BACKGROUND: Acute pulmonary embolism (APE) is a disorder involving the pulmonary circulation resulting from a blockage of the pulmonary artery. The present study aimed to investigate the effects of aspirin on the nuclear factor-κB (NF-κB) activity in a rat model of APE. METHODS: A total of 108 healthy male Sprague-Dawley rats were randomly assigned into six groups (n=18 rats per group): control group, sham operation group, APE model group, and low-, medium- and high-dose aspirin groups. Six, 24, and 72 hours after the induction of APE, rats in the low-, medium- and high-dose aspirin groups were given aspirin at a respective daily dose of 150, 300, and 600 mg/kg by gavage for three consecutive days. Rats in the other groups were treated with equal volumes of normal saline. Six rats in each group were anesthetized with 10％ chloral hydrate solution at each time point, and then the lung tissues were colected and analyzed using immunohistochemical staining. RESULTS: Positive immunohistochemical staining was present in the bronchial epithelial cells, alveolar cells, macrophages, and surrounding bronchial smooth muscle cells. When compared with the APE model group, the number of positive cells was significantly lower in the other groups at each time point (P<0.001). Statistically significant differences were also observed among the aspirin-treated groups at 6 hours (P<0.05,P<0.001). Compared with the APE model group, NF-κB protein expression was reduced in the other groups at each time point (P<0.05,P<0.001). Rats from the APE model group had thrombosis, damaged alveolar walls, and pulmonary hemorrhage, along with different degrees of infl ammatory cellular infiltration at each time point. However, pathological changes such as pulmonary hemorrhage and infiltration of inflammatory cells were attenuated after the aspirin treatment. CONCLUSION: Aspirin can significantly inhibit NF-κB activity in the lung of rats with APE in a dose-dependent manner, and can alleviate lung injury after APE.

By using the Medical Case Inquiry System and registries of infant's birth,the number of women with gestational diabetes mellitus(GDM)and the total number of women delivering in the First and Second Affiliated Hospital of Chongqing Medical University,Chongqing Xinqiao Hospital,and Chongqing Health Center For Women and Children from 2005 to 2009 were obtained.The data of 540 pregnant women with GDM were further analyzed.From 2005 to 2009,the incidence of GDM increased from 2.29% to 3.81 %(P<0.05).The diagnosis of GDM was made earlier by 28.0 weeks in 2009 compared with 31.3 weeks in 2005(P<0.05).Body mass index during GDM diagnosis manifested a growing trend(25.6-28.1 kg/m2),but no significance(P>0.05).From 2005 to 2009,the other related factors,including the average maternal age,the constituent ratio of women with advanced maternal age,pregnancy history,delivery history,and family history of diabetes showed insignificant changes(P>0.05).

Objective To prepare iRGD modified liposome(iRGD-LP)and evaluate their targeting efficiency in vitro and in vivo to colon cancer cell.Methods The iRGD-LP was prepared by film-ultrasonic method,its particle size and Zeta potential were evaluated.The cellular uptake efficiency of RKO cell to LP and iRGD-LP were evaluated in vitro and in vivo.Tumor spheroid model were constructed and the penetration efficiency of solid tumor were evaluated.Ectopic colon cancer nude mice model was constructed,and iRGD -LP distribution in the rat body were studied.Results The particle diameter of iRGD-LP was (109.4 ±12.9)nm with the Zeta potential of (4.2 ±1.47)mV.The cellular uptake efficiency of RKO cell to iRGD-LP were 3.2 times higher than that of LP(P<0.01).The tumor spheroid penetration test and iRGD-LP distribution in vivo imaging results showed iRGD-LP had the strongest fluorescence intensity.Conclusion The iRGD-LP might serve as a promising colon cancer delivery system of antitumor drugs.

Objective: To observe the effect of electroacupuncture (EA) pretreatment on the protein expression of c-fos in fastigial nucleus (FN) and lateral hypothalamus area (LHA) in rats with acute myocardial ischemia-reperfusion injury (MIRI), and to explore the role and mechanism of FN and LHA in EA at the Heart Meridian fighting against acute MIRI reaction. Methods: Seventy Sprague-Dawley rats were randomly divided into a sham operation group, a model group, an EA-Heart Meridian group and an EA-Lung Meridian group, with 14 rats in each group; an LHA lesion plus EA-Heart Meridian group (LHA+EA-Heart Meridian group) and a FN lesion plus EA-Heart Meridian group (FN+EA-Heart Meridian group), with 7 rats in each group. Except the sham operation group, the left anterior descending branch of coronary artery was ligated to establish acute MIRI rat models in the other 5 groups. In the three groups with EA-Heart Meridian treatment, Shenmen (HT 7) and Tongli (HT 5) were selected; Taiyuan (LU 9) and Lieque (LU 7) were selected in the EA-Lung Meridian group. All the EA groups received EA stimulation prior to modeling, with 1 mA in current intensity and 2 Hz in frequency, 20 min each time, once a day for a total of 7 d. The sham operation group and the model group did not receive EA stimulation. The electrocardiogram was observed in the rats to analyze the ST-segment deviation and cardiac arrhythmia score. The expression of c-fos protein in FN and LHA was detected by immunohistochemistry method. Results: Compared with the sham operation group, the ST-segment deviation, cardiac arrhythmia score and the expression of c-fos protein in the FN and LHA increased significantly in the model group (all P<0.05). Compared with the model group, the ST-segment deviation, cardiac arrhythmia score and the expression of c-fos protein in FN and LHA decreased significantly in the EA-Heart Meridian group (all P<0.05). Compared with the EA-Heart Meridian group, the ST-segment deviation and cardiac arrhythmia score increased significantly in the EA-Lung Meridian group, LHA+EA-Heart Meridian group and FN+EA-Heart Meridian group (all P<0.05); the expression of c-fos in FN increased significantly in the EA-Lung Meridian group and LHA+EA-Heart Meridian group (both P<0.05); the expression of c-fos in LHA increased significantly in the EA-Lung Meridian group and FN+EA-Heart Meridian group (both P<0.05). Conclusion: FN and LHA are involved in the mechanism of EA at Heart Meridian to improve the acute MIRI reactions, and the cerebellum may participate in the improvement of cardiac function by EA through the cerebellum-hypothalamus projection.

A HPLC method of analysis of Monascus citrinin was established. More than 30 strains of Monascus spp. were cultured in steamed rice at solid state or in MSG liquid medium composed of monosodium glutamate as sole nitrogen source and glucose as sole carbon to investigate their ability of producing citrinin. The results indicated that most of the Monascus strains are able to produce citrinin. MSG medium can be used as a specific culture medium to qualitatively identify if the strain is the potential citrinin producer. But to confirm whether the Monascus strains are potential citrinin producers, these strains should be cultured in several cultivation methods, as the culture states and culture conditions influence the citrinin production greatly.

Astrocytes maintain homeostasis of neuronal microenvironment, provide metabolic and trophic support to neurons and modulate neuronal responses to injury. Rotenone specifically inhibits mitochondrial complex I, and long exposure to rotenone may increase the risk for Parkinson's disease (PD) and cause Parkinsonism. However, little is known about the role of astrocytes in the process of rotenone-induced dopaminergic neuron injury. In order to investigate this issue, we used MN9D cells as a cell model of dopaminergic neurons and rotenone as a toxin to initiate mitochondrial deficiency. MN9D cells treated with the normal medium or astrocyte-conditioned medium (ACM) were exposed to different concentrations of rotenone for different time followed by cell viability measurement by MTT assay. Besides, various concentrations of ACM and temporally different treatments were devised to evaluate protective efficiency of ACM. Growth curve of cells in the normal medium or ACM was continuously assessed by cell counting for 8 d. The influence of rotenone and ACM on cellular oxidative stress was determined by DCFH-DA staining followed by flow cytometric analysis. Glutathione (GSH) content after treatment of ACM or rotenone was measured by GSH assay kit. Our results showed that rotenone decreased viability of MN9D cells in a dose-dependent manner and ACM treatment significantly attenuated rotenone toxicity at each concentration. No significant difference in growth rate was observed between the normal medium and ACM treatment. Four concentrations of ACM, namely 1/3ACM, 1/2ACM, 2/3ACM and pure ACM, all displayed protection, increasing cell viability to (124.15+/-0.79)%, (126.59+/-0.82) %, (125.84+/-0.61) % and (117.15+/-1.63) % of the cells exposed directly to rotenone, respectively. Treatment with ACM through the whole experiment except the initial 24 h, 24 h before or at the same time of rotenone addition all exerted protective effects, with cell viability being (110.11+/-2.52)%, (113.30+/-2.36) %, (114.42+/-2.00)% of the cells exposed directly to rotenone, respectively. Conversely, ACM treatment 12 h after rotenone addition had no protective effect, with cell viability being (102.54+/-1.36)% of the cells exposed directly to rotenone. Moreover, ACM treatment up-regulated GSH level in MN9D cells nearly twofold. Incubation with 100 nmol/L rotenone for 24 h depleted GSH level by nearly two thirds of the control, but ACM treatment mitigated the drop of GSH level, maintaining its content at (147.83+/-0.63)% of the control. Consistent with GSH change, rotenone administration resulted in a positive rate of 96.24% of DCF staining, implying a great extent of oxidative stress, whereas treatment with ACM reduced the extent of oxidative stress to a positive rate of 78.31%. Taken together, these findings suggest that astrocytes protect MN9D cells from oxidative stress caused by rotenone, and GSH partially accounts for the protection. Therefore, astrocytes may play a protective role in the process of PD.
Animals ; Astrocytes ; physiology ; Cells, Cultured ; Cytoprotection ; Glutathione ; analysis ; physiology ; Neurons ; drug effects ; metabolism ; Oxidative Stress ; Rats ; Rats, Sprague-Dawley ; Rotenone ; toxicity

OBJECTIVETo explore the relationship between alcohol intake and traditional Chinese medicine Syndrome type in patients with cardio-cerebral diseases.

METHODSStudy was conducted in 1013 selected inpatients with myocardial infarction (MI) or/and cerebral infarction (CI) by logistic multivariate regression analysis and comparison among groups.

RESULTSThe scores of blood stasis syndrome showed a decreasing tendency along the increasing of alcohol intake, but it cannot prove that taking alcohol could prevent blood stasis. The scores of dampness-heat syndrome increased in patients who had chronically taken alcohol in large dose.

CONCLUSIONDampness-heat syndrome induced by alcohol is one of the basic mechanisms of cardio-cerebral diseases. Alcohol intake should be restricted.

Adult ; Aged ; Aged, 80 and over ; Alcohol Drinking ; adverse effects ; Cerebral Infarction ; diagnosis ; etiology ; Diagnosis, Differential ; Female ; Humans ; Logistic Models ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Myocardial Infarction ; diagnosis ; etiology ; Surveys and Questionnaires

Animals ; Bone Marrow Cells ; Bone Marrow Transplantation ; Liver Cirrhosis, Experimental ; pathology ; surgery ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells ; Rats ; Rats, Sprague-Dawley

Abdominal Pain ; etiology ; Child ; Child, Preschool ; Endoscopy, Gastrointestinal ; Female ; Humans ; Male ; Purpura, Schoenlein-Henoch ; complications ; pathology

AIMTo develop a novel pulsatile drug delivery system of which the lag-time is controlled by an erodible plug (EP) and evaluate its release characteristics in vitro.

METHODSThe impermeable capsule body was prepared by fulfilling method and the drug tablet and the erodible plug were made by wet granulating compression. Tetramethylpyrazine phosphate (TMPP) pulsincap capsule was prepared by sealing the drug tablet and fillers inside the impermeable capsule body with the EP. The influence factors on the lag-time such as the EP pharmaceutical properties and the dissolution condition were investigated by dissolution testing.

RESULTSBoth the composition and the weight of EP influenced the lag-time of the tetramethylpyrazine phosphate pulsincap capsule significantly. The lag-time prior to the drug release was enhanced when the content of gel-forming excipient (hydroxypropylmethylcellulose, HPMC) in the EP or the weight of EP was increased. The hardness of EP showed minor influence on the lag-time. In addition, the lag-time was shortened when the paddle speed was higher, while the pH value of the dissolution medium exhibited no significant influence on it.

CONCLUSIONTo meet the chronotherapeutic requirements, a pulsatile drug delivery system with a suitable lag-time can be achieved by adjusting the composition and the EP weight.

Calcium Channel Blockers ; administration & dosage ; Capsules ; Delayed-Action Preparations ; Drug Delivery Systems ; Lactose ; analogs & derivatives ; Methylcellulose ; analogs & derivatives ; Oxazines ; Pyrazines ; administration & dosage ; Technology, Pharmaceutical