192 research outputs found
Performance evaluation of forwarding algorithms for generalized storage aware routing protocols
No full textThis thesis presents an investigation of the design and evaluation of the generalized storage aware routing (GSTAR) protocol proposed for use in the MobilityFirst future Internet architecture. The GSTAR protocol uses in-network storage to improve service quality and throughput in wireless access networks with varying radio link quality and/or disconnection. These gains are achieved using a combination of short-term buffering at routers to smooth out fluctuations in path quality along with delay-tolerant storage, to overcome total disconnection of the mobile device. The performance of the GSTAR protocol is evaluated for exemplary wireless access network scenarios using ns-3 based simulation models, and key design parameters are investigated. Each node in GSTAR maintains two kinds of topology information. The intra-partition graph contains information about path quality between nodes in the current partition of the network. The path quality is determined using two metrics: short term and long term expected transmission time (SETT and LETT). Every node compares these two metrics using the store/forward decision threshold and stores the data on finding that the path is degraded with the expectation that it may improve in the future. Inter-partition graph gives a probabilistic view of the connection patterns between nodes in the network. It is used in the event of disconnections or partitions. An ns-3 based simulation model is described which includes nodes with storage, hop-by-hop transport, time-varying wireless channels and mobile users with possible disconnection. The model is used to evaluate different forwarding algorithms in GSTAR. Using a baseline threshold scheme where packets are temporarily stored when SETT > 1.1 * LETT, it is shown that the resulting system achieves performance improvements over the baseline with no storage. The threshold algorithm is studied further to consider adaptive settings based on the moving average and other temporal filters of the SETT sequence. The results show that if link quality fluctuations are random, the moving average scheme works well, while an exponentially weighted moving average is recommended for on-off channels with periodic outages. Simulation results are provided in each case, showing the benefit of adaptive threshold settings over the baseline non-adaptive case considered in earlier work.M.S.Includes bibliographical referencesby Nehal Soman
sj-pdf-2-vmj-10.1177_1358863X231171948 – Supplemental material for Machine learning demonstrates top predictors of lipid-rich necrotic core modulation over 1 year in psoriasis
No full textSupplemental material, sj-pdf-2-vmj-10.1177_1358863X231171948 for Machine learning demonstrates top predictors of lipid-rich necrotic core modulation over 1 year in psoriasis by Christin G Hong, Haiou Li, Philip M Parel, Alexander R Berg, Nidhi Patel, Harry Choi, Heather L Teague, Eric Munger, Andrew J Buckler, Alexander V Sorokin and Nehal N Mehta in Vascular Medicine</p
sj-pdf-1-vmj-10.1177_1358863X231171948 – Supplemental material for Machine learning demonstrates top predictors of lipid-rich necrotic core modulation over 1 year in psoriasis
No full textSupplemental material, sj-pdf-1-vmj-10.1177_1358863X231171948 for Machine learning demonstrates top predictors of lipid-rich necrotic core modulation over 1 year in psoriasis by Christin G Hong, Haiou Li, Philip M Parel, Alexander R Berg, Nidhi Patel, Harry Choi, Heather L Teague, Eric Munger, Andrew J Buckler, Alexander V Sorokin and Nehal N Mehta in Vascular Medicine</p
Effect of hesperidin on renal complication in experimentally induced renal damage in diabetic sprague dawley rats
No full textPresent study was designed to evaluate in effect of Hesperidine on renal complication in Ischemia/reperfusion (I/R) induced renal damage in Sprague dawley diabetic rats. Hyperglycaemia is most probably a contributing factor in the development of ischaemic acute renal failure (ARF) in many patients. Both clinical and experimental data suggest that hyperglycaemia increases the risk of ARF. Type 2 Diabetes was induced in rats by a single intraperitoneal (i.p) injection of Streptozotocin (65 mg/kg, STZ) in overnight fasting rats followed by the i.p administration of Nicotinamide (110 mg/kg, NIC) after 15 minutes. After right nephrectomy, Hesperidine (100 mg/kg/day, p.o) was administered for 15 days. On the 16th day, ischemia was induced in contra lateral kidney for 45 min, followed by reperfusion for 24 hr. Renal function marker and oxidative parameter were estimated at the end of 24 hr reperfusion. At the end of experimental period the level of malondialdehyde formation/ lipid peroxidation (LPO) in kidney tissue and serum marker Creatinine, Urea and Uric acids were significantly increased. Whereas, the activity of biomarkers of oxidative stress such as reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) were found to be decreased significantly compared to control rats. Hesperidine improved the renal dysfunction and oxidative stress after renal ischemia/reperfusion injury in diabetic rats. In conclusion, Hesperidine shows potent may improve renal complication in I/R induced renal damage in type 2 diabetic rats.--------------------------------------------------------------------------------------------------------Pharmacology Department, Dharmaj Degree Pharmacy College, Petlad-Khambhat Road, Dharmaj, Anand-388430, Gujarat, India*Corresponding author, Email: [email protected]; Tel: +919825882522Cite This Article As: Jagdish Kakadiya, Divyang Patel, Nehal Shah. 2010. Effect of hesperidin on renal complication in experimentally induced renal damage in diabetic sprague dawley rats. J. Ecobiotechnol. 2(2): 45-50
Effect of Valsartan on Renal Marker, Nitrite and Histopathology of Kidney in Ischemia/Reperfusion Induced Renal Damage in Diabetic Rats
No full textPresent study was designed to evaluate the effect of Valsartan on renal marker, nitrite and histopathology of kidney in Ischemia/reperfusion induced renal damage in diabetic rats. Ischemia/reperfusion injury, which is commonly seen in the field of renal surgery or transplantation in diabetic condition, is a major cause of acute renal failure. Type 2 Diabetes was induced in rats by a single intraperitoneal (i.p) injection of Streptozotocin (65 mg/kg, STZ) in overnight fasting rats followed by the i.p administration of Nicotinamide (110 mg/kg, NIC) after 15 minutes. After right nephrectomy, Valsartan (8 mg/kg/day, p.o) was administered for 15 days. On the 16th day, ischemia was induced in contra lateral kidney for 45 min, followed by reperfusion for 24 hr. Renal function marker and histopathology were estimated at the end of 24 hr reperfusion. At the end of experimental period the level of nitrite in kidney tissue, serum marker Albumin and Blood urea nitrogen were significantly changed. Valsartan improved the renal dysfunction and nitrite after renal ischemia/reperfusion injury in diabetic rats. Light microscopic evaluation of the kidneys of the diabetic rats with I/R only showed tubular cell swelling, interstitial edema, tubular dilatation, and moderate to severe necrosis, whereas, Valsartan improve tubular dilation, loss of interstitial hemorrhage, and glomerular atrophy. In conclusion, Valsartan as a beneficial agent on renal marker, nitrite and histopathology of kidney in Ischemia/reperfusion induced renal damage in diabetic rats. -------------------------------------------------------------------Pharmacology Department, Dharmaj Degree Pharmacy College, Petlad-Khambhat Road, Dharmaj, Anand-388430, Gujarat, India*Corresponding author, Email: [email protected], Tel: +919825882522Â Cite This Article As: Jagdish Kakadiya, Nehal Shah. 2010. Effect of Valsartan on Renal Marker, Nitrite and Histopathology of Kidney in Ischemia/Reperfusion Induced Renal Damage in Diabetic Rats. J. Ecobiotechnol. 2(3): 12-17
Investigating the role of eukaryotic initiation factor 5B (eIF5B) in oral squamous cell carcinoma
No full textOral squamous cell carcinoma (OSCC) is a common malignancy of the mucosal epithelium affecting ~600,000 patients a year. Patient prognosis remains poor despite improvements in the therapeutic regime. Therefore, new therapeutic targets must be identified that improve the current standard of care. Regulation of mRNA translation plays a critical role in oncogenesis and cancer progression. Particularly, the IRES-mediated non-canonical translation of distinct mRNAs has been implicated in tumorigenesis. Eukaryotic initiation factor 5B (eIF5B) is a key factor that drives IRES-mediated translation of distinct anti-apoptotic proteins and is implicated in the pathophysiology of several malignancies. Single-cell RNAseq data analysis demonstrated that EIF5B is predominantly expressed in cancer cells compared to other cells in the tumor microenvironment. Further bioinformatic analyses revealed that higher EIF5B mRNA is correlated with poor patient prognosis for OSCC patients. Therefore, we aimed to establish the pre-clinical rationale for eIF5B as a therapeutic target for OSCC. Cell viability data suggested that RNAi-mediated eIF5B depletion significantly increased OSCC cell death under TRAIL treatment. eIF5B depletion also resulted in decreased levels of multiple antiapoptotic proteins. Bromodeoxyuridine (BrdU) incorporation, invasion, and wound healing assays suggested eIF5B depletion hinders proliferation, invasion and migration phenotypes, respectively. Western blot analysis revealed that proteins involved in ERK and NF-κΒ signalling, VEGF and HIF-1α, decreased upon eIF5B depletion. eIF5B depletion also resulted in the decrease of angiogenic biomarkers and endothelial tube formation, suggesting a role of eIF5B depletion in decreasing the angiogenic capability of OSCC cells. Stable eIF5B depletion was achieved with the use of shRNA. Under these conditions, eIF5B depletion increased cell death in the presence of cisplatin. Decreased invasion phenotypes were also observed using shRNA-mediated knockdown, setting up the pipeline to transition experiments into preclinical mouse models. Thus, my work has a strong potential to establish eIF5B as a therapeutic target for OSCC treatment
Performance Analysis of Network with Different Queuing Mechanisms in TCP/FTP and UDP/FTP Scenario
No full textSpectrin-Based Complex for Regulation of Signal Transducer and Activator of Transcription 3 Signaling and Heart Function
No full textMaladaptive cardiac remodeling is an important step in the progression of heart failure and is characterized by changes in cardiac chamber size, structure, and performance induced by a constellation of cell- and tissue-level factors. While great strides have been made in identifying membrane receptors, signaling molecules, and transcription factors involved in the remodeling process, fundamental questions remain about the molecular pathways linking extracellular stress cues to cellular reprogramming underlying progression of disease. Signal Transducer and Activator of Transcription 3 (STAT3) is a multifunctional transcription factor which regulates expression of gene programs important for inflammation, cell survival, and hypertrophy. While STAT3 signaling modulates cardiomyocyte function in response to ischemia and biomechanical stress, the molecular pathways that coordinate STAT3 activity is unclear. We hypothesized that βIV-spectrin, an actin associated cytoskeletal protein, coordinates a macromolecular complex with CaMKII and STAT3 to promote phosphorylation/activation of STAT3 at the cardiomyocyte submembrane. We believe that dysfunction of βIV-spectrin will induce cardiac malfunction downstream of STAT3. To understand the interaction between STAT3 and βIV-spectrin, novel mouse models expressing truncated βIV-spectrin protein lacking the validated CaMKII binding domain (qv3J), a cardiac-selective knockout (cKO) of βIV-spectrin, and wildtype littermates were used. Cardiac function was assessed by echocardiography at baseline and post Transverse Aortic Constriction (TAC). Levels of total and phosphorylated STAT3 and CaMKII were assessed in whole heart lysates by western blot, pull-down, and co-immunoprecipitation assays to measure relevant protein concentrations and interactions. Permeabilized cardiomyocytes were immunostained for βIV-spectrin, CaMKII, and STAT3 and protein localization was assessed by confocal microscopy to study the activation and localization of STAT3. βIV-spectrin cKO mice showed decreased heart function while qv3J mice displayed normal cardiac function at baseline and post TAC, compared to wildtype. Mice lacking βIV-spectrin/CaMKII/STAT3 interaction demonstrated abnormal STAT3 regulation and response to biomechanical stress. This study indicates the presence of a novel complex between βIV-spectrin and STAT3, thereby regulating the localization of STAT3 in cardiomyocytes. Future studies will address the specific role of STAT3 in pathology associated with spectrin-deficiency.The Ohio State University- College of EngineeringThe Ohio State University- Undergraduate Research OfficeA two-year embargo was granted for this item.Academic Major: Biomedical Engineerin
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