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D Bhatnagar

Publications and source records attributed to D Bhatnagar.

172 records · Page 10Linked to original sources
PubMedDate not supplied

Comparison of the enzymatic composition of cell-free extracts of non-aflatoxigenic Aspergillus parasiticus with respect to late stages of aflatoxin biosynthesis.

Cell-free extracts of fungal mycelia of two non-aflatoxigenic isolates of Aspergillus parasiticus (SRRC 163 and SRRC 2043) were examined for enzyme activities involved in the latter stages of aflatoxin biosynthesis. Post-microsomal fractions (105 Kxg supernatant) of both SRRC 163 (ATTC 56774) and SRRC 2043 were able to convert sterigmatocystin (ST) to O-methylsterigmatocystin (OMST); whereas the microsomal (105 Kxg pellet) preparation of only SRRC 163 was able to convert OMST to aflatoxin B1 (AFB1). A mixture of the microsomal fraction of SRRC 163 and post-microsomal fraction of SRRC 2043 converted ST to AFB1. Electrophoretic protein separations of the microsomal fractions of the two A. parasiticus isolates on non-denaturing or denaturing polyacrylamide gel electrophoresis (PAGE) provided equivalent protein profiles.

Aflatoxins↗
PubMedDate not supplied

Placebo-controlled trial of the effects of guar gum and metformin on fasting blood glucose and serum lipids in obese, type 2 diabetic patients.

Nineteen obese patients with Type 2 diabetes mellitus were treated for periods of 3 months with placebo, guar gum (5 g three times daily) and metformin (500 mg three times daily) in a randomized double-blind, double-placebo, cross-over study. Both active agents decreased fasting blood glucose from 11.4 +/- 3.7 mmol l-1 (mean +/- SD) to 8.6 +/- 2.8 mmol l-1 on metformin (p less than 0.001) and to 9.5 +/- 3.9 mmol l-1 on guar gum (p less than 0.01). Metformin significantly reduced the very low density lipoprotein (VLDL) cholesterol concentration from 0.62 (+0.73, -0.34) mmol l-1 (geometric mean (+SD, -SD)) to 0.43 (+0.58, -0.25) mmol l-1, (p less than 0.02), but unless hyperlipidaemia was present there were no changes in other serum lipid or lipoprotein levels. In patients with serum cholesterol greater than 6.5 mmol l-1 decreases in serum triglycerides from 3.29 (+3.27, -1.64) to 2.46 (+2.55, -1.25) mmol l-1 (p less than 0.02) occurred with metformin. In these patients guar gum produced a reduction in serum cholesterol (from 7.70 +/- 0.90 to 6.41 +/- 1.11 mmol l-1, p less than 0.01) due to an effect on low density lipoproteins. These differential effects may be important in planning therapy when hyperlipidaemia accompanies Type 2 diabetes.

Apolipoproteins B↗
PubMedDate not supplied

Double-blind placebo-controlled study of the effects of bezafibrate on blood lipids, lipoproteins, and fibrinogen in hyperlipidaemic type 1 diabetes mellitus.

The effects of bezafibrate 400 mg day-1 or placebo administered for 3 months, were compared in 36 patients with stable Type 1 diabetes and hypercholesterolaemia and/or hypertriglyceridaemia. Baseline characteristics of the 17 bezafibrate- and 19 placebo-treated patients were comparable in most respects with the exception of concentrations of fasting serum triglycerides and blood glucose which were lower (NS) and plasma fibrinogen which were higher (p less than 0.05), in those later treated with bezafibrate. Serum cholesterol concentrations decreased after 3 months bezafibrate treatment (from 7.1(0.2) (SE) to 6.3 (0.3) mmol l-1, p less than 0.05), predominantly due to a reduction in low density lipoprotein (LDL) cholesterol (from 4.8(0.3) to 4.2(0.3) mmol l-1, p less than 0.05). Over the same period bezafibrate reduced serum triglycerides from 1.78 (95% Cl 1.23-2.57) to 1.26(1.02-2.09) mmol l-1 (p less than 0.05), and plasma fibrinogen from 4.1(0.2) to 2.9(0.2) g l-1, p less than 0.001. Serum apolipoprotein B and apolipoprotein (a) showed no statistically significant changes. Overall there was no change in high density lipoprotein (HDL) cholesterol. However, in patients who were initially hypertriglyceridaemic there was significant increase in the cholesterol content of HDL and the HDL2-cholesterol subfraction (both p less than 0.05). After 3 months treatment with bezafibrate, fasting blood glucose levels were reduced from 8.5(1.1) to 6.4(0.7) mmol l-1, p less than 0.05, without any change in glycosylated haemoglobin (9.2(0.4) to 9.1(0.5)%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Serum lipoprotein(a) in patients heterozygous for familial hypercholesterolemia, their relatives, and unrelated control populations.

Serum lipoprotein(a) (Lp[a]) levels were significantly higher in 89 patients with heterozygous familial hypercholesterolemia (FH) (geometric mean, 22.7 mg/dl) than in 109 normocholesterolemic controls (10.0 mg/dl, p less than 0.05) and 40 controls (9.1 mg/dl, p less than 0.05) with similarly elevated low density lipoprotein cholesterol levels due to other primary hypercholesterolemias. To provide further evidence that the increased serum Lp(a) concentration was due to inheritance of the FH gene, 24 unaffected first-degree relatives were compared with their FH probands. Serum Lp(a) in affected individuals was significantly greater than in unaffected relatives (geometric means, 26.5 versus 13.7 mg/dl, respectively; p less than 0.05). Family membership exerted an effect on serum Lp(a) concentrations, indicating that other genetic influences were also operating, as is known to be the case in general populations. Serum Lp(a) in 30 of the FH patients, who had coronary heart disease, was not significantly different from 30 age- and sex-matched controls with FH but with coronary heart disease (geometric means, 23.6 versus 24.7 mg/dl, respectively). FH is associated with an increase in serum Lp(a). Elevated serum Lp(a) concentrations should probably now be regarded as a component of the clinical syndrome of FH. However, within our FH population Lp(a) did not distinguish those with clinically overt coronary heart disease from those without the disease.

Adult↗
PubMedDate not supplied

Relative clinical usefulness of glycosylated serum albumin and fructosamine during short-term changes in glycemic control in IDDM.

Serial changes in glycosylated blood proteins and direct measures of glycemia were studied in 100 subjects with insulin-dependent diabetes mellitus (IDDM) over a 6-wk period while attempts were made to improve glycemic control. All measures of glycemic control improved significantly (P less than .001). Mean +/- SE glycosylated hemoglobin (HbA1) fell from 9.1 +/- 0.2 to 8.0 +/- 0.1%, glycosylated serum albumin (GSA) from 9.8 +/- 0.4 to 7.3 +/- 0.3%, and fructosamine from 3.92 +/- 0.08 to 3.42 +/- 0.07 mM. Fasting blood glucose levels fell from 11.1 +/- 0.6 to 8.1 +/- 0.7 mM mean blood glucose levels from 12.5 +/- 0.3 to 8.8 +/- 0.03 mM, and the M value from 118 +/- 7 to 40 +/- 3 U. Mean percentage changes in direct measures of glycemia (32-66%) and GSA (29%) were greater than for fructosamine (11%) or HbA, (12%) levels (P less than .001). Furthermore, the correlation between the change in GSA and changes in direct measures of glycemia over the initial 2-wk period was significantly different from the corresponding correlations between direct measures of glycemia and fructosamine over this period (P less than .05-.01). Changes in GSA also correlated more closely than HbA1 or fructosamine did with direct measures of glycemia after 4 and 6 wk. The Spearman rank-correlation coefficient (rs) of absolute changes in GSA, fructosamine, and HbA1 after 2-6 wk ranged from 0.27 to 0.57, confirming that the three measures responded differently to changing glycemic control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Coronary stenting in diabetics: six months clinical and angiographic outcome.

The aim of this study was to assess the clinical and angiographic outcome of coronary stenting in diabetics as compared to non-diabetic patients. A total of 114 patients undergoing coronary angioplasty with stenting were prospectively evaluated. There were 30 diabetic (group A) and 84 non-diabetic (group B) patients. There were no significant differences in both the groups with respect to other risk factors and clinical characteristics. Both the groups were also comparable in terms of lesion morphology and stent types. The clinical endpoints were recurrent angina, reinfarction, cardiac death and need for target vessel revascularisation. The angiographic endpoint was angiographic restenosis at six months. There were 70 males and 44 female patients with a mean age of 55 +/- 12 years. Angiographic follow-up was completed in 85 (74.7%) patients which included 25 (83.3%) patients in group A and 60 (71.4%) in group B. Among clinical events at 30 days, the incidence of recurrent angina was 10.0 percent versus 8.3 percent (group A and B; p = NS) and incidence of reinfarction was 6.6 percent versus 5.9 percent (group A and B; p = NS), respectively. At six months, recurrent angina was seen in 16.6 percent versus 15.4 percent (p = NS) and reinfarction was seen in 10.0 percent versus 8.3 percent (p = NS) in group A and B, respectively. There were no deaths in either group. The angiographic restenosis rate was significantly higher in diabetics compared to non-diabetics (40.0% vs 23.3%; p = 0.02). The need for target vessel revascularisation was higher in diabetics as compared to non-diabetics (16.0% vs 6.6%; p = 0.03). We conclude that in spite of using coronary stents, the diabetics have higher restenosis rate and higher target vessel revascularisation rate than the non-diabetic patients.

Aged↗
PubMedDate not supplied

Study of events leading cellular senescence to human mammary epithelial cancer cells in vitro.

Role of various growth regulatory factors in inducing senescence in cultured HMEC cells have been investigated in ten cases of breast cancer. The histological grade of tumour cells is found to play significant role in controlling the proliferation and phenotypic charateristics of cultured HMEC cells during primary culture and also number of subsequent passages resulting in complete cellular senescence in them. Effects of conditioned media (CM) collected from primary and senescent cultures of these HMEC cells had also been studied on proliferation of their own HMEC cells used as target cells, to evaluate the role of various autocrine growth factors produced by them. Significant increase in proliferation of target cells was noticed on their exposure to CM from senescent cultures, while cessation of their proliferation was found on their exposure to CM from senscent cultures, suggesting that HMEC cells produce growth promoting factors during primary culture and growth inhibitory factors on subsequent passages, responsible for inducing features of cellular senescence in them. The role of epidermal growth factors (EGF) and transforming growth factors (TGF) alpha and beta as autocrine factors in inducing senescence of cultured HMEC cells were also investigated. Deletion of EGF from growth media initially caused decreased proliferation to target HMEC cells, followed by improvement in their proliferation. Supplementation of growth media by TGF-alpha induced significant increase in proliferation of target cells. Addition of epidermal growth factors receptor (EGFR) antibody to cells exposed to media devoid of EGF and media supplemented with TGF-alpha showed marked suppression of proliferation of target cells. The morphologic and phenotypic characteristics of target HMEC cells exposed to TGF-alpha were also found similar to those HMEC cells grown during primary culture, suggesting autocrine production of EGF and TGF-alpha by cultured HMEC cells during primary culture. Supplementation of TGF-beta to growth media induced marked suppression of proliferation to target cells along with morphologic and phenotypic features of terminal differntiation or senescence. Exposure of senescent cells to media supplemented with EGF and TGF-alpha could not induce their proliferation. This suggest that HMEC cells on subsequent passages undergo some genetic and phenotypic alterations resulting in production of growth inhibitory factor like TGF-beta which induces cessation of their proliferation alone with features of senescence.

Breast Neoplasms↗