Advance Parking Management System.

By looking towards scenario of today’s market and business; and approaches of peoples towards their standards ,to deal with the ever growing problem of parking management with issues like lack of space for parking, wastage of time to find parking space this paper proposes an advance solution for managing and monitoring free parking space and automated parking of the car. It aims at implementing smarter and better parking guidance mechanism with architecture which will settle within less land space and reduces significantly vehicle travel time and parking time

Study of drug prescription pattern among COPD patients admitted to medicine in-patient department of tertiary care hospital

Background: Drug utilization studies can provide insights into a pattern, quality, determinants and outcomes of drug use. COPD is one of the leading causes of death among Indian population and there is a lack of drug utilization studies in this field.Methods: A prospective, observational study was conducted among the patients admitted in inpatient department of medicine ward of Tertiary care hospital. Data has collected from COPD patients admission records. Parameters like demographic profile, common associated diseases, WHO core drug indicators and commonly prescribed drugs were assessed from the prescriptions.Results: A total 284 inpatient records were scrutinized. Out of 284 patients, 66.19% were male and 33.80% were female. Average numbers of drugs per prescription were 7. Mean age was 66.9 years. Antimicrobials (88.7%) were most commonly prescribed drugs followed by inhaled bronchodilators (84.5%).Conclusions: Study data highlights that average numbers of drugs prescribed were higher than WHO norms, antibiotics were commonly used, and drugs prescribed with brand names were higher than the generic names

Experimental evaluation of analgesic activity of PPAR γ agonists: pioglitazone and rosiglitazone

Background: To evaluate analgesic activity of pioglitazone and rosiglitazone by tail flick method in rats and acetic acid induced writhing method in mice.Methods: Albino wistar rats of either sex weighing 180-200 g and Swiss mice weighing 25-30 g were used. Study was conducted after approval from the Institutional Animal Ethics Committee. The tail flick method in rats described by D’Amour and Smith (1941) and acetic acid induced writhing in mice were used. The dose of pioglitazone and rosiglitazone were 20 mg/kg and 10 mg/kg respectively.Results: In tail flick method of analgesia, both, pioglitazone and rosiglitazone have analgesic activity which was statistically comparable to aspirin. In acetic acid induced writhing model of analgesia, the action of pioglitazone and rosiglitazone was significantly greater than the control group but it was less when compared to aspirin.Conclusions: Analgesic activity of pioglitazone and rosiglitazone was comparable to aspirin in tail flick model of analgesia in rats while it was significantly less when compared to tramadol. Analgesic activity of pioglitazone and rosiglitazone was significantly less than aspirin in acetic acid induced writhing method

Comparative assessment of antioxidant potential of different body parts of the yellow seahorse, Hippocampus kuda (Bleeker, 1852): source of traditional medicine

804-811Antioxidant potential of different body parts such as seahorse internal organs (SIO), skin with bones (SSB), bones (SB) and muscle tissues (SM) of cultured yellow seahorse, Hippocampus kuda was assessed in terms of total phenolic content (TPC), reducing power (RP), metal chelating activity (MCA), 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity, hydroxyl radical scavenging (HRS) and lipid peroxidation assay (LPX). In general, relatively elevated levels of TPC and other measured antioxidant activities were recorded in extracts from SIO and SM. Extract prepared from SIO exhibited significantly higher levels of TPC, RP, DPPH scavenging activity and LPX inhibition, while MCA and HRS activities were significantly higher in SM and SSB, respectively (P < 0.05). A significant difference in TPC and antioxidant activities between different body parts of seahorse was discernible. The results of the study revealed that internal organs and muscle tissues contribute significantly to the antioxidant potential in the H. kuda. Results obtained in the present investigation suggest that TPC and other antioxidant activities are dependent upon biochemical composition of individual body parts

Synergy of IL-21 and IL-15 in regulating CD8+ T cell expansion and function

Interleukin (IL)-21 is the most recently recognized of the cytokines that share the common cytokine receptor γ chain (γc), which is mutated in humans with X-linked severe combined immunodeficiency. We now report that IL-21 synergistically acts with IL-15 to potently promote the proliferation of both memory (CD44high) and naive (CD44low) phenotype CD8+ T cells and augment interferon-γ production in vitro. IL-21 also cooperated, albeit more weakly, with IL-7, but not with IL-2. Correspondingly, the expansion and cytotoxicity of CD8+ T cells were impaired in IL-21R−/− mice. Moreover, in vivo administration of IL-21 in combination with IL-15 boosted antigen-specific CD8+ T cell numbers and resulted in a cooperative effect on tumor regression, with apparent cures of large, established B16 melanomas. Thus, our studies reveal that IL-21 potently regulates CD8+ T cell expansion and effector function, primarily in a synergistic context with IL-15

LBH589, a deacetylase inhibitor, induces apoptosis in adult T-cell leukemia/lymphoma cells via activation of a novel RAIDD-caspase-2 pathway

Adult T-cell leukemia/lymphoma (ATLL), an aggressive neoplasm etiologically associated with human T-lymphotropic virus type-1 (HTLV-1), is resistant to treatment. In this study, we examined the effects of a new inhibitor of deacetylase enzymes, LBH589, on ATLL cells. LBH589 effectively induced apoptosis in ATLL-related cell lines and primary ATLL cells and reduced the size of tumors inoculated in SCID mice. Analyses, including with a DNA microarray, revealed that neither death receptors nor p53 pathways contributed to the apoptosis. Instead, LBH589 activated an intrinsic pathway through the activation of caspase-2. Furthermore, small interfering RNA experiments targeting caspase-2, caspase-9, RAIDD, p53-induced protein with a death domain (PIDD) and RIPK1 (RIP) indicated that activation of RAIDD is crucial and an event initiating this pathway. In addition, LBH589 caused a marked decrease in levels of factors involved in ATLL cell proliferation and invasion such as CCR4, IL-2R and HTLV-1 HBZ-SI, a spliced form of the HTLV-1 basic zipper factor HBZ. In conclusion, we showed that LBH589 is a strong inducer of apoptosis in ATLL cells and uncovered a novel apoptotic pathway initiated by activation of RAIDD

p53 Activation following Rift Valley Fever Virus Infection Contributes to Cell Death and Viral Production

Rift Valley fever virus (RVFV) is an emerging viral zoonosis that is responsible for devastating outbreaks among livestock and is capable of causing potentially fatal disease in humans. Studies have shown that upon infection, certain viruses have the capability of utilizing particular cellular signaling pathways to propagate viral infection. Activation of p53 is important for the DNA damage signaling cascade, initiation of apoptosis, cell cycle arrest and transcriptional regulation of multiple genes. The current study focuses on the role of p53 signaling in RVFV infection and viral replication. These results show an up-regulation of p53 phosphorylation at several serine sites after RVFV MP-12 infection that is highly dependent on the viral protein NSs. qRT-PCR data showed a transcriptional up-regulation of several p53 targeted genes involved in cell cycle and apoptosis regulation following RVFV infection. Cell viability assays demonstrate that loss of p53 results in less RVFV induced cell death. Furthermore, decreased viral titers in p53 null cells indicate that RVFV utilizes p53 to enhance viral production. Collectively, these experiments indicate that the p53 signaling pathway is utilized during RVFV infection to induce cell death and increase viral production

HTLV-1 Evades Type I Interferon Antiviral Signaling by Inducing the Suppressor of Cytokine Signaling 1 (SOCS1)

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of Adult T cell Leukemia (ATL) and the neurological disorder HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Although the majority of HTLV-1–infected individuals remain asymptomatic carriers (AC) during their lifetime, 2–5% will develop either ATL or HAM/TSP, but never both. To better understand the gene expression changes in HTLV-1-associated diseases, we examined the mRNA profiles of CD4+ T cells isolated from 7 ATL, 12 HAM/TSP, 11 AC and 8 non-infected controls. Using genomic approaches followed by bioinformatic analysis, we identified gene expression pattern characteristic of HTLV-1 infected individuals and particular disease states. Of particular interest, the suppressor of cytokine signaling 1—SOCS1—was upregulated in HAM/TSP and AC patients but not in ATL. Moreover, SOCS1 was positively correlated with the expression of HTLV-1 mRNA in HAM/TSP patient samples. In primary PBMCs transfected with a HTLV-1 proviral clone and in HTLV-1-transformed MT-2 cells, HTLV-1 replication correlated with induction of SOCS1 and inhibition of IFN-α/β and IFN-stimulated gene expression. Targeting SOCS1 with siRNA restored type I IFN production and reduced HTLV-1 replication in MT-2 cells. Conversely, exogenous expression of SOCS1 resulted in enhanced HTLV-1 mRNA synthesis. In addition to inhibiting signaling downstream of the IFN receptor, SOCS1 inhibited IFN-β production by targeting IRF3 for ubiquitination and proteasomal degradation. These observations identify a novel SOCS1 driven mechanism of evasion of the type I IFN antiviral response against HTLV-1

Prognostic Markers in Peripheral T-Cell Lymphoma

Based on their own experience and knowledge of the literature, the authors review the pathobiological characteristics of peripheral T-cell lymphomas (PTCLs), focusing on the available prognostic indicators. The International Prognostic Index (IPI), which is based on age, performance status, lactate dehydrogenase [LDH], stage, and extranodal involvement, appears to be efficient as a prognostic index for PTCLs, at least in part and especially for certain PTCL subtypes. However, it is not so satisfactory for the two commonest PTCLs, PTCL not otherwise specified (PTCL/NOS) and angioimmunoblastic T-cell lymphoma (AITL), for which novel scores, possibly based on the biologic features of the tumors, have been explored. An Italian cooperative group proposed a revision of the IPI for PTCL unspecified (PTCL-U), the Prognostic Index for PTCL-U (PIT), which includes age, performance status, LDH, and bone marrow involvement. The PIT apparently offered some advantages, but they were not confirmed in subsequent studies. A clinical-biological score (the Bologna score) was then proposed, including tumor proliferation and clinical features (age, LDH, and performance status). This score appears promising and offers the intriguing advantage of integrating biological and clinical elements, but independent validation on a large series is still warranted. More recently, gene expression profiling has been used to identify novel molecular prognostic factors. In particular, inactivation of the NFκB pathway, high expression of proliferation-associated genes, and cytotoxic molecular phenotype seem to be associated with a worse outcome. So far, however, none of these indicators has been validated in an independent series. Finally, various reports have dealt specifically with the prognostication of NK-derived tumors, including nasal and nasal-type lymphomas. Both the IPI and dedicated models have turned out to be of prognostic relevance for these tumors. In conclusion, although the IPI is somewhat effective for PTCL prognostication, novel scores that are more refined and possibly disease-specific are warranted. The validation process for several models, including clinical-pathological and molecular models, is now ongoing