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Introduction: Urinary tract infection is still one of the most common infections among all age groups. The causative microorgnisms of UTI and their sensitivity to different antibiotics varies in different areas, and changes with time. This necessitates periodic studies of the causative uropathogens and their antibiotic sensitivity pattern. Aim: To observe the profile of common uropathogens and their antibiotic sensitivity patterns to commonly used antimicrobial agents. Materials and Methods: A contemplative study was done at the department of Microbiology of Ad-din Women’s Medical College, Dhaka (AWMCH), Bangladesh, during January to December, 2017. Clean-catch midstream urine samples were collected from 7139 suspected urinary tract infection patients of different age and sex groups. Uropathogens were identified by standard microbiological techniques and antimicrobial susceptibility pattern was determined by Kirby Bauer Disc diffusion method following Clinical and Laboratory Standards Institute (CLSI) guidelines. Result: In this study, Out of 7139 patients, 1664 (23.3%) were growth positive for urine cultures. Majority of the patients (88.5%, 6315/7139) were female. The predominant isolate was E. coli 712 (42.8%), followed by Coagulase negative Staphylococcus (CONS) 589 (35.4%), Acinetobacter 126 (7.5%), Enterobacter spp. 72 (4.3%), Klebsiella spp. 62 (3.7%), Enterococcus spp. & Proteus spp. 16 (1.9%). Imipe­nem (92%), amikacin (83.8%), piperacillin- tazobactum (85.4%), gentamycin (69.4%), levofloxacin (65.6%) shows higher sensitivity to Gram negative bacteria, whereas high resistance to ampicillin (17%), cephradin (11.8%), cotrim (26%) and amoxiclav (28%) were observed. On the other hand, Gram positive bacteria showed high resistance to nalidixic acid (70-95%), erythromy­cin (68-90%), and high sensitivity to nitrofurantoin, meropenem, vancomycin and linezolid. Vancomycin, linezolid and nitrofurantoin for Gram positive bacteria and amikacin, meropenem, piperc

AIMS Diastolic Ca release (DCR) from sarcoplasmic reticulum (SR) Ca release channel ryanodine receptor (RyR2) has been linked to multiple cardiac pathologies, but its exact role in shaping divergent cardiac pathologies remains unclear. We hypothesize that the SR-mitochondria interplay contributes to disease phenotypes by shaping Ca signaling. METHODS AND RESULTS A genetic model of catecholaminergic polymorphic ventricular tachycardia (CPVT2 model of CASQ2 knockout) and a pre-diabetic cardiomyopathy model of fructose fed mice (FFD), both marked by DCR, are employed in this study. Mitochondria Ca (mCa) is modulated by pharmacologically targeting mitochondria Ca uniporter (MCU) or permeability transition pore (mPTP), mCa uptake and extrusion mechanisms, respectively. An MCU activator abolished Ca waves in CPVT2 but exacerbated waves in FFD cells. Mechanistically this is ascribed to mitochondria's function as a Ca buffer or source of reactive oxygen species (mtROS) to exacerbate RyR2 functionality, respectively. Enhancing mCa uptake reduced and elevated mtROS production in CPVT2 and FFD respectively. In CPVT2, mitochondria took up more Ca in permeabilized cells, and had higher level of mCa content in intact cells vs FFD. Conditional ablation of MCU in the CPVT2 model caused lethality and cardiac remodeling, but reduced arrhythmias in the FFD model. In parallel, CPVT2 mitochondria also employ upregulated mPTP-mediated Ca efflux to avoid mCa overload, as seen by elevated incidence of MitoWinks (an indicator of mPTP-mediated Ca efflux) vs FFD. Both pharmacological and genetic inhibition of mPTP promoted mtROS production and exacerbation of myocyte Ca handling in CPVT2. Further, genetic inhibition of mPTP exacerbated arrhythmias in CPVT2. CONCLUSION In contrast to FFD, which is more susceptible to mtROS-dependent RyR2 leak, in CPVT2 mitochondria buffer SR-derived DCR to mitigate Ca-dependent pathological remodeling and rely on mPTP-mediated Ca efflux to avoid mCa overload. SR-mitochondria interplay contributes to the divergent pathologies by disparately shaping intracellular Ca signaling. TRANSLATIONAL PERSPECTIVE It is well-established that RyR2 dysfunction is involved in a spectrum of pathological conditions including cardiac arrhythmias. In this study, two disease models marked by RyR2 dysfunction were employed to explore how the interplay between SR and mitochondria contributes to divergent cardiac pathologies. We found mitochondria act as essential Ca buffer to absorb SR-derived Ca to mitigate pathological remodeling in the genetic arrhythmic syndrome CPVT, but they are more susceptible to Ca overload or ROS-related exacerbation of RyR2 dysfunction in pre-diabetic cardiomyopathy. Thus, tailored therapies should be developed to target SR-mitochondria interplay in the aims of treating these diseases.