A Study to Evaluate the Effectiveness of Progressive Muscle Relaxation Technique on Job Stress among Workers in Sakthi Sugars Limited, Sakthinagar, Erode District

INTRODUCTION: The primary goal of the study was to assess the stress level of workers, Sakthi Sugars Limited, Sakthinagar. Researcher developed a structured teaching programme and educated to the workers about the progressive muscle relaxation technique .then the stress level was assessed among the workers, Sakthi Sugars Limited, Sakthinagar and was associated with demographic variables. STATEMENT OF THE PROBLEM: “A STUDY TO EVALUATE THE EFFECTIVENESS OF PROGRESSIVE MUSCLE RELAXATION TECHNIQUE ON JOB STRESS AMONG WORKERS IN SAKTHI SUGARS LIMITED, SAKTHINAGAR, ERODE DISTRICT” OBJECTIVES: 1. To assess the pretest and posttest level of job stress among the workers in Sakthi Sugars Limited, Sakthinagar, Erode. 2. To evaluate the effectiveness of progressive muscle relaxation technique on job stress. 3. To find out the association between job stress and selected demographic variables. METHODS: The research approaches adopted for this study was quantitative evaluative approach. The research design adopted for this study was Quasi – experimental (pre-experimental) design-one group pretest posttest design. The Non-Probability purposive sampling technique was used in this study. RESULT: ❖ The major findings of the study showed that the pretest mean job stress score related to cognition, emotional, time, physical and physiological, social support, spiritual, activities and finance are 7.35 (73.5%), 9.38 (67%), 8.98 (74.83%), 17.1 (71.25%), 7.33 (73.3%), 6.05 (75.63%), 8.52 (71%), and 7.45 (74.5%) respectively. ❖ The post test mean job stress score related to cognition 5.03 (50.3%), emotional 6.38 (45.57%), time 6.05 (50.42%), physical and physiological 11.52 (48%), social support 4.47 (44.7%) spiritual 3.57 (44.63%) activities 5.25 (43.75%) and finance 4.35 (43.5%). ❖ The pre test overall stress score {mild (8%), moderate (25%), severe (67%)} was higher than the posttest overall stress score {(mild (30%), moderate (60%), severe (10%) } ❖ The findings of the study showed that there is significant association between the level of job stress and demographic variables such as educational status, marital status, monthly income, years of experience and type of family. CONCLUSION: The findings of the study proved the need of psychiatric nurse to conduct a training programme regarding job stress among the workers. The study revealed that the level of job stress score was high in pretest than the posttest, after PMRT .They concluded that need for providing information regarding job stress through the mental health services

Hydrogen Sulfide and Neurogenic Inflammation in Polymicrobial Sepsis: Involvement of Substance P and ERK-NF-κB Signaling

Hydrogen sulfide (H2S) has been shown to induce transient receptor potential vanilloid 1 (TRPV1)-mediated neurogenic inflammation in polymicrobial sepsis. However, endogenous neural factors that modulate this event and the molecular mechanism by which this occurs remain unclear. Therefore, this study tested the hypothesis that whether substance P (SP) is one important neural element that implicates in H2S-induced neurogenic inflammation in sepsis in a TRPV1-dependent manner, and if so, whether H2S regulates this response through activation of the extracellular signal-regulated kinase-nuclear factor-κB (ERK-NF-κB) pathway. Male Swiss mice were subjected to cecal ligation and puncture (CLP)-induced sepsis and treated with TRPV1 antagonist capsazepine 30 minutes before CLP. DL-propargylglycine (PAG), an inhibitor of H2S formation, was administrated 1 hour before or 1 hour after sepsis, whereas sodium hydrosulfide (NaHS), an H2S donor, was given at the same time as CLP. Capsazepine significantly attenuated H2S-induced SP production, inflammatory cytokines, chemokines, and adhesion molecules levels, and protected against lung and liver dysfunction in sepsis. In the absence of H2S, capsazepine caused no significant changes to the PAG-mediated attenuation of lung and plasma SP levels, sepsis-associated systemic inflammatory response and multiple organ dysfunction. In addition, capsazepine greatly inhibited phosphorylation of ERK1/2 and inhibitory κBα, concurrent with suppression of NF-κB activation even in the presence of NaHS. Furthermore, capsazepine had no effect on PAG-mediated abrogation of these levels in sepsis. Taken together, the present findings show that H2S regulates TRPV1-mediated neurogenic inflammation in polymicrobial sepsis through enhancement of SP production and activation of the ERK-NF-κB pathway

Mitochondrial dysfunction and biogenesis: do ICU patients die from mitochondrial failure?

Mitochondrial functions include production of energy, activation of programmed cell death, and a number of cell specific tasks, e.g., cell signaling, control of Ca2+ metabolism, and synthesis of a number of important biomolecules. As proper mitochondrial function is critical for normal performance and survival of cells, mitochondrial dysfunction often leads to pathological conditions resulting in various human diseases. Recently mitochondrial dysfunction has been linked to multiple organ failure (MOF) often leading to the death of critical care patients. However, there are two main reasons why this insight did not generate an adequate resonance in clinical settings. First, most data regarding mitochondrial dysfunction in organs susceptible to failure in critical care diseases (liver, kidney, heart, lung, intestine, brain) were collected using animal models. Second, there is no clear therapeutic strategy how acquired mitochondrial dysfunction can be improved. Only the benefit of such therapies will confirm the critical role of mitochondrial dysfunction in clinical settings. Here we summarized data on mitochondrial dysfunction obtained in diverse experimental systems, which are related to conditions seen in intensive care unit (ICU) patients. Particular attention is given to mechanisms that cause cell death and organ dysfunction and to prospective therapeutic strategies, directed to recover mitochondrial function. Collectively the data discussed in this review suggest that appropriate diagnosis and specific treatment of mitochondrial dysfunction in ICU patients may significantly improve the clinical outcome

Role of protein kinase C and phosphoinositide 3-kinase-Akt in substance P-induced proinflammatory pathways in mouse macrophages

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Effect of hydrogen sulfide on the phosphatidylinositol 3-kinase-protein kinase B pathway and on caerulein-induced cytokine production in isolated mouse pancreatic acinar cells

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Substance P enhances NF-κB transactivation and chemokine response in murine macrophages via ERK1/2 and p38 MAPK signaling pathways

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