Hypovitamanosis D and non cardiac chest pain

Background: Recurrent atypical chest pain not due to cardiac illness is a very common condition in medical outpatient departments. Authors found that people consulting for atypical chest pain often have significant Vitamin D deficiency and correction of Vitamin D deficiency relieved patient symptoms. Hence authors carried out this study.Methods: Persons aged below 50 years were taken up for study. Those attending medical clinics with complaints of chest pain occurring more than two times were taken up for study. Cardiac illness was excluded by clinical examination and investigations. Those found to have low Vitamin D were taken up for study. 60,000 international units Vitamin D was administered orally weekly for 8 weeks. They were followed up twice weekly for three months and once monthly for three months.Results: Results were analyzed and charted. 120 subjects were taken up for study and duration of study was three years. Average age of the study group was 37.50 years and the average Vitamin D level was 15.75 nanogram/ml (ngm/ml). Duration of chest pain ranged from one week to one year. Most of the patients had migratory chest pain.Conclusions: As Vitamin D deficiency is a treatable medical condition it may be prudent to check Vitamin D levels in the patients presenting with recurrent atypical pain in the chest. It reduces the burden on the health care system and relieves the suffering of the patient. It may not be futile to check Vitamin D levels even in the patients with coronary artery disease who are suffering from atypical chest pain

Healthy blue man: congenital methemoglobinemia

Congenital methemoglobinemia, though often discussed in medical teachings is rarely encountered in clinical practice as the condition is asymptomatic. Here we present such a case and discuss in detail the clinical presentation of both congenital and acquired methemoglobinemia. We also outlined the management of the conditions. One should suspect methemoglobinemia when cyanosis is not being corrected by supplementing oxygen and and when the oxygen saturation is low by pulse oximetry and normal by arterial blood gas analysis. Treatment modalities for congenital methemoglobinemia is of cosmetic purpose, but timely intervention in acquired methemoglobinemia could be lifesaving. Methylene blue, Ascorbic acid and Riboflavin are drugs of choice

Density, dielectric and X-ray studies of Smectic A-Smectic A transitions

We report here the results of detailed density, dielectric and X-ray studies on three systems exhibiting different types of Smectic A-Smectic A transitions. It is found that although the layer spacing shows marked changes at the transitions, the corresponding density changes are extremely small. In every case studied, the dielectric anisotropy shows a pronounced decrease on going over to the lower temperature smectic A phase. This decrease can be correlated with the structural changes

Optineurin Is Required for CYLD-Dependent Inhibition of TNFα-Induced NF-κB Activation

The nuclear factor kappa B (NF-κB) regulates genes that function in diverse cellular processes like inflammation, immunity and cell survival. The activation of NF-κB is tightly controlled and the deubiquitinase CYLD has emerged as a key negative regulator of NF-κB signalling. Optineurin, mutated in certain glaucomas and amyotrophic lateral sclerosis, is also a negative regulator of NF-κB activation. It competes with NEMO (NF-κB essential modulator) for binding to ubiquitinated RIP (receptor interacting protein) to prevent NF-κB activation. Recently we identified CYLD as optineurin-interacting protein. Here we have analysed the functional significance of interaction of optineurin with CYLD. Our results show that a glaucoma-associated mutant of optineurin, H486R, is altered in its interaction with CYLD. Unlike wild-type optineurin, the H486R mutant did not inhibit tumour necrosis factor α (TNFα)-induced NF-κB activation. CYLD mediated inhibition of TNFα-induced NF-κB activation was abrogated by expression of the H486R mutant. Upon knockdown of optineurin, CYLD was unable to inhibit TNFα-induced NF-κB activation and showed drastically reduced interaction with ubiquitinated RIP. The level of ubiquitinated RIP was increased in optineurin knockdown cells. Deubiquitination of RIP by over-expressed CYLD was abrogated in optineurin knockdown cells. These results suggest that optineurin regulates NF-κB activation by mediating interaction of CYLD with ubiquitinated RIP thus facilitating deubiquitination of RIP

A Study of Load Carrying Capacity of cracked Weld Joint using Finite Element Analysis

Static Stress and dynamic modal analysis gives   the idea for strength of the joints.  Any failure in the analysis is catastrophic to the functioning of the structure/machine.  This can be eliminated by proper stress and dynamic analysis.  Cracks will happen in the welds after certain cycles of working. The present study is to find the effect of crack on load carrying capacity of the joint and its stress behaviour in the junction. The results shows parabolic reduction of strength with the propagation of crack which indicates failure propagation is more with increased cracking.  Also stress behaviour across the cross section also changes with the crack propagation and results shows maximum concentration at the bottom region which is totally different from the full contact problem