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One of the important aspects of supply chain management is inventory management because the cost of inventories in a supply chain accounts for about 30% of the value of the product. The main focus of this work is to study the performance of a single-product serial supply chain operating with a base-stock policy and to optimize the inventory (i.e. base stock) levels in the supply chain so as to minimize the total supply chain cost (TSCC), comprising holding and shortage costs at all the installations in the supply chain. A genetic algorithm (GA) is proposed to optimize the base-stock levels with the objective of minimizing the sum of holding and shortage costs in the entire supply chain. Simulation is used to evaluate the base-stock levels generated by the GA. The proposed GA is evaluated with the consideration of a variety of supply chain settings in order to test for its robustness of performance across different supply chain scenarios. The effectiveness of the proposed GA (in terms of generating base-stock levels with minimum TSCC) is compared with that of a random search procedure. In addition, optimal base-stock levels are obtained through complete enumeration of the solution space and compared with those yielded by the GA. It is found that the solutions generated by the proposed GA do not significantly differ from the optimal solution obtained through complete enumeration for different supply chain settings, thereby showing the effectiveness of the proposed GA.

Bipolar affective disorder and schizophrenia are severe behavioral disorders with a lifetime risk of \sim 1% in the population worldwide. There is evidence that these diseases may manifest the phenomenon of anticipation similar to that seen in diseases caused by trinucleotide repeat expansions. A recent report has implicated a potassium channel-coding gene, KCNN3, which contains a polymorphic CAG repeat in its coding region, in schizophrenia and bipolar disorder. We have tried to confirm these findings in Indian patients suffering from bipolar disorder and schizophrenia. No statistically significant evidence for the presence of an excess of longer alleles in the patient population, as compared to ethnically matched controls, was found. However, an analysis of the difference of allele sizes revealed a significantly greater number of patients with schizophrenia having differences of allele sizes \geq 5 when compared to normal controls. This finding may be of functional significance as the KCNN3 protein is thought to act as a tetramer, and a large difference in allele sizes would result in an asymmetric molecule with a different number of glutamine residues in each monomer.