AimsIndia is the diabetes capital with home to 69.1 million people with DM, the second highest number of cases after China. Recent epidemiological evidence indicates a rising DM epidemic across all classes, both affluent and the poor in India. This article reports on the prevalence of diabetes and pre-diabetes in the North Indian state of Punjab as part of a large household NCD Risk Factor Survey.MethodsA household NCD STEPS survey was done in the state of Punjab, India in a multistage stratified sample of 5127 individuals. All the subjects were administered the WHO STEPS questionnaire, anthropometric and blood pressure measurements. Every alternate respondent in the sample (n = 2499) was assayed for blood parameters.ResultsOverall prevalence of DM among the study participants was found out to be 8.3% (95% CI 7.3–9.4%) whereas prevalence of prediabetes was 6.3% (5.4–7.3%). Age group (45–69 years), marital status, hypertension, obesity and family history of DM were found to be the risk factors significantly associated with DM. Out of all persons with DM, only 18% were known case of DM or on treatment, among whom only about one-third had controlled blood glucose status.ConclusionsThe study reported high prevalence of diabetes, especially of undiagnosed cases amongst the adult population, most of whom have uncontrolled blood sugar levels. This indicates the need for systematic screening and awareness program to identify the undiagnosed cases in the community and offer early treatment and regular follow up.

The present study was intended to appraise the oxidant and antioxidant status in preeclampsia women. Seventy-seven preeclampsia women with severe variety having average B.P. of 170/140 mmHg with proteinuria; 47 preeclampsia women with mild variety having average B.P. of 138/100 mmHg were compared to 56 healthy pregnant women and 15 non-pregnant women for oxidant and antioxidant status. Lipid peroxidation was assessed by measuring malondialdehyde (MDA), and antioxidant status was assessed by measuring antioxidant enzymes N.B.; superoxide dismutase (SOD), glutathione peroxidase, catalase and vitamins viz; A, E, C and reduced glutathione (GSH). Lipid peroxidation was significantly higher in severe preeclampsia women. Antioxidant status was also compromised as is evident from decreased GSH levels and increased SOD activities not only in severe preeclampsia but also in normal pregnancy and mild preeclampsia women compared to non-pregnant women. Decreased antioxidant enzyme activity viz catalase and glutathione peroxidase was observed in pregnancy as compared to non-pregnant women. The levels of vitamin E which act as an antioxidant were significantly elevated in preeclampsia compared to that of normal pregnancy. These findings conclude that initially the oxidative stress due to pregnancy-induced hypertension is critically combated by the intricate defensive mechanism of natural antioxidant system of the body. It appears that this imbalance between oxidant and antioxidant is the effect of disease and not the causative factor.

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The present study was designed to evaluate the antimicrobial activity of six Indian spice extracts, namely clove, cinnamon, mustard, garlic, ginger and mint. All of these have been traditionally used in folk medicine, and are still used in the alternative system of health care. The antimicrobial activity of these commonly used Indian spices was tested against three potent foodborne pathogens, namely Escherichia coli,Staphylococcus aureus and Bacillus cereus, which are responsible for many health-related problems. These were tested using paper disc diffusion method, cup method and dilution method (qualitative). The results showed that the extracts of clove, cinnamon and mustard had good inhibitory action at 1% concentration, while garlic showed medium activity. At 3% concentration, complete bactericidal effect was achieved. Ginger and mint showed negligible antibacterial activity against these pathogens at the same concentration.

Animal models of copper toxicosis rarely exhibit neurological impairments and increased brain copper accumulation impeding the development of novel therapeutic approaches to treat neurodegenerative diseases having high brain Cu content. The aim of this study was to investigate the effects of intraperitoneally injected copper lactate (0.15 mg Cu/100 g body weight) daily for 90 days on copper and zinc levels in the liver and hippocampus, on biochemical parameters, and on neurobehavioral functions (by Morris water maze) of male Wistar rats. Copper-administered animals exhibited significantly decreased serum acetylcholinesterase (AChE) activity and impaired neuromuscular coordination and spatial memory compared to control rats. Copper-intoxicated rats showed significant increase in liver and hippocampus copper content (99.1 and 73 % increase, respectively), 40.7 % reduction in hepatic zinc content, and interestingly, 77.1 % increase in hippocampus zinc content with concomitant increase in copper and zinc levels in serum and urine compared to control rats. Massive grade 4 copper depositions and grade 1 copper-associated protein in hepatocytes of copper-intoxicated rats were substantiated by rhodanine and orcein stains, respectively. Copper-intoxicated rats demonstrated swelling and increase in the number of astrocytes and copper deposition in the choroid plexus, with degenerated neurons showing pyknotic nuclei and dense eosinophilic cytoplasm. In conclusion, the present study shows the first evidence in vivo that chronic copper toxicity causes impaired spatial memory and neuromuscular coordination, swelling of astrocytes, decreased serum AChE activity, copper deposition in the choroid plexus, neuronal degeneration, and augmented levels of copper and zinc in the hippocampus of male Wistar rats.

Genetic factors are implicated in pathogenesis of neonatal hyperbilirubinemia. In this nested case-control study, we determined 1) frequency of thymine-adenine (TA) n promoter polymorphism and Gly71Arg mutation in uridine diphosphoglucuronateglucuronosyltransferase 1A1 (UGT1A1) gene in neonates Ն35-wk gestation presenting with bilirubin levels Ն18 mg/dL and controls, 2) interaction among (TA) n promoter polymorphism, glucose-6-phosphate dehydrogenase (G6PD) gene mutations, and peak bilirubin. The number of TA repeats was assessed by PCR-single-strand conformation polymorphism (SSCP) analysis and Gly71Arg mutation by PCR-RFLP. Fifty samples of both mutations were verified with DNA sequencing. One hundred twenty-seven neonates were enrolled (77 hyperbilirubinemics, 50 controls). The incidence of (TA) n polymorphism was higher in babies with hyperbilirubinemia [89.6% vs. 50%, OR 8.63 (95% CI, 3.2-24.1)]. Gly71Arg mutation was not found either in hyperbilirubinemics or controls. A novel polymorphism (Ala72Pro) at codon position 72 of exon 1 was detected in all 50 samples (21 hyperbilirubinemics, 29 controls), which were sequenced. Presence of variant (TA) n promoter (adjusted OR, 10.6; 95% CI, 3.3-34.2), G6PD deficiency (adjusted OR, 20.6; 95% CI, 3.6 -117.3), and history of jaundice in sibling requiring phototherapy (adjusted OR, 12.6; 95% CI, 1.1-141.6) were independent risk factors for bilirubin levels Ն18 mg/dL. (Pediatr Res 65: 675-680, 2009) T he incidence and severity of neonatal hyperbilirubinemia is significantly higher in Asians, more so in North Indians, than in Caucasians (1,2). Despite all standard investigations, no cause is identified in 48 -58% of these cases (2,3). Genetic factors have been implicated in such situations; however, their contribution in Indian population has not been reported. Genetic variants involving red blood cell enzyme glucose-6-phosphate dehydrogenase (EC 1.1.1.49; G6PD) and bilirubin conjugating enzyme uridine diphosphoglucuronate-glucuronosyltransferase 1A1 (EC 2.4.1.17; UGT1A1) have been commonly associated with neonatal hyperbilirubinemia (4,5). The usual polymorphism described in Caucasians is additional thymine-adenine (TA) insertions in the normal sequence A(TA) 6 TAA of the TATAA box promoter of the UGT1A1 gene (6). However, in East Asians, missence mutations in the coding area of the UGT1A1 gene, especially G3 A transition at nucleotide position 211 of exon 1 (Gly71Arg) are the most common (7). The types, prevalence, and importance of various mutations of UGT1A1 gene vary across different regions of world.Hence, this study was conducted with the primary objective of determining the frequency of (TA) n promoter polymorphism and Gly71Arg mutation in the UGT1A1 gene in North Indian neonates Ն35-wk gestation presenting with serum total bilirubin (STB) Ն18 mg/dL. The secondary objective was to study the interaction among the presence of UGT1A1 gene polymorphisms, G6PD gene mutations, and peak STB levels. PATIENTS AND METHODSThis was a hospital-based nested case-co...

Copper is an essential micronutrient for physiological cell functioning and central nervous system (CNS) development. Indeed, it is a cofactor of many proteins and enzymes in a number of molecular pathways, including energy generation, oxygen transportation, hematopoiesis, cellular growth and metabolism, and signal transduction. This is because it serves as a catalyst of reduction-oxidation (redox) reactions in these processes. When copper is kept under control, bound to special proteins, it yields key properties. However, when it spirals out of control, it is exchanged among small compounds (it is loosely bound to them), and its redox activity makes it dangerous for cell viability, promoting oxidative stress. Copper homeostasis in the CNS is securely synchronized, and perturbations in brain copper levels are known to underlie the pathoetiology of wide spectrum of common neurodegenerative disorders, including Alzheimer's disease. The main objective of this review is to provide some of the most relevant evidence gleaned from recent studies conducted on animal models and humans, and to discuss the evidence as it pertains to a new concept: Aberrant copper metabolism, which appears to have a genetic basis, is a modifiable risk factor accelerating Alzheimer's disease and initiation/progression of cognitive deficits in a percentage of susceptible persons.

Kaler P, Prasad R. Molecular cloning and functional characterization of novel zinc transporter rZip10 (Slc39a10) involved in zinc uptake across rat renal brush-border membrane. Am J Physiol Renal Physiol 292: F217-F229, 2007. First published June 27, 2006 doi:10.1152/ajprenal.00014.2006.-Previously, in our laboratory a 40-kDa zinc transporter protein was purified and functionally reconstituted in proteoliposomes (Kumar R, Prasad R. Biochim Biophys Acta 1419: [23][24][25][26][27][28][29][30][31][32] 1999). Furthermore, we now report the identification of Slc39a10 cDNA encoding the 40-kDa zinc transporter protein by isolating a cloned DNA complementary to zinc transporter mRNA. cDNA was constructed from immunoenriched mRNA encoding the zinc transporter. cDNA was inserted into pBR322 using poly(dC)-poly(dG) tailing. Escherichia coli DH5␣ cells were transformed, and colonies were screened for zinc transporter cDNA by insertional inactivation. Plasmid DNA was purified from the ampicillin-sensitive clones, and the cDNA was sequenced from both strands. A basic local alignment research tool (BLAST) search of cDNA revealed that it belongs to the Slc39 gene family of zinc transporters and was designated as Slc39a10. Zinc transporter protein deduced on the basis of cDNA sequence was named rZip10 and consists of 385 amino acids with 9 predicted transmembrane domains. The Slc39a10 gene was abundantly expressed in both rat and human tissues. Increased extracellular zinc concentration resulted in upregulation of Slc39a10 in LLC-PK1 cells expressing rZip10, which was downregulated at higher zinc concentrations. These cells accumulated more zinc than control cells. rZip10-mediated zinc uptake activity was time-, temperature-, and concentration-dependent and saturable which followed Michaelis-Menten kinetics with a Km of 19.2 M and Vmax of 50 pmol⅐min Ϫ1 ⅐mg protein Ϫ1