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1.
Environ Health ; 18(1): 98, 2019 11 20.
Artigo em Inglês | MEDLINE | ID: mdl-31771610

RESUMO

BACKGROUND: Very few studies have focused on the relationship between ambient apparent temperature (AT) and admission of mental and behaviour disorders (MDs). Therefore, a time-series study was conducted in Yancheng, China, to explore the effects of AT on the daily emergency admissions of patients with MDs over the period of 2014-17. METHODS: A quasi-Poisson generalized linear model (GLM) combined with a distributed lag non-linear model (DLNM) was adopted to explore the associations after adjusting for time trend, day of the week, humidity, sunshine duration, rainfall, holidays and air pollutants. In the subgroup analysis, the modification effects of age and sex were also examined. RESULTS: Overall, 8438 cases of MDs emergency admissions were identified. With the apparent temperature with the minimum number of admissions (- 3.4 °C) serving as a reference, a positive correlation emerged between high AT and daily emergency admissions of patients with MDs in Yancheng, China, with the lagged effect of 1 to 5 days. The subgroup analysis demonstrated a positive relationship between AT and MDs emergency admissions among males and individuals younger than 45 years old, with no lagged effect. CONCLUSIONS: The results will provide important scientific evidence for mental health policy-makers and practitioners for possible intervention, especially among the vulnerable populations.

2.
Anesth Analg ; 110(3): 908-15, 2010 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-20185667
3.
Surg Neurol ; 71(5): 621-4; discussion 624-5, 2009 May.
Artigo em Inglês | MEDLINE | ID: mdl-18452979

RESUMO

In ancient times, awake craniotomy was used for trepanation to treat seizures and remove a variety of morbid conditions or even to permit the escape of evil air. In modern times, this technique was initially used for removal of epileptic foci with simultaneous application of brain mapping with electrical current. Further developments brought this technique into use for resection of tumors involving functional cortex. Recently, awake craniotomy has been described as an approach for removal of supratentorial tumors nonselectively, regardless of the involvement of eloquent cortex. It has been used in North America since the 1980s, then Europe, and recently has spread into Asia. Its spread to Asia could have significant impact based on the large population of patients and the low resource utilization associated with awake craniotomy.


Assuntos
Neoplasias Encefálicas/história , Neoplasias Encefálicas/cirurgia , Craniotomia/história , Craniotomia/métodos , Intercâmbio Educacional Internacional/história , Neurocirurgia/história , Neurocirurgia/métodos , Anestesia Local/história , Ásia , Encéfalo/patologia , Encéfalo/cirurgia , Mapeamento Encefálico/métodos , Educação Médica/história , Educação Médica/métodos , História do Século XVII , História do Século XIX , História do Século XX , História Antiga , Humanos , Intercâmbio Educacional Internacional/tendências , Neuronavegação/tendências , Trepanação/história , Vigília
4.
J Heart Lung Transplant ; 22(9): 979-85, 2003 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-12957607

RESUMO

BACKGROUND: Traditionally leukocytes have been viewed as the mediators and effectors of cell injury after tissue ischemia and reperfusion through the indiscriminate release of toxic cytokines and oxygen free radicals. This can be detrimental to functioning of the transplanted heart when reperfused after implantation. Paradoxically, evidence now suggests that certain cytotoxic cytokines and even oxygen free radicals can be cytoprotective in smaller concentrations. This study sought to determine whether cultured human monocytes can be pre-conditioned by brief hypoxia to protect cardiomyocytes from cell death after hypoxia and re-oxygenation. METHODS: Cultured human monocytes were exposed to transient hypoxia (10 minutes), after which we determined CD11b expression using flow cytometry. The 3 control groups comprised immunoglobulin G-negative controls, fMLP-positive controls, and virgin monocyte (VM) controls. We studied chick embryonic ventricular myocytes in a flow-through chamber while controlling flow rate, pH, O(2), and CO2 tension. We quantified cardiomyocyte viability using propidium iodide (5 micromol/liter). Cell systems of cardiomyocytes alone, cardiomyocytes and VM, human monocytes exposed to transient hypoxia before coculture with cardiomyocytes (PCHM-cardiomyocyte), and PCHM cocultured with anti-CD11b antibodies for 30 minutes before coculture with cardiomyocytes (CDHM-cardiomyocyte) were subjected to 1 hour of hypoxia and 3 hours of re-oxygenation, and cell death was determined. The experiment was repeated and the cell systems fixed, stained, and examined for monocytes adhering to cardiomyocytes. RESULTS: CD11b expression increased significantly with both transient hypoxia and fMLP (18.39% +/- 4.116%, n = 5, and 37.04% +/- 7.783%, n = 5, respectively, p < 0.05 vs VM 100%, n = 5). Coculture of cardiomyocytes with VM had no effects on cardiocyte death (40.6% +/- 6.1%, n = 6) compared with controls (46.5% +/- 4.0%, n = 10). The PCHM cocultured with cardiomyocytes significantly decreased cardiomyocyte death (25.2% +/- 4.7%, n = 6, p < 0.05). This protection was abrogated by the addition of CD11b-blocking antibodies to PCHM before coculture with cardiomyocytes (51.0% +/- 6.1%, n = 6, p < 0.05). The PCHM showed increased adhesion to cardiomyocytes (5.4 +/- 0.38/high-power [HP] field vs 0.67 +/- 0.24/HP field in VM, p < 0.05). The increased adhesion was abolished by CD11b-blocking antibody (0.78 +/- 0.28 vs 0.67 +/- 0.24 cells/HP field, p < 0.05). CONCLUSIONS: These results suggest that monocytes activated by transient hypoxia protect cardiomyocytes during hypoxia and re-oxygenation through expression of CD11b receptors. These cells seem to adhere to myocytes through this receptor to achieve this effect. The exact mechanism is unclear and requires further study. Autologous recipient monocytes may be pre-conditioned to protect the donor heart during reperfusion.


Assuntos
Antígeno CD11b/metabolismo , Monócitos/fisiologia , Reperfusão Miocárdica , Miócitos Cardíacos/fisiologia , Animais , Morte Celular , Hipóxia Celular , Linhagem Celular , Embrião de Galinha , Humanos , Monócitos/metabolismo , Miócitos Cardíacos/metabolismo
5.
J Pharmacol Exp Ther ; 301(3): 1012-9, 2002 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-12023532

RESUMO

Opioids generate free radicals that mediate protection in isolated cultured cardiomyocytes. We hypothesize that the nature of these radicals is nitric oxide, and that nitric oxide activates the protein kinase C (PKC) delta isoform. Through this signal transduction pathway, opiates protect cardiomyocytes during hypoxia and reoxygenation. Cell viability was quantified in chick embryonic ventricular myocytes with propidium iodide. Oxygen radicals were quantified using a molecular probe, 2',7'-dichlorofluorescin diacetate (DCFH-DA). After a 10-min infusion of the opioid delta receptor agonist BW373U86 (BW; 2 or 20 pM) and a 10-min drug-free period, cells were subjected to hypoxia for 1 h followed by reoxygenation for 3 h. BW produced a concentration-dependent reduction in cardiomyocyte death (2 pM, 35.3 +/- 3.9%, n = 5; 20 pM, 21.5 +/- 4.0%, n = 8, p < 0.05 versus controls) and attenuated oxidant stress compared with controls (43.3 +/- 4.2%, n = 8). The increase in DCFH-DA oxidation with BW before hypoxia was abolished by the specific nitric-oxide synthase inhibitors nitro-L-arginine methyl ester (L-NAME) or N(G)-monomethyl-L-arginine (L-NMMA) (100 microM each). L-NAME or L-NMMA blocked the protective effects of BW. BW selectively increased the activity of PKC delta isoform in the particulate fraction, and its protection was abolished by the selective PKC delta inhibitor rottlerin (1 microM). Similar to BW, infusion with 5 microM of the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP) reduced cardiomyocyte death (24.6 +/- 3.7, n = 8), and this protection was blocked by chelerythrine or rottlerin. Chelerythrine and rottlerin had no effect on BW-generated oxygen radicals before hypoxia, but they abolished the protection of SNAP. The nature of DCFH oxidation produced by opioid delta receptor stimulation is nitric oxide. Nitric oxide mediates cardioprotection via activating PKC delta in isolated myocytes.


Assuntos
Cardiotônicos/farmacologia , Radicais Livres/metabolismo , Isoenzimas/fisiologia , Miocárdio/enzimologia , Óxido Nítrico Sintase/fisiologia , Proteína Quinase C/fisiologia , Receptores Opioides delta/agonistas , Animais , Benzamidas/farmacologia , Morte Celular/efeitos dos fármacos , Morte Celular/fisiologia , Células Cultivadas , Embrião de Galinha , Inibidores Enzimáticos/farmacologia , Isoenzimas/metabolismo , Miocárdio/citologia , Miocárdio/metabolismo , Doadores de Óxido Nítrico/farmacologia , Óxido Nítrico Sintase/antagonistas & inibidores , Piperazinas/farmacologia , Proteína Quinase C-delta , Receptores Opioides delta/fisiologia
6.
Am J Physiol Heart Circ Physiol ; 282(4): H1395-403, 2002 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-11893576

RESUMO

Oxygen radicals and protein kinase C (PKC) mediate ischemic preconditioning. Using a cultured chick embryonic cardiomyocyte model of hypoxia and reoxygenation, we found that the oxygen radicals generated by ischemic preconditioning were H(2)O(2). Like preconditioning, H(2)O(2) selectively activated the epsilon-isoform of PKC in the particulate compartment and increased cell viability after 1 h of hypoxia and 3 h of reoxygenation. The glutathione peroxidase ebselen (converting H(2)O(2) to H(2)O) and the superoxide dismutase inhibitor diethyldithiocarbamic acid abolished the increased H(2)O(2) and the protection of preconditioning. PKC activation with phorbol 12-myristate 13-acetate increased cell survival; the protection of preconditioning was blocked by epsilonV(1-2), a selective PKC-epsilon antagonist. Similar to preconditioning, the protection of PKC activation was abolished by mitochondrial K(ATP) channel blockade with 5-hydroxydecanoate or by GABA receptor stimulation with midazolam or diazepam. In addition, PKC, mitochondrial ATP-sensitive K(+) (K(ATP)) channels, and GABA receptors had no effects on H(2)O(2) generated by ischemic preconditioning before prolonged hypoxia and reoxygenation. We conclude that H(2)O(2) opens mitochondrial K(ATP) channels and inhibits GABA receptors via activating PKC-epsilon. Through this signal transduction, preconditioning protects ischemic cardiomyocytes.


Assuntos
Antagonistas GABAérgicos/farmacologia , Coração/fisiologia , Peróxido de Hidrogênio/farmacologia , Isoenzimas/metabolismo , Miocárdio/enzimologia , Proteína Quinase C/metabolismo , Receptores de GABA/fisiologia , Animais , Bloqueadores dos Canais de Cálcio/farmacologia , Embrião de Galinha , Ácidos Decanoicos/farmacologia , Inibidores Enzimáticos/farmacologia , Fluoresceínas , Corantes Fluorescentes , Coração/efeitos dos fármacos , Coração/embriologia , Ventrículos do Coração/embriologia , Hidroxiácidos/farmacologia , Precondicionamento Isquêmico Miocárdico , Cinética , Proteínas de Membrana/efeitos dos fármacos , Proteínas de Membrana/fisiologia , Midazolam/farmacologia , Isquemia Miocárdica/fisiopatologia , Miocárdio/citologia , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/fisiologia , Canais de Potássio , Proteína Quinase C-épsilon , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia , Acetato de Tetradecanoilforbol/farmacologia , Função Ventricular
7.
Am J Physiol Heart Circ Physiol ; 282(4): H1380-6, 2002 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-11893574

RESUMO

The aims of this study were to determine whether preconditioning blocks cardiocyte apoptosis and to determine the role of mitochondrial ATP-sensitive K(+) (K(ATP)) channels and the protein kinase C epsilon-isoform (PKC-epsilon) in this effect. Ventricular myocytes from 10-day-old chick embryos were used. In the control series, 10 h of simulated ischemia followed by 12 h of reoxygenation resulted in 42 +/- 3% apoptosis (n = 8). These results were consistent with DNA laddering and TdT-mediated dUTP nick-end labeling (TUNEL) assay. Preconditioning, elicited with three cycles of 1 min of ischemia separated by 5 min of reoxygenation before subjection to prolonged simulated ischemia, markedly attenuated the apoptotic process (28 +/- 4%, n = 8). The selective mitochondrial K(ATP) channel opener diazoxide (400 micromol/l), given before ischemia, mimicked preconditioning effects to prevent apoptosis (22 +/- 4%, n = 6). Pretreatment with 5-hydroxydecanoate (100 micromol/l), a selective mitochondrial K(ATP) channel blocker, abolished preconditioning (42 +/- 2%, n = 6). In addition, the effects of preconditioning and diazoxide were blocked with the specific PKC inhibitors Gö-6976 (0.1 micromol/l) or chelerythrine (4 micromol/l), given at simulated ischemia and reoxygenation. Furthermore, preconditioning and diazoxide selectively activated PKC-epsilon in the particulate fraction before simulated ischemia without effect on the total fraction, cytosolic fraction, and PKC delta-isoform. The specific PKC activator phorbol 12-myristate 13-acetate (0.2 micromol/l), added during simulated ischemia and reoxygenation, mimicked preconditioning to block apoptosis. Opening mitochondrial K(ATP) channels blocks cardiocyte apoptosis via activating PKC-epsilon in cultured ventricular myocytes. Through this signal transduction, preconditioning blocks apoptosis and preserves cardiac function in ischemia-reperfusion.


Assuntos
Apoptose/fisiologia , Coração/fisiologia , Isoenzimas/metabolismo , Proteínas de Membrana/fisiologia , Reperfusão Miocárdica , Miocárdio/citologia , Proteína Quinase C/metabolismo , Alcaloides , Animais , Apoptose/efeitos dos fármacos , Benzofenantridinas , Células Cultivadas , Embrião de Galinha , Ácidos Decanoicos/farmacologia , Diazóxido/farmacologia , Coração/efeitos dos fármacos , Coração/embriologia , Hidroxiácidos/farmacologia , Ativação do Canal Iônico/efeitos dos fármacos , Ativação do Canal Iônico/fisiologia , Canais Iônicos/fisiologia , Precondicionamento Isquêmico Miocárdico , Proteínas de Membrana/efeitos dos fármacos , Fenantridinas/farmacologia , Canais de Potássio/efeitos dos fármacos , Canais de Potássio/fisiologia , Proteína Quinase C-épsilon , Acetato de Tetradecanoilforbol/farmacologia
8.
Curr Opin Anaesthesiol ; 15(2): 139-46, 2002 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-17019193

RESUMO

The purpose of this review is to describe in more detail ischemia reperfusion injury and preconditioning, and to speculate on the potential role of preconditioning in the care of critically ill patients. Current hemodynamic treatment of hypotension and hypoperfusion in critically ill patients is directed at ensuring essential organ perfusion by maintaining intravascular volume and cardiac output, and ensuring adequate oxygen delivery by maintaining arterial oxygen partial pressure and hemoglobin levels. However, morbidity and mortality remain high and new approaches to critically ill patients are required. Treatments are needed that can protect against organ ischemia during periods of low blood flow. In recent years, there has been a growing appreciation of the importance of ischemia reperfusion injury. Ischemia associated with reperfusion may result in greater injury than ischemia alone. Ischemic preconditioning is used to describe the protective effect of short periods of ischemia to an organ or tissue against longer periods of ischemia. Although first described in the myocardium, there is now evidence that this phenomenon occurs in a wide variety of organs and tissues, including the brain and other nervous tissue such as the retina and spinal cord, liver, stomach, intestines, kidney, and the lungs. Preconditioning therapy may offer a new avenue of treatment in critically ill patients. Both traditional preconditioning methods and pharmacologic agents that mimic or induce such preconditioning may be used in the future. Clinical trials of pharmacologic agents are underway in patients with coronary artery disease. Further trials of such methods and agents are needed in critically ill patients suffering from sepsis or multiorgan system failure.

9.
Pharmacology ; 64(1): 49-56, 2002 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-11731722

RESUMO

We wanted to determine whether oxygen radicals open the mitochondrial ATP-dependent potassium channels (K(ATP)) during an ischemic period to reduce cell death and oxidant stress. Chick embryonic cardiomyocytes were used. Cell viability was quantified with propidium iodide (5 microM), and free radicals was measured using 2',7'-dichlorofluorescein diacetate. Preconditioning was produced by 10 min of simulated ischemia followed by 10 min of reoxygenation. Acetylcholine (1 mM), infused for 10 min instead of preconditioning, reduced cell death similarly (24 +/- 5%, n = 7 and 18 +/- 2%, n = 7, respectively, vs. controls, 49 +/- 6%, n = 8). In control series, 60 min of simulated ischemia and 3 h of reoxygenation generated free radicals more than 300% above the baseline (ischemia: 3.63 +/- 0.58, reoxygenation: 3.66 +/- 0.47, n = 8). Preconditioning and acetylcholine markedly attenuated the oxidant stress during simulated ischemia (1.18 +/- 0.41, n = 6 and 1.34 +/- 0.60, n = 7 vs. controls 3.63 +/- 0.58, n = 8) and re-oxygenation (1.23 +/- 0.36, n = 6 and 1.50 +/- 0.59, n = 7 vs. controls 3.66 +/- 0.47, n = 8). The protection of acetylcholine was abolished with pretreatment with the antioxidant thiol reductant 2-mercaptopropionyl glycine and posttreatment with 5-hydroxydecanoate, a selective mitochondrial K(ATP) channel antagonist (37 +/- 7%, n = 7). These results demonstrate that oxygen radicals open mitochondrial K(ATP) channels, which mediates the acetylcholine-induced preconditioning effect, and that stimulation of this signaling pathway attenuates oxidant stress.


Assuntos
Acetilcolina/farmacologia , Radicais Livres/metabolismo , Isquemia Miocárdica/tratamento farmacológico , Canais de Potássio/efeitos dos fármacos , Tiopronina/farmacologia , Vasodilatadores/farmacologia , Análise de Variância , Animais , Morte Celular , Galinhas , Interações de Medicamentos , Precondicionamento Isquêmico Miocárdico , Estresse Oxidativo/efeitos dos fármacos
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