Anti-nociceptive and Anti-inflammatory Effects of the Leaf Extract of Vitex trifolia Linn. in Experimental Animals

The effect of Vitex trifolia Linn. (FamilyVerbenaceae) leaf extract was studied for the anti-nociceptive and anti-inflammatory activity in experimental animals. V. trifolia, 25 – 100 mg/kg administered orally for 3 days exhibited graded dose response equivalent to 21.95% - 89.90% protection in the tail flick latent test in rat. The V. trifolia leaf extract (50 and 100 mg/kg, p.o X 3 days) was effective in hot plate reaction time (64.05% and 112.97%, p\u3c 0.01 and p\u3c 0.001), analgesymeter induced mechanical pain (28.17% and 54.42%, p \u3c 0.01 and p \u3c 0.001) and acetic acid- induced writhing (26.68% and 51.79%, p \u3c 0.5 and p \u3c 0.05) in mice. The leaf extract of V. trifolia potentiated the analgesic activity with pentazocine (10 mg/kg, i.p.) and aspirin (25 mg/kg, i.p.). In the carrageenan- induced paw edema V. trifolia leaf extract (50 and 100 mg/kg, p.o X 3 days) decreased paw volume significantly (26.68% and 51.79%) and dose dependent anti-inflammatory activity in 1-3 hour time interval and potentiated with nimesulide (50 mg/kg, p.o.). In summary, this study demonstrates that leaf extract of V. trifolia has significant anti-nociceptive and anti-inflammatory activity

Azathioprine favourably influences the course of malaria

<p>Abstract</p> <p>Background</p> <p>Azathioprine triggers suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and exposure of phosphatidylserine at the erythrocyte surface. Eryptosis may accelerate the clearance of <it>Plasmodium</it>-infected erythrocytes. The present study thus explored whether azathioprine influences eryptosis of <it>Plasmodium</it>-infected erythrocytes, development of parasitaemia and thus the course of malaria.</p> <p>Methods</p> <p>Human erythrocytes were infected <it>in vitro </it>with <it>Plasmodium falciparum (P. falciparum) </it>(strain BinH) in the absence and presence of azathioprine (0.001 – 10 μM), parasitaemia determined utilizing Syto16, phosphatidylserine exposure estimated from annexin V-binding and cell volume from forward scatter in FACS analysis. Mice were infected with <it>Plasmodium berghei (P. berghei) </it>ANKA by injecting parasitized murine erythrocytes (1 × 10⁶) intraperitoneally. Where indicated azathioprine (5 mg/kg b.w.) was administered subcutaneously from the eighth day of infection.</p> <p>Results</p> <p><it>In vitro </it>infection of human erythrocytes with <it>P. falciparum </it>increased annexin V-binding and initially decreased forward scatter, effects significantly augmented by azathioprine. At higher concentrations azathioprine significantly decreased intraerythrocytic DNA/RNA content (≥ 1 μM) and <it>in vitro </it>parasitaemia (≥ 1 μM). Administration of azathioprine significantly decreased the parasitaemia of circulating erythrocytes and increased the survival of <it>P. berghei</it>-infected mice (from 0% to 77% 22 days after infection).</p> <p>Conclusion</p> <p>Azathioprine inhibits intraerythrocytic growth of <it>P. falciparum</it>, enhances suicidal death of infected erythrocytes, decreases parasitaemia and fosters host survival during malaria.</p

Automated sampling in upstream process development for accelerated access to Critical Process Parameters (CPPs) and Critical Quality Attributes (CQAs)

Please click Additional Files below to see the full abstract

GSU Event Portal

The GSU EVENT PORTAL is website where you can advertise, view and make a booking for event by anywhere. You can do your necessary work related to events by this website just within few minutes. This application is trying to very easy for user to find venue by Google map. Many of the online event websites are not supported in the mobile phones, this is one of the main drawback in present online event websites. We may come across replication of data. To overcome the problem, we came with a new online event portal which supports in any windows, android, iOS, etc. Our website provides events like audio functions, company events, college events, sports events, traditional events, and more. We are providing Create, Modify, Delete events by user and also admin. We provide offers on ticket purchases. Our main intention is to reduce time and cost. We provide regular notifications regarding events. We provide security for your data. We are planning to launch this portal in July first week

Market Analysis for Floral Rejuvenated Products in Hyderabad City of Telangana State, India

Flowers are an important part of Indian culture, and because of various religious practises, tonnes of flowers frequently collect in places of worship such temples, mosques, churches, and gurudwaras. They are also generated at weddings, flower markets, residential neighbourhoods, and other events. Unfortunately, the majority of these flowers are frequently dumped in garbage and water after being used, endangering the ecosystem. In order to reduce the effects caused by floral waste this can be converted into the production of value added products like incense sticks, compost, soaps, essential oils. Hence, to understand the market for these floral rejuvenated products, the present study was taken to analyse the source of awareness of users and factors influencing the users to purchase the floral rejuvenated products. Data was collected from 120 users in the Hyderabad city and analyzed using descriptive statistics, ANOVA Test and Factor analysis

Beneficial effect of aurothiomalate on murine malaria

<p>Abstract</p> <p>Background</p> <p>Premature death of <it>Plasmodium</it>-infected erythrocytes is considered to favourably influence the clinical course of malaria. Aurothiomalate has previously been shown to trigger erythrocyte death or eryptosis, which is characterized by cell membrane scrambling leading to phosphatidylserine exposure at the cell surface. Phosphatidylserine-exposing cells are rapidly cleared from circulating blood. The present study thus tested whether sodium aurothiomalate influences the intraerythrocytic parasite development <it>in vitro </it>and the clinical course of murine malaria <it>in vivo</it>.</p> <p>Methods</p> <p>Human erythrocytes were infected with <it>Plasmodium falciparum </it>BinH <it>in vitro </it>and mice were infected (intraperitoneal injection of 1 × 10⁶parasitized murine erythrocytes) with <it>Plasmodium berghei </it>ANKA <it>in vivo</it>.</p> <p>Results</p> <p>Exposure to aurothiomalate significantly decreased the <it>in vitro </it>parasitemia of <it>P. falciparum</it>-infected human erythrocytes without influencing the intraerythrocytic DNA/RNA content. Administration of sodium aurothiomalate <it>in vivo </it>(daily 10 mg/kg b.w. s.c. from the 8^thday of infection) enhanced the percentage of phosphatidylserine-exposing infected and noninfected erythrocytes in blood. All nontreated mice died within 30 days of infection. Aurothiomalate-treatment delayed the lethal course of malaria leading to survival of more than 50% of the mice 30 days after infection.</p> <p>Conclusions</p> <p>Sodium aurothiomalate influences the survival of <it>Plasmodium berghei</it>-infected mice, an effect only partially explained by stimulation of eryptosis.</p

Anti-malarial effect of gum arabic

<p>Abstract</p> <p>Background</p> <p>Gum Arabic (GA), a nonabsorbable nutrient from the exudate of <it>Acacia senegal</it>, exerts a powerful immunomodulatory effect on dendritic cells, antigen-presenting cells involved in the initiation of both innate and adaptive immunity. On the other hand GA degradation delivers short chain fatty acids, which in turn have been shown to foster the expression of foetal haemoglobin in erythrocytes. Increased levels of erythrocyte foetal haemoglobin are known to impede the intraerythrocytic growth of <it>Plasmodium </it>and thus confer some protection against malaria. The present study tested whether gum arabic may influence the clinical course of malaria.</p> <p>Methods</p> <p>Human erythrocytes were <it>in vitro </it>infected with <it>Plasmodium falciparum </it>in the absence and presence of butyrate and mice were <it>in vivo </it>infected with <it>Plasmodium berghei </it>ANKA by injecting parasitized murine erythrocytes (1 × 10⁶) intraperitoneally. Half of the mice received gum arabic (10% in drinking water starting 10 days before the day of infection).</p> <p>Results</p> <p>According to the <it>in vitro </it>experiments butyrate significantly blunted parasitaemia only at concentrations much higher (3 mM) than those encountered <it>in vivo </it>following GA ingestion (<1 μM). According to the <it>in vivo </it>experiments the administration of gum arabic slightly but significantly decreased the parasitaemia and significantly extended the life span of infected mice.</p> <p>Discussion</p> <p>GA moderately influences the parasitaemia and survival of <it>Plasmodium-</it>infected mice. The underlying mechanism remained, however, elusive.</p> <p>Conclusions</p> <p>Gum arabic favourably influences the course of murine malaria.</p

Shaping Neonatal Immunization by Tuning the Delivery of Synergistic Adjuvants via Nanocarriers

Adjuvanted nanocarrier-based vaccines hold substantial potential for applications in novel early-life immunization strategies. Here, via mouse and human age-specific in vitro modeling, we identified the combination of a small-molecule STING agonist (2′3′-cyclic GMP-AMP, cGAMP) and a TLR7/8 agonist (CL075) to drive the synergistic activation of neonatal dendritic cells and precision CD4 T-helper (Th) cell expansion via the IL-12/IFNγaxis. We further demonstrate that the vaccination of neonatal mice with quadrivalent influenza recombinant hemagglutinin (rHA) and an admixture of two polymersome (PS) nanocarriers separately encapsulating cGAMP (cGAMP-PS) and CL075 (CL075-PS) drove robust Th1 bias, high frequency of T follicular helper (TFH) cells, and germinal center (GC) B cells along with the IgG2c-skewed humoral response in vivo. Dual-loaded cGAMP/CL075-PSs did not outperform admixed cGAMP-PS and CL075-PS in vivo. These data validate an optimally designed adjuvantation system via age-selected small-molecule synergy and a multicomponent nanocarrier formulation as an effective approach to induce type 1 immune responses in early life

The nod-like receptor, Nlrp12, plays an anti-inflammatory role in experimental autoimmune encephalomyelitis

BACKGROUND: Multiple sclerosis (MS) is an organ-specific autoimmune disease resulting in demyelinating plaques throughout the central nervous system. In MS, the exact role of microglia remains unknown. On one hand, they can present antigens, skew T cell responses, and upregulate the expression of pro-inflammatory molecules. On the other hand, microglia may express anti-inflammatory molecules and inhibit inflammation. Microglia express a wide variety of immune receptors such as nod-like receptors (NLRs). NLRs are intracellular receptors capable of regulating both innate and adaptive immune responses. Among NLRs, Nlrp12 is largely expressed in cells of myeloid origins. It plays a role in immune inflammatory responses by negatively regulating the nuclear factor-kappa B (NF-κB) pathway. Thus, we hypothesize that Nlrp12 suppresses inflammation and ameliorates the course of MS. METHODS: We used experimental autoimmune encephalomyelitis (EAE), a well-characterized mouse model of MS. EAE was induced in wild-type (WT) and Nlrp12(−/−) mice with myelin oligodendrocyte glycoprotein (MOG):complete Freud’s adjuvant (CFA). The spinal cords of healthy and immunized mice were extracted for immunofluorescence and pro-inflammatory gene analysis. Primary murine cortical microglia cell cultures of WT and Nlrp12(−/−) were prepared with cortices of 1-day-old pups. The cells were stimulated with lipopolysaccharide (LPS) and analyzed for the expression of pro-inflammatory genes as well as pro-inflammatory molecule secretions. RESULTS: Over the course of 9 weeks, the Nlrp12(−/−) mice demonstrated increased severity in the disease state, where they developed the disease earlier and reached significantly higher clinical scores compared to the WT mice. The spinal cords of immunized WT mice relative to healthy WT mice revealed a significant increase in Nlrp12 messenger ribonucleic acid (mRNA) expression at 1, 3, and 5 weeks post injection. A significant increase in the expression of pro-inflammatory genes Ccr5, Cox2, and IL-1β was found in the spinal cords of the Nlrp12(−/−) mice relative to the WT mice (P < 0.05). A significant increase in the level of gliosis was observed in the spinal cords of the Nlrp12(−/−) mice compared to the WT mice after 9 weeks of disease (P < 0.05). Primary Nlrp12(−/−) microglia cells demonstrated a significant increase in inducible nitric oxide synthase (iNOS) expression (P < 0.05) and secreted significantly (P < 0.05) more tumor necrosis factor alpha (TNFα), interleukin-6 (IL-6), and nitric oxide (NO). CONCLUSION: Nlrp12 plays a protective role by suppressing inflammation during the development of EAE. The absence of Nlrp12 results in an increased inflammatory response

NLRX1 inhibits the early stages of CNS inflammation and prevents the onset of spontaneous autoimmunity

Nucleotide-binding, leucine-rich repeat containing X1 (NLRX1) is a mitochondria-located innate immune sensor that inhibits major pro-inflammatory pathways such as type I interferon and nuclear factor-κB signaling. We generated a novel, spontaneous, and rapidly progressing mouse model of multiple sclerosis (MS) by crossing myelin-specific T-cell receptor (TCR) transgenic mice with Nlrx1−/− mice. About half of the resulting progeny developed spontaneous experimental autoimmune encephalomyelitis (spEAE), which was associated with severe demyelination and inflammation in the central nervous system (CNS). Using lymphocyte-deficient mice and a series of adoptive transfer experiments, we demonstrate that genetic susceptibility to EAE lies within the innate immune compartment. We show that NLRX1 inhibits the subclinical stages of microglial activation and prevents the generation of neurotoxic astrocytes that induce neuronal and oligodendrocyte death in vitro. Moreover, we discovered several mutations within NLRX1 that run in MS-affected families. In summary, our findings highlight the importance of NLRX1 in controlling the early stages of CNS inflammation and preventing the onset of spontaneous autoimmunity