Thyroid disorders are one of the most frequent disorders affecting endocrine system. The present study aimed to identify the frequency of thyroid disorder in our locality at Duhok city. To do so, a total of one hundred patients and one hundred apparently healthy control individuals were enrolled in this study. Samples of venous blood (5 ml) were withdrawn from patients and control subjects and analysed. Clinical assessment was performed by a specialist and each patient provided with a document supporting preliminary clinical diagnosis. Measurements of serum TSH, T3, T4, and anti-thyroperoxidase antibodies (anti-TPO antibodies) serum levels were performed. All assays were conducted at Duhok central health laboratory. Out of the one hundred patients and the one hundred control groups, forty-two and thirty candidates were randomly selected, respectively. The mean TSH serum levels of 25.87 (uIU/ml) for the patients significantly differ from that of the control group 3.55 (uIU/ml) (p<0.001). However, T3 and T4 serum levels indicated no significant difference between the two categories. Moreover, there was statisticaly significant difference (p< 0.0001) between the patients and control groups when their mean serum anti-TPO concentrations were compared.  In conclusion, considerable number of subjects appeared to be candidates for deranged thyroid functions and is susceptible to autoimmune thyroid disorder.

(TEM) resistance gene. Results: Half of the cases involved were found to be caused by MRSA. All the tested isolates showed positive amplification bands for the presence of mec A gene and only 48.8% of these harbored TEM gene. The obtained results revealed high sensitivity of universal bacterial and TEM primers expressed as 97.6% and 100% respectively, while the sensitivity of mec A primer was limited to 60%. Conclusion:The phenotypic identification of MRSA revealed a higher incidence rate and that different molecular techniques can yield conflicting results and it can also be concluded that resistant due to beta-lactamase production can be a crucial factor added to the previously settled methicillin resistant due to mec A gene.

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The thyroid gland is frequently associated with autoimmune disease. It produces thyroid hormones responsible for controlling cellular metabolism. The current case control study  involved ninety subjects which were assigned into two equal-numbered groups of patients and apparently healthy controls. For laboratory evaluation, five millilitres of venous blood were withdrawn from individual participants, serum were collected and  stored at –20 oC to be analysed.  Immunoassay technique was used to measure the serum level of thyroid stimulating hormone (TSH), thyroxine (T4), and triiodothyronine (T3). While ELISA technique was used for measuring the serum levels of anti-thyroid peroxidase (anti-TPO) antibodies and IL-22. The results of the current study showed that, in  the patient group, thirty eight (84.44 %) subjects were diagnosed with hypothyroidism, represented by thirty five female (77.77 %) and three male (6.67 %); furthermore, seven individuals (15.56 %) were grouped as hyperthyroid patients and represented by five females  (11.11 %) and two males (4.45 %). The results also demonstrated that the serum  TSH levels  (12.04  ± 2.76) for the patients were significantly (p< 0.05) higher than that of the control group  (1.87 ± 0.15). Whereas, T3 and T4 mean serum levels ± SE were 2.05 nmol/l ±0.14; 100.66 nmol/l ± 4.76 and 2.14 nmol/l ± 0.07; 105.37 nmol/l ± 2.92 for patient and control categories, respectively. The findings of this work showed that mean serum level (IU/ml) of anti-thyroidperoxidase antibody in patient group differed significantly (P <0.05) in comparison to control group  (represented by 259.08±59.99 and 8.71 ±1.23, respectively). No statistical difference was non-significant when comparison involved mean serum concentration levels of IL-22 for patients (157.22 ng/ml ± 24.81) and controls (157.08 ng/ml ± 24.80). In conclusion: IL-22 cannot be proposed as an essential factor participating the development and/or the progression of autoimmune thyroid disease (AITD).