0.01).The dissolution of tablets from A and D manufacturers were same to each other while both of them were larger than those from B and C manufacture.CONCLUSIONS:The qualities of Warfarin sodium tablets from four manufacturers are different from one another.The quality of products from A and D manufacturers are superior to those from manufacturer B.The products from manufacturer C are the worst.

Aim: To study the effects of astragaloside IV on experimental ventricular remodeling in mice and its mechanism from matrix metalloproteinase aspect.Method: Ventricular remodeling in mice was induced by con-secutively subcutaneous injection of isoproterenol for 14 days.Astragaloside IV(40,80 mg/kg)and propranolol(40 mg/kg,positive control)were administered by gavage to mice.Echocardiography was used to observe the left ventricular end diastolic diameter(LVIDd),left ventricular end systolic diameter(LVIDs),fractional shortening(FS)and ejection fraction(EF).The myocardial pathological pattern was detected by HE staining.Expressions of matrix metalloproteinases(MMP2,MMP9)and tissue inhibitor of metalloproteinases(TIMP1,TIMP2)mRNA in myocardium were detected by RT-PCR.Activities of MMP2 and MMP9 were assayed by zymography.Results:Compared with those of control mice,LVIDd and LVIDs were increased,FS and EF were decreased in the model group.Myocardial injury and fibrosis existed in histop at hological slices of the model group.In addition,the mRNA expressions and activities of MMP2 and MMP9 were increased in the model group.However,there were no markable changes to TIMP1 and TIMP2.Treatment with astragaloside IV reduced LVIDd and LVIDs,increased FS and EF,attenuated myocardial injury,and down-regulated mRNA expressions and activities of MMP2 and MMP9 compared with the model group.Conclusion: Astragaloside IV can greatly improve ventricular remodeling and dysfunction via decreasing MMP2 and MMP9 mRNA expression and activities in cardiac ventricles.

Objective To simulate the process of hypoxic?ischemic brain injury at high altitude in a simulated cabin with plateau low pressure environment, and to prepare a rat model of cerebral injuries at different high altitudes. Method Thirty?two 0?day?old neonatal SD rats were divided into four groups, namely group A ( control group) and three test groups:group B (2000 m group), group C (4000 m group), and group D (6000 m group). The rats of control group were reared in a barrier environment. The rats of test groups were placed in a simulated cabin with plateau low pressure environment, and to prepare neonatal cerebral ischemia?hypoxia model by sport activities. The sport movements were carried out in the cabin in a swimming groove 60 min/d, and not less than 20 hours a day at high altitude low pressure environment. Zea Longa 5 point scale standard was used to determine the behavioral scores at the 3 th 7 th 11 th 15 th days, and samples were collected on the 15th day to observe red blood cell morphology using HE and 2, 3, 5?triphenyltetrazolium chloride ( TTC ) staining and ultrastructure by scanning electron microscopy. Result ( 1 ) The neurological scores of the test groups A, B, C were significantly different from that of the control group (P<0?05), and the scores of test group D and control group were very significantly different ( P <0?01 ) . ( 2 ) The histopathological examination using HE staining showed inflammatory cell infiltration in all rats of the test groups, and the extent of inflammatory cell infiltration was positively correlated with the increase of altitude. ( 3 ) The histopathology with TTC staining revealed prominent ischemia in the cerebral cortex of rats in the plateau hypoxic environment. ( 4 ) Scanning electron microscopy showed that the rat erythrocytes were cap?like in the group B, irregular in the group C, and zigzag shape in the group D. Conclusions In this study, a rat model of neonatal hypoxic?ischemic encephalopathy ( HIE) is successfully established by hypoxic cabin combined with sport activity. This model is stable, reliable, more closely mimicking the pathogenesis and clinical manifestation of neonatal HIE than models prepared with other methods, therefore, may be used in related research.

OBJECTIVETo evaluate the restoration of function after spinal cord injury (SCI) in patients of different ages who have underwent intraspinal transplantation of olfactory ensheathing cells (OECs).

METHODSOne hundred and seventy-one SCI patients were included in this study. Of them, 139 were male and 32 were female, with age ranging from 2 to 64 years (mean, 34.9 years). In all SCI patients the lesions were injected at the time of operation with OECs. According to their ages, the patients were divided into 5 groups: 51 years group (n = 14). The spinal cord function was assessed based on the American Spinal Injury Association (ASIA) Classification System before and 2 - 8 weeks after OECs transplantation. One-way ANOVA and q test were used for statistical analysis, and the data were expressed as mean +/- SD.

RESULTSAfter surgery, the motor scores increased by 5.2 +/- 4.8, 8.6 +/- 8.0, 8.3 +/- 8.8, 5.7 +/- 7.3 and 8.2 +/- 7.6 in 5 age groups respectively (F = 1.009, P = 0.404); light touch scores increased by 13.9 +/- 8.1, 15.5 +/- 14.3, 12.0 +/- 14.4, 14.1 +/- 18.5 and 24.8 +/- 25.3 respectively (F = 1.837, P = 0.124); and pin prick scores increased by 11.1 +/- 7.9, 17.2 +/- 14.3, 13.2 +/- 11.8, 13.6 +/- 13.9 and 25.4 +/- 24.3 respectively (F = 2.651, P = 0.035). Restoration of pin prick in > 51 years group was better than other age groups except 21 - 30 years group.

CONCLUSIONOECs transplantation can improve the neurological function of spinal cord of SCI patients regardless of their ages. Further research into the long-term outcomes of the treatment will be required.

Adolescent ; Adult ; Age Factors ; Child ; Child, Preschool ; Female ; Humans ; Male ; Middle Aged ; Olfactory Bulb ; cytology ; transplantation ; Spinal Cord ; physiology ; Spinal Cord Injuries ; surgery ; Treatment Outcome

BACKGROUND: Previous research demonstrated that a homozygous mutation of g.136372044G>A (S12N) in caspase recruitment domain family member 9 ( CARD9 ) is critical for producing Aspergillus fumigatus -induced ( Af -induced) T helper 2 (T H 2)-mediated responses in allergic bronchopulmonary aspergillosis (ABPA). However, it remains unclear whether the CARD9S12N mutation, especially the heterozygous occurrence, predisposes the host to ABPA. METHODS: A total of 61 ABPA patients and 264 controls (including 156 healthy controls and 108 asthma patients) were recruited for sequencing the CARD9 locus to clarify whether patients with this heterozygous single-nucleotide polymorphisms are predisposed to the development of ABPA. A series of in vivo and in vitro experiments, such as quantitative real-time polymerase chain reaction, flow cytometry, and RNA isolation and quantification, were used to illuminate the involved mechanism of the disease. RESULTS: The presence of the p.S12N mutation was associated with a significant risk of ABPA in ABPA patients when compared with healthy controls and asthma patients, regardless of Aspergillus sensitivity. Relative to healthy controls without relevant allergies, the mutation of p.S12N was associated with a significant risk of ABPA (OR: 2.69 and 4.17 for GA and AA genotypes, P = 0.003 and 0.029, respectively). Compared with patients with asthma, ABPA patients had a significantly higher heterozygous mutation (GA genotype), indicating that p.S12N might be a significant ABPA-susceptibility locus ( aspergillus sensitized asthma: OR: 3.02, P = 0.009; aspergillus unsensitized asthma: OR: 2.94, P = 0.005). The mutant allele was preferentially expressed in ABPA patients with heterozygous CARD9S12N , which contributes to its functional alterations to facilitate Af -induced T H 2-mediated ABPA development. In terms of mechanism, Card9 wild-type ( Card9WT ) expression levels decreased significantly due to Af -induced decay of its messenger RNA compared to the heterozygous Card9S12N . In addition, ABPA patients with heterozygous CARD9S12N had increased Af -induced interleukin-5 production. CONCLUSION Our study provides the genetic evidence showing that the heterozygous mutation of CARD9S12N , followed by allele expression imbalance of CARD9S12N , facilitates the development of ABPA.
Humans ; Aspergillosis, Allergic Bronchopulmonary/complications* ; Aspergillus fumigatus/genetics* ; Asthma/genetics* ; Aspergillus ; Mutation/genetics* ; CARD Signaling Adaptor Proteins/genetics*