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 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.

Objective To study the genetic polymorphisms of STR locus D20S85 and to obtain the genetic data of Guangdong Han, Guangxi Zhuang, Huadong Han,Neimenggu Han and Meng populations. Method Using PCR and silver - staining methods, the alleles of D20S85 locus were detected and analysed. Results 9 alleles and 35 genotypes were found in those populations. The highest allele frequency was D20S85* 6. The results of Hardy - Wein-berg equilibrium test showed that the genotype distributions observed in five populations were correspondent with the expected. The expected heterozygosity was 0.7720 - 0.7912; the exclusion probability of paternity was 0.7538-0.7594(triplet) and 0.3988 -0.4297 (biplet) ; the discrimination power 0.9175 -0.9272 and the polymorphism information content 0.7442 - 0.7656. Conclusion STR D20S85 locus is a useful genetic marker for forensic application .

The attempt of vitrectomy is to remove the lesion of vitreous body and relieve vitreous traction to retina.Whether the vitrectomy is successful or not depend on if exist a close adhesion between vitreous body and retina or a posterior vitreous detachment (PVD).The drug assisted vitrectomy is a new technique.These drugs can help surgeon to form PVD during surgery safely and effectively.The drug is utilized prior to vitreoretinal operation to promote the colliquate of vitreous body or dissolve of fibroplasia membrane of the vitreous body in order to release the traction between the posterior cortex of vitreous body and the inner limiting membrane of retina.The research advance in relevant drugs is reviewed in this article.

The severe hand,foot and mouth disease(HFMD) caused by Enterovirus 71 (EV71) has become a serious threat to children's health.It is an important issues which need to be faced and resolved by pediatrician and disease prevention and control system,especially pediatric critical care specialist.The pathogenesis of severe HFMD caused by EV71 has not been clearly defined so far,and the clinical treatmnent is controversial.So,to further explore the mechanism of EV71 infection in severe HFMD and explore new effective prevention and control methods,have important significance in reducing the mortality and improve the quality of life of patients with severe HFMD.

[Objective] To study the effect of family sickbed comprehensive nursing mode on patients with stroke.[Methods] 92 cases of discharged patients with cerebral apoplexy were selected between October 2010 and October 2011,and were divided into the observation group(52 cases)and the control group(40 cases).Among them,the observation group received the family sickbed comprehensive nursing intervention,which was conducted by community nurses.The control group received general discharge mode and did not accept community nursing intervention.As designed,patients were followed weekly or monthly after discharge.After three months the treatment efficacy and quality of life were assessed.[Results] After follow-up for 3 months,HAMD,NIHSS scores in the intervention group were lower than those of the control group,MMSE,FMA and BI scores were higher than those of the control group.The physical,psychological,social and environmental scorcs in the intervention group were higher than those in the control group.[Conclusions] Family sickbed comprehensive nursing of cerebral apoplexy patients during rehabilitation stage can not only save medical resources,but also facilitate to recovery of patients.

Peroxisome prolifreator-activated receptors (PPARs) are ligand-activated nuclear transcription factors, members of nuclear hormone receptor superfamily. PPARs play critical roles in growth, proliferation and apoptosis of variety of cells. Recently, PPAR ligands have been reported to ameliorate neuronal damage in neurodegenerative diseases including Alzheim- ers disease, Parkinsons disease,cerebral ischemia and multiple sclerosis. PPAR agonists may have potential values in treatment of neurodegenerative diseases. In this paper, we reviewed recent findings on PPARs′ neuroprotective actions and their underlying mechanisms.

Matrix metalloproteinases (MMPs) are a family of Zn~ 2+ -dependent endopeptidases targeting extracellular matrix (ECM) compounds as well as a number of other proteins. Their proteolytic activity acts as an effector mechanism of tissue remodeling in physiologic and pathologic conditions, and as modulator of inflammation. Recently, it has been reported that MMPs play an important role in nervous diseases including cerebral ischemia, Alzheimers disease,multiple sclerosis and Parkinson′s disease.

Aim To observe the effects of Xiatianwu tota l alkaloids ( XA ) on learning and memory impairment and the central cholinergic f unction in rats with quinolinic acid microinjected into bilateral hippocampus. Methods Alzheimers disease (AD) rat models were made by damagin g bilateral hippocampus with quinolinic acid (150 nmol in 2 ?l for each hippoca mpus). XA 0.25, 0.5, 1 mg?kg -1 was administrated ig from 1 week before model established to 3 weeks after model established. Y-maze was used to measur e the learning and memory ability. The activity of the acetylcholinesterase ( AC hE ) in hippocampus and the contents of acetylcholine ( ACh ) was determined by spectrophotometry. Results Microinjection of quinolinic acid in to the rats hippocampus induced learning and memory dysfunction (P