Objective To optimize the extraction conditions of Hyperici Perforate Herba, Coptidis Rhizoma, Schisandrae Chinensis Fructus, and Ziziphi Spinosae Semen forJinzao Yuanzhi Capsule.Methods Hyperin extraction rate was set as index, and HPLC was used for determination. The extraction conditions of ethanol concentration, ethanol quantity, extraction time and other factors were studied with orthogonal test and comparative test.Results Ethanol concentration and extracting times were remarkable factors in the test. The optimum extraction technology forJinzao Yuanzhi Capsule was to reflux and extract the materials with 8 times of 70% ethanol for 2 times, reflux extraction for 1.5 hours, filtration. Then 6 times of 70% ethanol was added for 1.5 hours’ reflux, filtering, and merging extracted liquid.Conclusion The optimum extraction technology is reasonable and feasible.

The system construction and work flow of automatic oral drug dispensing system(AODDS) in our hospital are introduced,its' advantages and disadvantages of the application are analyzed.After applying AODDS,drug dispensing speed and accuracy are significantly increased.AODDS is conducive to promote hospital pharmaceutical care and pharmacy quality administration.The application of AODDS in our hospital may be referred for other hospitals to select AODDS.

Accidents, Occupational ; Acute Disease ; Adolescent ; Adult ; Arsenic Poisoning ; Chemical Industry ; China ; Female ; Humans ; Male ; Middle Aged ; Young Adult ; Zinc

Diagnosis, Differential ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Phytotherapy ; Severe Acute Respiratory Syndrome ; drug therapy ; prevention & control

Animals ; Beer ; adverse effects ; Blood Glucose ; metabolism ; Diabetes Mellitus, Experimental ; metabolism ; Lipid Metabolism ; Male ; Physical Conditioning, Animal ; physiology ; Rats ; Rats, Wistar

BACKGROUND: Monoamine hypothesis has been demonstrated by researches. However, the correlation between the metabolite of plasma monoamine neurotransmitter and anti-depression treatment in patients with depression has less been reported.OBJECTIVE: To study the effect of different drugs on metabolite of plaama monoamine neurotransmitter, and the correlation between the metabolite of plasma monoamine neurotransmitter and anti-depression treatment in patients with depression.DESIGN: Case controlled study.SETTING: Neurological Department and Brain Institute of Nanjing Medical University.PARTICIPANTS: Forty patients with depression hospitalized in Nanjing Brain Hospital (depression group) were diagnosed with the second revised edition of China classification of mental diseases(CCMD-2) and the tenth edition of International classification of diseases. And the total score of Hanmilton rating scale for depression(HAMD) was more than 17. Healthy voluntary blood donators in the control group were from Nanjing Municipal Central Blood Station( n = 20).INTERVENTIONS: Antidepressant was used in the depression for 4 weeks: fluoxetine 20 mg per day; 5-serotonin selective reuptake inhibitor (SSRI) paroxetine 20 mg per day; venlafaxime 50- 100 mg per day;5-serotonin and morepinephrine selective reuptake inhibitor(SNRI) fluvoxamine 50-100 mg per day. High performance liquid chromatograpy(HPLC)was used to measure the level of metabolite of plasma monoamine neurotransmitter in patients with depression before and 42 week after treatment, and the HAMD was used to evaluate clinical effect of the patients.MAIN OUTCOME MEASURES: The levels of metabolites of plasma monoamine neurotransmitters in patients with depression: 5-hydroxyindoleace tic acid(5-HIAA), 3-methoxy-4-hydroxyphenylglycol(MHPG) and homovani llic acid(HVA) were measured before and 4th week after treatment.RESULTS: The levels of 5-HIAA, MHPG and HVA of the metabolites of plasma monoamine neurotransmitters in patients with depression before treatment [ (20.3±14.6), (124.8±103.6), (54.7±32.1) μg/L] were all lower than those in the normal control group[ (39.5±28.4), (334.5 ±107.3), (88.5±37.2) μg/L], with statistically significant differences (P＜0.05). After SSRI treatment, the 5-HIAA content[ (37.1±21.9)μg/L]was significantly increased as compared with that before treatment, whose difference indicated significant meaning ( P＜0.05), but the differences in MHPG and HVA had no significant meaning as compared with those before treatment(P＞0.05) . After SNRI treatment, 5-HIAA and MHPG contents [(35.4±25.2 ), (291.2±120.4) μg/L] both were significantly increased, which indicated significant difference as compared with those before treatment( P＜0.05); but HVA level had no significant changes.CONCLUSION:'The peripheral neurotransmitter metabolites in plasma can reflect their states in brain. The change of neurotransmitter metabolite in plasma can be regarded as an important reference index for the evaluation of depression.

OBJECTIVE:To study the apoptosis of human leukemic cells induced by Dihydroartemisinin and its molecular mechanism.METHODS:Human leukemia K562 cells were treated by Dihydroartemisinin.The inhibitory effect on cell proliferation was assayed by MTT.Fluorescence microscopy was applied to observe the presence of apoptosis.The expression of caspase-3 was assayed with reverse transcription-polymerase chain reaction(RT-PCR).Levels of mitochondrial and cytoplasmic cytochrome C were determined using Western blot.RESULTS:After treatment with Dihydroartemisinin for 48 hours,the IC50 values of human leukemia K562 cells were 8? 10-5mol? L-1 detected at a wavelength of 570nm by MTT.Distinct morphology changes of cell apoptosis such as karyopyknosis and conglomeration were observed by Hoechst33342/PI staining.RT-PCR assay showed the expression of Caspase-3.Western-blot detection showed the decrease of mitochondrial cytochrome C concentration but the positive expression of cytoplasmic cytochrome C concentration.CONCLUSION:Dihydroartemisinin could inhibit proliferation and induce apoptosis of human leakemic K562 cells,this may partially attributed to the promotion of the delivery of cyt-c and the activation of caspase-3.

BACKGROUND: Both epidermal growth factor (EGF) and insulin transfer their signals into cells by two primary signal transduction pathways,including phosphatidylinositol 3-kinase (PI3K) pathway and mitogen activated protein kinases (MAPK) pathway.But they have different physiological functions.OBJECTIVE: To comparatively assay the dynamic behaviors of phosphoproteomes between EGF and insulin signal transductions in mouse hepatocytes and find key signal proteins.DESIGN,TIME AND SETTING: Randomized grouping controlled observation experiment was performed in the laboratory of Molecular Biology,Luzhou Medical College between July 2005 and April 2006.MATERIALS: Hepatocytes were from Kunming mice of closed population.METHODS: The primarily cultured mouse hepatocytes were labeled with 32p isotope and then randomly divided into three groups: control,EGF-stimulated (received 10 μg/L EGF),and insulin-stimulated (received 100 nmol/L insulin) groups.MAIN OUTCOME MEASURES: After mouse hepatocytes were treated with EGF and insulin for 0,5,20,60 and 120 minutes,the dynamic behaviors of phosphoproteomes(I.e,phosphorylated level) between EGF and insulin signal transductions were comparatively analyzed by two-dimensional electrophoresis method.RESULTS: The categories of all phosphorylated proteins between EGF and insulin-stimulated phosphoproteomes had no apparent difference.The dynamic behaviors of phosphoproteomes of most proteins during EGF signal transduction are parallel with those during insulin stimulation,except the dynamic behaviors of 4 proteins are different significantly.CONCLUSION: Aforementioned 4 phosphorylated proteins were most probably the key members that could distinguish between two signal transduction pathways ornetworks,and determined their major physiological functions respectively.

BACKGROUND: It has been reported tbat there are rich expressions of serotonin transporter (5-HTT) in the cortical and limbic regions related to emotion and behavior in cerebrum. Regulation of the intensity and persistence of serotonergic nerve response can change the serotonergic neurotransmission, meanwhile, 5-HTT is also an important target for selective serotonin reuptake inhibitors (SSRIs).OBJECTIVE: To observe whether there is a correlation of 5-HTT gene polymorphism with plasma level of 5-HT and the clinical response of SSRIs in the population of Nanjing area.DESIGN: A case-control observation.SETTING: Department of Psychiatry, Brain Hospital of Nanjing Medical University.PARTICIPANTS: Totally 132 inpatients with depression in the Department of Psychiatry, Brain Hospital of Nanjing Medical University and 100 volunteer healthy blood donors were taken as the observational subjects between January 2001 and December 2003.METHODS: The genotype was analyzed with polymerase chain reaction (PCR) polymorphism analysis in the patients with depression and healthy subjects; plasma level of 5-HT was analyzed with high performance liquid chromatography-electrical chemistry detector (HPLC-ECD); and the clinical response to the antidepressants were assessed with Hamilton depression rating scale (HAMD).MAIN OUTCOME MEASURES: The analytical results of 5-HTT genotype frequency and allele frequency in both groups, and the relationship between 5-HTT genotype and plasma level of 5-HT before and after SSRIs treatment were observed.RESULTS: Blood samples were collected from all the 132 patients with depression and 100 normal healthy subjects, and they all finished the scale test and entered the analysis of results. ① There were no significant differences between the depression group and normal control group in the 5-HTT gene genotype frequencies (LL: 24.2%, LS: 44.7%, SS31.1%; LL:29.0%, LS: 47.0%, SS: 24.0%, x2=1.405 8, P ＞ 0.05) and allelefrequencies (L:46.59%, S: 53.41%; L: 52.5%, S: 47.5%, x2=0.696 2, P ＞ 0.05). ② The total score of HAMD had significant differences before treatment among the depressive patients of different genotypes (F=6.48, P=0.002 1). After 4-week treatment of SSRIs antidepressants, the total score of HAMD was significantly decreased, and there was significant difference in the decrease of score (F=3.38, P= 0.037). ③ The plasma level of 5-HT had significant differences before treatment among the depressive patients of different genotypes (F=5.38,P= 0.005 7). After 4-week treatment of SSRIs antidepressants, the plasma level of 5-HT was increased, and the increased level was significantly different among different genotypes (F=23.55, P ＜ 0.01).CONCLUSION: The 5-HTT polymorphism may be not associated with the attack of depression, but with the severity of depression and the clinical responses of SSRIs in the population of Nanjing area, and the genotype in this area may become a reference index for the realization of individualized treatment in patients with depression.

Objective To investigate the different distribution and expression of mammalian target of rapamycin complex (mTORC) in the kidney of diabetic nephropathy (DN) mice.Methods Fourteen eight-week-old male C57BL/6 mice were assigned to 2 groups: the control group ( n=7 ) and the streptozotocin ( STZ )-induced DN group ( n=7 ) . Blood and urinary variables including glucose , albumin, creatinine and albumin/creatinine ratio were assessed 2 weeks after STZ injection.Hematoxylin-eosin staining was performed for renal pathological analyses .The distributions of mTOR , phosph-ser2448-mTOR(p-mTOR), mTORC1(Raptor), mTORC2(Rictor) and phosph-ser240/244-S6K1 (p-S6K1) were determined by immunofluorescence.The expression levels of mTOR, p-mTOR, mTORC1(Raptor), mTORC2(Rictor), S6K1 and p-S6K1 were detected by Western blotting .Results Two weeks after STZ injection , the diabetic mice developed albuminuria (P<0.01) and renal hypertrophy (P<0.05).The immunofluorescence positive staining for mTOR , Raptor, and Rictor was distributed in the epithelial cells of proximal tubules , glomerular mesangium and capillary loops as well as the medullary collecting ducts of the control mouse kidney .These positive signals increased in the DN mouse kidney ( P<0.05).However, pS6K1 was not detected in the inner medulla of control mouse and p-mTOR was not found in the glomeruli of both control and DN mice .Conclusion mTORC is widely expessed in the mouse kidney and participates in the development of DN , whereas the 2448 serine phosphorylation of mTOR may be not implicated in the hyperglycemia mediated glomerular injury .