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This research aims to investigate the effectiveness of adapting Grice Maxims in teaching writing at undergraduate level, using a case study approach at Qurtuba University D. I. Khan. The study explores whether teaching writing by emphasizing the principles of relevance, quality, and clarity-which are the key principles of Grice Maxims can improve the quality of writing among undergraduate students. The population of the study is a class of 36 students of BS English enrolled in 2nd semester and 4 teachers who teach various subjects. The study employs a mixed-methods approach, which involves quantitative data collected through pre and post-tests from students, and qualitative data collected through interviews with teachers. The results suggest that using Grice Maxims in teaching writing has a positive impact on students' writing quality, as well as their perception of the writing process. The study concludes that incorporating Grice Maxims into the teaching of writing is a promising pedagogical approach that can enhance writing skills among undergraduate students.

Present study was conducted to develop and validate an Indigenous scale to assess the stressors experienced by obese people in different domains of their lives. Mixed method design and purposive sampling technique was used. A list of 29 items was generated after thorough review of the literature and from the details of the interviews conducted with the participants. Validation from expert clinical psychologists was obtained. Exploratory factor analysis (EFA) with oblimin rotation was run on a sample of 300 participants for current study. Confirmatory factor analysis on a separate sample of 400 participants yielded a good model fit and validated three-factor structure with fit indices ? 2 = 807.45 (df = 320, N = 300), p < .05, RMSEA = .062, CFI = .91 and TLI = .88. The Cronbach alpha valuewas.86 indicating strong internal consistency of the scale. The distress and Well-being subscales of Mental Health Inventory were utilized to assess the convergent and divergent Validity which yielded positive and negative correlation respectively affirming Stressor Scale for Obese people as a valid construct. The study is an initial step to highlight and understand the stressors experienced by obese people and its severity level. This will help doctors and mental health professional to devise effective management of obesity.

We attempt to analyse the form and content of major Native American plays to discuss their relationship with the traditional English drama and its content. By looking at plays of key Native American playwrights, we show that the Native American tradition goes against the English tradition of drama in its form by challenging the unities of time and place and characterization. It also brings in elements of Native American tradition of storytelling such as the blend of the sacred and the profane, the use of humor, the attitude towards facticity, to the tradition of drama to carve out a unique space for itself through which it attempts to challenge the dominant narratives of history, Native American culture, and at the same time highlight the problems the Native American nations face currently.

The complexity of signaling events and cellular responses unfolding in neuronal, glial, and immune cells upon traumatic brain injury (TBI) constitutes an obstacle in elucidating pathophysiological links and targets for intervention. We use array phosphoproteomics in a murine mild blunt TBI to reconstruct the temporal dynamics of tyrosine-kinase signaling in TBI and then scrutinize the large-scale effects of perturbation of Met/HGFR, VEGFR1, and Btk signaling by small molecules. We show Met/HGFR as a selective modifier of early microglial response and that Met/HGFR blockade prevents the induction of microglial inflammatory mediators, of reactive microglia morphology, and TBI-associated responses in neurons and vasculature. Both acute and prolonged Met/HGFR inhibition ameliorate neuronal survival and motor recovery. Early elevation of HGF itself in the cerebrospinal fluid of TBI patients suggests that this mechanism has translational value in human subjects. Our findings identify Met/HGFR as a modulator of early neuroinflammation in TBI with promising translational potential. ispartof: Cell Reports vol:41 issue:13 ispartof: location:United States status: published

Immune system molecules are expressed by neurons, often for unknown functions. We have identified IL-13 and its receptor IL-13Ra1 as neuronal, synaptic proteins in mouse, rat, and human brains, whose engagement upregulates the phosphorylation of NMDAR and AMPAR subunits and, in turn, increases synaptic activity and CREB-mediated transcription. We demonstrate that increased IL-13 is a hallmark of traumatic brain injury (TBI) in mice as well as in two distinct cohorts of human patients. We also provide evidence that IL-13 upregulation protects neurons from excitotoxic death. We show IL-13 upregulation occurring in several cohorts of human brain samples and in CSF. Thus, IL-13 is a previously unrecognized physiological modulator of synaptic physiology of neuronal origin, with implications for the establishment of synaptic plasticity and the survival of neurons under injury conditions. Furthermore, we suggest that the neuroprotection afforded through the upregulation of IL-13 represents a new entry point for interventions in the pathophysiology of TBI.

Background Blood-based biomarkers have proven to be a reliable measure of the severity and outcome of traumatic brain injury (TBI) in both murine models and patients. In particular, neuron-specific enolase (NSE), neurofilament light (NFL) and S100 beta (S100B) have been investigated in the clinical setting post-injury. Ethanol intoxication (EI) remains a significant comorbidity in TBI, with 30–40% of patients having a positive blood alcohol concentration post-TBI. The effect of ethanol on blood-based biomarkers for the prognosis and diagnosis of TBI remains unclear. In this study, we investigated the effect of EI on NSE, NFL and S100B and their correlation with blood–brain barrier integrity in a murine model of TBI. Methods We used ultra-sensitive single-molecule array technology and enzyme-linked immunosorbent assay methods to measure NFL, NSE, S100B and claudin-5 concentrations in plasma 3 hours post-TBI. Results We showed that NFL, NSE and S100B were increased at 3 hours post-TBI. Interestingly, ethanol blood concentrations showed an inverse correlation with NSE but not with NFL or S100B. Claudin-5 levels were increased post-injury but no difference was detected compared to ethanol pretreatment. The increase in claudin-5 post-TBI was correlated with NFL but not with NSE or S100B. Conclusions Ethanol induces an effect on biomarker release in the bloodstream that is different from TBI not influenced by alcohol. This could be the basis of investigations into humans.

Blood-based biomarkers have proven to be a reliable measure of traumatic brain injury (TBI) severity and outcome, in both murine models and patients. In particular, neuron-specific enolase (NSE) and neurofilament light (NFL) have been investigated in the clinical setting post injury. Ethanol intoxication (EI) remains a significant comorbidity in TBI, with 30-40% of patients having a positive blood alcohol level (BAC) post TBI. The effect of ethanol on blood-based biomarkers on the prognosis and diagnosis of TBI remain unclear. In this study, we investigated the effect of EI on NSE and NFL and their correlation with blood-brain barrier (BBB) integrity in a murine model of TBI. We have used ultra-sensitive single molecule array technology (SIMOA) and ELISA methods to measure NFL, NSE and Claudin-5 concentrations in plasma 3h post TBI. We showed that both NFL and NSE were increased 3h post TBI. However, ethanol blood concentrations only showed an inverse correlation with NSE, but not NFL. Claudin-5 levels were increased post injury, but no difference was detected in EI. The Claudin-5 increase post TBI was correlated with NFL, but not with NSE. Thus, the data indicate that ethanol has a confined effect on biomarker release in the bloodstream and neuronal biomarkers reflect a different pathophysiology upon TBI.

Traumatic brain injury (TBI) and ethanol intoxication (EI) frequently coincide, particularly in young subjects. However, the mechanisms of their interaction remain poorly understood. Among other pathogenic pathways, TBI induces glial activation and neuroinflammation in the hippocampus, resulting in acute and chronic hippocampal dysfunction. In this regard, we investigated the role of EI affecting these responses unfolding after TBI. We used a blunt, weight-drop approach to model TBI in mice. Male mice were pre-administered with ethanol or vehicle to simulate EI. The neuroinflammatory response in the hippocampus was assessed by monitoring the expression levels of >20 cytokines, the phosphorylation status of transcription factors and the phenotype of microglia and astrocytes. We used AS1517499, a brain-permeable STAT6 inhibitor, to elucidate the role of this pathway in the EI/TBI interaction. We showed that TBI causes the elevation of IL-33 , IL-1β , IL-38 , TNF-α , IFN-α , IL-19 in the hippocampus at 3h time point and concomitant EI results in the dose-dependent downregulation of IL-33 , IL-1β , IL-38 , TNF-α and IL-19 (but not of IFN-α ) and in the selective upregulation of IL-13 and IL-12 . EI is associated with the phosphorylation of STAT6 and the transcription of STAT6-controlled genes. Moreover, ethanol-induced STAT6 phosphorylation and transcriptional activation can be recapitulated in vitro by concomitant exposure of neurons to ethanol, depolarization and inflammatory stimuli (simulating the acute trauma). Acute STAT6 inhibition prevents the effects of EI on IL-33 and TNF-α , but not on IL-13 and negates acute EI beneficial effects on TBI-associated neurological impairment. Additionally, EI is associated with reduced microglial activation and astrogliosis as well as preserved synaptic density and baseline neuronal activity 7 days after TBI and all these effects are prevented by acute administration of the STAT6 inhibitor concomitant to EI. EI concomitant to TBI exerts significant immunomodulatory effects on cytokine induction and microglial activation, largely through the activation of STAT6 pathway, ultimately with beneficial outcomes.

Ethanol intoxication (EI) is a frequent comorbidity of traumatic brain injury (TBI), but the impact of EI on TBI pathogenic cascades and prognosis is unclear. Although clinical evidence suggests that EI may have neuroprotective effects, experimental support is, to date, inconclusive. We aimed at elucidating the impact of EI on TBI-associated neurological deficits, signaling pathways, and pathogenic cascades in order to identify new modifiers of TBI pathophysiology. We have shown that ethanol administration (5 g/kg) before trauma enhances behavioral recovery in a weight-drop TBI model. Neuronal survival in the injured somatosensory cortex was also enhanced by EI. We have used phospho-receptor tyrosine kinase (RTK) arrays to screen the impact of ethanol on TBI-induced activation of RTK in somatosensory cortex, identifying ErbB2/ErbB3 among the RTKs activated by TBI and suppressed by ethanol. Phosphorylation of ErbB2/3/4 RTKs were upregulated in vGlut2

Traumatic brain injury (TBI) induces a neuroinflammatory response resulting in astrocyte and microglia activation at the lesion site. This involves upregulation of neuroinflammatory genes, including chemokines and interleukins. However, so far, there is lack of knowledge on transcription factors (TFs) modulating this TBI-associated gene expression response. Herein, we analyzed activating transcription factor 3 (ATF3), a TF encoding a regeneration-associated gene (RAG) predominantly studied in peripheral nervous system (PNS) injury. ATF3 contributes to PNS axon regeneration and was shown before to regulate inflammatory processes in other injury models. In contrast to PNS injury, data on ATF3 in central nervous system (CNS) injury are sparse. We used Atf3 mouse mutants and a closed-head weight-drop-based TBI model in adult mice to target the rostrolateral cortex resulting in moderate injury severity. Post-TBI, ATF3 was upregulated already at early time points (i.e,. 1-4 h) post-injury in the brain. Mortality and weight loss upon TBI were slightly elevated in Atf3 mutants. ATF3 deficiency enhanced TBI-induced paresis and hematoma formation, suggesting that ATF3 limits these injury outcomes in wild-type mice. Next, we analyzed TBI-associated RAG and inflammatory gene expression in the cortical impact area. In contrast to the PNS, only some RAGs (Atf3, Timp1, and Sprr1a) were induced by TBI, and, surprisingly, some RAG encoding neuropeptides were downregulated. Notably, we identified ATF3 as TF-regulating proneuroinflammatory gene expression, including CCL and CXCL chemokines (Ccl2, Ccl3, Ccl4, and Cxcl1) and lipocalin. In Atf3 mutant mice, mRNA abundance was further enhanced upon TBI compared to wild-type mice, suggesting immune gene repression by wild-type ATF3. In accord, more immune cells were present in the lesion area of ATF3-deficient mice. Overall, we identified ATF3 as a new TF-mediating TBI-associated CNS inflammatory responses.

Ethanol intoxication is a risk factor for traumatic brain injury (TBI) but clinical evidence suggests that it may actually improve the prognosis of intoxicated TBI patients. We have employed a closed, weight-drop TBI model of different severity (2cm or 3cm falling height), preceded (-30min) or followed (+20min) by ethanol administration (5g/Kg). This protocol allows us to study the interaction of binge ethanol intoxication in TBI, monitoring behavioral changes, histological responses and the transcriptional regulation of a series of activity-regulated genes (immediate early genes, IEGs). We demonstrate that ethanol pretreatment before moderate TBI (2cm) significantly reduces neurological impairment and accelerates recovery. In addition, better preservation of neuronal numbers and cFos+cells was observed 7days after TBI. At transcriptional level, ethanol reduced the upregulation of a subset of IEGs encoding for transcription factors such as Atf3, c-Fos, FosB, Egr1, Egr3 and Npas4 but did not affect the upregulation of others (e.g. Gadd45b and Gadd45c). While a subset of IEGs encoding for effector proteins (such as Bdnf, InhbA and Dusp5) were downregulated by ethanol, others (such as Il-6) were unaffected. Notably, the majority of genes were sensitive to ethanol only when administered before TBI and not afterwards (the exceptions being c-Fos, Egr1 and Dusp5). Furthermore, while severe TBI (3cm) induced a qualitatively similar (but quantitatively larger) transcriptional response to moderate TBI, it was no longer sensitive to ethanol pretreatment. Thus, we have shown that a subset of the TBI-induced transcriptional responses were sensitive to ethanol intoxication at the instance of trauma (ultimately resulting in beneficial outcomes) and that the effect of ethanol was restricted to a certain time window (pre TBI treatment) and to TBI severity (moderate). This information could be critical for the translational value of ethanol in TBI and for the design of clinical studies aimed at disentangling the role of ethanol intoxication in TBI.

Plants are the primary reservoirs in food chain. They play a key role in the conversion of energy into food. The life on Earth is impossible without plants. With the increasing advances in different fields, the health of plants is deteriorating drastically. Heavy metals have become an environmental concern because of their adverse and detrimental effects on human life. Apart from that, one of the most important components of global change is increase in atmospheric nitrogen (N), which is threatening both the structure and function of the ecosystem. The N cycle is dominated by anthropogenic activity and the emission and deposition rates of N are expected to be doubled by 2050, which will greatly increase the number of regions potentially receiving damaging levels of N inputs. Another harmful air pollutant is the tropospheric ozone (O3) having negative impact on the growth and development of plants. Current concentration of O3 is decreasing the productivity of forest and crop yields. Future O3 concentration will increase if the current emission rate stays persistent. In addition, benzene; a volatile organic compound (VOC), is extracted from industries of petroleum and used widely as an additive or intermediate or solvent in many manufacturing industries. Ambient air pollution problems can be caused by the emission of benzene from many sources, even though several organizations and countries have standard guidelines on benzene use. A number of studies have been carried out to study the effect of petro-coke, cement, coal and dust, fly ash, automobile exhaust and other air-borne particulates on different physiological and morphological parameters in plants.

For centuries now, sugarcane is being cultivated and is acting as a source of sugar production. This production is the source of many breeding programs all around the world. The sugarcane straw usually considered as trash is normally burned or is left in the soil depending on the harvesting system. There is an immense amount of straw being wasted yearly. Besides utilizing the straw for energy production or its requirement, there are a lot of other agronomic benefits that enhance the possibility of the straw blanket placed/left on the ground including protection of soil avoiding erosion, increasing organic ratio of content of carbon in the soil, inhibition of growth of weed, recycling of nutrients in textile fiber, and soil water reduction. Although consumption of sugarcane is very popular worldwide, certain factors are to be kept in mind regarding postharvest storage of stalk that involves enzymatic browning. This chapter focuses on ways sugarcane straw can be utilized as a primary source for the production of products having great agronomic value. Balancing the pros of keeping sugarcane fields with a percentage of straw, which significantly outnumber the cons, economists are keen to find out beneficial properties and economic aspects of keeping straw on the ground rather than using it all as possible energy source. The most challenging factor is to maintain the straw quality rendering it useful.

The abrupt increases in temperature as well as increasing population density are two major factors, which are threatening the world’s food security. A holistic approach is needed to address this situation to overcome the risk of food paucity. Therefore the agricultural scientists worldwide need to develop the coordinated research efforts covering all disciplines that encroach on agricultural productivity to minimize the unpleasant effects of climatic changes within the available natural resources. For this, a stress-tolerant germplasm coupled with natural resource management as well as policy interventions should be devised to ensure crop productivity under unpredictable environmental conditions. The countries that are located in temperate zones may extract some benefit from this change in temperature whereas the countries located in the tropical and subtropical regions have an increased vulnerability towards the effects of rising temperature.