Background: Intra-abdominal adhesions are fibrous bands that develop after abdominal surgery or inflammation and cause mortality and morbidity following surgeries. This study aimed to assess the effects of bupivacaine, saline and two doses of lidocaine, after peritoneal lavage and to compare their effects in reducing abdominal adhesions in rat. Methods: In a blinded, randomised, placebo-controlled clinical trial, 50 female rats were anaesthetised and the parietal peritoneum was scratched to induce punctate bleeding. The rats were randomly assigned to five groups: saline, lidocaine 2% (3 and 6 mg/kg), bupivacaine 0.25% (2 mg/kg) and control (no irrigation). The peritoneal cavity was irrigated with the appropriate solution during laparotomy. Two weeks later, re-laparotomy was performed. The quantity, quality, severity and scores of adhesions were recorded and compared. Results: The quantity and quality of adhesions were significantly higher in the control group than in the lidocaine (6 mg/kg) and bupivacaine groups. The quality of the adhesions was higher in the normal saline group than in the lidocaine (6 mg/kg) and bupivacaine groups. The severity of adhesions between the lidocaine 3 and 6 mg/kg groups and between the lidocaine 3 mg/ kg and saline groups was lower than that in the control group. Conclusion: Using lidocaine (6 mg/kg) and bupivacaine lavage in first laparotomy reduces abdominal peritoneal obstruction because of the formation of adhesion bands.

Objectives: This study was undertaken to evaluate AmpC β-lactamase-producing Escherichia coli urine isolates and to characterize the frequency of plasmid-mediated AmpC (pAmpC)-encoding genes. Methods: Antimicrobial susceptibility tests were performed using the disk diffusion technique. AmpC β-lactamase production was assessed with a phenotypic inhibitor-based method. The presence of 6 pAmpC-encoding cluster genes was detected by multiplex polymerase chain reaction (PCR). Results: The proportion of antibiotic resistance of E. coli isolates ranged from 7.4% to 90.5%, and more than half (51.6%) of the total isolates were multidrug-resistant (MDR). Among the 95 E. coli isolates, 60 (63.2%) were found to be cefoxitin-resistant, but only 14 (14.7%) isolates were confirmed as AmpC β-lactamase-producers. In the PCR assay, pAmpC-encoding genes were found in 15 (15.8%) isolates, and blaDHA was the most prevalent type. However, blaFOX, blaMOX, and blaACC genes were not detected in the isolates. Conclusion Our findings contributed valuable information concerning antibiotic resistance, confirmatory phenotypic testing for AmpC production, and pAmpC β-lactamase gene content in E. coli isolates in southwestern Iran. The level of MDR recorded in AmpC-producing strains of this study was worrying; therefore, implementing strong infection control approaches to reduce the MDR burden is recommended.

INTRODUCTIONChildhood-onset proximal spinal muscular atrophies (SMAs) are an autosomal recessive, clinically heterogeneous group of neuropathies characterised by the selective degeneration of anterior horn cells. SMA has an estimated incidence of 1 in 10,000 live births. The causative genes are survival motor neuron (SMN) gene and neuronal apoptosis inhibitory protein (NAIP) gene. Deletions of the telomeric copy of SMN gene (SMN1) have been reported in 88.5% to 95% of SMA cases, whereas the deletion rate for NAIP gene (NAIP) is between 20% and 50% depending on the disease severity. The main objective of this study was to genetically characterise the childhood onset of SMA in Iran.

MATERIALS AND METHODSMolecular analysis was performed on a total of 75 patients with a clinical diagnosis of SMA. In addition to common PCR analysis for SMN1 exons 7 and 8, we analysed NAIP exons 4 and 5, along with exon 13, as a internal control, by bi-plex PCR.

RESULTSThe homozygous-deletion frequency rate for the telomeric copy of SMN exons 7 and 8 in all types of SMA was 97%. Moreover, exons 5 and 6 of NAIP gene were deleted in approximately 83% of all SMA types. Three deletion haplotypes were constructed by using SMN and NAIP genotypes. Haplotype A, in which both genes are deleted, was seen in approximately 83% of SMA types I and II but not type III. It was also found predominantly in phenotypically severe group with an early age of onset (i.e., less than 6-month-old). We also report 34 of our prenatal diagnosis.

CONCLUSIONSTo our knowledge, the present study is the first one giving detailed information on SMN and NAIP deletion rates in Iranian SMA patients. Our results show that the frequency of SMN1 homozygous deletions in Iran is in agreement with previous studies in other countries. The molecular analysis of SMA-related gene deletion/s will be a useful tool for pre- and postnatal diagnostic.

Age of Onset ; Child, Preschool ; Cyclic AMP Response Element-Binding Protein ; genetics ; Female ; Gene Deletion ; Humans ; Iran ; Male ; Muscular Atrophy, Spinal ; etiology ; genetics ; physiopathology ; Nerve Tissue Proteins ; genetics ; Neuronal Apoptosis-Inhibitory Protein ; genetics ; RNA-Binding Proteins ; genetics ; SMN Complex Proteins ; Survival of Motor Neuron 1 Protein