The use of suboptimal concentrations of sodium hypochlorite and didecyldimonium chloride can lead to the evolution of antibiotic-resistant Pseudomonas strains.
Background Acute lymphoblastic leukemia (ALL) is the most well‐known sort of leukemia in children. In spite of favorable survival rates, some patients relapse and achieve a poor outcome. Methods We analyzed miR‐125b and Bcl‐2 expressions in pediatric patients with ALL and evaluated their clinical utility as molecular markers for the prediction of disease outcomes. Results Downregulation of miR‐125b and increased Bcl‐2 expression levels in pediatric patients with ALL were associated with poor prognosis at diagnosis. At day 28 of induction, miR‐125b was significantly increased, whereas Bcl‐2 was downregulated. Loss of miR‐125b during diagnosis and its elevation after therapy are strongly correlated with short leukemia‐free survival and worse survival. Moreover, the combination of miR‐125b with Bcl‐2 markers can clearly enhance the prediction of the disease outcome. Finally, a univariate analysis highlighted the independent prognostic value of miR‐125 in a pediatric patient with ALL. Conclusions miR‐125b and Bcl‐2 together are potent predictors for the prognosis and, therefore, can be used as therapeutic targets in childhood ALL.
The relationship between hepatitis B virus (HBV) infection, severity of liver disease, frequency of infection, and degree of gastric lesions was not yet fully investigated in Egyptian patients. The present work was performed on 100 Egyptian patients with HBV from the National Hepatology and Tropical Medicine Institute and 70 healthy volunteers as control group. The participants were subjected to full medical history taking, clinical examination, and laboratory investigations. All patients were positive for HBV surface antigen (HBV sAg), HBV DNA, and negative for hepatitis C virus antibodies. The severity of the liver disease was assessed using Child-Pugh scoring system. Screening of all participants for Ag in stool was performed. Biopsy specimens were taken from the gastric lesions of -infected patients for histopathological examination. The mean age of the patients and control group were 34.9 and 33.4 years, respectively. The levels of the liver enzymes were statistically higher in HBV patients than the control group. Ag in stool was detected in 45.7% of the control group, and a higher percentage (60%) was detected in the patients group. Chronic gastritis with glandular atrophy and metaplasia was found in 15.6% of patients of Child-Pugh A, 70% of Child-Pugh B, and 100% of Child-Pugh C. It could be concluded that the prognosis of the liver disease significantly influences the severity of the gastric pathology in infection.
Emerging hepatocellular carcinoma (HCC) has been sequentially reported in chronic hepatitis C virus (HCV) treated with direct-acting antivirals (DAAs). Homeobox transcript antisense RNA (HOTAIR), an oncogene, has been reported to be associated with cancer. We investigated the predictive value of lnc-HOTAIR for HCC surveillance in chronic HCV patients following DAAs therapy. The expression levels of lnc-HOTAIR and ATG-7 genes were measured in 220 with chronic HCV, following a DAAs based therapy for 12 weeks, the patients were followed-up for attentive surveillance of HCC for 12 months after starting DAAs. In terms of lnc-HOTAIR, patients with HCC and high viral load had significantly higher median expression levels of HOTAIR of (68 vs. 24; p = .001) and (94 vs. 52; p = .001), respectively. Moreover, the median expression level of ATG-7 was higher in those who developed HCC (114 vs. 51; p = .001). The expression of lnc-HOTAIR and ATG-7 are significant predictors of the development of HCC in HCV-4 infected patients treated with DAAs, with a cutoff value of 37 and 86, respectively. The increased expression levels of lnc-HOTAIR more than 68 in HCC patients following DAAs were correlated with poorer disease outcomes compared to those with lower expression levels; however, ATG-7 expression levels more than 114 were correlated with worse overall survival but not the progression-free one. We suggest that high expression levels of lnc-HOTAIR could serve as a risk assessment biomarker for HCC before and during DAAs course therapy in Chronic HCV-4 patients, and should be rigorously taken into consideration before DAAs.
Extended-spectrum β-lactamases (ESβLs) pose a serious problem in the treatment of urinary tract infections (UTIs). The ESβL-producing organism is an expanding global health problem. Therefore, screening for ESβL, detection of their drug-resistance pattern, and molecular characterization should be a continuous process. The present study was performed to determine the antibiotic resistance profile and the genetic characterization of ESβL isolates from hospital-and community-acquired UTIs. Two hundred fifty Enterobacteriaceae isolates were obtained from urine samples of outpatient clinic attendants and hospitalized patients at Kasr Al-Aini Hospital. By phenotypic screening tests, 100 ESβL isolates were detected among the studied groups. Furthermore, detection of beta-lactamase (bla) cefotaxime (CTX)-M, sulfhydryl variable, and temoneira ESβL genes was investigated by polymerase chain reaction. A subset of 25 CTX-M-positive isolates was further identified by gene sequencing technology. Among the 100 ESβL isolates, 66% were Escherichia coli and 34% were Klebsiella spp. There was no statistical difference in the prevalence of ESβL Enterobacteriaceae in community-acquired versus hospital-acquired UTIs. The susceptibility of all ESβL isolates to carbapenems was the most prevalent finding. In addition, all ESβL E. coli isolates were susceptible to fosfomycin, whereas all community-acquired ESβL isolates were susceptible to nitrofurantoin. A total of 98% of the ESβL isolates harbored bla-CTX-M genes, with CTX-M-15 being the most prevalent. It could be concluded that ESβL production is present at a high rate among Egyptian patients with hospital-and community-acquired UTI. The high prevalence of bla-CTX-M may suggest it as a candidate for molecular screening of ESβL.
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