A Detailed Analogy of Network Simulators � NS1, NS2, NS3 and NS4

Networking is a field of Computer Science where the researchers are dependent on simulators and simulation as the devices used in networking are very costly and complex. It is not easily possible to establish a computer network in real world easily, also direct installation of network devices and cables is not feasible. A simulator is a low cost mechanism which can be used to deploy a network and implement protocols and test the feasibility of the network. NS aka Network Simulator is one such low cost tool, which is available as open source software to network designers. With time simulators have evolved and now Network simulators can simulate wireless networks and advanced mobile networks. The Network Simulator evolution took place with the methodologies and coding technologies. Medium level language like C++ was used in NS1 and later in NS2 we started using easy modeling language like OTCL and C++. In NS3 we can now do coding with more powerful language Python, it also has support for OTCL and C++. High level and advanced language like P4 is the recent one to be used in NS4. The network simulators are now more powerful and fast, as compared to earlier generations of simulators. This paper talks about these advancements that have taken place in the history of Network Simulators and future scopes of NS

School environment assessment tools to address behavioural risk factors of non-communicable diseases: A scoping review

We aimed to identify, describe and analyse school environment assessment (SEA) tools that address behavioural risk factors (unhealthy diet, physical inactivity, tobacco and alcohol consumption) for non-communicable diseases (NCD). We searched in MEDLINE and Web of Science, hand-searched reference lists and contacted experts. Basic characteristics, measures assessed and measurement properties (validity, reliability, usability) of identified tools were extracted. We narratively synthesized the data and used content analysis to develop a list of measures used in the SEA tools. Twenty-four SEA tools were identified, mostly from developed countries. Out of these, 15 were questionnaire based, 8 were checklists or observation based tools and one tool used a combined checklist/observation based and telephonic questionnaire approach. Only 1 SEA tool had components related to all the four NCD risk factors, 2 SEA tools has assessed three NCD risk factors (diet/nutrition, physical activity, tobacco), 10 SEA tools has assessed two NCD risk factors (diet/nutrition and physical activity) and 11 SEA tools has assessed only one of the NCD risk factor. Several measures were used in the tools to assess the four NCD risk factors, but tobacco and alcohol was sparingly included. Measurement properties were reported for 14 tools. The review provides a comprehensive list of measures used in SEA tools which could be a valuable resource to guide future development of such tools. A valid and reliable SEA tool which could simultaneously evaluate all NCD risk factors, that has been tested in different settings with varying resource availability is needed

SOME RESULT IN ORDERED METRIC SPACES FOR RATIONAL TYPE EXPRESSIONS

In this paper, we prove some fixed point theorems for mappings involving rational expression in the framework of metric spaces endowed with a partial order using a class of pairs of functions satisfying certain assumptions. Our result generalize and extend some known results appeared in [6], [14], [15]

Pathophysiology of acute experimental pancreatitis: Lessons from genetically engineered animal models and new molecular approaches

The incidence of acute pancreatitis is growing and worldwide population-based studies report a doubling or tripling since the 1970s. 25% of acute pancreatitis are severe and associated with histological changes of necrotizing pancreatitis. There is still no specific medical treatment for acute pancreatitis. The average mortality resides around 10%. In order to develop new specific medical treatment strategies for acute pancreatitis, a better understanding of the pathophysiology during the onset of acute pancreatitis is necessary. Since it is difficult to study the early acinar events in human pancreatitis, several animal models of acute pancreatitis have been developed. By this, it is hoped that clues into human pathophysiology become possible. In the last decade, while employing molecular biology techniques, a major progress has been made. The genome of the mouse was recently sequenced. Various strategies are possible to prove a causal effect of a single gene or protein, using either gain-of-function (i.e., overexpression of the protein of interest) or loss-of-function studies (i.e., genetic deletion of the gene of interest). The availability of transgenic mouse models and gene deletion studies has clearly increased our knowledge about the pathophysiology of acute pancreatitis and enables us to study and confirm in vitro findings in animal models. In addition, transgenic models with specific genetic deletion or overexpression of genes help in understanding the role of one specific protein in a cascade of inflammatory processes such as pancreatitis where different proteins interact and co-react. This review summarizes the recent progress in this field. Copyright (c) 2005 S. Karger AG, Basel

Src Dependent Pancreatic Acinar Injury Can Be Initiated Independent of an Increase in Cytosolic Calcium

Several deleterious intra-acinar phenomena are simultaneously triggered on initiating acute pancreatitis. These culminate in acinar injury or inflammatory mediator generation in vitro and parenchymal damage in vivo. Supraphysiologic caerulein is one such initiator which simultaneously activates numerous signaling pathways including non-receptor tyrosine kinases such as of the Src family. It also causes a sustained increase in cytosolic calcium- a player thought to be crucial in regulating deleterious phenomena. We have shown Src to be involved in caerulein induced actin remodeling, and caerulein induced changes in the Golgi and post-Golgi trafficking to be involved in trypsinogen activation, which initiates acinar cell injury. However, it remains unclear whether an increase in cytosolic calcium is necessary to initiate acinar injury or if injury can be initiated at basal cytosolic calcium levels by an alternate pathway. To study the interplay between tyrosine kinase signaling and calcium, we treated mouse pancreatic acinar cells with the tyrosine phosphatase inhibitor pervanadate. We studied the effect of the clinically used Src inhibitor Dasatinib (BMS-354825) on pervanadate or caerulein induced changes in Src activation, trypsinogen activation, cell injury, upstream cytosolic calcium, actin and Golgi morphology. Pervanadate, like supraphysiologic caerulein, induced Src activation, redistribution of the F-actin from its normal location in the sub-apical area to the basolateral areas, and caused antegrade fragmentation of the Golgi. These changes, like those induced by supraphysiologic caerulein, were associated with trypsinogen activation and acinar injury, all of which were prevented by Dasatinib. Interestingly, however, pervanadate did not cause an increase in cytosolic calcium, and the caerulein induced increase in cytosolic calcium was not affected by Dasatinib. These findings suggest that intra-acinar deleterious phenomena may be initiated independent of an increase in cytosolic calcium. Other players resulting in acinar injury along with the Src family of tyrosine kinases remain to be explored. © 2013 Mishra et al

The University of California San Francisco, Brain Metastases Stereotactic Radiosurgery (UCSF-BMSR) MRI Dataset

The University of California San Francisco Brain Metastases Stereotactic Radiosurgery (UCSF-BMSR) dataset is a public, clinical, multimodal brain MRI dataset consisting of 560 brain MRIs from 412 patients with expert annotations of 5136 brain metastases. Data consists of registered and skull stripped T1 post-contrast, T1 pre-contrast, FLAIR and subtraction (T1 pre-contrast - T1 post-contrast) images and voxelwise segmentations of enhancing brain metastases in NifTI format. The dataset also includes patient demographics, surgical status and primary cancer types. The UCSF-BSMR has been made publicly available in the hopes that researchers will use these data to push the boundaries of AI applications for brain metastases.Comment: 15 pages, 2 tables, 2 figure

Acute cholecystitis with massive upper gastrointestinal bleed: A case report and review of the literature

BACKGROUND: Cystic artery pseudoaneurysm is a rare complication following cholecystitis. Its presentation with upper gastrointestinal hemorrhage (UGIH) is even rarer. Thirteen patients with cystic artery pseudoaneurysm have been reported in the literature but only 2 of them presented with UGIH alone. CASE PRESENTATION: We report a 43-year-old woman who developed a cystic artery pseudoaneurysm following an episode of acute cholecystitis. She presented with haematemesis and melaena associated with postural symptoms. Upper gastrointestinal endoscopy revealed a duodenal ulcer with adherent clots in the first part of the duodenum. Ultrasonography detected gallstones and a pseudoaneurysm at the porta hepatis. Selective hepatic angiography showed two small pseudoaneurysms in relation to the cystic artery, which were selectively embolized. However, the patient developed abdominal signs suggestive of gangrene of the gall bladder and underwent an emergency laparotomy. Cholecystectomy with common bile duct exploration along with repair of the duodenal rent, and pyloric exclusion and gastrojejunostomy was done. CONCLUSION: This case illustrates the occurrence of a rare complication (pseudoaneurysm) following cholecystitis with an unusual presentation (UGIH). Cholecystectomy, ligation of the pseudoaneurysm and repair of the intestinal communication is an effective modality of treatment

Taking stock of carbon dioxide removal policy in emerging economies: developments in Brazil, China, and India

Deliberately removing carbon dioxide from the atmosphere is an important element of bringing mitigation pathways in line with the climate goals of the Paris Agreement. To reach global net-zero CO2 emissions and limit global warming to 1.5°C with no or limited overshoot, global mitigation pathways assessed by IPCC’s Sixth Assessment Report require some world regions to achieve net-negative CO2 emissions with large-scale carbon dioxide removal (CDR) deployment. This raises important questions about the availability and feasibility of CDR deployment in different societal and political contexts. This paper therefore combines an analysis of CDR deployment in a sample of scenarios from the IPCC AR6 database with a bottom-up analysis of the state of CDR governance and policy in countries considered key in scaling up CDR capacity and not yet covered by existing research. In particular, the paper focuses on Brazil, China, and India as important emerging economies and large emitters. We highlight the expected use of CDR methods in those regions in scenarios and systematically assess and compare the level of CDR regulation and innovation across these countries. This comparative perspective has the potential to broaden the understanding of existing and emerging CDR policies and politics. The synthesis of the case studies provides three key contributions to existing literature: First, we explore the state of CDR governance and policymaking in key emerging economies. As in OECD countries, there is a notable lack of CDR regulation and innovation to enable the scale of CDR required in the short- and medium term. Second, we identify that repurposing policies is a key type of emerging CDR policymaking in these countries targeting CDR methods in the land use, land use change and forestry (LULUCF) sector. We find that the repurposing efforts strengthen the level of regulation and innovation for this group of methods. Third, we explore three building blocks (regional differentiation, delay of upscaling, sustainability thresholds) of plausible CDR deployment narratives that could help bridge integrated assessment models and comparative case studies in future research

Inhibitors of Bcl-2 protein family deplete ER Ca2+ stores in pancreatic acinar cells

Physiological stimulation of pancreatic acinar cells by cholecystokinin and acetylcholine activate a spatial-temporal pattern of cytosolic [Ca+2] changes that are regulated by a coordinated response of inositol 1,4,5-trisphosphate receptors (IP3Rs), ryanodine receptors (RyRs) and calcium-induced calcium release (CICR). For the present study, we designed experiments to determine the potential role of Bcl-2 proteins in these patterns of cytosolic [Ca+2] responses. We used small molecule inhibitors that disrupt the interactions between prosurvival Bcl-2 proteins (i.e. Bcl-2 and Bcl-xl) and proapoptotic Bcl-2 proteins (i.e. Bax) and fluorescence microfluorimetry techniques to measure both cytosolic [Ca+2] and endoplasmic reticulum [Ca+2]. We found that the inhibitors of Bcl-2 protein interactions caused a slow and complete release of intracellular agonist-sensitive stores of calcium. The release was attenuated by inhibitors of IP3Rs and RyRs and substantially reduced by strong [Ca2+] buffering. Inhibition of IP3Rs and RyRs also dramatically reduced activation of apoptosis by BH3I-2′. CICR induced by different doses of BH3I-2′ in Bcl-2 overexpressing cells was markedly decreased compared with control. The results suggest that Bcl-2 proteins regulate calcium release from the intracellular stores and suggest that the spatial-temporal patterns of agonist-stimulated cytosolic [Ca+2] changes are regulated by differential cellular distribution of interacting pairs of prosurvival and proapoptotic Bcl-2 proteins