Clinical Profile and Outcome of Young Infants With Hypernatremic Dehydration Presenting to the Emergency Department.

OBJECTIVES: The aim of this study was to evaluate the clinical profile and outcome of young infants presenting to the pediatric emergency department with hypernatremic dehydration. METHODS: A prospective observational study was conducted at a tertiary care teaching hospital over a period of 18 months. All outborn sick young infants aged 2 months or younger who presented to the emergency department with symptoms and signs of possible sepsis and/or dehydration were screened, and those with hypernatremia were enrolled in the study. Those infants born at less than 37 weeks of gestation and gross congenital anomaly were excluded. Hypernatremic dehydration was defined as serum sodium levels (Se Na+)higher than 145 mEq/L. Variables used in the study were defined as per standard definitions. Acute kidney injury was defined and staged using serum creatinine as per modified neonatal Kidney Disease Improving Global Outcome guidelines. Clinical presentation, laboratory parameters, and comorbidities were compared among outcome groups (survived and died). RESULTS: Of 1124 outborn young infants who met the eligibility criteria for screening, 63 were diagnosed to have hypernatremic dehydration and 55 were enrolled. The hospital-based period prevalence of hypernatremic dehydration in young infants was 4.89%. The median age of presentation was 17 days (10-30). Male-to-female ratio was 1.1:1. Seventy-three percent were first in birth order. Feeding pattern showed 61.8%, 30.9%, and 7.3% of infants were exclusively breastfed, top fed, and mixed fed, respectively. The median serum sodium at the time of admission was 160 (153.5-167) mg/dL. Three (5.5%) infants had mild, 39 (70.9%) had moderate, and 13 (23.6%) had severe hypernatremic dehydration. There was statistically significant correlation between median platelet count with severity of hypernatremic dehydration. The mean time taken to correct serum sodium level was 3.30 ± 1.60 days. The case fatality rate was 41.8%. Those who died had statistically more severe hypernatremic dehydration, acute kidney injury, sepsis, and need for ventilation. CONCLUSIONS: Acute kidney injury stage 3, shock, and need for ventilation are associated with poor outcome in infants with hypernatremic dehydration.

A study of serum brain-derived neurotrophic factor level in individuals with obsessive compulsive disorder and their first-degree relatives as compared to the healthy population.

Background: The nosological tradition in psychiatry defines diagnostic criteria for disorders based on expert consensus than objective biological markers reflecting underlying neurobiological correlates. Endophenotypes have been researched as heritable biological markers that can be quantified and defined to represent intermediate measures of a psychiatric illness. In obsessive-compulsive disorder (OCD), various putative biomarkers such as neuropsychological, neurophysiological, neuroradiological, brain-derived neurotrophic factor (BDNF), etc., have been explored. Aim: The study aimed to compare levels of serum BDNF in individuals with OCD and their unaffected first-degree relatives (FDR) with healthy controls (HC). Methods: This cross-sectional study compared serum BDNF levels in medication-free/naive individuals with OCD (n = 30) to their FDR (n = 30) and age-sex matched HC (n = 30). Intergroup comparison was done using analysis of variance (ANOVA) and post-hoc Tukey's test. Correlation analysis was conducted to find the relationship of sociodemographic and clinical correlates to serum BDNF as well as dimensional subtypes of OCD. Results: No significant difference in BDNF levels was observed between OCD and HC (P = 0.13) but a significantly higher level was found in the FDR group compared to age-sex matched HC (P = 0.02). Conclusion: BDNF levels may have a complex interplay influencing the genetic inheritance and clinical manifestations of OCD. Further research is required before considering it a viable biomarker.

Efforts to cope with CBME in COVID-19 era to teach biochemistry in medical college.

The COVID-19 outbreak has shut down universities and prompted the teaching faculty to move to online resources. In view of upcoming of new Medical Council of India (MCI) curriculum and outbreak of COVID-19 pandemic, keeping pace with medical education became a challenge. To keep on par with learning activities of undergraduate students during this period, the teaching faculty adopted the use of online resources. E-learning tools were utilized to engage first-year undergraduate students and satisfy majority of aspects of Competency-Based Undergraduate Medical Curriculum/Education (CBMC/E) in Biochemistry.

Single-Nucleotide Polymorphism on Exon 17 of Insulin Receptor Gene Influences Insulin Resistance in PCOS: A Pilot Study on North Indian Women.

Polycystic ovarian syndrome (PCOS), a major cause of infertility, is also strongly associated with insulin resistance. Defects in insulin receptor signaling are considered as one of the major molecular pathogeneses for insulin resistance. To investigate the possible mechanism of this signaling defect at genetic level, single-nucleotide polymorphism (SNP) [His 1085 C/T] at the exon 17 of insulin receptor gene (INSR) was studied in this pilot study. Polymerase chain reaction was performed on leucocytic DNA of women diagnosed with PCOS, selected from the outpatient department of Safdarjung Hospital, New Delhi, using suitable primer to amplify a region on INSR. An equal number of age-matched healthy women were selected as controls. SNP analysis was performed with restriction enzyme length polymorphism technique using Pm II enzyme. Serum insulin level was measured by ELISA kit and HOMA-IR was calculated mathematically. A higher frequency of the CC genotype was observed in PCOS women than in controls. Also, HOMA-IR, a tool for estimating insulin resistance, was significantly high in PCOS women with the CC genotype. C1008T SNP at exon 17 of INSR is associated with insulin resistance in Indian women with PCOS. Presence of CC genotype (C1085T) could be developed as a marker for insulin resistance and metabolic complications in PCOS women.

Lipids of erythrocyte membranes of COPD patients: a quantitative and qualitative study.

Chronic obstructive pulmonary disease (COPD) is characterized by inflammation of lung parenchyma and pulmonary hypoxemia with a proven systemic component. Tobacco smoke is the most important risk factor and plasma membrane plays a major role in the disease pathology and progression. The properties of biological membranes are a function of their lipid composition. Any change in its composition may lead to the pathophysiology. In COPD research, erythrocytes are emerging as a new therapeutic venture, as their shape and properties change in the disease. Therefore we studied the lipid composition of the erythrocyte membranes of COPD patients. The study included 30 patients having COPD, 10 healthy smokers and 10 non-smokers. Erythrocytes were separated from peripheral blood and their membranes prepared, followed by estimation of proteins, cholesterol and phospholipids. Individual phospholipids were identified and separated by TLC and fatty acid composition determined by gas chromatography. The data were analyzed statistically and P < 0.05 was considered significant. Our results demonstrate that in very severe COPD, proteins decrease, whereas phospholipids and cholesterol contents increase significantly, which showed a consistent negative correlation with FEV1%. The fatty acid analysis showed preponderance towards saturated fatty acids mainly arachidic and behenic acid, suggesting a decrease in membrane fluidity or a closer packing of lipid rafts. We are the first to report about preponderance of saturated fatty acids in plasma membrane of erythrocytes of COPD patients which may decrease the membrane fluidity and possibly impair the functions of the plasma membrane in the disease.

Normalization of deranged signal transduction in lymphocytes of COPD patients by the novel calcium channel blocker H-DHPM.

Investigations on the role of intracellular Ca(2+) ion concentration in the mechanism of development of COPD in smokers and non-smokers were carried out. The intracellular Ca(2+) levels were found to be increased in human lymphocytes in patients with COPD as compared to non-smokers and smokers without COPD. The investigations reveal an association in altered intracellular Ca(2+) regulation in lymphocytes and severity of COPD, by means of significant activation of Protein kinase C and inducible nitric oxide synthase (iNOS). The effect of a novel calcium channel blocker ethyl 4-(4'-heptanoyloxyphenyl)-6-methyl-3,4-dihydropyrimidin-2-one-5-carboxylate (H-DHPM) as a potential candidate for the treatment of COPD was also investigated. H-DHPM treated cells showed a decrease in intracellular Ca(2+) level as compared to the control cells. Molecular studies were carried out to evaluate the expression profile of NOS isoforms in human lymphocytes and it was shown that H-DHPM decreases the increased iNOS in COPD along with reestablishing the normal levels of endothelial nitric oxide synthase (eNOS). The results of H-DHPM were comparable with those of Amlodipine, a known calcium channel blocker. Calcium channel blocker H-DHPM proves to be a potential candidate for the treatment of COPD and further clinical studies are required to prove its role in the treatment of pulmonary hypertension (PH).

Prevention of benzene-induced genotoxicity in bone marrow and lung cells: superiority of polyphenolic acetates to polyphenols.

Previous investigations carried out in our laboratory have highlighted that 7,8-diacetoxy-4-methylcoumarin demonstrates a mechanism-based inhibition of cytochrome P450 (Cyt-P450) activities such as microsome-mediated aflatoxin B1 (AFB1) epoxidation, dealkylation of alkylated resorufin, and toxicokinetics of benzene. 7,8-Diacetoxy-4-methylcoumarin, quercetin pentaacetate, and ellagic acid peracetate were also found to be effective in giving the protection of AFB1-induced genotoxicity in rat's bone marrow and lung cells possibly due to acetylation of Cyt-P450 apoprotein mediated by acetoxy drug: protein transacetylase. Later, this transacetylase was identified as calreticulin, and the acetyltransferase function of calreticulin was appropriately termed calreticulin transacetylase. In this communication, we have focused on the superiority of several classes of polyphenolic acetates to polyphenols in the modification of Cyt-P450-linked mixed function oxidases (MFOs) such as 7-ethoxyresorufin O-deethylase (EROD) and pentoxyresorufin O-dealkylase (PROD). Special attention has also been focused on benzene-induced genotoxicity in bone marrow and lung cells. Results clearly indicated that polyphenolic acetates demonstrated time-dependent inhibition of Cyt-P450-linked MFOs, while parent polyphenols failed to demonstrate the same. Polyphenolic acetates were found to be more superior to polyphenols in preventing benzene-induced micronuclei formation. The pattern of inhibition of Cyt-P450-dependent MFOs and benzene-induced micronuclei formation by polyphenolic acetates was found in tune with their specificities to calreticulin transacetylase. These results further substantiated that inhibition of Cyt-P450-linked MFOs and benzene-induced genotoxicity in bone marrow and lung cells by polyphenolic acetates are mediated by the action of calreticulin transacetylase that catalyzes the acetylation of concerned proteins.