Prevalence of alcohol dependence syndrome in the patients of acute pancreatitis: A cross-sectional study.

Background: Acute pancreatitis (AP) is the main reason for mortality and morbidity. Numerous studies have shown a link between chronic alcohol usage and AP. However, there are few studies on the percentage of patients developing AP as a result of dependent patterns of drinking and associated risk factors. Aim: This study aimed to study the prevalence and impact of risk factors of alcohol dependence syndrome with AP patients hospitalized in tertiary care facilities. Materials and Methods: This is a cross-sectional observational study. Sociodemographic and clinical data were taken from patients with AP after consent. Eighty-five patients with AP who met the inclusion criteria were involved after each participant had clinical evaluation using the modified Marshall score, the Alcohol Use Disorder Identification Test, and the Severity of Alcohol Dependence Questionnaire (SAD-Q). The outcomes were tabulated and analyzed using Statistical Package for the Social Sciences (SPSS) software. Results: 38.8% of patients with AP were found to have features of alcohol dependence syndrome. Higher values of mean corpuscular volume (MCV), serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), Gamma-glutamyl transferase (GGT), and uric acid were associated with a greater propensity to have AP. The severity of alcohol dependence syndrome and AP was not associated. Conclusion: AP is potentially a fatal disease. In this study, 38.8% of AP patients had alcohol dependence syndrome. There was no statistical association between the severity of AP and alcohol dependence syndrome, though high values of MCV, SGOT, SGPT, and GGT were at greater risk of developing AP. As a result, alcohol dependence syndrome should be examined in all individuals with AP.

Childhood trauma and bipolar affective disorder: Is there a linkage?

Bipolar affective disorder (BPAD) is a major psychiatric illness impairing the quality of life. The etiology of BPAD is influenced by different factors possibly related to gene-environment interactions. Approximately 30% to 50% of individuals with BPAD have experienced some traumatic event in childhood. Serious adverse experiences that children may suffer early in life are often described as childhood trauma (CT). It includes physical, emotional, and sexual abuse and physical and emotional neglect. CT is linked with an elevated risk of developing BPAD. Childhood adversities play a role in modulating the early onset of illness, increased number of depressive episodes, increased suicide attempts, and other clinical severity of BPAD. Hospital-based studies comprising heterogeneous populations had researched the specific role of each trauma subtype as a predisposing factor for BPAD. Identifying and addressing CT through early intervention methods may prevent the future development of chronic disorders like BPAD. This review article is an attempt to explore and highlight the existing literature regarding the association of different subtypes of CT with BPAD.

Jugaad: An indi-genius problem-solving approach.

Jugaad, "an inexpensive innovation to meet an expensive need" has caught the attention of the global industry as a frugal innovative concept worth exploring. Relevant literature was reviewed to understand psychosocial factors related to Jugaad. A conceptual framework was developed based on available evidence. Jugaad is an effective approach aimed at functional problem-solving in a resource-constrained environment. Possible drawbacks need to be kept in mind while utilizing this approach.

Physiological alterations and regulation of heterocyst and nitrogenase formation in Het(-) Fix(-) mutant strain of Anabaena variabilis.

Physiological alterations and regulation of heterocyst and nitrogenase formation have been studied in Het(-) Fix(-) mutant strain of diazotrophic cyanobacterium Anabaena variabilis. Het(-) Fix(-) mutant strain of A. variabilis has been isolated by N-methyl-N'-nitro-N"-nitrosoguanidine (NTG) mutagenesis and was screened with the penicillin enrichment (500 microg ml(-1)). Growth, heterocyst differentiation, nitrogenase and glutamine synthetase (biosynthetic and transferase), (14)CO(2)-fixation, nitrate reductase (NR), nitrite reductase (NiR), glucose-6-phosphate dehydrogenase (G6PDH), and isocitrate dehydrogenase (IDH) activities, and NO(3)(-), NO(2)(-), and NH(4)(+) uptake and whole cell protein profile in different metabolic conditions were studied in the Het(-) Fix(-) mutant strain taking wild-type A. variabilis as reference. Het(-) Fix(-) mutant strain was incapable of assimilating elemental nitrogen (N(2)) due to its inability to form heterocysts and nitrogenase and this was the reason for its inability to grow in BG-11(0) medium (free from combined nitrogen). In contrast, wild-type strain grew reasonably well in the absence of combined nitrogen sources and also showed heterocyst differentiation (8.5%) and nitrogenase activity (10.8 etamol C(2)H(4) formed microg(-1) Chl a h(-1)) in N(2)-medium. Wild-type strain also exhibited higher NR, NiR, and GS activities compared to its Het(-) Fix(-) mutant strain, which may presumably be due to acquisition of high uptake of NO(3)(-), NO(2)(-), and NH(2)(+). Wild-type strain in contrast to its Het(-) Fix(-) mutant strain also exhibited high level of G6PDH, IDH, and (14)CO(2) fixation activities. Low levels of G6PDH and IDH activities in Het(-) Fix(-) mutant strain further confirmed the lack of heterocyst differentiation and nitrogenase activity in the Het(-) Fix(-) mutant strain.NR, NiR, and GS activities in both the strains were energy-dependent and the energy required is mainly derived from photophosphorylation. Furthermore, it was found that de novo protein synthesis is necessarily required for the activities of NR, NiR, and GS in both wild-type and its Het(-) Fix(-) mutant strain.

Regulation of potassium uptake in the sodium-resistant (NaCl(r)) and thalium-resistant (TlCl(r)) mutant strain of diazotrophic cyanobacterium Anabaena variabilis.

A thalium chloride-resistant (TlCl(r)) mutant strain and a sodium chloride-resistant (NaCl(r)) mutant strain of the diazotrophic cyanobacterium Anabaena variabilis have been isolated by spontaneous and chemical mutagenesis by using TlCl, a potassium (K(+)) analog, and nitrosoguanidine (NTG), respectively. The TlCl(r) mutant strain was found to be defective in K(+) transport and showed resistance against 10 microM TlCl. However, it also showed sensitivity against NaCl (LD(50), 50 m M). In contrast, neither wild-type A. variabilis nor its NaCl(r) mutant strain could survive in the presence of 10 microM TlCl and died even at 1 microM TlCl. The TlCl(r) mutant strain exhibited almost negligible K(+) uptake, indicating the lack of a K(+) uptake system. High K(+) uptake was, however, observed in the NaCl(r) mutant strain, reflecting the presence of an active K(+) uptake system in this strain.DCMU, an inhibitor of PS II, inhibited the K(+) uptake in wild-type A. variabilis and its TlCl(r) and NaCl(r) mutant strains, suggesting that K(+) uptake in these strains is an energy-dependent process and that energy is derived from photophosphorylation. This contention is further supported by the inhibition of K(+) uptake under dark conditions. Furthermore, the inhibition of K(+) uptake by KCN, DNP, and NaN(3) also suggests the involvement of oxidative phosphorylation in the regulation of an active K(+) uptake system. The whole-cell protein profile of wild-type A. variabilis and its TlCl(r) and NaCl(r) mutant strains growing in the presence of 50 m M KCl was made in the presence and absence of NaCl. Lack of transporter proteins in TlCl(r) mutant strain suggests that these proteins are essentially required for the active transport and accumulation of K(+) and make this strain NaCl sensitive. In contrast, strong expression of the transporter proteins in NaCl(r) mutant strain and its weak expression in wild-type A. variabilis is responsible for their resistance and sensitivity to NaCl, respectively. Therefore, it appears that the increased salt tolerance of the NaCl(r) mutant strain was owing to increased K(+) uptake and accumulation, whereas the salt sensitivity of the TlCl(r) mutant strain was owing to the lack of K(+) uptake and accumulation.