TCP Concurrent Echo Program using Fork and Thread

In networking, client-server model plays a vital role in exchanging information between processes. Client-server model predominantly relies on socket programming. Sockets allow communication between processes on same or different machines. Servers in the client-server model are of two types- Iterative and Concurrent. This paper describes about the elementary socket function for TCP client/server. An implementation of TCP Echo program for concurrent server using fork and thread is also given. DOI: 10.17762/ijritcc2321-8169.160410

Structure and chromosomal location of the bovine gene for the heart muscle isoform of cytochrome c oxidase subunit VIII

We have isolated the bovine COX8H gene for the heart/muscle isoform of cytochrome c oxidase (COX) subunit VIII from a library of bovine genomic DNA cloned into lambda EMBL3. Primer extension assays on bovine heart mRNA mapped the 5′ ends of COX8H transcripts to a CA dinucleotide 62-bp upstream from the ATG codon. The gene thus spans 1565-bp and comprises two exons and one large intron of 1227 bp. Exon 1 encodes the 5′ untranslated region, a 24-amino acid presequence, and the first 13 amino acids of the mature COX VIII-H protein. Exon 2 encodes the remainder of the cDNA: amino acids 14 to 46 plus the 66-bp 3′ untranslated region. The exon-intron boundaries matched the consensus splice junction sequences. Two protein polymorphisms were seen: an Ala/Val polymorphism at position-6 in the presequence and the previously noted Lys/Arg polymorphism at residue 7 of the mature protein. A Taq I polymorphism occurs in the intron. The COX8H gene was mapped by bovine x rodent somatic cell hybrid mapping panels to bovine (BTA) Chromosome (Chr) 25 with 100% concordancy. BTA25 is conserved relative to the long arm of human (HSA) Chr 11, which contains COX8, the gene for the single human COX VIII subunit that is homologous to the liver isoform.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47018/1/335_2004_Article_BF00303255.pd

Towards the clinical implementation of pharmacogenetics in bipolar disorder.

BackgroundBipolar disorder (BD) is a psychiatric illness defined by pathological alterations between the mood states of mania and depression, causing disability, imposing healthcare costs and elevating the risk of suicide. Although effective treatments for BD exist, variability in outcomes leads to a large number of treatment failures, typically followed by a trial and error process of medication switches that can take years. Pharmacogenetic testing (PGT), by tailoring drug choice to an individual, may personalize and expedite treatment so as to identify more rapidly medications well suited to individual BD patients.DiscussionA number of associations have been made in BD between medication response phenotypes and specific genetic markers. However, to date clinical adoption of PGT has been limited, often citing questions that must be answered before it can be widely utilized. These include: What are the requirements of supporting evidence? How large is a clinically relevant effect? What degree of specificity and sensitivity are required? Does a given marker influence decision making and have clinical utility? In many cases, the answers to these questions remain unknown, and ultimately, the question of whether PGT is valid and useful must be determined empirically. Towards this aim, we have reviewed the literature and selected drug-genotype associations with the strongest evidence for utility in BD.SummaryBased upon these findings, we propose a preliminary panel for use in PGT, and a method by which the results of a PGT panel can be integrated for clinical interpretation. Finally, we argue that based on the sufficiency of accumulated evidence, PGT implementation studies are now warranted. We propose and discuss the design for a randomized clinical trial to test the use of PGT in the treatment of BD

Convergent functional genomic studies of omega-3 fatty acids in stress reactivity, bipolar disorder and alcoholism

Omega-3 fatty acids have been proposed as an adjuvant treatment option in psychiatric disorders. Given their other health benefits and their relative lack of toxicity, teratogenicity and side effects, they may be particularly useful in children and in females of child-bearing age, especially during pregnancy and postpartum. A comprehensive mechanistic understanding of their effects is needed. Here we report translational studies demonstrating the phenotypic normalization and gene expression effects of dietary omega-3 fatty acids, specifically docosahexaenoic acid (DHA), in a stress-reactive knockout mouse model of bipolar disorder and co-morbid alcoholism, using a bioinformatic convergent functional genomics approach integrating animal model and human data to prioritize disease-relevant genes. Additionally, to validate at a behavioral level the novel observed effects on decreasing alcohol consumption, we also tested the effects of DHA in an independent animal model, alcohol-preferring (P) rats, a well-established animal model of alcoholism. Our studies uncover sex differences, brain region-specific effects and blood biomarkers that may underpin the effects of DHA. Of note, DHA modulates some of the same genes targeted by current psychotropic medications, as well as increases myelin-related gene expression. Myelin-related gene expression decrease is a common, if nonspecific, denominator of neuropsychiatric disorders. In conclusion, our work supports the potential utility of omega-3 fatty acids, specifically DHA, for a spectrum of psychiatric disorders such as stress disorders, bipolar disorder, alcoholism and beyond

A processed pseudogene with an intact coding sequence for rat liver cytochrome c oxidase subunit VIc

The biogenesis of eukaryotic cytochrome c oxidase involves the coordinate expression of nuclear and mitochondrial genes. Very little information is available on the gene structure of nuclear-coded cytochrome c oxidase subunits in mammalian systems. We report here the isolation and complete nucleotide sequence determination of a processed pseudogene for cytochrome c oxidase subunit VIc from rat liver. The pseudogene lacks introns and the coding region is intact with no deleterious lesions; however, there are 7 amino acid (aa) differences when compared to the sequence derived from cDNA clones. The pseudogene has the potential to code for a protein of 76 aa, containing a putative 3 aa N-terminal presequence when compared to the mature bovine heart VIc subunit. Potential regulatory regions, including a TATA box, are present in the 5′-flanking region

A processed pseudogene with an intact coding sequence for rat liver cytochrome c oxidase subunit VIc

The biogenesis of eukaryotic cytochrome c oxidase involves the coordinate expression of nuclear and mitochondrial genes. Very little information is available on the gene structure of nuclear-coded cytochrome c oxidase subunits in mammalian systems. We report here the isolation and complete nucleotide sequence determination of a processed pseudogene for cytochrome c oxidase subunit VIc from rat liver. The pseudogene lacks introns and the coding region is intact with no deleterious lesions; however, there are 7 amino acid (aa) differences when compared to the sequence derived from cDNA clones. The pseudogene has the potential to code for a protein of 76 aa, containing a putative 3 aa N-terminal presequence when compared to the mature bovine heart VIc subunit. Potential regulatory regions, including a TATA box, are present in the 5'-flanking region

Expression of Cytochrome P-450 and Albumin Genes in Rat Liver: Effect of Xenobioticst

Thioacetamide, a hepatocarcinogen and an inhibitor of heme synthesis, blocks the phenobarbitone- mediated increase in the transcription of cytochrome P-450b+e messenger RNA in rat liver. This property is also shared by CoCl, and 3-amino-l,2,4-triazole, two other inhibitors of heme synthesis. Thus, it appears feasible that heme may serve as a positive regulator of cytochrome P-450b+e gene transcription. Thioacetamide enhances albumin messenger RNA concentration, whereas phenobarbitone decreases the same. However, these changes in albumin messenger RNA concentration are not accompanied by corresponding changes in the transcription rates. Therefore, drug-mediated changes in albumin messenger RNA concentration are due to posttranscriptional regulation. The property of thioacetamide to enhance the albumin messenger RNA concentration is not shared by CoC1, and 3-amino- 1,2,4-triazole. Therefore, heme does not appear to be a regulatory molecule mediating the reciprocal changes brought about in the concentrations of cytochrome P-450b+e and albumin messenger RNAs