Tuple board: a new distributed computing paradigm for mobile ad hoc networks

In this project, we introduce a new distributed computing paradigm called tuple board which is based on the tuple space abstraction originated by Gelernter and the blackboard architecture popular in distributed artificial intelligence. Most prominent implementations of tuple space systems including JavaSpaces and T-Spaces follow a centralized architecture where the space itself resides on a server, akin to a database server. Recently, researchers have attempted to develop decentralized architectures for tuple space systems. Some work includes LIME and PeerSpaces. In our opinion, the traditional implementation of tuple spaces is not well suited for ad hoc networks where devices frequently lose network access. The tuple space architecture attempts to provide persistent storage of tuples irrespective of the state of nodes in the network. While persistence may be easily implemented in centralized systems such as JavaSpaces, achieving this end in a purely decentralized environment would require complex replication schemes. This would place undue overhead on the resource-constrained devices that are typical for ad hoc networks. In the architecture used in this project the availability of tuples is determined by the state of devices participating in the network. At any given point of time, only the tuples contained in devices that are active in the network are available on the tuple board. As part of the project, a specific instance of the tuple board architecture was realized using the Anhinga Infrastructure. The system, called Anhinga Board, uses the M2MI protocol for the implementation of tuple board semantics. To demonstrate the Anhinga Board, a collaborative conference information system, consisting of tuple board based applications running on attendees devices, vendors devices, and the conference center s devices, was also developed

A study on Renal Failure in Chronic Liver Disease patients

INTRODUCTION: Renal failure is a challenging complication in patients with advanced cirrhosis. Patients with cirrhosis are susceptible to develop AKI which is associated with poor prognosis. Pathogenesis of renal dysfunction in CLD is complex. AIM OF THE STUDY: To identify the precipitating /risk factors associated with the renal failure in patients with chronic liver disease and the assess the outcome of renal failure on mortality in a period of 2 weeks duration. STUDY DESIGN: Prospective study. METHODS AND MATERIALS: All the patients with chronic liver disease and renal failure were included irrespective of age, sex, etiology. Patients with primary renal pathology were excluded from the study. Totally 40 patients were studied prospectively in the period of 6 months (Jan 2016 - June 2016) in Thanjavur Medical College. Patients were followed for 2 weeks (early hospitalization) with detailed history, examination and investigations include cbc, Rbs, serial renal function tests monitoring, S.electrolytes, liver function tests, prothrombin time, Urine analysis, Ascitic fluid analysis, USG Abdomen, UGI scopy, Blood culture, urine culture. Child pugh score and MELD score calculated for all the patients. Finally the outcome of the patient is assessed for 2 weeks. RESULTS: In this prospective study, we found that UGI bleed followed by SBP are the major precipitating events for renal failure in CLD. Other precipitating factors are infections, drugs, paracentesis etc., Totally 8 patients died which is 20% mortality. Alcohol is the main etiology for liver disease. High MELD score (>32) with P value 3.2 mg/dl) with P value < 0.02 has significant association with mortality in patients with CLD with renal failure. CONCLUSION: All the patients with CLD should be monitored for renal parameters for progressive risk of developing renal failure. We conclude that early identification, intervention and treating the risk factors for renal failure can prevent / reduce the mortality in early hospitalisation (2 weeks). MELD score, Child pugh Score, S. creatinine has significant co-relation with the short term mortality in early hospitalisation (2 weeks) as evidenced in the study. As many patients got either discharged/died during the study period, we could follow up patients only for 2 weeks duration. Long term mortality need to be assessed

An array of simple, fast, and safe approaches to visualizing fine cellular structures in free-hand sections of stem, leaf, and fruit using optical microscopy

A wide array of free-hand-sectioning-based optical microscopy techniques that are simple, safe, and inexpensive, yet allows quick and easy identification of specific cell types and cellular components with unprecedented resolution are presented using leaf (Saintpaulia ionantha and Schefflera actinophylla), stem (Vitis vinifera and V. labruscana), and fruit (Vitis vinifera) tissues.&nbsp; The objective of this study was to generate contrast and capture high quality cellular images of various plant organs either via infusing basic fuchsin, a xylemic dye into organs or using naturally pigmented organs by employing the classic technique of free-hand sectioning.&nbsp; Also, images were obtained via post-staining free-hand sections of organs without any dye infusion.&nbsp; Leaves injected with dye revealed its strikingly regular and hierarchical reticulate venation structure.&nbsp; The free-hand sections of healthy and water-stressed leaf petioles, and stems and pedicels prepared from organs either infused with basic fuchsin or post-stained with safranin displayed exceptional cellular details.&nbsp; These included the xylic and phloic transport systems positioned around the central parenchymatous pith, their tissue pattern in each system, and occlusion of xylem vessels by the parenchymatous tissues (tylosis).&nbsp; The free-hand sections of fruit revealed fine details of its translucent mesocarp embedded with vasculature of varied architecture, and seed morphology.&nbsp; Free-hand sections of naturally chromated petioles illustrated its internal structure pertaining to anthocyanin accumulating cells and crystals in superb details, and particularly, the most visually spectacular images of trichomes.&nbsp; Since observations of internal structures of plants constitute the foundations of plant biology, the microscopy techniques illustrated in this study can be of great interest and benefit to both addressing fundamental questions in plant biology and curiosity-driven research

Immune Responses of Systemic and Mucosal Lymphoid Organs to Pnu-Imune Vaccine as a Function of Age and the Efficacy of Monophosphoryl Lipid A as an Adjuvant

A murine model system was established to study immune responses to the Pnu-Imune vaccine, which is made up of 23 different pneumococcal capsular polysaccharides. In this animal model, antibody-forming cell responses to 21 of 23 individual polysaccharides in the vaccine were detected. The Pnu-Imune vaccine elicited good antibody responses from the spleens and mesenteric lymph nodes (MLN) of young mice, whereas a variety of other peripheral lymph nodes were unresponsive. The immunoglobulin M plaque-forming cell (PFC) response in the spleen to the Pnu-Imune vaccine (given intraperitoneally or subcutaneously) decreased dramatically with increasing age. However, the spleen and MLN differed in their susceptibility to an age-associated decline in immune function. While the PFC responses in the spleen declined with age, the PFC response in the mucosa-associated MLN did not decline with age but instead remained constant over the entire age span of 4 to 28 months studied. These studies showed that the spleen, peripheral lymph nodes, and MLN did not demonstrate parallel age-associated defects in antibody responses to pneumococcal polysaccharides when the antigen was administered systematically. Also, the deficient splenic antibody response to Pnu-Imune vaccine in aged mice could be enhanced by injecting a combination of Pnu-Imune vaccine and the nontoxic adjuvant monophosphoryl lipid A. Moreover, an immunoglobulin G response was induced when the immunogen was a mixture of vaccine and adjuvant

Multiple Regulatory Mechanisms Control B-1 B Cell Activation

B-1 cells constitute a unique subset of B cells identified in several species including mice and humans. B-1 cells are further subdivided into B-1a and B-1b subsets as the former but not the later express CD5.The B-1a subset contributes to innate type of immune responses while the B-1b B cell subset contributes to adaptive responses. B-1 cell responses to B cell receptor (BCR) as well as Toll-like receptor (TLR) ligation are tightly regulated due to the cross-reactivity of antigen specific receptors on B-1 cells to self-antigens. B-1 cells are elevated in several autoimmune diseases. CD5 plays a major role in down regulation of BCR responses in the B-1a cell subset. Reduced amplification of BCR induced signals via CD19 and autoregulation of BCR and TLR responses by B-1 cell produced IL-10 appear to have a role in regulation of both B-1a and B-1b B cell responses. Siglec G receptors and Lyn kinase also regulate B-1 cell responses but their differential role in the two B-1 cell subsets is unknown

Inhibition of Bruton Tyrosine Kinase Reduces Neuroimmune Cascade and Promotes Recovery after Spinal Cord Injury

Microglia/astrocyte and B cell neuroimmune responses are major contributors to the neurological deficits after traumatic spinal cord injury (SCI). Bruton tyrosine kinase (BTK) activation mechanistically links these neuroimmune mechanisms. Our objective is to use Ibrutinib, an FDA-approved BTK inhibitor, to inhibit the neuroimmune cascade thereby improving locomotor recovery after SCI. Rat models of contusive SCI, Western blot, immunofluorescence staining imaging, flow cytometry analysis, histological staining, and behavioral assessment were used to evaluate BTK activity, neuroimmune cascades, and functional outcomes. Both BTK expression and phosphorylation were increased at the lesion site at 2, 7, 14, and 28 days after SCI. Ibrutinib treatment (6 mg/kg/day, IP, starting 3 h post-injury for 7 or 14 days) reduced BTK activation and total BTK levels, attenuated the injury-induced elevations in Iba1, GFAP, CD138, and IgG at 7 or 14 days post-injury without reduction in CD45RA B cells, improved locomotor function (BBB scores), and resulted in a significant reduction in lesion volume and significant improvement in tissue-sparing 11 weeks post-injury. These results indicate that Ibrutinib exhibits neuroprotective effects by blocking excessive neuroimmune responses through BTK-mediated microglia/astroglial activation and B cell/antibody response in rat models of SCI. These data identify BTK as a potential therapeutic target for SCI

DIURETIC POTENTIAL OF AERVA LANATA AND ECBOLIUM LIGUSTRINUM ROOT EXTRACTS

Based on the ethnobotanical importance as diuretics Aerva lanata and Ecbolium ligustrinum were selected for presentscreening. Experiment was carried out on male wister strain albino rats using furosemide as standard drug. 20mg/kg and200mg/kg oral doses are selected for standard and test respectively. For quantifying the diuretic activity the urine output,urine pH, sodium, potassium and chloride levels in the urine are measured. The diuretic index value of Ecbolium ligustrinumis 1.70 and nearer to the standard furosemide value 1.80. Aerva lanata group shows less diuretic index of 1.49 compared tostandard. The ratio of the concentration of sodium ions to the potassium ions in control group was found to be 1.39 and theratio for standard, Aerva lanata and Ecbolium ligustrinum are 1.78, 1.49 and 1.68 respectively. Ecbolium ligustrinumaffected the amount of urine excreted and also the electrolyte concentration in urine. The present study concluded that rootsof Aerva lanata and Ecbolium ligustrinum are having diuretic nature

Primary Antibody Responses to Thymus-Independent Antigens in the Lungs and Hilar Lymph Nodes of Mice

B lymphocytes from the pulmonary lymphoid tissues were stimulated with a variety of thymus-independent (TI) antigens by intratracheal (i.t.) immunization. Immune responses in the lungs and hilar lymph nodes (HLN), which are part of the localized lymphoid tissue, as well as in the spleen, the systemic lymphoid organ, were studied. Thus, primary i.t. immunization of mice with the TI-1 antigen trinitrophenyl-lipopolysaccharide (TNP-LPS) elicited both antigen-specific and polyclonal plaque-forming cell responses from HLN, lung, and splenic B lymphocytes. These responses appeared as early as 3 days after immunization and declined by day 7. Similar immunization with another TI-1 antigen, TNP-Brucella abortus, resulted in anti-TNP responses in both pulmonary and systemic lymphoid tissues, although the kinetics of the antibody response were different than those to TNP-LPS. Interestingly an i.t. immunization with a TI-2 antigen, TNP-Ficoll, failed to induce an anti-TNP PFC response from HLN and lung B cells, although there was good antibody formation from splenic B cells. Antibody response to TNP-Ficoll was restored in pulmonary tissues when mice were immunized with TNP-Ficoll mixed with unconjugated B. abortus. In conclusion, our results indicate that TI-1 and TI-2 antigens differ in their ability to induce antibody responses in the pulmonary lymphoid tissues. The inability of TNP-Ficoll to elicit an antibody response in pulmonary lymphoid tissues has significance in the development of vaccines containing bacterial polysaccharides

Interleukin-10 Mediated Autoregulation of Murine B-1 B-Cells and Its Role in \u3cem\u3eBorrelia hermsii\u3c/em\u3e Infection

B cells are typically characterized as positive regulators of the immune response, primarily by producing antibodies. However, recent studies indicate that various subsets of B cells can perform regulatory functions mainly through IL-10 secretion. Here we discovered that peritoneal B-1 (B-1P) cells produce high levels of IL-10 upon stimulation with several Toll-like receptor (TLR) ligands. High levels of IL-10 suppressed B-1P cell proliferation and differentiation response to all TLR ligands studied in an autocrine manner in vitro and in vivo. IL-10 that accumulated in cultures inhibited B-1P cells at second and subsequent cell divisions mainly at the G1/S interphase. IL-10 inhibits TLR induced B-1P cell activation by blocking the classical NF-kappaB pathway. Co-stimulation with CD40 or BAFF abrogated the IL-10 inhibitory effect on B-1P cells during TLR stimulation. Finally, B-1P cells adoptively transferred from the peritoneal cavity of IL-10-/- mice showed better clearance of Borrelia hermsii than wild-type B-1P cells. This study described a novel autoregulatory property of B-1P cells mediated by B-1P cell derived IL-10, which may affect the function of B-1P cells in infection and autoimmunity