Comprometimento organizacional no IFPB

20f.O presente cen?rio mundial apresenta in?meras mudan?as que t?m impactos diretos e imediatos na forma de agir de cada indiv?duo (Bauman, 2007). No que tange os estudos na ?rea do comprometimento organizacional concentram-se em uma linha de pesquisa com maior ?nfase no relacionamento entre o funcion?rio e a organiza??o, n?o apenas em organiza??es empresariais mais tamb?m as organiza??es p?blicas-educacionais. A educa??o ? um dos pilares que rege a sociedade, constatando a necessidade de melhorar a qualidade de ensino o governo criou os Institutos Federais, que est?o aumentando de forma acelerada devido ao crescimento veloz e a contrata??o de muito servidores, impossibilitando assim o processo de sele??o adequado para as contrata??es, o que poderia p?r em risco o rendimento dos servidos e consequentemente da institui??o, sendo assim surgia a necessidade de estudar o comprometimento organizacional dos servidores, em especifico nos Institutos Federais da Para?ba, varia de acordo com as caracter?sticas relativas ao perfil. Diante desta problem?tica, o presente artigo busca formas que possibilitem a cria??o de novas pol?ticas nas quais visando melhorar o rendimento dos servidores atrav?s das an?lises dos seus perfis, tendo em vista a boa presta??o de servi?o. Foi utilizada uma abordagem quantitativa caracterizada como explorat?ria e descritiva. O instrumento de pesquisa ? a escala EBACO, os question?rios foram aplicados online, a partir da? foram obtidas 647 respostas. Atrav?s dos resultados, foi vi?vel ponderar algumas variantes do comprometimento dos servidores, utilizando o teste de hip?tese, analisando diferentes grupos, obtendo resultados satisfat?rios para a organiza??o

The inhibitory efect of Ph?1? toxin on diabetic neuropathic pain involves the CXCR4 chemokine receptor.

Background: Diabetic neuropathy is a common cause of painful diabetic neuropathy (PDN). C-X-C chemokine receptor type 4 (CXCR4) expression is increased in peripheral nerve samples from diabetes patients, suggesting a role for CXCR4 in PDN. Therefore, we evaluated the effects of Ph?1?, ?-conotoxin MVIIA, and AMD3100 in a model of streptozotocin (STZ)-induced PDN in rodents and na?ve model of rats with the activation of the CXCR4/stromal cell-derived factor 1 (SDF-1) signal. Methods: Diabetic neuropathy was induced by intraperitoneal (ip) injection of STZ in Wistar rats. Na?ve rats were intrathecally injected with SDF-1 to test the CXCR4/SDF-1 signal. The effects of Ph?1? intrathecal (it), ?-conotoxin MVIIA intrathecal (it), and AMD3100 intraperitoneal (ip) on rat hypersensitivity, IL-6, and the intracellular calcium [Ca2+]i content of diabetic synaptosomes were studied. Results: The drugs reduced the hypersensitivity in diabetic rats. SDF-1 (1.0 ?g/it) administration in na?ve rats induced hypersensitivity. Ph?1? (100 pmol/it) or AMD3100 (2.5 ?g/ip) reduced this hypersensitivity after 2 h treatments, while ?-conotoxin MVIIA did not have an effect. IL-6 and [Ca2+]i content increased in the spinal cord synaptosomes in diabetic rats. The drug treatments reduced IL-6 and the calcium influx in diabetic synaptosomes. Conclusions: Ph?1?, ?-conotoxin MVIIA, and AMD3100, after 2 h of treatment of STZ-induced PDN, reduced hypersensitivity in diabetic rats. In na?ve rats with CXCR4/SDF-1 activation, the induced hypersensitivity decreased after 2 h treatments with Ph?1? or AMD-3100, while ?-conotoxin MVIIA did not affect. The inhibitory effects of Ph?1? on PDN may involve voltage-dependent calcium channels

Assessment of cardiometabolic risk factors, physical activity levels, and quality of life in stratified groups up to 10 years after bariatric surgery.

Obesity is a highly prevalent chronic metabolic disease, with an increasing incidence, and is currently approaching epidemic proportions in developing countries. Ouraim was to evaluate the activity levels, quality of life (QoL), clinical parameters, laboratory parameters, and cardiometabolic risk factors afterbariatric surgery (BS).We classified78 patients who underwentBS into four groups, as follows: Those evaluated 1?2 years after BS (BS2), 2?4 years after BS (BS4), 4?6 years after BS (BS6), and 6?10 years after BS (BS+6). Body weight (BW), body mass index (BMI), comorbidities associated with obesity (ACRO), physical activity level, and QoL were evaluated. Patients exhibited improvements in BW, BMI, cardiometabolic risk, hypertension, dyslipidemia, and diabetes and significant changes in lipid profiles in the first postoperative yearafter BS.The physical activity level inthe BS2, BS4, and BS6 groups was increased, compared with that in the first postoperative year, with a decrease in International Physical Activity Questionnaire scores at 1 year in the BS2 (207.50 30.79), BS4 (210.67 33.69), and BS6 (220.00 42.78) groups. The QoL of patients in theBS2 and BS4 groups was excellent and that of patients in the BS4 and BS+6 groupswas very good. These findings suggest that BS promoted improved physical activity levels and QoL and reduced comorbidities in patients with morbid obesity

Phoneutria toxin PnTx3-5 inhibits TRPV1 channel with antinociceptive action in an orofacial pain model.

Capsaicin, an agonist of TRPV1, evokes intracellular [Ca2+] transients and glutamate release from perfused trigeminal ganglion. The spider toxin PnTx3-5, native or recombinant is more potent than the selective TRPV1 blocker SB-366791 with IC50 of 47???0.18?nM, 45???1.18?nM and 390???5.1?nM in the same experimental conditions. PnTx3-5 is thus more potent than the selective TRPV1 blocker SB-366791. PnTx3-5 (40?nM) and SB-366791 (3??M) also inhibited the capsaicin-induced increase in intracellular Ca2+ in HEK293?cells transfected with TRPV1 by 75???16% and 84???3.2%, respectively. In HEK293?cells transfected with TRPA1, cinnamaldehyde (30??M) generated an increase in intracellular Ca2+ that was blocked by the TRPA1 antagonist HC-030031 (10??M, 89% inhibition), but not by PnTx3-5 (40?nM), indicating selectivity of the toxin for TRPV1. In whole-cell patch-clamp experiments on HEK293?cells transfected with TRPV1, capsaicin (10??M) generated inward currents that were blocked by SB-366791 and by both native and recombinant PnTx3-5 by 47???1.4%; 54???7.8% and 56???9.0%, respectively. Intradermal injection of capsaicin into the rat left vibrissa induced nociceptive behavior that was blocked by pre-injection with either SB-366791 (3 nmol/site i.d., 83.3???7.2% inhibition) or PnTx3-5 (100 fmol/site, 89???8.4% inhibition). We conclude that both native and recombinant PnTx3-5 are potent TRPV1 receptor antagonists with antinociceptive action on pain behavior evoked by capsaicin