Objective Study analyzes mutation in mtDNA (Mitochondrial DNA) among diabetic women with PCOS in non-diabetic diabetic women and compared with the healthy control. Women with known case of hyperandrogenism, ovulatory dysfunction and/or polycystic ovaries were selected and anthropometric and demographic variables were collected during their clinical visit. Biochemical estimation of glucose, FSH, LH, estradiol (E2), and insulin levels were analyzed. Mutational analysis of mt-tRNA genes of each individual was compared with the updated consensus Cambridge sequence. The mtDNA content was determined in triplicate using SYBR green PCR mastermix. Results The clinical and biochemical characteristics of participants showed no statistical difference in age and/or FSH, PRL, E2, PRGE or fasting glucose value between patients of different groups. Women with PCOS-D had significantly higher LH, LH/FSH, TT and fasting insulin levels and HOMA-IR with respect to the control group. Ten different type of mutation were seen in POCS group. Most of these mutations were confined to evolutionarily conserved region. The mtDNA copy numbers were considerably lower PCOS group irrespective of diabetic status. To conclude, the current study inferred that the mutations occur in the mitochondrial genome, mt-tRNA in specific, are the important causal factor in PCOS.

Generally, treatment of urinary tract infection (UTI) in children is a difficult task, due to development of high resistance against antibiotics. The object of this study is to investigate the greatest causative microorganisms, their susceptibility and resistance to antibiotics in children suffering from UTI in Baghdad. A total of 810 urine samples were collected from suspected cases of UTI in children patients of ages (1 day to 12 years) of both sexes. Urine specimens were examined by urinalysis and cultured for isolation of microbial agents. In this study, Bacterial growth was obtained in 202 samples (24.39%) out of 810 urine samples. Various pathogenic organisms were isolated, which represented by A) Gram-Negative bacilli include Escherichia coli (41.58%), Enterobacter spp. (13.68%), Proteus Mirabilis (12.78%), Acinetobacter spp. (4.45%), Providencia spp. (4.45%), Pseudomonas aeruginosa (3.46), Klebsiella pneumoniae (2.47%), Citrobacter spp.(0.49%), Salmonella Spp.(0.49%), B) Gram- Positive cocci: Staphylococcus aureus (11.38%), Enterococcus faecalis (1.98%) and Streptococcus agalactiae (1.48%) C) Candida albicans (0.9%).). According to antibiotic susceptibility test, mostly the isolates were resistant to Nalidixic acid (67.05%), cefotaxime (59.40%) and cefepime (50.49%). Mostly Gram-Negative bacilli were responsible for UTI, and maximum recurrent isolated bacteria were Escherichia coli. The isolated bacteria were found to be sensitive to Imipenem, Amikacin, and ciprofloxacin. Therefore, the selection of antibiotic therapy in UTI should depend on the native sensitivity form of the infecting organism.

Background/aim:A chronic neuroinflammation of disease with unknown cause and variable clinical development is multiple sclerosis (MS).Interleukin-23 (IL-23) is a constituent of the IL-12 cytokine family that has shown through development of T helper type 17 (Th17) cells development could play a chief role in the inflammatory autoimmune responses in multiple sclerosis (MS).Objective:A goal of studyis to assess IL-23 level in serum in Iraqi patients with multiple sclerosis (MS) in comparison with healthycontrol group.Methods:blood sampleswere taken from 45patients with multiple sclerosis and 30 healthy controls. IL-23 level in the serum wasassessed by Enzyme-Linked immunosorbent assay (ELISA).Results:: IL-23 level in the serum taken from affected persons was found to be significantly hiegher than its level in the serum of control group (P<0.05). We also observed significantlyhigher IL-23 serumlevels in females than males within patients group (P. Value=0.0349).Conclusions:Theresults show the increasinglevel ofIL-23 in patients with multiple sclerosis which confirms a role for IL-23 in MSsuggestedcould be a particularbiomarker and thecurative goalin MS therapythrough inhibiting.

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