OBJECTIVETo explore acute effects of SO(2) and NO(2) on mortality in the six cities of China.

METHODSSurveillance data on daily air quality, meteorology and the cause of death were collected from January 1, 2007 to December 31, 2009 in Beijing, Tianjin, Xi'an, Shanghai, Guangzhou and Wuhan. Generalized additive model was used to explore the relationship between the daily average concentration of SO(2) and NO(2) and daily mortality, after adjusting the effects of long-term and seasonal trend and weather conditions.

RESULTSIn Beijing, Tianjin, Xi'an, Shanghai, Guangzhou and Wuhan, the daily average concentration of SO(2) and NO(2) were in the range of 39.8-59.5 µg/m(3) and 41.4-60.1 µg/m(3) respectively; the daily mortality for non-accidental were 174.5, 101.4, 27.7, 108.4, 50.6, 17.8, cardiovascular were 86.9, 53.3, 12.8, 34.8, 16.3, 8.1 and respiratory were 18.3, 8.6, 2.6, 18.6, 9.0, 1.8 respectively. The daily average concentration of SO(2) were negatively correlated with daily average temperature in Beijing, Tianjin, Xi'an and Wuhan (the correlation coefficients were -0.66, -0.73, -0.67 and -0.39 respectively, P<0.05). The daily average concentration of SO(2) were negativeiy correlated with relative humidity in Tianjin, Shanghai and Wuhan (the correlation coefficients were -0.26, -0.46 and -0.28 respectively, P<0.05). The daily average concentration of NO(2) were negative correlated with daily average temperature in Beijing, Tianjin, Xi'an and Wuhan (the correlation coefficients were -0.27, -0.49, -0.45 and -0.38 respectively, P<0.05). When the day concentration of SO(2) increased every 10 µg/m(3), the non-accidental mortality in Tianjin and Wuhan raised 0.44%(95%CI: 0.11%-0.78%) and 0.96%(95%CI: 0.22%-1.72%) respectively. When the 1 day-lag concentration of SO(2) increased every 10 µg/m(3), the non-accidental mortality in Shanghai, Guangzhou and Wuhan raised 0.28% (95% CI: 0.02%-0.54% ), 0.41% (95% CI: 0.04%-0.79% ) and 1.14% (95% CI: 0.44%-1.84%) respectively. When the day and 1 day-lag concentration of SO(2) increased every 10 µg/m(3), the non-accidental mortality and the cardiovascular mortality at the six cities scale raised 0.40% (95% CI: 0.13%-0.67%) and 0.48% (95% CI: 0.11%-0.85%) respectively. When the day concentration of NO2 increased every 10 µg/m(3), the non-accidental mortality in Beijing, Tianjin, Shanghai, Guangzhou and Wuhan raised 0.60% (95% CI: 0.26%-0.95%), 0.96% (95% CI: 0.29%-1.64%), 0.43% (95% CI: 0.09%-0.78%), 1.17%(95%CI: 0.69%-1.66%) and 1.23%(95%CI: 0.19%-2.28%) respectively; the cardiovascular mortality in Beijing, Tianjin, Xi'an, Guangzhou and Wuhan raised 0.83% (95% CI: 0.34%-1.32%), 1.09% (95% CI: 0.25%-1.94%), 1.98% (95% CI: 0.00%-4.01%), 1.52% (95% CI: 0.70%-2.36%) and 2.04% (95% CI: 0.54%-3.56%) respectively. When the 1 day-lag concentration of NO(2) increased every 10 µg/m(3), the non-accidental mortality in Guangzhou and Wuhan raised 0.97% (95% CI: 0.49%-1.46%) and 1.67% (95% CI: 0.66%-2.70%)respectively; the cardiovascular mortality in Guangzhou and Wuhan raised 1.06% (95% CI: 0.24%-1.89%)and 2.42% (95% CI: 0.97%-3.89%) respectively. When the day and 1 day-lag concentration of NO(2) increased every 10 µg/m(3), the non-accidental mortality and the cardiovascular mortality at the six cities scale raised 0.81% (95% CI: 0.35%-1.28%), 1.03% (95% CI: 0.40%-1.66%) respectively.

CONCLUSIONExposure to SO(2) and NO(2) was significantly associated with daily non-accidental morality and cardiovascular morality at the multi-city scale in China.

Air Pollution ; adverse effects ; China ; Cities ; Humans ; Mortality ; Nitric Oxide ; adverse effects ; Particulate Matter ; Sulfur Dioxide ; adverse effects ; Temperature ; Weather

OBJECTIVETo detect the protective effect of ligustrazine hydrochloride on homocysteine-injured ECV304 cells.

METHODIn the in vitro study, human umbilical vein endothelial cells were selected as objects, with homocysteine as the molding agent, to judge the injury degree by monitoring NOS and NO contents. Based on that, the best homocysteine concentration in ECV304 cells, the best reaction time could be determined, and an endothelial cell injury model was established. After adding ligustrazine hydrochloride, NOS and NO contents in injured endothelial cells were determined to observe the protective effect of ligustrazine hydrochloride.

RESULTIt was proved that the optimal concentration of homocysteine on injured ECV304 cell was 1 mmol x L(-1), the best reaction time was 48 h. An injured endothelial cell model was established. At the same time, positive drug nitroglycerin and ligustrazine hydrochloride displayed a protection effect on injured ECV304 cells, NOS and NO formation were significantly increased compared with the model group.

CONCLUSIONLigustrazine hydrochloride has a protective effect on homocysteine-injured ECV304 cells. The model established in this study can be used to screen anti-myocardial ischemia drugs targeting at an endothelial cell protective agent.

Cytoprotection ; drug effects ; Homocysteine ; adverse effects ; Human Umbilical Vein Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase ; biosynthesis ; Pyrazines ; pharmacology

OBJECTIVEBlood transfusion saves lives but may also increase the risk of injury. The objective of this review was to evaluate the possible adverse effects related to transfusion of red blood cell (RBC) concentrates stored for prolonged periods.

DATA SOURCESThe data used in this review were mainly from PubMed articles published in English up to February 2015.

STUDY SELECTIONClinical and basic research articles were selected according to their relevance to this topic.

RESULTSThe ex vivo changes to RBC that occur during storage are collectively called storage lesion. It is still inconclusive if transfusion of RBC with storage lesion has clinical relevance. Multiple ongoing prospective randomized controlled trials are aimed to clarify this clinical issue. It was observed that the adverse events related to stored RBC transfusion were prominent in certain patient populations, including trauma, critical care, pediatric, and cardiac surgery patients, which leads to the investigation of underlying mechanisms. It is demonstrated that free hemoglobin toxicity, decreasing of nitric oxide bioavailability, and free iron-induced increasing of inflammation may play an important role in this process.

CONCLUSIONIt is still unclear whether transfusion of older RBC has adverse effects, and if so, which factors determine such clinical effects. However, considering the magnitude of transfusion and the widespread medical significance, potential preventive strategies should be considered, especially for the susceptible recipients.

Blood Preservation ; adverse effects ; Erythrocyte Transfusion ; adverse effects ; Erythrocytes ; metabolism ; physiology ; Humans ; Nitric Oxide ; metabolism ; Time Factors

Adult ; Dimethylformamide ; adverse effects ; Glutathione ; blood ; Humans ; Male ; Methanol ; adverse effects ; Nitric Oxide ; blood ; Occupational Exposure ; Oxygen ; metabolism ; Superoxide Dismutase ; blood ; Surveys and Questionnaires ; Toluene ; adverse effects

OBJECTIVETo study the changes of nitric oxide(NO) and nitric-oxide synthase(NOS) in the development of cold-induced hypertension (CIH).

METHODSSixty male Sprague-Dawley adult rats were used. Thirty were exposed to cold (4 +/- 1) degrees C as cold-treated group while the other 30 were at (25 +/- 1) degrees C as controls, 4 hours a day for 6 weeks for both groups. Systolic blood pressure (SBP) and heart rate were measured twice every week. Each group was further subdivided into three groups, 10 rats each. A subgroup of the cold-treated and control rats were sacrificed at 2, 4 and 6 week. Plasma was saved to measure superoxide dismutase (SOD) and malondiadehycle (MDA), while heart was homogenated to measure NO, NOS.

RESULTS1 SBP increased during 6 weeks of exposure to cold. From the second week, SBP of cold-treated group [(94.16 +/- 3.81) mm Hg] was significantly greater than that of control group [(88.77 +/- 4.45 mm Hg), P<0.01]. The highest SBP level was achieved at the sixth week [(116.78 +/- 3.79)mm Hg, P<0.01]. 2 Compared to the control group, SOD in cold-treated group decreased significantly from the second week, and maintained throughout the time of exposure to cold (P<0.05). MDA levels did not differ significantly between cold-treated and control groups though it increased mildly during 6 weeks of cold exposure (P>0.05). Heart NOS in cold-treated group decreased significantly from the fourth week to the sixth week. And a mild decrease was observed in heart NO of cold-treated group during 6 weeks of exposure (P>0.05).

CONCLUSIONCold-induced hypertension is induced in rats after repeated exposure to cold. The levels of NOS, NO decrease accordingly to the rise of blood pressure. This indicates that the dysfunction of NO and NOS is involved in the development of CIH.

Animals ; Cold Temperature ; adverse effects ; Disease Models, Animal ; Hypertension ; etiology ; metabolism ; Male ; Malondialdehyde ; blood ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood

Adult ; Aged ; Dust ; analysis ; Humans ; Middle Aged ; Niacin ; therapeutic use ; Nitric Oxide ; blood ; Nitric Oxide Synthase ; blood ; Occupational Exposure ; analysis ; prevention & control ; Silicon Dioxide ; adverse effects

AIMTo observe the changes of nitric oxide synthase (NOS) activity and nitric oxide (NO) content of hippocampus including their time course and region distribution character in rat during the process of formalin-induced inflammatory pain as well as the pain behavior of rat.

METHODSThe pain threshold (PT) was determined by radiant heat-induced tail flick test. NOS expression in the hippocampus was determined by using NADPH-d histochemical staining. NO production in hippocampus was determined by assaying NO3- and NO2-.

RESULTSSubcutaneous injection of formalin elicited nociceptive behavioural response and led to decrease in PT of rat. The number and staining degree of NADPH-d positive neurons began to increase at 6 h after the formalin injection in CA1, CA2 - 3 and DG of hippocampus as well as NO content, which increased most obviously at 12 h and returned to control level at 48 h.

CONCLUSIONFormalin-induced inflammatory pain could induce the elevation of NOS activity in CA1, CA2 - 3 and DG of hippocampus with a certain time course, which further led to a increase of NO production in hippocampus.

Animals ; Formaldehyde ; adverse effects ; Hippocampus ; metabolism ; Inflammation ; chemically induced ; metabolism ; Male ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase ; metabolism ; Pain ; chemically induced ; metabolism ; Pain Threshold ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo reveal interventions for chronic cyclosporine A nephrotoxicity (CCN) and provide new targets for further studies, we analyzed all relevant studies about interventions in renal cell apoptosis.

DATA SOURCESWe collected all relevant studies about interventions for cyclosporine A (CsA)-induced renal cell apoptosis in Medline (1966 to July 2010), Embase (1980 to July 2010) and ISI (1986 to July 2010), evaluated their quality, extracted data following PICOS principles and synthesized the data.

STUDY SELECTIONWe included all relevant studies about interventions in CsA-induced renal cell apoptosis no limitation of research design and language) and excluded the duplicated articles, meeting abstracts and reviews without specific data.

RESULTSThere were three kinds of intervention, include anti-oxidant (sulfated polysaccharides, tea polyphenols, apigenin, curcumin, spirulina, etc), biologics (recombinant human erythropoietin (rhEPO), a murine pan-specific transforming growth factor (TGF)-beta-neutralizing monoclonal antibody1D11, cartilage oligomeric matrix protein (COMP)-angiopoietin-1 and hepatocyte growth factor (HGF) gene), and other drugs (spironolactone, rosiglitazone, pirfenidone and colchicine). These interventions significantly improved the CCN, renal cell apoptosis and renal dysfunction through intervening in four apoptotic pathways in animals or protected renal cells from apoptosis induced by CsA and increased cell survival through respectively four pathways in vitro.

CONCLUSIONSThere are three group interventions for CCN. Especially anti-oxidant drugs can significantly improve CCN, renal cell apoptosis and renal dysfunction. Many drugs can improve CCN through intervening in Fas/Fas ligand or mitochondrial pathway with sufficient evidences. Angiotensin II, nitric oxide (NO) and endoplasmic reticulum (ER) pathways will be new targets for CCN.

Animals ; Apoptosis ; drug effects ; Chronic Disease ; Cyclosporine ; adverse effects ; Humans ; Immunosuppressive Agents ; adverse effects ; Kidney ; drug effects ; pathology ; Mitochondria ; physiology ; Nitric Oxide ; physiology ; Signal Transduction ; fas Receptor ; physiology

The aim of this study was to investigate the influences of heme oxygenase-1, carbon monoxide and nitricoxide synthase, nitrogen monoxide systems on vascular remodeling of injured balloon carotid artery in rabbits and the intercorrelations among the two systems after balloon angioplasty. Seventy rabbits were randomly divided into seven groups, i. e., control group, SH group, Chol group, Arg group, L-NAME group, Hem group, and Znpp group. The control group received normal chow, while all the rabbits the rest six groups received 1.5% cholesterol diet. Among the six test groups, to those in Chol group and SH group nothing else was added except the 1.5% cholesterol. L-arginine or L-nitro-arginine methylester was added to those in the Arg group and in the L-NAME group with drinking water. Hemin or zincprotoporphyrin IX was added to those in Hem group and in Znpp group by injecting the medicine into the abdominal cavity. After two weeks, the experimental groups underwent balloon injury at one side common carotid artery. Compared to Chol group, the HO-1 activity and CO production increased significantly. The intima area was reduced distinctly in Hem group, while there were opposite results in Znpp group. Compared with that in Chol group, the NF-kappaB activity of Arg group and Hem group were lower significantly. That of L-NAME group and Znpp group were higher significantly. Compared with that in the Chol group, the cNOS activity and NO production were eleveated markedly in Arg group while they were decreased markedly in L-NAME group. The intima area was reduced significantly in Arg group, while in L-NAME group they were not different from those in Chol group. These results suggested that the reciprocal relationship between HO-1/CO and NOS/NO system in restenosis may play the inhibitory role against neointimal proliferation and vascular wall remodeling after balloon angioplasty.
Animals ; Carbon Monoxide ; metabolism ; Carotid Arteries ; metabolism ; pathology ; physiopathology ; Catheterization ; adverse effects ; Heme Oxygenase-1 ; metabolism ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; metabolism ; Nitric Oxide Synthase Type III ; metabolism ; Rabbits ; Random Allocation

Inhaled NO (iNO) has been shown to have beneficial effects on decreasing pulmonary inflammation, increasing function of surfactant and improving lung growth in prematurely born animal models. iNO has been gradually applied in the neonatal intensive care unit since its first use for persistent pulmonary hypertension (PPHN) in the early 1990's. Although many research findings have shown the benefits of iNO for hypoxic respiratory failure (HRF) of preterm infants, there is no certain evidence to support the routine use of iNO in premature infants. According to recent literature, the mechanism of iNO therapy, treatment scheme, iNO effectiveness and safety in premature infants were reviewed in this article, so as to provide bases for the clinical use of this treatment.
Administration, Inhalation ; Humans ; Hypoxia ; complications ; Infant, Newborn ; Infant, Premature ; Nitric Oxide ; administration & dosage ; adverse effects ; Respiratory Insufficiency ; drug therapy