Влияние корпоративной культуры на создание комфортных эмоционально-психологических условий труда в коллективе

Объем работы 90 стр., таблиц – 8, источников – 53. Корпоративная культура, социально-психологический климат, эмоционально-психологический климат, психологическая атмосфера, уровень, удовлетворенность, внутренние коммуникации. Актуальность проблем, освещаемых в работе, связана с развитием рыночной экономики. Неизбежный рост конкурентной среды стимулирует компании к более эффективному использованию ресурсов, в том числе и человеческих. Актуальным становится формирование на предприятии корпоративной культуры высокого уровня. Объектом исследования является корпоративная культура организации. Предметом – влияние элементов культуры на эмоционально-психологический климат организации. Цель ВКР – разработка проектных рекомендаций по совершенствованию элементов корпоративной культуры цифровой типScope of work page 90, table – 8, source – 53. Corporate culture, socio-psychological climate, emotional-psychological climate, psychological climate, level, satisfaction, internal communication. The relevance of the problems outlined in the work connected with the development of a market economy. The inevitable growth of a competitive environment encourages companies to make more effective use of resources, including human. Actual there is a formation of enterprise corporate culture of high level. The object of research is corporate culture of the organization. Subject – the influence of cultural elements on the emotional and psychological climate of the organization. The purpose of the WRC – development of design recommendations for improving elements of corporate culture digital typog

Status Update and Interim Results from the Asymptomatic Carotid Surgery Trial-2 (ACST-2)

Objectives: ACST-2 is currently the largest trial ever conducted to compare carotid artery stenting (CAS) with carotid endarterectomy (CEA) in patients with severe asymptomatic carotid stenosis requiring revascularization. Methods: Patients are entered into ACST-2 when revascularization is felt to be clearly indicated, when CEA and CAS are both possible, but where there is substantial uncertainty as to which is most appropriate. Trial surgeons and interventionalists are expected to use their usual techniques and CE-approved devices. We report baseline characteristics and blinded combined interim results for 30-day mortality and major morbidity for 986 patients in the ongoing trial up to September 2012. Results: A total of 986 patients (687 men, 299 women), mean age 68.7 years (SD ± 8.1) were randomized equally to CEA or CAS. Most (96%) had ipsilateral stenosis of 70-99% (median 80%) with contralateral stenoses of 50-99% in 30% and contralateral occlusion in 8%. Patients were on appropriate medical treatment. For 691 patients undergoing intervention with at least 1-month follow-up and Rankin scoring at 6 months for any stroke, the overall serious cardiovascular event rate of periprocedural (within 30 days) disabling stroke, fatal myocardial infarction, and death at 30 days was 1.0%. Conclusions: Early ACST-2 results suggest contemporary carotid intervention for asymptomatic stenosis has a low risk of serious morbidity and mortality, on par with other recent trials. The trial continues to recruit, to monitor periprocedural events and all types of stroke, aiming to randomize up to 5,000 patients to determine any differential outcomes between interventions. Clinical trial: ISRCTN21144362. © 2013 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved

Second asymptomatic carotid surgery trial (ACST-2): a randomised comparison of carotid artery stenting versus carotid endarterectomy

Background: Among asymptomatic patients with severe carotid artery stenosis but no recent stroke or transient cerebral ischaemia, either carotid artery stenting (CAS) or carotid endarterectomy (CEA) can restore patency and reduce long-term stroke risks. However, from recent national registry data, each option causes about 1% procedural risk of disabling stroke or death. Comparison of their long-term protective effects requires large-scale randomised evidence. Methods: ACST-2 is an international multicentre randomised trial of CAS versus CEA among asymptomatic patients with severe stenosis thought to require intervention, interpreted with all other relevant trials. Patients were eligible if they had severe unilateral or bilateral carotid artery stenosis and both doctor and patient agreed that a carotid procedure should be undertaken, but they were substantially uncertain which one to choose. Patients were randomly allocated to CAS or CEA and followed up at 1 month and then annually, for a mean 5 years. Procedural events were those within 30 days of the intervention. Intention-to-treat analyses are provided. Analyses including procedural hazards use tabular methods. Analyses and meta-analyses of non-procedural strokes use Kaplan-Meier and log-rank methods. The trial is registered with the ISRCTN registry, ISRCTN21144362. Findings: Between Jan 15, 2008, and Dec 31, 2020, 3625 patients in 130 centres were randomly allocated, 1811 to CAS and 1814 to CEA, with good compliance, good medical therapy and a mean 5 years of follow-up. Overall, 1% had disabling stroke or death procedurally (15 allocated to CAS and 18 to CEA) and 2% had non-disabling procedural stroke (48 allocated to CAS and 29 to CEA). Kaplan-Meier estimates of 5-year non-procedural stroke were 2·5% in each group for fatal or disabling stroke, and 5·3% with CAS versus 4·5% with CEA for any stroke (rate ratio [RR] 1·16, 95% CI 0·86–1·57; p=0·33). Combining RRs for any non-procedural stroke in all CAS versus CEA trials, the RR was similar in symptomatic and asymptomatic patients (overall RR 1·11, 95% CI 0·91–1·32; p=0·21). Interpretation: Serious complications are similarly uncommon after competent CAS and CEA, and the long-term effects of these two carotid artery procedures on fatal or disabling stroke are comparable. Funding: UK Medical Research Council and Health Technology Assessment Programme

Plasma and cellular fibronectin: distinct and independent functions during tissue repair

Fibronectin (FN) is a ubiquitous extracellular matrix (ECM) glycoprotein that plays vital roles during tissue repair. The plasma form of FN circulates in the blood, and upon tissue injury, is incorporated into fibrin clots to exert effects on platelet function and to mediate hemostasis. Cellular FN is then synthesized and assembled by cells as they migrate into the clot to reconstitute damaged tissue. The assembly of FN into a complex three-dimensional matrix during physiological repair plays a key role not only as a structural scaffold, but also as a regulator of cell function during this stage of tissue repair. FN fibrillogenesis is a complex, stepwise process that is strictly regulated by a multitude of factors. During fibrosis, there is excessive deposition of ECM, of which FN is one of the major components. Aberrant FN-matrix assembly is a major contributing factor to the switch from normal tissue repair to misregulated fibrosis. Understanding the mechanisms involved in FN assembly and how these interplay with cellular, fibrotic and immune responses may reveal targets for the future development of therapies to regulate aberrant tissue-repair processes

Thyroid hormone action on mitochondria

Measurements of fluorescence at >420 nm and extracted NADPH in mitochondria obtained from the livers of hypothyroid rats show that the addition of Pi, ADP and glutamate rapidly reduces over 90% of the total reducible intrinsic pyridine nucleotides in State 3, compared with 20% in normals. The total fluorescence intensity change and reducible NADP + is about twice normal in hypothyroid mitochondria. Adding 6–30 µM l -thyroxine to hypothyroid mitochondria in vitro decreases and delays the substrate-induced reduction of pyridine nucleotides, and excludes both NADP + from such reduction and NADPH from oxidation by added ADP + Pi, without changing the high NADP(H) content. The correcting actions of the hormone are rapidly reversed by albumin, probably by binding free hormone. Changes in respiration do not appear to account for these observations. There is indirect evidence for decreased phosphorylation of added ADP in hypothyroid mitochondria, and a correction by added hormone. The hormonal actions on NADP(H) redox reactions are not reproduced by 1 to 6 µM dinitrophenol in vitro . l -Thyroxine appears to specifically block the participation of NADP (H) in redox reactions in mitochondria from hypothyroid rats, perhaps by effecting a sequestration of the nucleotide, by inhibiting the pyridine nucleotide transhydrogenase, or by activating an energy-linked process that competes with transhydrogenation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44803/1/10863_2004_Article_BF00761448.pd

Guidelines for management of ischaemic stroke and transient ischaemic attack 2008

This article represents the update of the European Stroke Initiative Recommendations for Stroke Management. These guidelines cover both ischaemic stroke and transient ischaemic attacks, which are now considered to be a single entity. The article covers referral and emergency management, Stroke Unit service, diagnostics, primary and secondary prevention, general stroke treatment, specific treatment including acute management, management of complications, and rehabilitation

Second harmonic imaging: a new ultrasound technique to assess human brain tumour perfusion

Background: Second harmonic imaging is a new ultrasound technique that allows evaluation of brain tissue perfusion after application of an ultrasound contrast agent. Objective: To evaluate the potential of this technique for the assessment of abnormal echo contrast characteristics of different brain tumours. Methods: 27 patients with brain tumours were studied. These were divided into four groups: gliomas, WHO grade III–IV (n = 6); meningiomas (n = 9); metastases (n = 5); and others (n = 7). Patients were examined by second harmonic imaging in a transverse axial insonation plane using the transtemporal approach. Following intravenous administration of 4 g (400 mg/ml) of a galactose based echo contrast agent, 62 time triggered images (one image per 2.5 seconds) were recorded and analysed off-line. Time–intensity curves of two regions of interest (tumour tissue and healthy brain tissue), including peak intensity (PI) (dB), time to peak intensity (TP) (s), and positive gradient (PG) (dB/s), as well as ratios of the peak intensities of the two regions of interest, were derived from the data and compared intraindividually and interindividually. Results: After administration of the contrast agent a marked enhancement of echo contrast was visible in the tumour tissue in all patients. Mean PI and PG were significantly higher in tumour tissue than in healthy brain parenchyma (11.8 v 5.1 dB and 0.69 v 0.16 dB/s; p < 0.001). TP did not differ significantly (37.1 v 50.2 s; p = 0.14). A tendency towards higher PI and PG as well as shorter TP was apparent in malignant gliomas. When comparing different tumour types, however, none of these variables reached significance, nor were there significant differences between malignant and benign tumours in general. Conclusions: Second harmonic imaging not only allows identification of brain tumours, but may also help in distinguishing between different tumour types. It gives additional and alternative information about tumour perfusion. Further studies are needed to evaluate the clinical potential of this technique in investigating brain tumours—for example in follow up investigations of patients undergoing radiation or chemotherapy—especially in comparison with neuroradiological and neuropathological findings

Tissue transglutaminase in fibrosis - more than an ECM crosslinker

Tissue transglutaminase (TG2) is upregulated in the pathogenesis of a wide variety of chronic diseases. In this review special emphasis will be placed on fundamental mechanisms underlying the critical role of TG2 in fibroproliferative disorders. TG2 is best known for its cross-linking capacities in the extracellular space but has many critical and multifaceted roles beyond protein cross-linking, which are driven by the conformation and specific localization of the molecule. As extracellular crosslinker TG2 promotes fibrotic disease through the storage of latent TGF-β1 in a stiffened extracellular matrix (ECM). As membrane-bound cell adhesion cofactor and signaling protein and intracellular crosslinker or G-protein, TG2 promotes fibrotic disease through cell survival and profibrotic pathway activation on a signaling, transcriptional and translational level. Similarities between the roles that TG2 plays in scar tissue and in the tumor stroma suggest that a deeper understanding of key common pathways in disease pathogenesis and progression might lead to the identification of novel treatment targets and the development of new drugs and diagnostic methods