Background/Purpose: This work aimed to assess the impact of different etiologies
of acute pancreatitis (AP) and vitamin D receptor (VDR) TaqI rs731236 gene polymorphism
on the severity of AP.
Methods: This case-control study included 70 patients with AP and 40 healthy controls.
Etiologies of AP were identified by imaging, ANA, cytomegalovirus (CMV)
IgM, coxsackie B virus IgM, and IgG4. Genotyping of VDR TaqI rs731236 polymorphism,
Laboratory tests and severity scores using Ranson, BISAP, Atlanta and
APACHE II scores were determined.
Results: The age in AP patients was 36.03 ± 10.76, and females were 85.7%. The
etiologies of AP were as follows: biliary (51.4%), coxsackievirus (22.9%), autoimmune
(14.3%), post-ERCP (8.6%) and 2.9% were idiopathic. The TT genotype of
VDR polymorphism was significantly more common in AP than control (P = .001)
and allele T dominated in AP group (OR = 2; 95% CI: 0.665–5.64). Most cases
showed low severity scores with significant differences among etiologies and VDR
genotypes. Biliary pancreatitis showed highest percentages of severe AP. However,
etiologies and VDR polymorphism were not predictors of severity.
Conclusion: Etiology of AP could have impact on the disease severity. VDR gene
polymorphism increases the risk of AP. Neither the etiology nor VDR gene polymorphism
could predict AP severity.

Hospital-acquired infections represent a serious public health problem in all countries. It is clear that monitoring of the hospital
environment is an essential element in the control and a part of the policy for preventing nosocomial infections. It allows a better
understanding of the microbial ecology for the purpose of conducting preventive and corrective actions. &e aims of this work
were to determine the percentage of bacterial contamination of environmental samples and to identify potential nosocomial
pathogens isolated from environments of seven referral hospitals from 2009 to 2015. By using the swab technique, 12863 samples
were collected. Qualitative and quantitative cultures were performed. &e organisms were primarily identified by colony
morphology, microscopy of Gram stain, and standard biochemical tests. 25.6% of total samples showed contamination (93% was
monomicrobial and 7.0% was polymicrobial). &e predominant species was coagulase-negative staphylococcus (CNS) (32%),
followed by methicillin-resistant S. aureus (MRSA) (26%) and then K. pneumonia (10.6%). &e percentage of contamination
varied among the covered hospitals and according to the year of monitoring with highly statistically significant difference
(p value < 0.001). Direct contact with environmental surfaces or equipment transmits the majority of nosocomial infection. Major
nosocomial pathogens have been identified. Hospital managers and healthcare bodies must be aware of the reality of the concept
of environmental bacterial tanks and the need for respect of biocleaning procedures and choice of biocleaning tools.

Background: Methicillin resistance in S. aureus is caused by the acquisition of mecA gene,
that encodes an additional ß-lactam-resistant penicillin-binding protein, termed PBP2a. PVL
toxin is one of many toxins produced by S.aureus. Objectives: to evaluate the efficacy of
phenotypic methods and detection of mec A gene with PCR for detection of MRSA and to
assess the incidence of PVL gene in MRSA and all S. aureus isolates Methods: 576
patients from Assiut University Hospitals were enrolled in this study were classified into
community acquired infection group (CAI) and Hospital acquired infection group
(HAI)culture and PCR were done for all samples Results: 92 s.aureus isolates detected
MRSA were 62 (67.4%) of all S.aureus infections, They were 30 (65.2 %) of CAI and 32
(69.6 %) of HAI, The prevalence of PVL genes, The prevalence of PVL genes in CAI
isolates was 10.9%. None of HAI isolates had PVL gene. Conclusion: The presence of
PVL gene cannot be used as a sole marker for CA-MRSA and further studies are
required to find a reliable marker or combination of markers to facilitate the recognition
of CA- MRSA strains.

Occult Hepatitis B infection (OBI), defined as the presence of serum HBV DNA without detectable HBsAg, can be classified into seropositive OBI [anti-HBc and/or anti-hepatitis B surface (anti- HBs) positive] and seronegative OBI (anti-HBc and anti- HBs negative). We examined the role of anti-HBc as a screening test for OBI in HCV patients with chronic liver diseases and evaluated the possible impact of OBI on liver disease progression. 90 patients with hepatitis C related chronic liver diseases (CLD) and negative for HBsAg were divided into three equal groups; chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). Patients were tested for anti-HBc by ELISA and by PCR for S-gene. Total anti-HBc was found in 26 patients (28.9%). 8 patients (8.9%) had positive serum HBV DNA. Of these, 2 were positive for anti-HBc and 6 negative for anti-HBc. No correlation between OBI and severity of HCV related CLD was observed. In conclusion, as OBI was not associated with total anti-HBc, it is invaluable surrogate marker for OBI detection

Occult Hepatitis B infection (OBI), defined as the presence of serum HBV DNA without detectable HBsAg, can be classified into seropositive OBI [anti-HBc and/or anti-hepatitis B surface (anti- HBs) positive] and seronegative OBI (anti-HBc and anti- HBs negative). We examined the role of anti-HBc as a screening test for OBI in HCV patients with chronic liver diseases and evaluated the possible impact of OBI on liver disease progression. 90 patients with hepatitis C related chronic liver diseases (CLD) and negative for HBsAg were divided into three equal groups; chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). Patients were tested for anti-HBc by ELISA and by PCR for S-gene. Total anti-HBc was found in 26 patients (28.9%). 8 patients (8.9%) had positive serum HBV DNA. Of these, 2 were positive for anti-HBc and 6 negative for anti-HBc. No correlation between OBI and severity of HCV related CLD was observed. In conclusion, as OBI was not associated with total anti-HBc, it is invaluable surrogate marker for OBI detection

Abstract: Nicotine neuronal interactions exert an adverse potential in some brain regions and a significant link has been established between tobacco smoke/nicotine and vascular impairment. This work addresses nicotine impact on various components of the substantia nigra compacta (SNc) in rat. Twenty adult male Albino rats were divided equally into two groups: Group I, vehicle-control group (received saline [1 ml/kg body weight intra peritoneally] for 11 days). Group II; nicotine group (received 1.5 mg/kg body weight/day Sc) for 11 days. Nicotine levels were detected in the serum. Specimens were taken from the mid brain, processed and examined using biochemical, immunohistochemical, ultrastructural and morphometric techniques. In nicotine group, biochemical analysis revealed reduction in total antioxidant capacity (TAC), decrease in dopamine and malondialdehyde (MDA) levels. The mean number of light cells, and the mean surface area of nerve cells/field were significantly reduced, with an increase of dark cells were found in nicotine group compared to control. Immunoreactivity in nicotine group revealed an increase in neuronal α-synuclein, reduction in tyrosine hydroxylase enzyme, an increase in caspase 3 and ultrastructure changes suggestive of neuronal apopto. The blood capillaries were markedly affected. Nicotine induced endothelial and pericytic apoptotic changes, irregular lumena and indistinct endothelial junctional complex. Nicotine administered subcutaneously in a small dose may have a deleterious effect on SNc, mainly involving dopaminergic neurons and blood capillaries. This effect seems to be secondary to an oxidative stress that might be produced by reduced TAC and increased MDA levels. 

Occult Hepatitis B infection (OBI), defined as the presence of serum HBV DNA without detectable HBsAg, can be classified into seropositive OBI [anti-HBc and/or anti-hepatitis B surface (anti- HBs) positive] and seronegative OBI (anti-HBc and anti- HBs negative). We examined the role of anti-HBc as a screening test for OBI in HCV patients with chronic liver diseases and evaluated the possible impact of OBI on liver disease progression. 90 patients with hepatitis C related chronic liver diseases (CLD) and negative for HBsAg were divided into three equal groups; chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC). Patients were tested for anti-HBc by ELISA and by PCR for S-gene. Total anti-HBc was found in 26 patients (28.9%). 8 patients (8.9%) had positive serum HBV DNA. Of these, 2 were positive for anti-HBc and 6 negative for anti-HBc. No correlation between OBI and severity of HCV related CLD was observed. In conclusion, as OBI was not associated with total anti-HBc, it is invaluable surrogate marker for OBI detection

Enteroaggregative Escherichia coli (EAEC) is a common diarrhoeagenic human pathogen, isolated
from patients in both developing and industrialized countries, that is becoming increasingly
resistant to many frontline antibiotics. In this study, we screened 50 E. coli strains from children
presenting with diarrhea at the outpatients clinic of Assiut University Children’s Hospital, Egypt.
We show that all of these isolates were resistant to multiple classes of antibiotics and identified
two as being typical EAEC strains. Using whole genome sequencing, we determined that both
isolates carried, amongst others, blaCTX-M and blaTEM antibiotic resistance genes, as well as many
classical EAEC virulence determinants, including the transcriptional regulator, AggR. We demonstrate
that the expression of these virulence determinants is dependent on AggR, including aar,
which encodes for a repressor of AggR, Aar. Since biofilm formation is the hallmark of EAEC
infection, we examined the effect of Aar overexpression on both biofilm formation and AggRdependent
gene expression. We show that whilst Aar has a minimal effect on AggR-dependent
transcription it is able to completely disrupt biofilm formation, suggesting that Aar affects these
two processes differently. Taken together, our results suggest a model for the induction of
virulence gene expression in EAEC that may explain the ubiquity of EAEC in both sick and healthy
individuals.
ARTICLE HISTORY
Received 28 August 2020
Revised 24 November 2020
Accepted 1 December 2020
KEYWORDS
EAEC; antibiotic resistance;
virulence; bacterial gene
regulation; genome
sequencing
Introduction
Diarrhoeagenic Escherichia coli strains are important
human pathogens, which cause considerable morbidity
and mortality around the globe, particularly amongst
infants and children in developing countries. These
pathogens are classified into different pathotypes,
which include enteroaggregative E. coli (EAEC), enterohaemorrhagic
E. coli (EHEC), enteroinvasive E. coli
(EIEC), enteropathogenic E. coli (EPEC), enterotoxigenic
E. coli (ETEC) and diffuse adhering E. coli
(DAEC), based on their disease characteristics and specific
adherence patterns [1]. Enteroaggregative
Escherichia coli (EAEC) is a commonly isolated
human pathogen that is responsible for causing mucoid
diarrhea in patients from both industrialized and developing
countries [2–5]. EAEC has been shown to elicit
travelers’ diarrhea, pediatric diarrhea, impairment of
pediatric growth and cognition, and even extraintestinal
infections, such as urinary tract infections
and septicemia [4,6–11]. In addition, EAEC strains
have b

Enteroaggregative Escherichia coli (EAEC) is a common diarrhoeagenic human pathogen, isolated
from patients in both developing and industrialized countries, that is becoming increasingly
resistant to many frontline antibiotics. In this study, we screened 50 E. coli strains from children
presenting with diarrhea at the outpatients clinic of Assiut University Children’s Hospital, Egypt.
We show that all of these isolates were resistant to multiple classes of antibiotics and identified
two as being typical EAEC strains. Using whole genome sequencing, we determined that both
isolates carried, amongst others, blaCTX-M and blaTEM antibiotic resistance genes, as well as many
classical EAEC virulence determinants, including the transcriptional regulator, AggR. We demonstrate
that the expression of these virulence determinants is dependent on AggR, including aar,
which encodes for a repressor of AggR, Aar. Since biofilm formation is the hallmark of EAEC
infection, we examined the effect of Aar overexpression on both biofilm formation and AggRdependent
gene expression. We show that whilst Aar has a minimal effect on AggR-dependent
transcription it is able to completely disrupt biofilm formation, suggesting that Aar affects these
two processes differently. Taken together, our results suggest a model for the induction of
virulence gene expression in EAEC that may explain the ubiquity of EAEC in both sick and healthy

Interferon--inducible protein-10 (IP-10), is an inflammatory cytokine produced by different subsets of the immune cells and induces chemotaxis, apoptosis, growth of cells and angiostasis after binding to its receptor CXCR3. Inflammatory disorders, involving infectious diseases, immune dysfunction, and tumour growth have been linked to changes in CXCL10 levels. We aimed to investigate serum levels of IP-10 in chronic HBV infected patients undergoing treatment with entecavir and possible correlation with response to therapy. A total of 53 chronic HBV infected patients and 25 healthy controls were enrolled in this study. Patients included 20 with cirrhosis and 33 non-cirrhotic individuals. All patients received 0.5 mg/day entecavir and serum IP-10 level was determined by ELISA at baseline and at week 24 of treatment. mRNA expression of CXCR3 of PBMC was assessed by real-time polymerase chain reaction (RT-PCR). Response to therapy was achieved in 27/33 (81.8%) non-cirrhotic and 14/20 (70%) cirrhotic patients. Mean serum IP-10 levels was higher in patients than healthy controls, and cirrhotic patients had higher IP-10 than non-cirrhotic patients (520 vs 293.5 pg/ml; P<0.005). Response to treatment was associated with decreased IP-10 levels. Before treatment, the mean level in non-cirrhotic patients was 235±54 pg/ml, which decreased to 95±34 pg/ml (P<0.005) at week 24 of treatment. Similarly, in the cirrhotic group, IP-10 decreased from 458±42 pg/ml to 354±25 pg/ml (P <0.05) after 24 weeks of treatment. On the other hand, no change in IP-10 levels was observed for patients who did not respond to treatment. Interestingly, IP-10 levels correlated with PBMC’s expression of CXCR3 mRNA (r= 0.448, P = 0.004), ALT level (r=0.273, P =0.048), liver fibrosis score 4 (FIB-4) (r=0.664, P = 0.01) and HBV DNA level (r=0.762, P =0.0001). In conclusion; IP10 may be used to predict response to therapy in HBV-infected patients