Background: The mandatory month is Ramadan on Muslim's fasting. Muslims cease from ingestion of food and water starting onset to grass widower to who wants to be fasting in this month that's according to the lunar calendar; so many immunological, physiological and biochemical changes may happen. Objective: To evaluate some vitamins, hormones and immunological markers in the first and the 28th day of fasting. Patients and Methods: Twenty five healthy adult male who were subjected to this study. The age range was 24-49 years with mean ± SD (31.6±7.07). Body weight, BMI, serum glucose, total cholesterol, high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), very low density lipoprotein-cholesterol (VLDL-C), triglyceride (TG), aspartate amino transferase (AST), alanine amino transferase (ALT), alkaline phosphatase (ALP), total serum bilirubin (TSB), serum creatinine, blood urea, serum electrolytes (Na, K, Cl,) haemoglobin concentration (Hb), haematocrit, vitamin -D, testosterone and C-reactive protein (CRP) were estimated in the 1st day and the 28th day of Ramadan month. The while-interval of study was 27 days. Human privacy, statistical analyses and P value were used. Results: Serum glucose, LDL, ALT, TSB, serum creatinine, blood urea, vitamin D and CRP were significantly decreased in 28th day of fasting (P=0.0002, P=0.005, P=0.009, P=0.00004, P=0.013, P=0.0074, P=0.0109, respectively). There were no significance change in total cholesterol, VLDL-C, TG, AST, ALP, K, Cl, Hb, haematocrit, testosterone (P>0.05). While HDL-C and serum Na were increased significantly in this study (P= 0=0.004, P=0.0214, respectively). Conclusion: Consuming two meals per a day during month of Ramadan has a balancing effect on biochemical, enzymes and CRP in fasted men.

No abstract

Public swimming pools, if not treated well could work as a reservoir of many microorganisms that cause infections among swimmers. Conjunctivitis is one of those common infections that resulted from microbial and non-microbial agents, microbial conjunctivitis caused by viral (mainly Human adenovirus HAdVs) and bacterial infections. This study aims to investigate the prevalence of microbial causative agents of swimming pool conjunctivitis and evaluating the swimming pools in terms of health and the extent of contamination in Erbil province. Eighty-eight specimens were isolated and identified from the swimmers showing signs and symptoms of swimming pool conjunctivitis from different public swimming pools in Erbil city from January to the end of February 2020. Sample identified using bacteriological methods, serology test, and nested PCR for detection of HAdVs. The swimmers samples consisted of 60 males and 28 females, and they were aged between 16-56 years. The obtained results showed that, out of 88 samples, 36 (40.91%) detected as a viral infection and 29 (32.95%) as bacterial infection, while, 23 (26.13%) showed no growth (non-microbial infection). Frequency of swimming pool conjunctivitis among male and female was 60 (68.2%) and 28 (31.8%) respectively. Depending on the obtained results, it can be concluded that conjunctivitis could result from viral, bacterial, and non-microbial agents, a viral infection is the main cause followed by a bacterial infection, also public swimming pools are not a safe place and swimmers are subjected to infection by different pathogens.

No abstract

Forty five isolates of Proteus mirabilis were identified among 600 samples taken from patients with urinary tract infection from different hospitals in Erbil City. Isolates were identified from urine sample by using cultural, morphological and biochemical characteristics and confirmed confirmed by VITEK 2 systems. Antibiotic sensitivity testing was done for all isolates by using fifteen antibiotic types which included Amikacin (AK), Ampicillin (AMP), Aztreonam (AT), Chloramphenicol (C), Cephalothin (CEP), Ciprofloxacin (CIP), Ceftriaxone (CTR), Cefotaxime (CTX) Fosfomycin (FOX), Gentamicin (GEN), Imipenem (IMP), Nalidixic acid (NA), Norfloxacin (NOR), Piperacilin (PI) and Tobramycin (TOB). IMP was the most effective antibiotic against isolated of P. mirabilis. The resistance rate of the isolates toward these antibiotics were 8.8% for CIP, 11% for AT, 11% for FOX, 15.5% for NOR, 17.7% for TOB, 20% for AK, 22% for PI, 26% for CTR, 28.8% for CTX, 33% for NA, 35.5% for GEN, 44% for C, and 62% for AMP respectively. To control the antibiotic resistance of the tested P. mirabilis isolates, curing of plasmid DNA was conducted using tetracycline and elevated temperature at 46 o C, two most resistance isolates were chosen for this purpose P32, and P40, then treated with different concentrations of tetracycline (0.5, 1, 1.5, 2, 2.5, 3, 3.5, and 4) µg/ml separately. The MIC for tetracycline was 2.5µg/ml and SMIC 2µg/ml was used as a curing agent. The genes encoded resistance to ampicillin, chloramphenicol, cephalothin, ceftriaxone, cefotaxime, gentamicin and tobramycin were cured from P32 and the percentage of curing was (46.6%), while amikacin, chloramphenicol, ciprofloxacin and gentamicin resistance genes were cured from P40 isolate and the curing percent was (26.6%).The results confirmed by conducting gel electrophoresis and revealed that tetracycline DOI: 10.24086/cuesj.si.2017.n2a5 47 removed plasmid of P32, while it had no effect on plasmid of P40. On the other hand, elevated temperature used also as curing agent and the results revealed that resistance to amikacin, ampicillin, chloramphenicol, cephalothin, ceftriaxone, gentamicin and tobramycin genes were cured from P32 and the curing percent was (46.6%), while genes encoding amikacin, ampicillin, chloramphenicol, ciprofloxacin, ceftriaxone, cefotaxime, fosfomycin, gentamicin, nalidixic acid, norfloxacin and tobramycin were cured from P40 isolate with the percentages of (73.3%) after incubating the isolates at 46 o C. It is clear that elevated temperature is the most efficient method than tetracycline. The results confirmed by conducting gel electrophoresis and showed that both tested isolates lost their plasmids after incubation at 46 o C.