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The reactive power demand of the induction generator is significantly increased when the generator runs close to the rated operating point. The losses are increased due to the increased reactive power flow. Due to the limitation of converter ratings in the doubly fed induction generator (DFIG) system, power clipping may occur at turbine-rated conditions. In this paper, an optimum strategy for reactive power flow in the DFIG scheme is proposed to capture maximum wind power with minimum total losses. The proposed strategy considers the machine-copper loss, converters' loss, and filter loss. Reasonable values for converter ratings are investigated and compared. The modeling of the DFIG-based wind turbine along with its control scheme is designed in Matlab/Simulink environment. Simulation results are presented to ensure the validity and feasibility of the proposed strategy for reactive power management.Index Terms-doubly fed induction generator, reactive power management, loss minimization of wind generation schemes, and wind-based distributed generation.

Background: Although recent meta-analyses indicates a consistent significant inverse relation of serum 25 (OH) D and the prevalence of gestational diabetes mellitus (GDM), the mechanism is unclear and conflicting opinions continue to be reported. Objectives: The objectives are: 1) comparison of vitamin D status in diabetic and non-diabetic pregnant women; 2) trying to determine the level of vitamin D associated with GDM, and its sensitivity and specificity; 3) determination of the relation of hypovitaminosis D with insulin resistance. Subjects and Methods: One hundred consecutive pregnant women (<28 weeks gestational period) from the attendants of the out-patient clinic at our hospital were diagnosed for GDM by glucose tolerance test (GTT) (75 g 2 h). Among them, 40 patients met the inclusion criteria for this study (group I). As a comparative group, another 40 pregnant ladies were included, 20 of them (group II) had pre-gestational type II DM, and the other 20 (group III) had normal glucose tolerance (NGT) as a control. For all the participants, we estimated fasting blood glucose, fasting serum insulin, homeostasis model assessment of (HOMA-IR and HOMA-B), quantitative insulin sensitivity check index (QUICKI), and serum 25-OH vit D. The ROC curve analysis was used to determine the optimal threshold value of vit D in relation to DM. Results: Compared to the control group, the diabetic patients showed a statistically significant increase in the levels of fasting glucose, 1-hour postprandial glucose, 2-hour post prandial glucose, fasting insulin, and HOMA-IR, (P=0.000 for all). None of the diabetic patients showed optimal vit D level. Vit D insuficiency (10 -29 ng/ml) was found in 32.5% of patients in group I, 55% in group II, and 50% in group III. Vit D deficiency (<10 ng/ml) was found in 67.5% of patients in group I, 45% in group II, and 0% in group III. Significant negative correlation was found for vit D with fasting insulin and FBS. The AUC for 25 OH vit D was 97%, CI was 95% and p-value was 0.0001. The sensitivity, specificity, and positive and negative predictive values of 25 OH vit D in GDM versus control persons were 97%, 90%, 95.1%, 94.7% respectively at a cut-off level <22 ng/ml. Conclusions: Although it might seem premature to draw a sharp relation between hypovi- taminosis D and GDM, this study showed the importance of vit D in GDM, the need for supplementation below 22 ng/ml, and the role of hypovitaminosis D in increasing insulin resistance. Further randomized studies with vit D supplementation are recommended.