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Looking at the particular dimensionality of pre-service teachers' passion regarding instructing through combining frameworks regarding academic scientific disciplines and company therapy.
INTRODUCTION Acinetobacter baumannii is an opportunistic pathogen that causes nosocomial infections with high mortality. Treatment options are limited owing to its resistance to numerous antibiotics. Here, we sought to determine the antibiotic susceptibilities of A. baumannii isolates, investigate clonal relationship among the strains, and determine the frequency of beta-lactamase resistance genes. METHODOLOGY The identification and antibiotic susceptibilities of 69 A. baumannii strains were determined using a BD-Phoenix automated system. The presence of blaOXA-2, blaOXA-10, blaOXA-23, blaOXA-24/40, blaOXA-51, blaOXA-58, blaTEM, blaSHV, blaIMP, blaVIM, and blaGIM genes were investigated using polymerase chain reaction (PCR), and clonal relatioships among the isolates were determined using pulsed-field gel electrophoresis (PFGE). RESULTS All strains were resistant to ampicillin-sulbactam, gentamicin, cefepime, ciprofloxacin, and ceftriaxone. While 65 of the 69 strains (94.2%) were resistant to piperacillin-tazobactam, amikacin, imipenem, and meropenem, all strains were susceptible to tigecycline and colistin. The frequencies of blaOXA-51, blaOXA-23, blaTEM, blaOXA-2, blaVIM, and blaSHV were 100%, 94.2%, 53.6%, 21.7%, 14.5%, and 2.9%, respectively. Based on PFGE results, 56 of the 69 strains were clonally related, and the clustering rate was 81.2%. No common outbreak isolate was detected. CONCLUSIONS The most prevalent OXA genes were blaOXA-51, blaOXA-23, and blaOXA-2. Furthermore, blaTEM, blaSHV, and blaVIM, which are common in Enterobacterales and Pseudomonas spp, were detected, suggesting horizontal gene transfer had occurred between bacteria. No single clone outbreak was detected by PFGE. However, multiclonal spread and the high clustering rate suggest cross-contamination. Therefore, in future, more effective infection control measures must be implemented. Copyright (c) 2019 Nergis Asgin, Baris Otlu, Elcin Kal Cakmakliogullari, Nafia Canan Gursoy, Betul Demir.INTRODUCTION Clostridium chauvoei (C. chauvoei) is an anaerobic, histotoxic Gram-positive, bacterium causing fatal myonecrosis in livestock with high mortalities. The disease is common in dairy animals, but little is known about the pathophysiology of the disease in exotic (non-native) animals kept under local conditions in Pakistan. RP-102124 METHODOLOGY Diagnosis of blackleg was made based on hematological and serum biochemical analysis, PCR, necropsy and histopathology. RESULTS Clinically sick animals exhibited fever, lameness, subcutaneous gaseous swelling and edema particularly in hindquarter and front legs. Hematological analysis showed increases in erythrocyte sedimentation rate and reduces in number of red blood cells, packed cell volume, leukocytes and differential leukocyte count. Serum aspartate aminotransferase, lactate dehydrogenase, alkaline phosphates, alanine aminotransferase, urea, creatinine, creatine kinase, and creatinine phosphokinase were significantly (P less then 0.05) higher in the infected ahaffar, Narmeen Tariq, Abdul Qayyum, Gamal Wareth.INTRODUCTION Over the past decades, prevalence of biofilm-forming Staphylococcus aureus strains has significantly increased in urinary tract infections. The aim of this study was to investigate prevalence of biofilm forming and adhesion encoding genes and to analyze distribution of different agr and spa types in S. aureus isolates. METHODOLOGY In the present study, 75 S. aureus isolates obtained from patients with urinary tract infections were examined for susceptibility to antimicrobial agents. Adhesion, biofilm, and spa encoding genes were detected by PCR screening; agr types were determined using multiplex PCR. RESULTS Among the 75 isolates, 72% were biofilm producers and 28% were non-biofilm producers. Notably, the ability to produce biofilm was higher among MRSA strains ompared to MSSA strains. The most prevalent biofilm forming gene was icaD (77.3%), followed by icaA (76%), icaB (57.3%) and icaC (50.7%). Adhesion genes clfA, clfB, fnbB, can, fnbA, ebp and bap were detected in 94.7%, 92%, 68%, 64%, 64%, 60% and 5.3% of the isolates, respectively. The spa types t426 and t7789 were found among the non-MDR isolates. It was found that t790, t084, t7789 and t325 spa types were biofilm producers, while t426 and t1339 spa types were non-biofilm producers. CONCLUSION Biofilm encoding genes icaD and spa type t790 and agr type III were the most prevalent factors among MDR biofilm producer isolates. The study emphasized that identification of genes and characterization of molecular types involved in biofilm formation should be considered. Copyright (c) 2019 Mehdi Goudarzi, Anis Mohammadi, Anahita Amirpour, Maryam Fazeli, Mohammad Javad Nasiri, Ali Hashemi, Hossein Goudarzi.In this study, we evaluated the function and regulation of the long non-coding RNA (lncRNA) FAM83H-AS1 in triple-negative breast cancer (TNBC). Our data show that the FAM83H-AS1 levels are increased in human TNBC cells and tissues. Proliferation, migration, and invasion of TNBC cells are decreased by FAM83H-AS1 suppression, but increased by FAM83H-AS1 overexpression. Bioinformatics analysis revealed that miR-136-5p is a potential target of FAM83H-AS1. MiR-136-5p expression is decreased in TNBC tissues, and its overexpression suppresses TNBC cell proliferation, migration, and invasion. MiR-136-5p suppression reverses the FAM83H-AS1 silencing-mediated inhibition of TNBC cell proliferation, migration, and invasion, suggesting that FAM83H-AS1 exerts its oncogenic effect by inhibiting miR-136-5p. Our data identify metadherin (MTDH) as the target gene of miR-136-5p, and demonstrate that the MTDH expression is increased in human TNBC tissues, which induces proliferation, migration, and invasion of TNBC cells. Importantly, our in vivo data show that FAM83H-AS1 also promotes tumor growth in TNBC mouse xenografts. Together, our results demonstrate that FAM83H-AS1 functions as an oncogenic lncRNA that regulates miR-136-5p and MTDH expression during TNBC progression, and suggest that targeting the FAM83H-AS1/miR-136-5p/MTDH axis may serve as a novel therapeutic target in TNBC.
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