotryptic activity of proteasomes but not aspartic proteases. However, proplasmepsin processing is not blocked by other cysteine protease inhibitors, nor by the proteasome inhibitor lactacystin. Processing is also not blocked by aspartic protease inhibitors. This inhibitor profile suggests that unlike most other aspartic proteases, proplasmepsin maturation may not be autocatalytic in vivo, but instead could require the action of an unusual processing enzyme. Compounds that block processing are expected to be potent antimalarials.

Amino Acid Sequence↗
PubMed1997

Evidence that cobalt-carbon bond homolysis is coupled to hydrogen atom abstraction from substrate in methylmalonyl-CoA mutase.

Methylmalonyl-CoA mutase catalyzes the isomerization of methylmalonyl-CoA to succinyl-CoA. It is dependent on the cofactor, coenzyme B12 or adenosylcobalamin, for activity. The first step in this, and other coenzyme B12-dependent reactions, is postulated to be homolysis of the Co-C bond of the cofactor. Methylmalonyl-CoA mutase accelerates the rate of Co-C bond homolysis by a factor of approximately 10(12). The strategy employed by the enzyme for the remarkable labilization of this bond is not known. Using UV-visible stopped-flow spectrophotometry, we demonstrate that the Co-C homolysis rate in the presence of protiated substrate has a rate constant of >600 s(-1) at 25 degrees C. In the presence of [CD3]methylmalonyl-CoA, this rate decreases to 28 +/- 2 s(-1). These results suggest that Co-C bond homolysis is coupled to hydrogen atom abstraction from the substrate and that the intrinsic binding energy of substrate may be a significant contributor to catalysis by methylmalonyl-CoA mutase.

Acyl Coenzyme A↗
PubMed1997

Magnetic field effects on coenzyme B12-dependent enzymes: validation of ethanolamine ammonia lyase results and extension to human methylmalonyl CoA mutase.

Enzymes with radical-pair intermediates have been considered as a likely target for purported magnetic field effects in humans. The bacterial enzyme ethanolamine ammonia lyase and the human enzyme methylmalonyl-CoA mutase catalyze coenzyme B12-dependent rearrangement reactions. A common step in the mechanism of these two enzymes is postulated to be homolysis of the cobalt-carbon bond of the cofactor to generate a spin-correlated radical pair consisting of the 5'-deoxyadenosyl radical and cob(II)alamin [Ado. Cbl(II)]. Thus, the reactions catalyzed by these enzymes are expected to be sensitive to an applied magnetic field according to the same principles that control radical pair chemical reactions. The magnetic field effect on ethanolamine ammonia lyase reported previously has been corroborated independently in one of the authors' laboratory. However, neither the human nor the bacterial mutase from Propionibacterium shermanii exhibits a magnetic field effect that could be greater than about 15%, considering the error limit imposed by the uncertainty of the coupled assay. Our studies suggest that putative magnetic field effects on physiological processes are not likely to be mediated by methylmalonyl-CoA mutase.

Cobamides↗
PubMed1997

The Yin-Yang of cobalamin biochemistry.

The cobalamins are B12 cofactors with a reactive cobalt-carbon bond at their core and support the activity of two mammalian enzymes that are both medically important. The reactive organometallic bond of the cofactor can be cleaved either homolytically or heterolytically, but what determines how the enzymes control the fate of this bond?

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1997

Sequence analysis of the coding region of human methionine synthase: relevance to hyperhomocysteinaemia in neural-tube defects and vascular disease.

Elevated homocysteine (Hcy) levels are observed in two apparently unrelated diseases: neural-tube defects (NTD) and premature vascular disease. Defective human methionine synthase (MS) could result in elevated Hcy levels. We sequenced the coding region of MS in 8 hyperhomocysteinaemic patients (4 NTD patients and 4 patients with pregnancies complicated by spiral arterial disease, SAD). We identified only one mutation resulting in an amino acid substitution: an A-->G transition at bp 2756, converting an aspartic acid (D919) into a glycine (G). We screened genomic DNA for the presence of this mutation in 56 NTD patients, 69 mothers of children with NTD, 108 SAD patients and 364 controls. There was no increased prevalence of the GG and AG genotypes in NTD patients, their mothers or SAD patients. The D919G mutation does not seem to be a risk factor for NTD or vascular disease. We then examined the mean Hcy levels for each MS genotype. There was no correlation between GG- or AG-genotype and Hcy levels. The D919G mutation is thus a fairly prevalent, and probably benign polymorphism. This study, though limited, provides no evidence for a major involvement of MS in the aetiology of homocysteine-related diseases such as NTD or vascular disease.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗