To Overcome Communication Challenges in Distributed/Virtual Scrum Teams

The purpose of this research is to give an overview of a scrum in distributed teams and to suggest ways overcome communication challenges in such projects. In this research proposal, the latest available research on a scrum in distributed teams will be thoroughly analyzed and evaluated to know the possible solutions for communication problems in distributed teams. A review of the literature suggested scrum is widely accepted agile methodology in software projects and also it works best within collocated teams. However, the literature review also proposes that lack of proper communication is one of the main challenge faced by distributed scrum teams which needs more research. Effective communication among teams is fundamental to the agile approach in which proper and continuous feedback are absolutely necessary to improve team productivity and software quality. It is important to have right communication tool, trust among team members, organized daily scrum meetings, proper coordination, less time zone difference between locations and no language barrier to have effective communication within virtual scrum teams. Due to progression in technology scrum projects are going distributed as there are many benefits to the organizations. A brief literature review will be conducted to study the research problem which will provide valuable solutions to the communication issues in distributed teams. This research paper will be very useful to other researchers to solve the other challenges of a scrum in distributed projects

G, N, and P Gene-based Analysis of Chandipura Viruses, India

An encephalitis outbreak in 2003 in children from India was attributed to Chandipura virus. Sequence analyses of G, N, and P genes showed 95.6%–97.6% nucleotide identity with the 1965 isolate (G gene, 7–11 amino acid changes); N and P genes were highly conserved

Genetic divergence of Chikungunya viruses in India (1963-2006) with special reference to the 2005-2006 explosive epidemic

Re-emergence of Chikungunya (CHIK), caused by CHIK virus, was recorded in India during 2005-2006 after a gap of 32 years, causing 1.3 million cases in 13 states. Several islands of the Indian Ocean reported similar outbreaks in the same period. These outbreaks were attributed to the African genotype of CHIK virus. To examine relatedness of the Indian isolates (IND-06) with Reunion Island isolates (RU), full-genome sequences of five CHIK virus isolates representative of different Indian states were determined. In addition, an isolate obtained from mosquitoes in the year 2000 (Yawat-2000), identified as being of the African genotype, and two older strains isolated in 1963 and 1973 (of the Asian genotype), were sequenced. The IND-06 isolates shared 99.9 % nucleotide identity with RU isolates, confirming involvement of the same strain in these outbreaks. The IND-06 isolates shared 98.2 % identity with the Yawat-2000 isolate. Of two crucial substitutions reported for RU isolates in the E1 region, M269V was noted in the Yawat-2000 and IND-06 isolates, whereas D284E was seen only in the IND-06 isolates. The A226V shift observed with the progression of the epidemic in Reunion Island, probably associated with adaptation to the mosquito vector, was absent in all of the Indian isolates. Three unique substitutions were noted in the IND-06 isolates: two (T128K and T376M) in the Nsp1 region and one (P23S) in the capsid protein. The two Asian strains showed 99.4 % nucleotide identity to each other, indicating relative stability of the virus. No evidence of recombination of the Asian and African genotypes, or of positive selection was observed. The results may help in understanding the association, if any, of the unique mutations with the explosive nature of the CHIK outbreak

Comparison of etiology of sporadic acute and fulminant viral hepatitis in hospitalized patients in Pune, India during 1978-81 and 1994-97

Objective: To determine and compare the etiology of sporadic acute and fulminant viral hepatitis in two groups of patients 16 years apart. Methods: Serologic diagnostic tests for hepatitis A, B, C, D and E, and cytomegalovirus infection were carried out in 276 patients during 1994-1997 (Group A) and 206 patients during 1978-1981 (Group B). Results: Among children, hepatitis A virus was the major etiologic agent (81.6% in Group A and 51.4% in Group B), followed by hepatitis E virus (12.2%, 46.4%) and hepatitis B virus (5.4%, none). Among adults, hepatitis E virus was the main causative agent (42.4% in Group A and 71.2% in Group B) followed by HBV (28%, 25.5%) and hepatitis A virus (10.6%, 3.5%). Delta hepatitis was found only in Group A. No viral cause was found in 25% of patients in Group A and 13.5% patients in Group B. Conclusions: Hepatitis E virus is a major cause of sporadic acute and fulminant hepatitis. There has been an increase in hepatitis A in adults who developed fulminant hepatic failure. Our data points to the emergence of hepatitis A in adults and emergence of delta virus infection. Hepatitis C virus was unimportant in causing sporadic hepatitis

The Elevated Susceptibility to Diabetes in India: An Evolutionary Perspective

India has rapidly become a “diabetes capital” of the world, despite maintaining high rates of under-nutrition. Indians develop diabetes at younger age and at lower body weights than other populations. Here, we interpret these characteristics in terms of a “capacity–load” model of glucose homeostasis. Specifically, we assume that glycemic control depends on whether the body’s “metabolic capacity,” referring to traits, such as pancreatic insulin production and muscle glucose clearance, is able to resolve the “metabolic load” generated by high levels of body fat, high dietary glycemic load, and sedentary behavior. We employ data from modern cohorts to support the model and the interpretation that elevated diabetic risk among Indian populations results from the high metabolic load imposed by westernized lifestyles acting on a baseline of low metabolic capacity. We attribute this low metabolic capacity to the low birth weight characteristic of Indian populations, which is associated with short stature and low lean mass in adult life. Using stature as a marker of metabolic capacity, we review archeological and historical evidence to highlight long-term declines in Indian stature associated with adaptation to several ecological stresses. Underlying causes may include increasing population density following the emergence of agriculture, the spread of vegetarian diets, regular famines induced by monsoon failure, and the undermining of agricultural security during the colonial period. The reduced growth and thin physique that characterize Indian populations elevate susceptibility to truncal obesity, and increase the metabolic penalties arising from sedentary behavior and high glycemic diets. Improving metabolic capacity may require multiple generations; in the meantime, efforts to reduce the metabolic load will help ameliorate the situation

POMK regulates dystroglycan function via LARGE-mediated elongation of matriglycan

Matriglycan [-GlcA-β1,3-Xyl-α1,3-]n serves as a scaffold in many tissues for extracellular matrix proteins containing laminin-G domains including laminin, agrin, and perlecan. Like-acetylglucosaminyltransferase-1 (LARGE1) synthesizes and extends matriglycan on α-dystroglycan (α-DG) during skeletal muscle differentiation and regeneration; however, the mechanisms which regulate matriglycan elongation are unknown. Here, we show that Protein O-Mannose Kinase (POMK), which phosphorylates mannose of core M3 (GalNac-β1,3-GlcNac-β1,4-Man) preceding matriglycan synthesis, is required for LARGE1-mediated generation of full-length matriglycan on α-DG (~150 kDa). In the absence of Pomk in mouse skeletal muscle, LARGE1 synthesizes a very short matriglycan resulting in a ~90 kDa α-DG which binds laminin but cannot prevent eccentric contraction-induced force loss or muscle pathology. Solution NMR spectroscopy studies demonstrate that LARGE1 directly interacts with core M3 and binds preferentially to the phosphorylated form. Collectively, our study demonstrates that phosphorylation of core M3 by POMK enables LARGE1 to elongate matriglycan on α-DG, thereby preventing muscular dystrophy

Dinosaurs reveal the geographical signature of an evolutionary radiation

Dinosaurs dominated terrestrial ecosystems across the globe for over 100 million years and provide a classic example of an evolutionary radiation. However, little is known about how these animals radiated geographically to become globally distributed. Here, we use a biogeographical model to reconstruct the dinosaurs’ ancestral locations, revealing the spatial mechanisms that underpinned this 170-million-year-long radiation. We find that dinosaurs spread rapidly initially, followed by a significant continuous and gradual reduction in their speed of movement towards the Cretaceous/Tertiary boundary (66 million years ago). This suggests that the predominant mode of dinosaur speciation changed through time with speciation originally largely driven by geographical isolation—when dinosaurs speciated more, they moved further. This was gradually replaced by increasing levels of sympatric speciation (species taking advantage of ecological opportunities within their existing environment) as terrestrial space became a limiting factor. Our results uncover the geographical signature of an evolutionary radiation