p38 MAPK mediates cardiovascular and behavioral responses induced by central IL-1β and footshock in conscious rats

INTRODUCTION Sharing characteristics of stress mediators[1], cen-tral interleukin-1β (IL-1β) is very important in cardio-vascular and behavioral responses to stressors[2-4]. Itcan induce similar hypertensive responses to stress viacardiovascular regulatory regions[5]. We observed pre-viously that central IL-1β mediated cardiovascular re-sponses to some stressful stimuli, such as conditionedfear stimuli and footshock[6]. Many stressful stimulimay increase IL-1β mRNA expression and …     

认真实施“一法一例” 抓好母婴保健工作

沈阳市人大、市政府高度重视《中华人民共和国母婴保健法》和《辽宁省母婴保健条例》的贯彻实施，认真抓好宣传工作，建立起一支高素质的执法队伍，加强监督执法的力度，清理整顿了母婴保健技术服务市场，使该市的妇幼卫生工作向法制化管理迈出了一大步     

ARDS数据库标准字段集专家共识(2022年版)

急性呼吸窘迫综合征(acute respiratory distress syndrome, ARDS)是急危重症医学领域研究的重点和难点, 病死率居高不下。近年来我国开展的ARDS临床研究逐渐增多, 以美国国立健康研究院临床研究登记网站(clinicaltrials.gov)为例, 2016年以前我国注册的ARDS研究只有26项, 而近5年新注册的研究已达43项。然而, 我国ARDS临床研究的数量和质量与欧美相比仍存在差距, 特别是支撑临床研究的电子数据管理系统(Electronic Data Capture System, EDC), 存在起步晚、质量参差不齐和使用普及不够的缺点。     

Differential Effects of Anesthetics on Mitochondrial KATP Channel Activity and Cardiomyocyte Protection

Background: Mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels play a pivotal role in mediating cardiac preconditioning. The effects of intravenous anesthetics on this protective channel have not been investigated so far, but would be of importance with respect to experimental as well as clinical medicine.

Methods: Live cell microscopy was used to visualize and measure autofluorescence of flavoproteins, a direct reporter of mitoKATP channel activity, in response to the direct and highly selective mitoKATP channel opener diazoxide, or to diazoxide following exposure to various anesthetics commonly used in experimental and clinical medicine. A cellular model of ischemia with subsequent hypoosmolar trypan blue staining served to substantiate the effects of the anesthetics on mitoKATP channels with respect to myocyte viability.

Results: Diazoxide-induced mitoKATP channel opening was significantly inhibited by the anesthetics R-ketamine, and the barbiturates thiopental and pentobarbital. Conversely, urethane, 2,2,2-trichloroethanol (main metabolite of [alpha]-chloralose and chloral hydrate), and the opioid fentanyl potentiated the channel-opening effect of diazoxide, which was abrogated by coadministration of chelerythrine, a specific protein kinase C inhibitor. S-ketamine, propofol, xylazine, midazolam, and etomidate did not affect mitoKATP channel activity. The significance of these modulatory effects of the anesthetics on mitoKATP channel activity was substantiated in a cellular model of simulated ischemia, where diazoxide-induced cell protection was mitigated by R-ketamine and the barbiturates, while urethane, 2,2,2-trichloroethanol, and fentanyl potentiated myocyte protection.     

Roles of Carbon Monoxide in Leukocyte and Platelet Dynamics in Rat Mesentery during Sevoflurane Anesthesia

Background: Heme oxygenase 1 (HO-1), induced by a variety of stressors, provides endogenous carbon monoxide (CO) and bilirubin, both of which play consequential roles in organs. The current study aimed to examine whether induction of HO-1 and its by-products modulated endothelial interaction with circulating leukocytes and platelets evoked by sevoflurane anesthesia in vivo.

Methods: Rats, pretreated with or without hemin, were anesthetized with sevoflurane in 100% O2, and lungs were mechanically ventilated. Platelets labeled with carboxyfluorescein diacetate succinimidyl ester and leukocyte behavior in mesenteric venules were visualized during sevoflurane anesthesia at 1,000 frames/s using intravital ultrahigh-speed intensified fluorescence videomicroscopy. To examine the mechanisms for the effects of HO-1 on leukocyte and platelet behavior, these studies were repeated with superfusion of either CO, bilirubin, or N[omega]-nitro-l-arginine methyl ester (l-NAME).

Results: As reported previously, the elevation of sevoflurane concentration evoked adhesive responses of leukocytes, concurrent with platelet margination and rolling. Pretreatment with hemin, a HO-1 inducer, prevented such sevoflurane-elicited changes in the microvessels. These changes were restored by zinc protoporphyrin IX, a HO inhibitor, and repressed by CO but not by bilirubin. During sevoflurane anesthesia, however, nitric oxide suppression by l-NAME deteriorated microvascular flows irrespective of the presence or absence of the HO-1 induction.     

Consumption of Soy Diet before Nerve Injury Preempts the Development of Neuropathic Pain in Rats

Background : A previous report using a partial sciatic nerve ligation (PSL) model for neuropathic pain in rats demonstrated that consumption of soy-containing diets preoperatively and postoperatively suppressed development of mechanical and heat allodynia, as well as hyperalgesia. The current study examined whether dietary soy suppresses these neuropathic sensory disorders when consumed either before or after PSL injury.

Methods : Male Wistar rats were grouped into seven different feeding regimens. These rats were fed SOY (RMH-1000, PMI Feeds, St. Louis, MO), a diet containing 85% soy protein since weaning, and were then switched to noSOY (Bio-Serv Co., Frenchtown, NJ), a diet devoid of soy at certain time points before PSL injury (14, 7, 1 days, or 15 and 0 h). Postoperatively, these rats were fed SOY or noSOY diets. Levels of mechanical and heat allodynia and hyperalgesia were determined preoperatively and 3, 8, and 14 days after PSL injury.

Results : Compared with groups fed preoperative noSOY, consumption of SOY before PSL injury significantly blunted postoperative levels of allodynia and hyperalgesia. Administering the SOY diet both before and after PSL injury provided no additional suppression of neuropathic pain. No pain suppression was noted in rats fed a noSOY diet preoperatively and SOY diet after PSL injury. Switching from SOY to noSOY feeding within 15 h of PSL injury was sufficient to allow for the full development of allodynia and hyperalgesia.     

Mild Hypercapnia Induces Vasodilation via Adenosine Triphosphate-sensitive K+ Channels in Parenchymal Microvessels of the Rat Cerebral Cortex

Background: Carbon dioxide is an important vasodilator of cerebral blood vessels. Cerebral vasodilation mediated by adenosine triphosphate (ATP)-sensitive K+ channels has not been demonstrated in precapillary microvessel levels. Therefore, the current study was designed to examine whether ATP-sensitive K+ channels play a role in vasodilation induced by mild hypercapnia in precapillary arterioles of the rat cerebral cortex.

Methods: Brain slices from rat cerebral cortex were prepared and superfused with artificial cerebrospinal fluid, including normal (Pco2 = 40 mmHg; pH = 7.4), hypercapnic (Pco2 = 50 mmHg; pH = 7.3), and hypercapnic normal pH (Pco2 = 50 mmHg; pH = 7.4) solutions. The ID of a cerebral parenchymal arteriole (5-9.5 [mu]m) was monitored using computerized videomicroscopy.

Results: During contraction to prostaglandin F2[alpha] (5 x 10-7 m), hypercapnia, but not hypercapnia under normal pH, induced marked vasodilation, which was completely abolished by the selective ATP-sensitive K+ channel antagonist glibenclamide (5 x 10-6 m). However, the selective Ca2+-dependent K+ channel antagonist iberiotoxin (10-7 m) as well as the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (10-4 m) did not alter vasodilation. A selective ATP-sensitive K+ channel opener, levcromakalim (3 x 10-8 to 3 x 10-7 m), induced vasodilation, whereas this vasodilation was abolished by glibenclamide.     

IMPROVING ACCESS TO HEALTH SERVICES IS STRATEGIC PRIORITY OF PRODUCTIVITY DEVELOPMENT

As one of the basic human rights, health is an important guarantee for productivity. The authors introduce the Andersen's behavioral model of health service use,as well as the conception and classification of access to health services based on the model. Meanwhile,the relative guidelines and the impact on the health reform of China are discussed, compared with America's and China's. This paper propounds three strategic priority of productivity development.