श्री रामदरश मिश्र के कहानी साहित्य में युगीन यथार्थ

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Understanding Tourism Dynamics Using GIS and Forecasting Model in Banswara District, Rajasthan, India

Understanding the tourism dynamics of an area involves a rigorous literature review, interviewing the local people and experts, and visiting the sites. This also involves getting acquainted with the transport network of the area to know about the accessibility to the tourism destination, which ultimately helps in preparing a suitable plan for tourism development by creating tourist circuits. Forecasting tourism demand with the help of past data helps put a better picture in front of planners and administration so they can plan more efficiently. Thus, a proper understanding of tourism dynamics requires a holistic vision. The present study tried to understand the tourism dynamics of Banswara district in Rajasthan state, India, by using forecasting techniques and GIS. This twin methodology used in this study highlights the fact that Banswara tourism is at its incipient stage and that there is a substantial prospect of religious, historical, and nature-based tourism in this area. Few of the sites are well connected with the road network, and thus, by taking connectivity into account, tourist circuits are designed

The CI-FLOW Project: A System for Total Water Level Prediction from the Summit to the Sea

Kildow et al. (2009) reported that coastal states support 81% of the U.S. population and generate 83 percent [$11.4 trillion (U.S. dollars) in 2007] of U.S. gross domestic product. Population trends show that a majority of coastal communities have transitioned from a seasonal, predominantly weekend, tourist-based economy to a year-round, permanently based, business economy where industry expands along shorelines and the workforce commutes from inland locations. As a result of this transition, costs associated with damage to the civil infrastructure and disruptions to local and regional economies due to coastal flooding events are escalating, pushing requirements for a new generation of flood prediction technologies and hydrologic decision support tools

Global patient outcomes after elective surgery: prospective cohort study in 27 low-, middle- and high-income countries.

BACKGROUND: As global initiatives increase patient access to surgical treatments, there remains a need to understand the adverse effects of surgery and define appropriate levels of perioperative care. METHODS: We designed a prospective international 7-day cohort study of outcomes following elective adult inpatient surgery in 27 countries. The primary outcome was in-hospital complications. Secondary outcomes were death following a complication (failure to rescue) and death in hospital. Process measures were admission to critical care immediately after surgery or to treat a complication and duration of hospital stay. A single definition of critical care was used for all countries. RESULTS: A total of 474 hospitals in 19 high-, 7 middle- and 1 low-income country were included in the primary analysis. Data included 44 814 patients with a median hospital stay of 4 (range 2-7) days. A total of 7508 patients (16.8%) developed one or more postoperative complication and 207 died (0.5%). The overall mortality among patients who developed complications was 2.8%. Mortality following complications ranged from 2.4% for pulmonary embolism to 43.9% for cardiac arrest. A total of 4360 (9.7%) patients were admitted to a critical care unit as routine immediately after surgery, of whom 2198 (50.4%) developed a complication, with 105 (2.4%) deaths. A total of 1233 patients (16.4%) were admitted to a critical care unit to treat complications, with 119 (9.7%) deaths. Despite lower baseline risk, outcomes were similar in low- and middle-income compared with high-income countries. CONCLUSIONS: Poor patient outcomes are common after inpatient surgery. Global initiatives to increase access to surgical treatments should also address the need for safe perioperative care. STUDY REGISTRATION: ISRCTN5181700

New mechanistic insights, novel treatment paradigms, and clinical progress in cerebrovascular diseases

The past decade has brought tremendous progress in diagnostic and therapeutic options for cerebrovascular diseases as exemplified by the advent of thrombectomy in ischemic stroke, benefitting a steeply increasing number of stroke patients and potentially paving the way for a renaissance of neuroprotectants. Progress in basic science has been equally impressive. Based on a deeper understanding of pathomechanisms underlying cerebrovascular diseases, new therapeutic targets have been identified and novel treatment strategies such as pre- and post-conditioning methods were developed. Moreover, translationally relevant aspects are increasingly recognized in basic science studies, which is believed to increase their predictive value and the relevance of obtained findings for clinical application.This review reports key results from some of the most remarkable and encouraging achievements in neurovascular research that have been reported at the 10th International Symposium on Neuroprotection and Neurorepair. Basic science topics discussed herein focus on aspects such as neuroinflammation, extracellular vesicles, and the role of sex and age on stroke recovery. Translational reports highlighted endovascular techniques and targeted delivery methods, neurorehabilitation, advanced functional testing approaches for experimental studies, pre-and post-conditioning approaches as well as novel imaging and treatment strategies. Beyond ischemic stroke, particular emphasis was given on activities in the fields of traumatic brain injury and cerebral hemorrhage in which promising preclinical and clinical results have been reported. Although the number of neutral outcomes in clinical trials is still remarkably high when targeting cerebrovascular diseases, we begin to evidence stepwise but continuous progress towards novel treatment options. Advances in preclinical and translational research as reported herein are believed to have formed a solid foundation for this progress

Recurrent hypoglycemia increases oxygen glucose deprivation-induced damage in hippocampal organotypic slices

► Diabetes is a risk factor for cerebral ischemia and heart disease. ► A major side effect of intensive therapy for diabetics is recurrent hypoglycemia. ► Recurrent hypoglycemic episodes exacerbate post-ischemic cerebral damage. ► This effect is independent of hormonal fluctuations. More than 65% of mortality among diabetics is due to stroke and heart disease. The major side effect of intensive therapy in both type 1 and type 2 diabetics is recurrent hypoglycemic episodes (RH). Our previous study in a rat model of insulin-requiring diabetes indicated that RH exacerbates cerebral ischemic damage. Studies related to RH in hypoglycemia unawareness suggest that RH may be deleterious to outcome following cerebral ischemia owing to systemic effects, since hormonal response to hypoglycemia is impaired following RH. The goal of the present study was to determine if RH increases oxygen-glucose deprivation (OGD)-induced damage in hippocampal organotypic slices, which are devoid of systemic influence. Hippocampal slices cultured in ex vivo conditions for 9–10 days were exposed to ten 30-min episodes of “hypoglucose” (to mimic the hypoglycemic condition) medium (1.06 mM) twice a day. Slices were exposed to OGD 12 h after the last hypo/normo-glucose exposure. OGD in control slices resulted in 60% neuronal death. The percentage of cell death in RH-treated slices was significantly higher by 24% than in control slices. The results demonstrate that RH can affect brain cells in the absence of humoral influence. In conclusion, the previous exposure of hippocampal slices to RH exacerbates OGD-induced damage. Understanding the mechanism by which RH increases ischemic damage in diabetics will help improve outcome following stroke

Role of reactive oxygen species and protein kinase C in ischemic tolerance in the brain

It is now understood that the mechanisms leading to neuronal cell death after cerebral ischemia are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia, and that reperfusion following cerebral ischemia contributes substantially to ischemic injury. It is now well accepted that central to ischemic/reperfusion-induced injury is what occurs to mitochondria hours to days following the ischemic insult. For many years, it has been established that reactive oxygen species (ROS) and reactive nitrogen species (RNS) promote lipid, protein, and DNA oxidation that affects normal cell physiology and eventually leads to neuronal demise. In addition to oxidation of neuronal molecules by ROS and RNS, a novel pathway for molecular modifications has risen from the concept that ROS can activate specific signal transduction pathways that, depending on the insult degree, can lead to either normal plasticity or pathology. Two examples of these pathways could explain why lethal ischemic insults lead to the translocation of protein kinase Cdelta (deltaPKC), which plays a role in apoptosis after cerebral ischemia, or why sublethal ischemic insults, such as in ischemic preconditioning, lead to the translocation of epsilonPKC, which plays a pivotal role in neuroprotection. A better understanding of the mechanisms by which ROS and/or RNS modulate key protein kinases that are involved in signaling pathways that lead to cell death and survival after cerebral ischemia will help devise novel therapeutic strategies

Protein kinase C and synaptic dysfunction after cardiac arrest

It is now understood that the mechanisms leading to neuronal cell death after cardiac arrest (CA) are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia. It has been suggested that decreases in electrophysiological activities precede the morphologic deterioration in postischemic CA1 neurons and that this deterioration may be one cause for delayed cell death. The link between synaptic dysfunction and cardiac arrest is evident by the fact that about 50% of long-term survivors of cardiac arrest exhibit impaired mental abilities, manifested as learning impairment, memory disturbance. Since PKC is known to be a key player in synaptic function and has been implicated in promoting cell death after cerebral ischemia, it is a logical candidate as a modulator of synaptic derangements after CA. In this review, we provide an overview of synaptic dysfunction following CA and the putative role of PKC on this dysfunction