Evaluation of serum mineral micronutrients (Zn, Cu, Fe, Mg) and their correlation with clinical parameters (gingival index, probing pocket depth, clinical attachment loss) in chronic periodontitis patients

Background: Nutrition especially micro-mineral nutrients plays a major role in the etiology of chronic periodontitis. Serum levels of micro-mineral nutrients can be used as markers for the incidence of periodontitis and may also be used as indicators for dietary supplementation. Aims and Objectives: The aim of the study was to estimate the serum levels of Zn, Cu, Fe, and Mg of chronic periodontitis patients and normal healthy controls., to measure the clinical parameters (gingival index, probing pocket depth [PPD], and clinical attachment loss) in chronic periodontitis patients and normal healthy controls., to compare the levels of serum Zn, Cu, Fe, and Mg levels of chronic periodontitis patients and healthy controls and to correlate the levels of serum micronutrients with clinical parameters (gingival index, PPD, and clinical attachment loss) in chronic periodontitis patients and healthy controls. Materials and Methods: A total of 110 subjects, 55 subjects with chronic periodontitis and 55 healthy control subjects in the age group 35–65 years were selected for the study. Serum micronutrient levels of Cu, Fe, Zn, Mg, and the clinical parameters were measured. Results: Serum concentrations of Cu and Fe showed statistically significant increase and serum Zn and Mg showed a significant decrease in peridontitis patients as compared to normal healthy controls. Copper and Fe showed a significant positive correlation and Zn and Mg showed a significant negative correlation with clinical parameters (gingival index, PPD, and clinical attachment loss). Conclusion: The present study supports and extends the view that the assessment of serum mineral micronutrient can serve as possible biomarkers or indicators for an inflammatory condition like chronic periodontitis

Regulation of mammary gland branching morphogenesis by the extracellular matrix and its remodeling enzymes.

A considerable body of research indicates that mammary gland branching morphogenesis is dependent, in part, on the extracellular matrix (ECM), ECM-receptors, such as integrins and other ECM receptors, and ECM-degrading enzymes, including matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs). There is some evidence that these ECM cues affect one or more of the following processes: cell survival, polarity, proliferation, differentiation, adhesion, and migration. Both three-dimensional culture models and genetic manipulations of the mouse mammary gland have been used to study the signaling pathways that affect these processes. However, the precise mechanisms of ECM-directed mammary morphogenesis are not well understood. Mammary morphogenesis involves epithelial 'invasion' of adipose tissue, a process akin to invasion by breast cancer cells, although the former is a highly regulated developmental process. How these morphogenic pathways are integrated in the normal gland and how they become dysregulated and subverted in the progression of breast cancer also remain largely unanswered questions

Site-Directed Mutations and the Polymorphic Variant Ala160Thr in the Human Thromboxane Receptor Uncover a Structural Role for Transmembrane Helix 4

The human thromboxane A2 receptor (TP), belongs to the prostanoid subfamily of Class A GPCRs and mediates vasoconstriction and promotes thrombosis on binding to thromboxane (TXA2). In Class A GPCRs, transmembrane (TM) helix 4 appears to be a hot spot for non-synonymous single nucleotide polymorphic (nsSNP) variants. Interestingly, A160T is a novel nsSNP variant with unknown structure and function. Additionally, within this helix in TP, Ala1604.53 is highly conserved as is Gly1644.57. Here we target Ala1604.53 and Gly1644.57 in the TP for detailed structure-function analysis. Amino acid replacements with smaller residues, A160S and G164A mutants, were tolerated, while bulkier beta-branched replacements, A160T and A160V showed a significant decrease in receptor expression (Bmax). The nsSNP variant A160T displayed significant agonist-independent activity (constitutive activity). Guided by molecular modeling, a series of compensatory mutations were made on TM3, in order to accommodate the bulkier replacements on TM4. The A160V/F115A double mutant showed a moderate increase in expression level compared to either A160V or F115A single mutants. Thermal activity assays showed decrease in receptor stability in the order, wild type>A160S>A160V>A160T>G164A, with G164A being the least stable. Our study reveals that Ala1604.53 and Gly1644.57 in the TP play critical structural roles in packing of TM3 and TM4 helices. Naturally occurring mutations in conjunction with site-directed replacements can serve as powerful tools in assessing the importance of regional helix-helix interactions

Determinants of Infant Mortality in Older ASEAN Economies

Infant mortality in the Association of Southeast Asian Nations (ASEAN) has been declining, yet disparities remain between the nations. This paper therefore explores the determinants of infant mortality in the older ASEAN-4 economies, Malaysia, Thailand, Indonesia and the Philippines using an Autoregressive Distributed Lag (ARDL) Error Correction Model framework. The key findings of the study are: First, there is evidence of long-run relationships among infant mortality, education, female fertility, income and access to healthcare. Second, the determinants of infant mortality vary between countries. Female fertility emerged as the main determinant of infant mortality in Malaysia, while access to healthcare matter for infant mortality in Indonesia, and to a lesser extent for the Philippines. The income effect is significant for reducing infant mortality in Malaysia, while female education is important for Indonesia and Thailand. Third, the speed of adjustment of infant mortality rate is comparatively low in ASEAN-4