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Background: Urinary tract infections (UTIs) are commonly detected in several hospitals and typical medical health centres. The antibiotic policy must be updated based on current knowledge about causative agents and their antibiotic susceptibility patterns. The goal of this study was to find out exactly how frequently microbes cause urinary infections and their antibiotic susceptibility patterns. Methods: Mid-stream urine samples were analyzed microscopically for a routine examination, and bacterial pathogens were isolated by conventional culture method using Chromogenic UTI media and MacConkey agar culture media. A group of biochemical parameters were utilized for bacterial identification and characterization. Finally, in vitro antimicrobial susceptibility was performed by the Kirby- Bauer disc diffusion methods against 14 commercially available antibiotics. Results: A total of 1288 clinical samples from UTI patients were obtained aseptically, with 398 showing positive growth with a range of bacteria. Females have a higher prevalence of UTI than males. E. coli was the most common pathogen found (82.86%), followed by Enterococcus faecalis (8.44%), Klebsiella pneumoniae (5.63%), Pseudomonas aeruginosa (2.81%), and Proteus mirabilis (0.26%). The majority of the bacteria had a high sensitivity to Meropenem (98.25%); moderate sensitivity to Amoxicillin, Azithromycin, Ciprofloxacin, Gentamicin, Levofloxacin, Ceftriaxone, Cefepime, and Nitrofurantoin; and low sensitivity (20%) to Cefixime, Cephradine, Cefuroxime, Clindamycin, and Trimethoprime. Conclusion: These findings have clinical and epidemiological implications, improving study to identify causative pathogens and pathogen sensitivity patterns in urinary tract infections, as well as clinicians' knowledge of how to choose the best antibiotics and, ultimately, contributing to patient diagnosis and treatment.
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Background: Outcome of drainage operation for chronic pancreatitis are variable. The present study is taken to observe effect of longitudinal pancreatico-jejunostomy (LPJ) on pain control and pancreatic function in chronic pancreatitis in our setting.Material & Methods:Thirty-three patients who underwent LPJ for symptomatic chronic pancreatitis for one year period presented with abdominal pain (100%), steatorrhoea (30.3%), diabetes (66.7%) and weight loss (78.8%). Definitive diagnosis was made on the basis of ultrasonography and MRCP findings. LPJ (Partingtong-Rochelle) operation was done in all patients. Pain (using visual analoge scale), glycemic status (using FBS, 2hABF, HbA1c), body weight, serum zinc levels (as a marker of exocrine function), and serum insulin level (as a marker of endocrine function) were measured immediately after admission and 3 months after operation.Results:Three months after operation pain was completely disappeared in 23 (69.7%) patients, it persisted in different grade in 10 (30.3%) patients and the pain reduction rate was significant. Twenty two patients who had diabetes prior to surgery, their glycemic status significantly decreased and serum insulin level significantly increased (preoperative; 7.1�1 礥/L, postoperative; 14.3�礥/L) in 22 patients with DM after surgery. Serum zinc level increased (preoperative; 80.8�.5 礸/dl, postoperative; 85.3�.7 礸/dl) 3 months after surgery but the difference was not significant (p=0.571). However the body weight of all patients were significantly increased after operation.Conclusions:LPJ reduces abdominal pain and improves both exocrine and endocrine function in patient with chronic pancreatitis. Serum zinc levels can be considered as a tool of exocrine function.
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Malaria, caused by the Plasmodium parasite is still a health problem worldwide due to resistance of the pathogen to current anti-malarials. The search for new anti-malarial agents has become more crucial with the emergence of chloroquine-resistant Plasmodium falciparum strains. Protein kinases such as mitogen-activated protein kinase (MAPK), MAPK kinase, cyclin-dependent kinase (CDK) and glycogen synthase kinase- 3(GSK-3) of parasitic protozoa are potential drug targets. GSK-3 is an enzyme that plays a vital role in multiple cellular processes, and has been linked to pathogenesis of several diseases such as type II diabetes and Alzheimer's disease. In the present study, the antiplasmodial property of LiCl, a known GSK-3 inhibitor, was evaluated in vivo for its antimalarial effect against mice infected with Plasmodium berghei. Infected ICR mice were intraperitoneally administered with LiCl for four consecutive days before (prophylactic test) and after (suppressive test) inoculation of P. berghei-parasitised erythrocytes. Results from the suppressive test (post-infection LiCl treatment) showed inhibition of erythrocytic parasitemia development by 62.06%, 85.67% and 85.18% as compared to nontreated controls for the 100 mg/kg, 300 mg/kg and 600 mg/kg dosages respectively. Both 300 mg/kg and 600 mg/kg LiCl showed similar significant (P<0.05) suppressive values to that obtained with chloroquine-treated mice (86% suppression). The prophylactic test indicated a significantly (P<0.05) high protective effect on mice pre-treated with LiCl with suppression levels relatively comparable to chloroquine (84.07% and 86.26% suppression for the 300 mg/kg and 600 mg/kg LiCl dosages respectively versus 92.86% suppression by chloroquine). In both the suppressive and prophylactic tests, LiCl-treated animals survived longer than their non-treated counterparts. Mortality of the non-treated mice was 100% within 6 to 7 days of parasite inoculation whereas mice administered with LiCl survived beyond 9 days. Healthy non-infected mice administered with 600 mg/ kg LiCl for four consecutive days also showed decreased mortality compared to animals receiving lower doses of LiCl; three of the seven mice intraperitoneally injected with the former dose of LiCl did not survive more than 24 h after administration of LiCl whereas animals given the lower LiCl doses survived beyond four days of LiCl administration. To date, no direct evidence of anti-malarial activity in vivo or in vitro has been reported for LiCl. Evidence of anti-plasmodial activity of lithium in a mouse infection model is presented in this study.