Complete excision with staged reconstruction in the treatment of earlobe keloid after ear piercing.
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Biomedical subjects
Publications and source records attributed to P Yadav.
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OBJECTIVES: A cross sectional study was conducted to find the prevalence of coronary risk factors in non-insulin dependent diabetic (NIDDM) patients and to compare and co-relate these risk factors in type II diabetics with and without electrocardiographic and/or symptomatic evidence of coronary heart disease (CHD). METHODS: One hundred sixty-seven consecutive NIDDM patients (77 males, and 90 females) attending the diabetic clinic at Dr. RML Hospital, New Delhi were studied. Only known NIDDM cases, already on treatment and without any history of ketosis or congestive heart failure were included. Coronary risk factors comprising of age, gender, duration and treatment for diabetes, smoking, physical activity, hypertension, truncal obesity, lipids, microalbuminuria (semiquantitative) and glycemic control have been particularly ascertained in all the cases. The data was analysed using 'Epi Info version 6.0'. RESULTS: The mean age of patients was 53.12 year and 8.86 year was the mean duration of diabetes. 28.6% of the diabetic men were found to be currently smoking and/or consuming alcohol, 82% were involved in sedentary physical activity and 20.4% had family history of CHD. Central obesity was observed in 46.7% of the cases; more so in females. 31.74% of cases were hypertensive; more females than males had hypertension (33.8% vs 30%). Poor glycemic control (HbA1c > = 9.5%) was seen in 16.8% of the cases. In about 52.5% of the total group hypertriglyceridemia was noted. Microalbuminuria could be found in 35.93%. CHD was diagnosed in 15.57% of cases in this study. CONCLUSIONS: The present study revealed that high levels of serum cholesterol (p = 0.000004), LDL (p = 0.00003), HbA1c (p = 0.002), microalbuminuria (p = 0.000006) and hypertension (p = 0.00006) are significant associates of CHD in NIDDM (both the sexes). Among the female NIDDM cases, in addition BMI (p = 0.01), Waist-hip ratio (WHR) (p = 0.003) and low HDL level (p = 0.008) are important correlates of CHD. Multiple logistic regression analysis was used to allow for confounding between variables. Microalbuminuria alone entered the 'best' model for CHD prediction. Other risk factors, though significant, provided inadequate models for CHD prediction.
Cadmium induced lipid peroxidation (LPO) and the activity of antioxidant enzymes after the administration of a single dose of CdCl2 (0.4 mg kg-1 body wt, i.p.) was studied in rat erythrocytes. Cd intoxication increased erythrocyte LPO along with a decrease in superoxide dismutase (SOD) up to three days of Cd treatment. The decrease in erythrocyte catalase (CAT) activity was marked within 9 h of Cd intoxication. After three days of Cd treatment, LPO decreased towards normal, along with an increase in erythrocyte SOC and CAT activity. Blood glutathione (GSH) decreased significantly within 24 h of Cd treatment, followed by an increase towards normal. Erythrocyte glutathione S-transferase (GST) activity increased up to 10 days of Cd intoxication, probably in an attempt to reduce Cd toxicity. Serum glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase (SALP) and serum bilirubin increased up to 10 days of Cd intoxication. Blood urea increased significantly up to three days, followed by a decrease towards normal. The results show that Cd induced LPO was associated with a decrease in antioxidant enzymes and GSH in erythrocytes; as these antioxidants increase in erythrocytes with recovery from Cd intoxication, the Cd induced LPO reversed towards normal. The increase in the SGPT, SALP and serum bilirubin correlated with LPO. The results suggest that Cd intoxication induces oxidative stress and alters the antioxidant system, resulting in oxidative damage to rat erythrocytes.
Monoclonal antibodies were raised to the idiotype of a gonadotropin releasing hormone (GnRH) specific antibody, one of which was found to bind specifically to GnRH receptors present on pituitary gonadotrophs, placental syncytiotrophoblasts and testicular Leydig cells. These observations were confirmed by Western and ligand blotting as well as by the ability of the antibody to induce an increase in intracellular Ca++ in a mouse gonadotroph cell-line viz., alpha T3-1.
Alloxan-induced diabetic rats were treated with insulin (i.p.) or with Capparis decidua powder as a hypoglycaemic agent mixed with diet. The effect was assessed on lipid peroxidation (LPO) and the antioxidant defense system in rat tissues. The increased levels of blood glucose in diabetes produce superoxide anions and hydroxyl radicals in the presence of transition metal ions which cause oxidative damage to cell membranes. The heart tissue showed an increased lipid peroxidation (LPO) in diabetic rats while no significant change was observed in the liver and kidney. The treatment with C. decidua lowered LPO in these tissues even more effectively than insulin-treated rats. The superoxide dismutase (SOD) activity increased in the heart and kidneys in the diabetic group of rats probably to increase dismutation of superoxide anions. However, treatment with C. decidua decreased SOD activity in the liver and kidney and was comparable to control rats. Catalase (CAT) activity was not significantly affected in any of the tissues in diabetic and insulin-treated animals, however, CAT activity markedly increased in tissues with C. decidua treatment. Total and Se-dependent glutathione peroxidase (GSH-Px) in the heart was markedly lowered in diabetic rats which recovered with insulin as well as with C. decidua treatment. The increase in GSH-Px and CAT activity with C. decidua treatment may lower H2O2 toxicity and reduce oxidative stress in diabetes. However, glutathione (GSH) content in the heart and kidney and glutathione reductase (GSH-R) activity in all the tissues studied increased in diabetic rats while treatment with insulin lowered GSH content and GSH-R activity in these tissues. The treatment with C. decidua also decreased GSH-R activity in the kidney and heart which resulted in the decrease in GSH content in these tissues. The changes such as the increase in kidney and heart SOD may be an adaptive response in order to neutralize superoxide anions. The increase in GSH content and GSH-R activity in the tissue are in response to neutralize superoxide anions and to counteract oxidative stress in diabetes. Glutathione S-transferase (GST) was not significantly affected in diabetic rat tissue, however, heart GST increased with antidiabetic treatments. The increase in glucose-6-phosphate dehydrogenase (G6PDH) in the kidney and heart of diabetic rats subsequently decreased with C. decidua treatment. The increase in G6PDH in tissues may increase NADPH generation required for GSH-R activity and GSH production. It is suggested that these changes initially counteract the oxidative stress in diabetes, however, a gradual decrease in the antioxidative process may be one of the factors which results in chronic diabetes. The data indicate that C. decidua may have potential use as an antidiabetic agent and in lowering oxidative stress in diabetes.
Cadmium (Cd)-induced oxidative damage in erythrocytes causes loss of membrane function by enhancing lipid peroxidation (LPO) and altering the erythrocyte antioxidant system. Vitamin E and/or selenium (Se) was administered to rats, prior to Cd intoxication, in order to prepare the animals to withstand oxidative assault. The treatment with Cd increased LPO in erythrocytes while animals pretreated with vitamin E and/or Se prior to Cd treatment showed decreased LPO as compared with animals given Cd alone. The erythrocyte SOD and CAT activities decreased significantly with Cd treatment. The pretreatment with vitamin E and/or Se prior to Cd administration partially reversed such changes. The erythrocytes showed a marked depletion in glutathione (GSH) content with Cd treatment. The antioxidant treatments before Cd administration helped to maintain the erythrocyte GSH content. The erythrocyte glutathione reductase (GSH-R) activity increased markedly when treatments with vitamin E and Se were applied. The GSH-R activity was not observed to decrease in animals treated with antioxidant prior to Cd intoxication, which may mean that the replenishment of erythrocyte GSH content is via GSH-R. The glutathione-S-transferase (GST) activity increased significantly with Cd intoxication; however, treatment with antioxidants prior to Cd treatment decreased erythrocyte GST activity. The results show that Cd-induced LPO decreased the antioxidant capability of the erythrocytes, causing erythrocyte membrane damage.
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Antidiabetic treatment with powdered fruit of Capparis decidua decreased alloxan induced lipid peroxidation (LPO) significantly in erythrocytes, kidney and heart. Erythrocyte superoxide dismutase (SOD) activity decreased while the kidney and heart SOD increased in diabetic animals. These alterations in SOD were counteracted by insulin as well as with powdered fruit of C. decidua. Increased catalase (CAT) activity in erythrocytes, liver, kidney and heart with C. decidua treatment indicate that the treatment may neutralize H2O2 toxicity by its increased decomposition by CAT. Result shows that treatment with C. decidua lowers alloxan induced LPO and alters SOD and CAT enzymes to reduce oxidative stress.
Cadmium may induce oxidative damage in different tissues by enhancing peroxidation of membrane lipids and altering the antioxidant system of the cells. The peroxidative damage to the cell membrane may cause injury to cellular components due to the interaction of metal ions with the cell organelles. The treatment with Cd (0.4 mg/kg body wt, ip) significantly increased lipid peroxidation (LPO) in heart within 3 h of the Cd injection, while the increase in kidney and liver followed 6 to 12 h after Cd intoxication. The antioxidant enzymes and other antioxidants provide protection to the cells against oxidative damage. The superoxide dismutase (SOD) activity increased in heart, kidney and liver within 24 h of Cd intoxication. The CAT activity increased significantly in heart 9 h after Cd injection; however, no significant change in CAT activity was observed in kidney and liver tissues. The GSH content and the activity of GR decreased in heart, kidney and liver 72 h after Cd administration, which has been suggested to be the cause for increased LPO in the tissues. The hexose monophosphate (HMP) shunt enzymes generate NADPH required for the activity of GR which may affect the GSH content in the tissues. The generalised decrease in glucose 6-phosphate dehydrogenase (G6PDH) and 6 phospho gluconate dehydrogenase (6PGDH) at 9 h followed by an increase in these enzymes in tissues 72 h after Cd intoxication suggest that the production of NADPH by the HMP shunt is required to reduce the oxidative damage. The results show that Cd induced LPO in the tissues and the condition was partially counteracted by the antioxidant system.
Effect of zinc and cadmium on lipid peroxidation and catalase activity in liver, heart, brain and testis was determined in order to characterise the interaction of zinc with cadmium. Zinc and cadmium both increased lipid peroxidation significantly in the tissues studied. In animals pretreated with zinc prior to cadmium administration, significant decrease in lipid peroxidation in liver was observed. Lipid peroxidation was not affected significantly in testis but a significant increase was observed in heart and brain tissues. Catalase activity in testis increased significantly by zinc treatment with or without cadmium administration.
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Ascogregarina culicis and Ascogregarina taiwanensis are common gregarine parasites of Aedes aegypti and Aedes albopictus mosquitoes, respectively. These mosquito species are also known to transmit dengue and Chikungunya viruses. The sporozoites of these parasites invade the midgut epithelial cells and develop intracellularly and extracellularly in the gut to complete their life cycles. The midgut is also the primary site for virus replication in the vector mosquitoes. Therefore, studies were carried out with a view to determine the possible role of these gregarines in the vertical transmission of dengue and Chikungunya viruses from larval to adult stage. Experiments were performed by exposing first instar mosquito larvae to suspensions containing parasite oocysts and viruses. Since Ascogregarina sporozoites invade the midgut of first instar larvae, the vertical transmission was determined by feeding the uninfected first instar larvae on the freshly prepared homogenates from mosquitoes, which were dually infected with viruses and the parasite oocysts. Similarly, the role of protozoan parasites in the vertical transmission of viruses was determined by exposing fresh first instar larvae to the dried pellets of homogenates prepared from the mosquitoes dually infected with viruses and the parasite oocysts. Direct vertical transmission and the vertical transmission of CHIK virus through the oocyst of the parasites were observed in the case of Ae. aegypti mosquitoes. It is suggested that As. culicis may have an important role in the maintenance of CHIK virus during the inter-epidemic period.
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