Study and Analysis of Fluid Filled Abnormalities in Retina Using OCT Images

Visual impairment is one of the most regularly happening infections in human. The reason being variation from the normal in the different layers of retina because of strange measure of liquid either abundance aggregation or shortage. This paper targets recognizing and assessing the different abnormalities that could be earlier stages to visual deficiency. The proposed target is achieved by means of implementation using Digital Image Processing Technique, starting from preprocessing to classification at various stages. Not restricting to binary classification as normal or abnormal, the proposed system also extends its capacity to classify the input image as Cystoid Macular Edema (CME), Choroidal Neo Vascular Membrane (CNVM), Macular Hole (MH) and normal images. The preprocessing methodology implemented filters to remove the speckle noises which are most common in ultrasound-based imaging system. Random forest classifier was utilized for classifying the input features and also seems to be promising on par with the various existing methodologies

ROLE OF SUBSTANCE P IN PANCREATITIS AND ASSOCIATED DISEASES

Substance P (SP) is a neuropeptide that has its place in the tachykinin family and helps in the transmission of neurogenic signals. SP is also a neuromodulator that plays a crucial part in pain during inflammatory processes. It is produced by the capsaicin-sensitive unmyelinated C fibers sensory neurons by the central and peripheral nervous systems. Substance P is known as a critical primary responder to most of the extreme stimuli, i.e., specifically those with the ability to destabilize the biological integrity. Hence, SP can be considered as an instantaneous system for defense, stress, healing, etc. SP is known to perform a vital role in neurogenic inflammation and the pathophysiology of acute pancreatitis. Out of these, neurogenic inflammation is responsible for acute interstitial pancreatitis as a result of oedema. SP binds itself to the G-protein coupled neurokinin-1 receptor and causes plasma leakage, cell proliferation, and invasion resulting in pancreatic cancer. SP along with comparable neuropeptides seems to be crucial targets with the capability of satisfying several unfulfilled medical requisites. This review article mainly focuses on compiling the available evidence to show that SP could be a novel therapeutic target for pancreatic diseases, and more exploration into the SP signaling pathways is the call of the hour

Inhibition of cystathionine-γ-lyase-mediated hydrogen sulfide production in LPS-stimulated RAW 264.7 macrophages by polyherbal extract

111-117The polyherbal formulation chandraprabha vati (CV) comprising 29 herbs is traditionally used as an anti-inflammatory agent for arthritis and urinary ailments in Indian Siddha medicine. Earlier, we reported that lipopolysaccharide (LPS) induced apoptosis in RAW 264.7 macrophages is mediated by hydrogen sulfide (H2S), a potential target for many inflammatory diseases. Here, we hypothesized that pretreatment with CV decreases H2S level and thereby alleviate the inflammatory conditions induced by LPS in RAW 264.7 macrophages, and this protective effect occurs through alterations in cystathionine-γ-lyase (CSE), a H2S synthesizing enzyme. Accordingly, we evaluated the anti-inflammatory effect of CV in LPS-stimulated RAW 264.7 macrophages in vitro. The CV pretreatment followed by 12 h of LPS-stimulation showed significantly decreased TNF-α, H2S production possibly through CSE gene expression and NF-кB activation compared to the non pretreated macrophages. Our results further confirm that the polyherbal extract chandraprabha vati may be a useful therapy for inflammatory disorders by reducing H2S levels

Inhibition of cystathionine-γ-lyase-mediated hydrogen sulfide production in LPS-stimulated RAW 264.7 macrophages by polyherbal extract

The polyherbal formulation chandraprabha vati (CV) comprising 29 herbs is traditionally used as an anti-inflammatory agent for arthritis and urinary ailments in Indian Siddha medicine. Earlier, we reported that lipopolysaccharide (LPS) induced apoptosis in RAW 264.7 macrophages is mediated by hydrogen sulfide (H2S), a potential target for many inflammatory diseases. Here, we hypothesized that pretreatment with CV decreases H2S level and thereby alleviate the inflammatory conditions induced by LPS in RAW 264.7 macrophages, and this protective effect occurs through alterations in cystathionine-γ-lyase (CSE), a H2S synthesizing enzyme. Accordingly, we evaluated the anti-inflammatory effect of CV in LPS-stimulated RAW 264.7 macrophages in vitro. The CV pretreatment followed by 12 h of LPS-stimulation showed significantly decreased TNF-α, H2S production possibly through CSE gene expression and NF-кB activation compared to the non pretreated macrophages. Our results further confirm that the polyherbal extract chandraprabha vati may be a useful therapy for inflammatory disorders by reducing H2S levels

LPS-induced apoptosis is partially mediated by hydrogen sulphide in RAW 264.7 murine macrophages

Abstract Lipopolysaccharide (LPS) induces apoptosis in murine macrophages through the autocrine secretion of tumor necrosis factor (TNF)-α and nitric oxide (NO). LPS-induced inflammation in murine macrophages is associated with hydrogen sulfide (H2S) production. In this present study, we reported the novel role of H2S in LPS-induced apoptosis and its underlying molecular mechanism specifically at late phases in murine macrophage cells. Stimulation of RAW 264.7 macrophages with LPS resulted in a time- and dose-dependent induction of apoptosis. We observed that the LPS-induced early apoptosis (associated with TNF-α secretion) in macrophages was not inhibited in the presence of H2S inhibitor (DL-propargylglycine), whereas early apoptosis was absent in the presence of TNF receptor antibody. Interestingly, LPS-induced late apoptosis paralleled with H2S production was reduced in the presence of H2S inhibitor but not with TNF receptor antibody. The late apoptotic events mediated by H2S and not the TNF-α induced early apoptosis correlated significantly with the induction of p53 and Bax expression in LPS-induced macrophages. Thus, it is possible that RAW 264.7 murine macrophages treated with LPS mediated early apoptosis through TNF-α and the late apoptotic events through the production of H2S

Inhibition of cystathionine-γ-lyase-mediated hydrogen sulfide production in LPS-stimulated RAW 264.7 macrophages by polyherbal extract

The polyherbal formulation chandraprabha vati (CV) comprising 29 herbs is traditionally used as an anti-inflammatory agent for arthritis and urinary ailments in Indian Siddha medicine. Earlier, we reported that lipopolysaccharide (LPS) induced apoptosis in RAW 264.7 macrophages is mediated by hydrogen sulfide (H2S), a potential target for many inflammatory diseases. Here, we hypothesized that pretreatment with CV decreases H2S level and thereby alleviate the inflammatory conditions induced by LPS in RAW 264.7 macrophages, and this protective effect occurs through alterations in cystathionine-γ-lyase (CSE), a H2S synthesizing enzyme. Accordingly, we evaluated the anti-inflammatory effect of CV in LPS-stimulated RAW 264.7 macrophages in vitro. The CV pretreatment followed by 12 h of LPS-stimulation showed significantly decreased TNF-α, H2S production possibly through CSE gene expression and NF-кB activation compared to the non pretreated macrophages. Our results further confir

Thermal co-reduction approach to vary size of silver nanoparticle: its microbial and cellular toxicology

In recent years, silver nanoparticles (AgNPs) have attracted considerable interest in the field of food, agriculture and pharmaceuticals mainly due to its antibacterial activity. AgNPs have also been reported to possess toxic behavior. The toxicological behavior of nanomaterials largely depends on its size and shape which ultimately depend on synthetic protocol. A systematic and detailed analysis for size variation of AgNP by thermal co-reduction approach and its efficacy toward microbial and cellular toxicological behavior is presented here. With the focus to explore the size-dependent toxicological variation, two different-sized NPs have been synthesized, i.e., 60 nm (Ag60) and 85 nm (Ag85). A detailed microbial toxicological evaluation has been performed by analyzing minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), diameter of inhibition zone (DIZ), growth kinetics (GrK), and death kinetics (DeK). Comparative cytotoxicological behavior was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. It has been concluded by this study that the size of AgNPs can be varied, by varying the concentration of reactants and temperature called as ``thermal co-reduction'' approach, which is one of the suitable approaches to meet the same. Also, the smaller AgNP has shown more microbial and cellular toxicity

The Lysophosphatidic Acid Type 2 Receptor Is Required for Protection Against Radiation-Induced Intestinal Injury

Background & Aims: We recently identified lysophosphatidic acid (LPA) as a potent antiapoptotic agent for the intestinal epithelium. The objective of the present study was to evaluate the effect of octadecenyl thiophosphate (OTP), a novel rationally designed, metabolically stabilized LPA mimic, on radiation-induced apoptosis of intestinal epithelial cells in vitro and in vivo. Methods: The receptors and signaling pathways activated by OTP were examined in IEC-6 and RH7777 cell lines and wild-type and LPA1 and LPA2 knockout mice exposed to different apoptotic stimuli. Results: OTP was more efficacious than LPA in reducing gamma irradiation-, camptothecin-, or tumor necrosis factor α/cycloheximide-induced apoptosis and caspase-3-8, and caspase-9 activity in the IEC-6 cell line. In RH7777 cells lacking LPA receptors, OTP selectively protected LPA2 but not LPA1 and LPA3 transfectants. In C57BL/6 and LPA1 knockout mice exposed to 15 Gy gamma irradiation, orally applied OTP reduced the number of apoptotic bodies and activated caspase-3-positive cells but was ineffective in LPA2 knockout mice. OTP, with higher efficacy than LPA, enhanced intestinal crypt survival in C57BL/6 mice but was without any effect in LPA2 knockout mice. Intraperitoneally administered OTP reduced death caused by lethal dose (LD)100/30 radiation by 50%. Conclusions: Our data indicate that OTP is a highly effective antiapoptotic agent that engages similar prosurvival pathways to LPA through the LPA2 receptor subtype. © 2007 AGA Institute

Regulation of vascular endothelial growth factor receptor 2 trafficking and angiogenesis by Golgi localized t-SNARE syntaxin 6

Vascular endothelial growth factor receptor 2 (VEGFR2) plays a key role in physiologic and pathologic angiogenesis. Plasma membrane (PM) levels of VEGFR2 are regulated by endocytosis and secretory transport through the Golgi apparatus. To date, the mechanism whereby the VEGFR2 traffics through the Golgi apparatus remains incompletely characterized. We show in human endothelial cells that binding of VEGF to the cell surface localized VEGFR2 stimulates exit of intracellular VEGFR2 from the Golgi apparatus. Brefeldin A treatment reduced the level of surface VEGFR2, confirming that VEGFR2 traffics through the Golgi apparatus en route to the PM. Mechanistically, we show that inhibition of syntaxin 6, a Golgi-localized target membrane-soluble N-ethylmaleimide attachment protein receptor (t-SNARE) protein, interferes with VEGFR2 trafficking to the PM and facilitates lysosomal degradation of the VEGFR2. In cell culture, inhibition of syntaxin 6 also reduced VEGF-induced cell proliferation, cell migration, and vascular tube formation. Furthermore, in a mouse ear model of angiogenesis, an inhibitory form of syntaxin 6 reduced VEGF-induced neovascularization and permeability. Our data demonstrate the importance of syntaxin 6 in the maintenance of cellular VEGFR2 levels, and suggest that the inhibitory form of syntaxin 6 has good potential as an antiangiogenic agent