Woven design data transmission using TTL logic for 128 hooks electronic cardless jacquard

A new electronic cardless handloom weaving apparatus which is an alternate to mechanical jacquard has been developed in order to improve the productivity and to reduce the occupational stress of the handloom weaver. The main objective of this development is to retain the features of the handloom with comfortable weaving and reduced laborious work. This development is based on embedded system to control the warp yarn vertical movement. The conventional punched cards are replaced by multimedia memory card file system. The shedding effect is programmatically controlled through miniature stepper motors. The new apparatus is found to be highly versatile for introducing variety of weaving patterns

Adsorption of Chromium Ions by Acid Activated Low Cost Carbon-Kinetic,Thermodynamic and Equilibrium Studies

A carbonaceous adsorbent prepared from an indigenous waste, by acid treatment was tested for its efficiency in removing metal ions. The process parameters studied include agitation time, initial metal ions concentration, carbon dose, pH and temperature. The adsorption followed first order reaction equation and the rate is mainly controlled by intra-particle diffusion. Freundlich and Langmuir isotherm models were applied to the equilibrium data. The adsorption capacity (Qm) obtained from the Langmuir isotherm plot were found to around 30 mg/g at an initial pH of 7.0. The temperature variation study showed that the metal ions adsorption is endothermic and spontaneous with increased randomness at the solid solution interface. Significant effect on adsorption was observed on varying the pH of the metal ion solutions. The Langmuir and Freundlich adsorption isotherms obtained, positive ΔH0 value, pH dependent results and desorption of metal ions in mineral acid suggest that the adsorption of metal ions on BBC involves chemisorption as well as physisorption mechanism

Current Treatment of Venous Thromboembolism

Venous thromboembolism (VTE), comprising deep vein thrombosis and pulmonary embolism, is a common disorder with at least 250,000 new events occurring each year in the United States alone. Treatment of VTE entails anticoagulation, which is achieved initially with the use of a parenterally administered anticoagulant followed by a more prolonged course of treatment with an oral vitamin K antagonist. The duration of anticoagulation depends on the clinical assessment of the benefit-risk ratio of prolonged anticoagulation versus the risk of recurrent events. In this review, we discuss some of the issues that we believe are among the most critical unanswered questions in the management of VTE in the present era

Adsorption of Chromium Ions by Acid Activated Low Cost Carbon-Kinetic,Thermodynamic and Equilibrium Studies

Abstract: A carbonaceous adsorbent prepared from an indigenous waste, by acid treatment was tested for its efficiency in removing metal ions. The process parameters studied include agitation time, initial metal ions concentration, carbon dose, pH and temperature. The adsorption followed first order reaction equation and the rate is mainly controlled by intra-particle diffusion. Freundlich and Langmuir isotherm models were applied to the equilibrium data. The adsorption capacity (Q m ) obtained from the Langmuir isotherm plot were found to around 30 mg/g at an initial pH of 7.0. The temperature variation study showed that the metal ions adsorption is endothermic and spontaneous with increased randomness at the solid solution interface. Significant effect on adsorption was observed on varying the pH of the metal ion solutions. The Langmuir and Freundlich adsorption isotherms obtained, positive H 0 value, pH dependent results and desorption of metal ions in mineral acid suggest that the adsorption of metal ions on BBC involves chemisorption as well as physisorption mechanism

Coagulation Abnormalities and Thrombosis in Patients Infected with SARS-CoV-2 and Other Pandemic Viruses

The world is amid a pandemic caused by severe acute respiratory syndrome-coronavirus 2. Severe acute respiratory syndrome-coronavirus causes serious respiratory tract infections that can lead to viral pneumonia, acute respiratory distress syndrome, and death. Some patients with coronavirus disease 2019 (COVID-19) have an activated coagulation system characterized by elevated plasma levels of d-dimer - a biomarker of fibrin degradation. Importantly, high levels of D-dimer on hospital admission are associated with increased risk of mortality. Venous thromboembolism is more common than arterial thromboembolism in hospitalized COVID-19 patients. Pulmonary thrombosis and microvascular thrombosis are observed in autopsy studies, and this may contribute to the severe hypoxia observed in COVID-19 patients. It is likely that multiple systems contribute to thrombosis in COVID-19 patients, such as activation of coagulation, platelet activation, hypofibrinolysis, endothelial cell dysfunction, inflammation, neutrophil extracellular traps, and complement. Targeting these different pathways may reduce thrombosis and improve lung function in COVID-19 patients

Excess of heme induces tissue factor-dependent activation of coagulation in mice

An excess of free heme is present in the blood during many types of hemolytic anemia. This has been linked to organ damage caused by heme-mediated oxidative stress and vascular inflammation. We investigated the mechanism of heme-induced coagulation activation in vivo. Heme caused coagulation activation in wild-type mice that was attenuated by an anti-tissue factor antibody and in mice expressing low levels of tissue factor. In contrast, neither factor XI deletion nor inhibition of factor XIIa-mediated factor XI activation reduced heme-induced coagulation activation, suggesting that the intrinsic coagulation pathway is not involved. We investigated the source of tissue factor in heme-induced coagulation activation. Heme increased the procoagulant activity of mouse macrophages and human PBMCs. Tissue factor-positive staining was observed on leukocytes isolated from the blood of heme-treated mice but not on endothelial cells in the lungs. Furthermore, heme increased vascular permeability in the mouse lungs, kidney and heart. Deletion of tissue factor from either myeloid cells, hematopoietic or endothelial cells, or inhibition of tissue factor expressed by non-hematopoietic cells did not reduce heme-induced coagulation activation. However, heme-induced activation of coagulation was abolished when both non-hematopoietic and hematopoietic cell tissue factor was inhibited. Finally, we demonstrated that coagulation activation was partially attenuated in sickle cell mice treated with recombinant hemopexin to neutralize free heme. Our results indicate that heme promotes tissue factor-dependent coagulation activation and induces tissue factor expression on leukocytes in vivo. We also demonstrated that free heme may contribute to thrombin generation in a mouse model of sickle cell disease

C1 inhibitor deficiency enhances contact pathway–mediated activation of coagulation and venous thrombosis

C1 inhibitor (C1INH) is a multifunctional serine protease inhibitor that functions as a major negative regulator of several biological pathways, including the contact pathway of blood coagulation. In humans, congenital C1INH deficiency results in a rare episodic bradykinin-mediated swelling disorder called hereditary angioedema (HAE). Patients with C1INH deficiency–associated HAE (C1INH-HAE) have increased circulating markers of activation of coagulation. Furthermore, we recently reported that patients with C1INH-HAE had a moderate but significant increased risk of venous thromboembolism. To further investigate the impact of C1INH deficiency on activation of coagulation and thrombosis, we conducted studies using patient samples and mouse models. Plasmas from patients with C1INH-HAE had significantly increased contact pathway–mediated thrombin generation. C1INH-deficient mice, which have been used as a model of C1INH-HAE, had significantly increased baseline circulating levels of prothrombin fragment 1+2 and thrombin-antithrombin complexes. In addition, whole blood from C1INH-deficient mice supported significantly increased contact pathway–mediated thrombin generation. Importantly, C1INH-deficient mice exhibited significantly enhanced venous, but not arterial, thrombus formation. Furthermore, purified human C1INH normalized contact pathway–mediated thrombin generation and venous thrombosis in C1INH-deficient mice. These findings highlight a key role for endogenous C1INH as a negative regulator of contact pathway–mediated coagulation in humans and mice. Further, this work identifies endogenous C1INH as an important negative regulator of venous thrombus formation in mice, complementing the phenotype associated with C1INH-HAE

Building the foundation for a community-generated national research blueprint for inherited bleeding disorders: research priorities for mucocutaneous bleeding disorders

BACKGROUND: Excessive or abnormal mucocutaneous bleeding (MCB) may impact all aspects of the physical and psychosocial wellbeing of those who live with it (PWMCB). The evidence base for the optimal diagnosis and management of disorders such as inherited platelet disorders, hereditary hemorrhagic telangiectasia (HHT), hypermobility spectrum disorders (HSD), Ehlers-Danlos syndromes (EDS), and von Willebrand disease (VWD) remains thin with enormous potential for targeted research. RESEARCH DESIGN AND METHODS: National Hemophilia Foundation and American Thrombosis and Hemostasis Network initiated the development of a National Research Blueprint for Inherited Bleeding Disorders with extensive all-stakeholder consultations to identify the priorities of people with inherited bleeding disorders and those who care for them. They recruited multidisciplinary expert working groups (WG) to distill community-identified priorities into concrete research questions and score their feasibility, impact, and risk. RESULTS: WG2 detailed 38 high priority research questions concerning the biology of MCB, VWD, inherited qualitative platelet function defects, HDS/EDS, HHT, bleeding disorder of unknown cause, novel therapeutics, and aging. CONCLUSIONS: Improving our understanding of the basic biology of MCB, large cohort longitudinal natural history studies, collaboration, and creative approaches to novel therapeutics will be important in maximizing the benefit of future research for the entire MCB community

A machine learning approach to predict mortality due to immune-mediated thrombotic thrombocytopenic purpura

Background: Mortality due to immune-mediated thrombotic thrombocytopenic purpura (iTTP) remains significant. Predicting mortality risk may potentially help individualize treatment. The French Thrombotic Microangiopathy (TMA) Reference Score has not been externally validated in the United States. Recent advances in machine learning technology can help analyze large numbers of variables with complex interactions for the development of prediction models. Objectives: To validate the French TMA Reference Score in the United States Thrombotic Microangiopathy (USTMA) iTTP database and subsequently develop a novel mortality prediction tool, the USTMA TTP Mortality Index. Methods: We analyzed variables available at the time of initial presentation, including demographics, symptoms, and laboratory findings. We developed our model using gradient boosting machine, a machine learning ensemble method based on classification trees, implemented in the R package gbm. Results: In our cohort (n = 419), the French score predicted mortality with an area under the receiver operating characteristic curve of 0.63 (95% CI: 0.50-0.77), sensitivity of 0.35, and specificity of 0.84. Our gradient boosting machine model selected 8 variables to predict acute mortality with a cross-validated area under the receiver operating characteristic curve of 0.77 (95% CI: 0.71-0.82). The 2 cutoffs corresponded to sensitivities of 0.64 and 0.50 and specificities of 0.76 and 0.87, respectively. Conclusion: The USTMA Mortality Index was acceptable for predicting mortality due to acute iTTP in the USTMA registry, but not sensitive enough to rule out death. Identifying patients at high risk of iTTP-related mortality may help individualize care and ultimately improve iTTP survival outcomes. Further studies are needed to provide external validation. Our model is one of many recent examples where machine learning models may show promise in clinical prediction tools in healthcare