The effects of Perilla Frutescens (L) Britt stem and Progesteroune on endometrium carbonic anhydrase were estimated; with 80 mice, by means of colorimatric method. It was found that both of them can increase the activity of the enzyme. and the effects increased with the increase of the doses. When the dosage of progesterone increased from 0.1ml/d to 9ml/d, the carbonic anhydrase activity (EU/gm) increased from 22.9 to 74.7, and simila fly, when the dosage of perilla frutescens (L) Britt stem increased from 0.05ml/d to 0.3 ml/d, the enzyme activity (EU/gm) increased from 22.1 to 55.5.

Objective To study the tissue pathology and the expression of related factors during renal tubular-interstitial fibrosis in aristolochic acid (AA) nephropathy in rat. Methods 46 male Wistar rats were randomly divided into 2 groups. The test group consisted of 26 rats which were gavaged with the extract of Caulis Aristolochiae Manshuriensis (CAM) (AA 20mg?kg -1 ?d -1 ); the control group consisted of 20 rats which were given with equal volume of potable water. At the end of 4th, 8th, 12th week, the kidneys of each rat were separately harvested. The HE, PAS and Masson staining were used to analyze the degree of tubular damage and interstitial fibrosis, and immunohistochemical method was applied to assess the protein expression of proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), transforming growth factor-?_1 (TGF-?_1) in the renal specimens. The mRNA expression of VEGF, endothelin-1 (ET-1), bone morphogenetic protein-7 (BMP-7) in renal tissue were determined by RT-PCR respectively. Results A severe renal tubular-interstitial damage and an early fibrosis were observed at the end of 12th week, and the interstitial fibrotic area was 31.36%. The protein expression of PCNA was increased at 4th week, but down-regulated after 8th week; the expression of TGF-?_1 and VEGF was increased at 4th week, while TGF-?_1 was maintatined on a high level with passage of time, but VEGF decreased gradually. The mRNA expression of VEGF and ET-1 increased notably at 4th week, slightly decreased after 8th week, but maintained at a high level. The BMP-7 declined slowly with the progression of pathological changes, reaching its lowest level at 12th week. Conclusion The mechanism of the rapid progression of fibrosis in AAN might be the renal result of severe impairment of regeneration of epithelial cells, lowering of expression of factors of promoting repair and inhibiting fibrosis, while the expression of factors of promoting fibrosis was maintained at a highlevel.

Objective To investigate the pathological characters of capillaries in tubulointerstitial nephropathy,and to study the expression of vascular endothelial growth factor(VEGF)and proliferation cell nuclear antigen(PCNA)in capillary endothelial cells in aristolochic acid-induced nephropathy in rat.Methods 46 male Wistar rats were randomly divided into 2 groups,the model group was composed of 26 rats which were gavaged with the extract of Caulis Aristolochiae Manshuriensis(aristolochic acid AA 20mg/kg?d),and the control group consisted of 20 rats which were treated with equal volume of potable water.The rats were sacrificed in batches at the end of 4th,8th and 12th weeks,and the blood samples were collected from abdominal aorta for the tests of renal functions.The kidney of each rat was harvested.The renal tissues were stained with HE,PAS,and Masson's technique for the analysis of degree of tubulointerstitial injury,interstitial fibrosis,and peritubular capillary(PTC),and the expressions of both VEGF and PCNA were morphologically observed and immunohistochemically analyzed.Results In the model group,the level of serum creatinine/body weight increased markedly,the renal pathological changes consisted of severe acute renal tubulointerstitial damage with cloudy swelling of tubule,degeneration,and exfoliation.With prolongation of feeding time,the damage progressively aggravated,and showed a remarkable tubulointerstitial injury.The interstitial fibrosis area was 31.36% at the end of 12th week.The renal capillaries showed thickening of vessel wall,narrowing of the vessel cavity,obstruction or hyalinization of some capillaries.There was focal infiltration of inflammatory cells around the injured vessels.But there was no apparent change in the globules compared with that in control group.The PTC dwindled in caliber or distorted,and the PTC density decreased significantly in models,especially in the region of tubular damage or interstitial fibrosis.The expression of VEGF showed compensatory up-regulation at the 4th week,but it was down-regulated gradually.The expression of PCNA was up-regulated at the 4th week,but down-regulated after 8th week,and only a few basement membrane naked tubular cells showed positive expression at 12th week.Conclusion AA could induce injury and loss of capillaries of the kidney.The decrease in capillary density might contribute to the impairment of renal function and progressive interstitial fibrosis,and the relative deficiency of VEGF expression may be related to PTC injury,which is one of the causes of chronic progression of aristolochic acid nephropathy.

After a descrption of the background of patron-driven acquisition ( PDA) or demand-driven acquision (DDA) and its short-term loan model, purchase model, auto-purchase model, librain-purchase model, and evi-dence-based acquisition model, the total amount of resources in common PDA platform, PDA models and their users were analyzed.The key problems in PDA implementation were pointed out, such as formulation of criteria for the development of resources, control of funds, mangement of MARC data, and assessment of PDA project, and sug-gestions were put forward for their solution .

OBJECTIVE: To investigate the pathogenic mechanism of aristolochic acid nephropathy (AAN) by observing the renal tubular injury and the change of the expression of bone morphogenetic protein-7 (BMP-7) mRNA in renal tissue of rats induced by aristolochic acid (AA), an active constituent in Caulis Aristolochiae Manshuriensis (CAM). METHODS: Forty-six male Wistar rats were randomly divided into normal control group (n=20) and AA-treated group (n=26). Rats in AA-treated group were intragastrically administered with AA 20 mg/(kg.d), and rats in control group were treated with equal volume of potable water. At the end of the 4th, 8th and 12th week of administration, the 24 h-urine was collected by metabolic cage for detecting the activity of N-acetyl-beta-D-glucosaminidase (NAG) and the blood samples were obtained from abdominal aorta for detecting serum creatinine (SCr). Pathological change and the degree of injury of the kidneys were observed by microscopy. The expression of proliferative cell nuclear antigen (PCNA) was detected by immunohistochemical method, and mRNA expression of bone morphogenetic protein-7 (BMP-7) in the renal tissue was detected by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Compared with the normal control group, the activity of NAG and the ratio of SCr vs body weight were markedly increased in rats of the AA-treated group after treatment (P<0.05 and P<0.01). Pathological section of renal tissue showed that most renal tubules had cloudy swelling, and vacuolar degenerating in tubular epithelial cells, with brush border dropping off, and parts of tubular basement membrane were exposed. The degrees of injuries were aggravated depending on treating time. The tubulointerstitial injury (TI) parameter in rats of AA-treated group was higher than that of the normal control group. The positive expression of PCNA was observed in the damaged tubular cells. The proliferation index of PCNA was significantly increased after 4- and 8-week treatment (P<0.01), but was decreased after 12-week treatment (P<0.05). The mRNA expression of BMP-7 was markedly decreased in the AA-treated group compared with the normal control group after 4-week treatment (P<0.05), and decreased with the extension of treatment time. CONCLUSION: AA can induce injury of the renal tubules, impair the cell regeneration, and inhibit the expression of BMP-7 mRNA in renal tissue. This may be one of the pathogenic mechanisms of AAN.

Objective:To investigate the relationship between Toxoplasma infection and schizophrenia by comparing the clinical symptoms between the antitoxoplasma-seropositive and seronegative patients with schizophrenia.Methods: Six hundred cases of first-episode schizophrenia were examined the serum reactivity to IgG antitoxoplasma antibody by Enzyme Linked Immunosorbent Assay (ELISA). And the clinical symptoms of the schizophrenic patients were scored by use of Positive and Negative Syndrome Scale (PANSS). Results: Compared to IgG-seronegative schizophrenia, IgG-seropositive schizophrenia group was higher in the positive subscale score, the positive component score, the excitement component score, and the cognitive component score(20.8?4.2与19.4?3.4,P

Objective To evaluate the effect of early clinical interference strategies on preventing the conversion of acute pancreatitis to the severe form and aggravation of severe acute pancreatitis(SAP).Methods The patients with acute pancreatitis admitted to this hospital were divided into two therapeutic phases by different therapeutic methods from January 2001 to December 2008.Patients in the first phase(from January 2001 to December 2004) were treated by the routine management,and the second phase(from January 2005 to December 2008) by the routine management combined with early clinical interference strategies.Then,the ratio of conversion from acute pancreatitis to SAP and prognosis of SAP between two phases were compared.Results Compared with the first phase,the rate of aggravation of acute pancreatitis was significantly decreased in the second phase(4.48% vs.21.18%),the average healing time of SAP,the incidences of systemic and local complications and the mortality of pancreatitis were reduced(P

Objective To investigate the relationship between COX-2 and Ki-67 proliferation index, bax, microvascular density(MVD)and CD44v6 respectively. Methods The expression of COX-2,Ki-67, bax, MVD (labelled by CD34) and CD44v6 were examined by immunohistochemistry PV method and tissue chip method in 101 cases of cervical carcinomas epithelium. Results The expression of COX-2 in cervical carcinomas has positive correlation with Ki-67, MVD and CD44v6, but has no correlation with bax. Conclusion The probable mechanisms are related with neovascularization, cell proliferation and cell adherence, but not related with the expression of bax.

Objective To explore the applicability of the histological features of plexiform bone and osteon banding to species identification. Methods 35 ground cross sections of the tibial midshaft collected from 10 human cadavers, 10 pigs, 5 cattle, 5 dogs, and 5 sheep, were observed under light microscope at 100-fold magnification. Results Plexiform bone and osteon banding were mostly observed in nonhuman bones, whereas rarely in human bones. Additionally, histological structures also varied with different individuals within a species. Conclusion The plexiform bone and osteon banding are the two important characteristics for certifying nonhuman bone in species identification.

AIM: To study the role of acylation stimula ting protein (ASP) in the differentiation of 3T3-F442A preadipocytes. METHODS: Differentiation of 3T3-F442A preadipocytes was induced by ASP. The morphological changes were observed by Oil-Red O staining and the di fferentiation rate was compared. TG synthesis and TG mass in these cells were al so assayed. DNA synthesis was measured by -TdR incorporation. A typical differentiation inducer, insulin, was used as a positive control to compare thes e results. RESULTS: (1) 3T3-F442A preadipocytes were induced to differentia te by ASP alone. Fat droplets were clearly visible in the cytoplasm of 3T3-F442A cells. The differentiation rate was high (90%), but no significant difference w as observed, compared with that in insulin group (95%). (2) In ASP group, TG syn thesis and TG mass were significantly increased, both of them were higher than t hat in control group (P0.05). CONCLUSION: As a new adipocytes hormone, ASP plays an important biological role in the differentiation of preadipocytes.