Branch atheromatous disease (BAD) is a deep cerebral infarction at the entrance or the origin of perforating artery because of atherosclerosis causing lumen stenosis or occlusion. It is common in clinical practice and there is often a clinical feature of progression or fluctuation in the acute phase. Its prognosis is poor and it will bring a heavy burden to the family and society. Therefore, the early intervention for patients with BAD is very important. This article reviews the treatment of BAD.

The pathological changes of the damages on many vital organs during acute obstructive cholangitis were observed in 45 rats under optical and electron microscopy.The morphological changes of the vital organs were characterized by disturbance of blood circulation,degeneration and/or necrosis of the tissues and cells,and inflammatory reactions.The hepatic damage appeared earlier and more severe thna the other organs during acute obstructive cholangitis.

Objective To observe the PML protein expression of hepatocellar carcinoma tissue and cells lines and As 2 O3 regulate its expression .Methods Immunohistochemistry was used to examine the PML protein expression of hepatocellar carcinoma tissue . Western blot analysis were used to observe PML protein expression of hepatocellar carcinoma tissue of 12 cases ,5 hepatocellar car-cinoma cell lines ,such as HuH7 ,HepG2 ,Hep3B ,SMMC-7721 ,MHC97H .Western blot analysis was used to detected the PML pro-tein expression of these hepatocellar carcinoma cell lines after 72-96 h treated with 0 .25 μg/mL of As2 O3 .Results Immunohisch-enmical staining showed that the PML protein was expressed in both cytoplasm and nucleus ,did not well-distributed in hepatocellar carcinoma cells .There was no significant differences of PML protein expressed among differently differentiated stages of hepatocel-lar carcinoma cells .Western blot analysis found that hepatocellar carcinoma tissues of 12 cases with hepatocellar carcinoma ex-pressed PML protein ,and there was significant difference of PML protein expressed among 12 cases suffer with hepatocellar carci-noma .hepatocellar carcinoma cell lines ,such as HuH7 ,HepG2 ,Hep3B ,SMMC-7721 and MHC97H all expressed PML protein ,and there was little difference of PML protein expressed among hepatocellar carcinoma cell lines .The PML protein expression of HuH7 ,HepG2 ,Hep3B ,SMMC-7721 and MHC97H cell after 72-96 h treated with 0 .25 μg/mL of As2O3 significant decreased . Conclusion Hepatocellar carcinoma tissue and cells may express PML protein ,and As2 O3 may regulate this protein expression as well .PML protein may be the target molecule of As2 O3 treating HCC .

Objective To evaluate the effectiveness of Moxifloxaein in treatment of multidrug-resistant(MDR)pulmonary tuberculosis.Methods 65 MDR pulmonary Mycobacterium tuberculosis patients were randomized divided into two groups,separately receiving the regimens of contained Moxifloxacin0.4 qd or Levofloxacin 0.6 qd six drugs treatment accompanying with aminoglycosides,prothionamide,pasiniazid,pyrazinamide,ethambutol and clarithromyein from 2003—2005y in Guangzhou chest hospital.The treatment outcomes were evaluated when study executed one and half year later.Results 35 patients in moxifloxacin group had 27 cases cured,and 30 patients in levofloxacin group had 19 cases cured.The success rates were 77.1% versus 63.3%(P=0.222).The time to sputum culture conversion were (1.9?0.7)months and 3.0?1.8 months(P=0.035).Bacillary susceptible to levofloxacin,good adherence,radi- ographic extent less than one lung,and use of moxifloxacin were independent predictors of favorable outcome(odds ratios,7.3 to 21.4).Conclusion Moxifloxacin was found have a better bactericidal activity in vivo and less side effects. Its efficacy was higher than levofloxacin when incorporated into muhidrug regimens used for treatment of MDR tuberculosis.

Objective To construct markless gene deletion mutant at the clpP loci on the chromosome of Streptococcus mutans(S.mutans).Methods ASp resistance gene was amplified by PCR,to construct the Sp resistance cassette where the Sp resistance gene was flanked with two loxP site.After the clpP gene was cloned into the pGEM-T-Easy TA cloning vector,it was digested and linked with the Sp resistance cassette,yielding homologous recombination vector pIB △ clpP-Sp.The vector was linearized and used for the transformation of S.mutans UA159,with transformants selected on TPY plates containing Sp.The selected strain was transformed with the thermosensitive plasmid pCrePA to excise the Sp resistance gene.The pCre-PA was then easily eliminated at nonpermissive temperature,resulting in a markless mutant strain carrying a deletion at the clpP loci,which was verified by PCR and DNA sequencing.Results The result of the PCR analysis and DNA sequencing indicated that a part of the clpP gene was deleted.There was a loxP at this loci without the Sp resistance gene.Conclusion The markless clpP-deletion mutant of S.mutans was constructed successfully,which laid a foundation for further study of its biological function and its influence on the cariogenicity of S.mutans.

Objective To research whether the inhibitory oligonucleotides could improve the immune status of the BXSB mice. The purpose was to provide a valuable direction for treating systemic lupus erythematosus. Methods 3-month-old BXSB lupus mice were divided into three groups (including inhibitory oligonucleotides group, saline group and blank control group). The 24 hours urine proteins were determined before treatment. After treatment,the urine protein, anti-dsDNA, peripheral blood lymphocytes apoptosis and immune complex in renal glomeruli were measured. Results Before treatment,the urine proteins had no statistical differences among the three groups ( P > 0.05 ).After treatment,the urine protein, anti-dsDNA levels in inhibitory oligonucleotides group were significantly lower than that of control group(P < 0.01 ). Apoptosis of peripheral blood lymphocytes in inhibitory oligonucleotides group was significantly higher than that of control group( P < 0.05 ) ,immune complex in renal glomeruli in inhibitory oligonucleotides group was significantly lower than that of the other groups ( P < 0.05 ). Compared with saline group, inhibitory oligonucleotides had prolonged life period of BXSB mice ( P < 0.01 ). Conclusion The inhibitory oligonucleotides could improve immune status of BXSB, and could put off the disease progression.

BACKGROUND: Contacting with blood, most of polymer materials lead to different extents of blood coagulation, which limits their clinical application. Therefore, developing polymer materials with excellent anticoagulant property has become a key to clinical study of bioartificial liver materials.OBJECTIVE: To in vitro detect the blood dompatibility of polyacrylamide grafted polypropylene (PP) membrane (PP-g-AAm), a novel artificial liver reactor material.METHODS: Prior to and after modification, hemolytic test, prothrombin time and activated partial thromboplastin time tests of PP membrane were performed; blood platelet CD62P and CD63 expression rates were determined by flow cytometry, and platelet adhesion on PP and PP-g-AAm membranes by scanning electron microscopy.RESULTS AND CONCLUSION: The hemolysis ratio of PP and PP-g-AAm membranes was 1.32% and 1.46%, respectively.Compared with PP-g-AAm membrane, prothrombin time and activated partial thromboplastin time of PP membrane weremarkedly shorter (P < 0.05). CD62P and CD63 expression rates in the PP-g-AAm membrane were significantly lower than PP membrane (P < 0.05). Scanning electron microscopy results revealed that there were obvious changes of platelets adhering to these two membranes, but platelets adhering to PP-g-AAm membrane were fewer than PP membrane. These results indicate that PP-g-AAm membrane exhibits good blood compatibility.

Objective: To observe the effect of moxibustion on the expression of N-methyl-D-aspartic acid (NMDA) receptor subtype 2B (NR2B) in the hippocampus of rheumatoid arthritis (RA) rats, and to explore the analgesic mechanisms of moxibustion in RA treatment. Methods: Sixty male Sprague-Dawley rats were randomly divided into a normal group, a model group, a moxibustion group, a moxibustion + NMDA receptor antagonist (AP-5) group, and a moxibustion + NMDA receptor agonist (NMDA) group, with 12 rats in each group. Except for the normal group, rats in the other four groups were treated with complete Freund's adjuvant in a windy, cold, and damp environment to replicate RA models. Rats in the moxibustion group received suspended moxibustion with moxa sticks at Shenshu (BL23) and Zusanli (ST36), and the two points were used alternately. After intraperitoneal injection of AP-5 or NMDA, rats in the moxibustion + AP-5 group and the moxibustion + NMDA group received the same moxibustion intervention as in the moxibustion group, once a day for 15 d. The thermal withdrawal latency (TWL) of rats in each group was detected before and after modeling and after the 15-day intervention. After the 15-day intervention, hematoxylin-eosin staining was performed to observe the pathological changes in knee joints. The real-time fluorescence quantitative polymerase chain reaction method was used to detect the mRNA expression of NR2B in the hippocampus; Western blotting assay was used to detect the protein and the phosphorylated protein expression of hippocampal NR2B. Results: The synovial tissue was proliferated, the synovial lining was significantly thickened, the pannus was formed, and the cartilage and bone tissues were significantly damaged in the model group. After intervention, the pathological morphology of the knee joints in the moxibustion group, the moxibustion + AP-5 group, and the moxibustion + NMDA group was significantly improved, and the improvement in the moxibustion + AP-5 group was more notable than that in the moxibustion + NMDA group. Compared with the normal group, the TWL was significantly decreased (P<0.01), and the mRNA, protein, and phosphorylated protein expression levels of hippocampal NR2B were significantly increased in the model group (P<0.01). Compared with the model group, the TWL of each intervention group was significantly increased (P<0.01 or P<0.05), and the mRNA, protein, and phosphorylated protein expression levels of hippocampal NR2B were significantly decreased (P<0.01). Compared with the moxibustion group, the TWL was significantly increased (P<0.01), and the mRNA, protein, and phosphorylated protein expression levels of hippocampal NR2B were significantly decreased in the moxibustion + AP-5 group (P<0.01); the TWL was significantly decreased (P<0.01), and the mRNA, protein, and phosphorylated protein expression levels of hippocampal NR2B were significantly increased in the moxibustion + NMDA group (P<0.01). Conclusion: Moxibustion reduces hyperalgesia in RA inflammatory rats. The analgesic effect may be related to the decrease in the expression and phosphorylation levels of NR2B in the hippocampus.

Objective To clarify the anatomical and pathlogical implications of Denonvilliers' fascia.Method In this study,thirty pelvic specimens (17 males and 13 females) were incised through the median sagittal plane and carried for regional anatomy study; Denonvilliers' fascia was identified by immunohistochemistry.Results Denonvilliers' fascia could be found in all male specimens:it had an anterior leaf and a posterior leaf,with the anterior one attaching to seminal vesicle,seminiferous duct,prostate and the bottom of bladder firmly.The fascia originated at the fold of the peritoneum and ended at the perineum fascia,fusing into the pelvic parietal fascia laterally.It was not obvious in females,only to find a thin and transparent membrane between vagina and rectum.The maximum height of Denonvilliers' fascia in left pelvis was (3.2 ± 0.3) cm,compared with (3.3 ± 0.3) cm in the right pelvis (t =0.965,P ＞ 0.05).Immunohistochemistry study revealed that there was no lymph node in the fascia and its lateral parts were enriched of nerve fibers,which were few in its middle part.Conclusions The unique anatomical and pathlogical characteristics of Denonvilliers' fascia are of vital importance to the avoidance of nerve injury during rectal surgery.

ObjectiveTo explore linkage relationship between polymorphisms of (AC)n (AT)xTy and mutations in the β-globin gene in patients with mild β-thalassemia.MethodsThe subjects were 89 mild β-thalassemia patients with known mutations and 110 healthy subjects from People's Hospital of Baoan District of Shenzhen from February 2009 to July 2010.Genomic DNA was extracted from peripheral leukocytes.Sequence of the BP1 binding site upstream of the β-globin gene was amplified by polymerase chain reaction,polymorphisms of (AC)n (AT)xTy were determined by DNA sequencing.Allelic frequencies of (AC)n (AT)xTy between mild β-thalassemia patients and healthy subjects were compared using x2 test.Mutation rates between two groups were also compared using x2 test for subjects carrying same haplotype. Linkage relationship was conducted according to allelic frequencies and mutations. Results Analysis of the (AC)n(AT) xTy polymorphisms of the BP1 binding site upstream of the β-globin gene showed 9 different genotypes: (AC)2( AT)7T7,( AC)2( AT)8T5,( AC)3( AT)7T5,( AC)2( AT)9T5,( AC)2(AT)8T9,(AC)3(AT)8T5,(AC)2(AT)10T3,(AC)2(AT)7T5 and (AC)2(AT)11T3.The (AC)2(AT)7T7 and (AC)2 (AT)8T5 genotypes were common for patients with mild β-thalassemia.Allele frequencies of (AC)2(AT)7T7,(AC)3 ( AT)7T5 and ( AC)2( AT)8T9 were 38.8％ (69/178),11.8％(21/178),9.0％ ( 16/178 ) for mild β-thalassemia patients,and 24.1％ ( 53/220),5.4％ ( 12/220),3.2％(7/220)for healthy subjects, respectively, there were significant differences between mild β-thalassemia patients and healthy subjects (x2 =9.966,4.371,6.093,P ＜ 0.05 ).Allele frequency of (AC)2(AT)9T5 was 10.1％ (18/178) and 33.2％ (73/220) for mild β-thalassemia patients and healthy subjects,frequency of (AC)2 (AT)9T5 was significandy lower in mild β-thalassemia patients than in healthy subjects (x2 =29.691,P ＜0.01 ).Allele frequency of (AC)2(AT)8T5 was 25.3％ (45/178) and 29.1％(64/220) for mild β-thalassemia patients and healthy subjects,there wasn't significant difference between patients and healthy subjects (x2 =0.718,P ＞0.05).The mutation rates of codon41/42(-TTCT) and IVSⅡ-654(C→T) were 59％ (10/17) and 29％ (5/17) for mild β-thalassemia patients carrying (AC)2(AT)7T7 allele,and 29％ (4/14) and 57％ (8/14) for patients carrying ( AC)2 (AT)8T5 allele.There were not significant differences between codon41/42(-TTCT) mutation rate and IVS-Ⅱ-654(C→T) mutation rate (x2 =2.982,2.333,P ＞ 0.05 ) for mild β-thalassemia patients carrying ( AC)2 ( AT)7T7 and ( AC)2(AT)8T5 allele.ConclusionsAllele of (AC)2(AT)7T7,(AC)3(AT)7T5 and (AC)2(AT)8T9 are in linkage disequilibrium with β-thalassemia.Most mild β-thalassemia patients carrying (AC)2 (AT)7T7 allele are caused by codon41/42 (-TTCT) mutation in the β-globin gene,and IVS-Ⅱ-654 (C→T) is a major mutation for patients carrying (AC)2(AT)8T5 allele.