Ophthalmic complications of injectable facial fillers.

The recently published mini-review article by Miotti is an effort to clarify various aspects regarding the choice between fat grafts and fillers in facial aesthetic surgery. One of the complications associated with the administration of fillers is the possibility of vascular injury and spread of the dermal filler into the orbit, causing unexpected effects at a site distant from that of the initial injection, including ophthalmoplegia, ptosis and even visual compromise. Acute vision loss following filler injection is a devastating complication, occurring in up to 0.

Bidirectional link between periodontitis and systemic inflammation in diabetic retinopathy.

Periodontitis is independently associated with numerous lifestyle diseases. Diabetic patients have approximately threefold increased odds of periodontitis, which in turn increases the risk of systemic inflammation. The study by Thazhe Poyil is an effort to establish the inflammatory link between diabetic re-tinopathy (DR) and periodontitis based on the periodontal inflamed surface area in diabetic patients with and without DR.

Nutrition interventions and clinical outcomes of pregnant women with gestational diabetes mellitus: More than meets the eye.

In the retrospective study by Luo regarding clinical outcomes in gestational diabetes mellitus (GDM), the results are statistically significant in favour of the benefits of individualized nutrition interventions enumerated therein. The study has provided important evidence to improve maternal and child health in the Asian population. The methods, however, appear to have considerable limi-tations, wherein the time point of diagnosis of GDM, severity of GDM, selection bias, compliance to therapy, important maternal covariates, observable microvascular abnormalities and the confounding effect of added insulin have not been considered.

Type II PtdIns 4-kinase β associates with CD4-p56lck complex and is involved in CD4 receptor signaling.

Type II phosphatidylinositol (PtdIns) 4-kinases are involved in the synthesis of PtdIns 4-phosphates and modulate various cell functions like, intracellular signaling, cytoskeletal rearrangements, vesicular trafficking, and pathogen invasion. In CD3 receptor activated T cells, a type II PtdIns 4-kinase β is recruited to CD3 receptor zeta and plays a role in intracellular calcium release and probably in actin cytoskeleton reorganization. T cell receptor mediated activation is supported by CD4 receptor.

Piperine inhibits type II phosphatidylinositol 4-kinases: a key component in phosphoinositides turnover.

Piperine has been shown to have anti-inflammatory properties. The molecular mechanisms by which it mediates anti-inflammatory activities remain elusive. Type II phosphatidylinositol 4-kinase(s) are key components in FcεRI receptor-mediated signaling leading to inflammatory mediators release in RBL-2H3 cells.

Type II phosphatidylinositol 4-kinases interact with FcεRIγ subunit in RBL-2H3 cells.

Ligation of high-affinity IgE receptor I (FcεRI) on RBL-2H3 cells leads to recruitment of FcεRI and type II phosphatidylinositol 4-kinases (PtdIns 4-kinases) into lipid rafts. Lipid raft integrity is required for the activation of type II PtdIns 4-kinases and signal transduction through FcεRIγ during RBL-2H3 cell activation. However, the molecular mechanism by which PtdIns 4-kinases are coupled to FcεRI signaling is elusive.

Fyn kinase regulates type II PtdIns 4-kinases in RBL 2H3 cells.

Type II phosphatidylinositol 4-kinases are implicated in FcεRI-mediated signaling cascades leading to release of inflammatory molecules. Cross-linking of FcεRI on RBL 2H3 cells results in protein tyrosine phosphorylation and activation of type II PtdIns 4-kinase activity. Protein tyrosine kinase(s) that phosphorylate type II PtdIns 4-kinase(s) in RBL 2H3 cells remains elusive and is being addressed in this manuscript.

Sanguinarine suppresses IgE induced inflammatory responses through inhibition of type II PtdIns 4-kinase(s).

The effects of sanguinarine on IgE mediated early signaling mechanisms leading to inflammatory mediators release were investigated. Pretreatment of RBL 2H3 cells with sanguinarine inhibited IgE induced activation of type II PtdIns 4-kinase activity. Concomitant with type II PtdIns 4-kinase inhibition, sanguinarine also inhibited IgE induced degranulation and β hexosaminidase release in RBL 2H3 cells.

Perception of young doctors towards service to rural population in Bihar.

With the launch of National Rural Health Mission (NRHM), rural health is being given more attention than ever before but health of the rural population is still in the hands of handful of qualified doctors. To know the willingness of young doctors to serve rural population and factors associated with their decision, 176 participants (101 students and 75 interns) of a medical college of Bihar were interviewed during the period July 2005 to December 2006. Only 9.

Neurotoxicity of the anticoagulant-selective E149A-activated protein C variant after focal ischemic stroke in mice.

Wild type (WT) activated protein C (APC) and cytoprotective-selective APC variants such as 3K3A-APC (<10% anticoagulant but normal cytoprotective activity) are neuroprotective in murine focal ischemic stroke models. Here we compared the neuroprotective effects of the anticoagulant-selective E149A-APC variant (>3-fold increased anticoagulant activity but defective cytoprotective activities) to those of the cytoprotective-selective 5A-APC variant (<10% anticoagulant activity). After transient distal middle cerebral artery occlusion, mice received a vehicle, E149A-APC or 5A-APC at 0.

Type II phosphatidylinositol 4-kinase(s) in cell signaling cascades.

Phosphorylated derivatives of phosphatidylinositol (PtdIns) are key components of many signaling cascades. Many isoforms of PtdIns kinases, PtdIns phosphate kinases and phosphatases use these lipids in amazing networks of signaling cascades that are yet to be understood fully. PtdIns 4-kinase(s) phosphorylates PtdIns at the 4th -OH position of inositol head group and are classified in to type II and III PtdIns 4-kinases.