Objective To investigate the clinical significance of serum lactate dehydrogenase (LDH) and its isoenzymes,M or H subunits in the retreated patients with multiple myeloma(MM).Methods 141 medical records of retreated patients with multiple myeloma were collected,and the relationship of LDH and its isoenzymes,subunits with DS staging system,ISS staging system,creatinine,bone marrow plasma cell percentage,immunoglobulin and microglobin was analyzed.Results Serum total LDH activity was not significantly related to DS staging system and ISS staging system.LDH1 percentages was negatively correlated with ISS staging system (P＜0.01),and LDH4 percentages positively associated with ISS staging system (P＜0.05).LDH activity,absolute value of LDH1 ,LDH2,LDH3,LDH4,and H subunits were positively linked to serum creatinine in myeloma kidney disease patients with renal inadequacy (P＜0.05).Both percentage and absolute value of LDH5 were negatively correlated with bone marrow plasma cell percentage (P＜0.01 and P＜0.05 respectively).Conclusion The detection of serum LDH isoenzyme is more valuable than total LDH activity in retreated patients with multiple myeloma.

Objective: To develop an HPLC-ELSD method for the simultaneous determination of six saponins constituents including notoginsenoside R1, ginsenoside Rg1, ginsenoside Re, ginsenoside Rb1, ginsenoside Rc and ginsenoside Rd in Xinling pills.Methods: HPLC-ELSD was used, and the chromatographic separation was performed on an Agilent Eclipse XBD-C18 column (150 mm×4.6 mm,5 μm) with acetonitrile-water as the mobile phase with gradient elution at the flow rate of 1.0 ml·min-1, the column temperature was maintained at 20℃, the drift tube temperature was 60℃, and the gas pressure was 4.00 bar.Results: Notoginsenoside R1, ginsenoside Rg1, ginsenoside Re, ginsenoside Rb1, ginsenoside Rc and ginsenoside Rd was linear within the range of 0.30-6.00μg(r=0.999 5), 1.14-22.80μg (r=0.999 6), 0.17-3.40 μg (r=0.999 7), 0.81-16.20 μg (r=0.999 7), 0.08-1.60 μg (r=0.999 8) and 0.07-1.40 μg (r=0.999 8), respectively.The average recovery was 98.23%, 97.98%, 99.14%, 99.15%, 98.72% and 98.37%, and the RSDs were 1.56%, 1.31%, 1.16%, 1.07%, 0.73% and 0.92%(n=6), respectively.Conclusion: The method is convenient, accurate and reproducible in the quality control of saponins components in Xinling pills

AIM:To study the effects of transforming growth factor-β_1 (TGF-β_1) on cell apoptosis,cell cycle,production of endogenous TGF-β_1,expressions of P27~(Kip1),cyclin E and bcl-2 mRNA levels in NB4 cells. METHODS:Apoptotic morphological changes were observed by Wright-Giemsa staining. Cell cycle and apoptosis were detected with flow cytometry. Semiquantitative RT-PCR was used to examine the mRNA levels of endogenous TGF-β_1,P27~(Kip1),cyclin E and bcl-2. RESULTS:TGF-β_1 significantly restrained the growth and promoted the apoptosis of NB4 cells. The blockage of NB4 cells treated by TGF-β_1 at concentration of 5 μg/L was in G1 phase. Endogenous TGF-β_1 mRNA expression in NB4 cells was up-regulated when the concentration of exogenous TGF-β_1 was <5 μg/L. Meanwhile,the expression of endogenous TGF-β_1 mRNA was down-regulated when the concentration of exogenous TGF-β_1 was 10 μg/L. After treated with TGF-β_1 at concentration of 5 μg/L,P27~(Kip1) mRNA expression in NB4 cells was up-regulated,cyclin E and bcl-2 were reduced. CONCLUSION:TGF-β_1 is able to induce apoptosis and cell cycle distribution abnormally in NB4 cells by (1) Up-regulation of endogenous TGF-β_1,so that NB4 cells was induced into apoptosis through consequently high expression of P27~(Kip1). (2) TGF-β_1 may lead to cell cycle arrest by inhibiting the expression of cyclin E directly,or by inhibiting the activity of cyclin E through the increased expression of P27~(Kip1). (3) Down-regulation of bcl-2 induces apoptosis of NB4 cells.

Objective To observe the synthesis of TLR2 protein and mRNA expression in Kupffer cells(KCs). Methods BALB/C mice were used to make model of partial hepatic ischemia/reperfusion (I/R) injury. After injury, KCs were isolated with two-steps in situ perfusion technique. The synthesis of TLR2 protein was determined by flow cytometric analysis (FCM) and real time reverse transcription(polymerase) chain reaction (Real Time RT-PCR) was used to analyse its gene expression in KC. Results The expression of TLR2mRNA and synthesis of protein in KC were significantly higher in experimental group, compared with sham group (protein expression: 9.19?0.43 % vs 1.52 ?0.24%, P

Objective To investigate the diagnosis and treatment of ectopic opening of the common bile duct in the duodenal bulb.Methods The clinical data of 3 patients who were admitted to the Binzhou People's Hospital and 9 patients who were admitted to the Tianjin People's Hospital from January 2006 to December 2013 with ectopic opening of the common bile duct in the duodenal bulb were retrospectively analyzed.Seven patients had choledocholithiasis and 5 had stenosis at the end of common bile duct.The medical histories and clinical features in patients were analyzed and routine blood test and serum liver function test were done.All the patients received the endoscopic retrograde cholangiopancreatography (ERCP) examination and were cured.All the patients were followed up via outpatient examination and telephone interview up to August 2014.Results Six patients had histories of cholangitis recurrence and 2 had histories of duodenal ulcer recurrence.All the patients had pain in the right hypochondriac region of the abdomen.Seven patients had fever,chills,skin yellowing sclera and tenderness in the right hypochondriac region of the abdomen.The levels of alkaline phosphatase (ALP) and glutamyltranspeptidase (GGT) in 11 patients,the levels of TBil and DBil in 8 patients and the count of WBC in 7 patients were increased.(1) The results of ERCP showed as follows:there was no papillar opening at the second and third segment of duodenum.The crack-like opening located at the duodenal post-bulb with rough and erosive mucosal surfaces and intermittent outflow of bile.Duodenal ulcer was detected in 5 patients and duodenal bulb metamorphosis in 3 patients.All the 12 patients received successfully intubations.(2)The results of retrograde cholangiography showed as follows:the end of common bile duct of 12 patients was taper and sickle-shaped.Intra-and extrahepatic bile duct dilation was detected in 10 patients,choledocholithiasis in 7 patients and clear findings for the pancreatic duct in 5 patients.Among the 12 patients,8 received balloon dilation (5 with stenosis at the end of common bile duct,3 with choledocholithiasis),3 received laparoscopic common bile duct exploration (LCBDE) combined with cholangioenterostomy due to diameter of stone more than 1.5 cm and ectopic opening stenosis of the common bile duct in the duodenal bulb.One patient was treated by percutaneous transhepatic cholangiography (PTC) lithotomy of common bile duct after unsuccessful ERCP without bleeding and pancreatitis-related complications.The symptoms of cholangitis in 3 patients were alleviated after balloon dilation,2 patients had recurrence of cholangitis and were cured by Roux-en-Y cholangioenterostomy.The mean open surgery time and mean duration of postoperative hospital stay in 5 patients were 85 minutes (range,60-150 minutes) and 10 days (range,8-14 days),respectively.All the 12 patients were followed up with a median time of 38 months (range,8-90 months).During the follow-up,10 patients survived well without recurrence of cholangitis and cholelithiasis.Two patients had recurrence of cholangitis at postoperative month 2 and month 14,including 1 patient with the recurrence of common bile duct sand-like stones,and they were readmitted to hospital and treated by Roux-en-Y cholangioenterostomy without recurrence by follow-up.Conclusions The clinical symptoms of ectopic opening of the common bile duct in the duodenal bulb included recurrence of cholangitis,duodenal ulcer history,pain in the right hypochondriac region of the abdomen,skin yellowing sclera,abnormal liver function,crack-like openings in the duodenal bulb by ERCP examination with outflow of bile,cholangiography-guided taper and sickle-shaped end of common bile duct.The treatment should be aimed at the concomitant diseases.

Objective To analyze the clinical manifestation of diffusive alveolar hemorrhage in acute leukemia induction therapy.Methods Clinical data of two diagnosed cases of diffusive alveolar hemorrhage secondary to acute leukemia were collected.Clinical data of eight cases of diffusive alveolar hemorrhage secondary to acute leukemia which were published were also collected by searching in Medline database.The clinical manifestation,diagnosis,strategy of differential diagnosis and treatment of diffusive alveolar hemorrhage secondary to acute leukemia were analyzed.Results Diffusive alveolar hemorrhage was a rare but fatal complication of acute leukemia.The common clinical manifestations included hemoptysis,progressive dyspnea and progressive decrease in concentration of hemoglobin.The analysis of blood gas showed type Ⅰ respiratory failure.The manifestations of chest computed tomography included diffusive ground glass opacity and infiltration of parenchyma.The bronchoalveolar lavage fluid was bloody.And lung biopsy showed congestion of alveoli and capillaritis.The detection for pathogens,vasculitis related antibodies,brain natrium peptide were negative.The mortality of those cases was 40 ％ (4/10).Corticosteroids therapy was effective.The mortality of patients received corticosteroids therapy was 25 ％ (2/8).Conclusion Diffusive alveolar hemorrhage is a rare but fatal complication of acute leukemia.The mortality is high.The key points of therapy are early diagnosis and corticosteroids therapy.

BACKGROUND: Effective treatment for severed acute radiation sickness (over 8 Gy) has not been obtained at present. Mesenchymal stem cells, which are shown to secrete hematopoietic cytokines and support hematopoietic progenitors, play an important role in cute radiation sickness. OBJECTIVE: To investigate the therapeutic potential of non-adherent bone marrow-derived stem cells in the treatment of acute radiation injury induced by 8.5 Gy X-ray irradiation, as wel as the mechanisms involved. METHODS: Non-adherent marrow-derived stem cells from the long bone of fetal limbs were col ected for analyzing surface antigens, cel cycle, osteogenic and adipogenic differentiation potential, and expressions of vascular endothelial growth factors and Annexin A2. After being exposed to 8.5 Gy total body irradiation, BALB/C mice were randomly assigned into transplantation group and control group. Mice in the transplantation group were given 3×106 CFDA-SE labeled human non-adherent bone marrow-derived stem cells, and those in the control group were given 0.3 mL normal saline. Then, the survival rate, peripheral white blood cells at different time, pathologic change and angiogenesis of the bone marrow were observed. RESULTS AND CONCLUSION: After X-ray irradiation, transplanted non-adherent mesenchymal stem cells appeared to have a homing to the site of injury. The survival rate of mice in the transplantation group was much higher than that in the control group. Compared with the control group, the white blood cells in the transplantation group decreased more slowly while recovered more rapid: the nadir appeared at day 14 after transplantation while it recovered within 30 days. The bone marrow of mice in the transplantation group regenerated more actively and had more hematopoietic islands than those in the control group on day 21. In addition, bone marrow angiogenesis of the transplantation group was more obvious than that of the control group. In conclusion, human fetal non-adherent bone marrow-derived stem cells could promote bone marrow angiogenesis in a mouse model of acute radiation injury, through which they could play an important role in tissue regeneration of acute radiation injury.

The evolution of hepatocellular carcinoma (HCC) is a compound process which involves many kinds of genes and transductional pathways. The expression of the peptidyl-proplyl-isomerase PIN1 gene, the mutation in exon 3 of beta-catenin and its correspondent abnormal expression and their roles in the hepatocellular carcinogeneisis were investigated. Among 29 pair cases of HCC and non-carcinoma tissues, the expression of PIN1 gene was detected by immunochemical staining. Mutations in exon 3 of beta-catenin gene and differential expression of beta-catenin gene were investigated by the methods of PCR-SSCP, direct sequencing and immunohistochemical technique as well. The results indicated: (1) 44.8% (13/29) cases of HCC presented higher level of PIN1 gene expression than non-cancerous tissues (chi2=32.63, P<0.05), especially in cytoplasm and nucleus, while there was lower level of PIN1 expression in non-cancerous tissues; (2) 58.6% (17/29) HCC tissues showed beta-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated beta-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated beta-catenin protein accumulation with lower level or trace of PIN1 expression (chi2=0.00, P>0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of beta-catenin, and accompanied by beta-catenin protein accumulation. There was no mutation in non-cancerous tissues. All the mutation presented in tissues with low level of PIN1 expression. There was no mutation of beta-catenin gene in tissues with high PIN1 expression level (chi2=58.12, P<0.05). So it was postulated that the increase of PIN1 gene expression could promote hepatocellular carcinogenesis via a way different from beta-catenin gene mutation.

The evolution of hepatocellular carcinoma (HCC) is a compound process which involves many kinds of genes and transductional pathways. The expression of the peptidyl-proplyl- isomerase PIN1 gene, the mutation in exon 3 of β-catenin and its correspondent abnormal expression and their roles in the hepatocellular carcinogeneisis were investigated. Among 29 pair cases of HCC and non-carcinoma tissues, the expression of PIN1 gene was detected by immunochemical staining. Mutations in exon 3 of β-catenin gene and differential expression of β-catenin gene were investigated by the methods of PCR-SSCP, direct sequencing and immunohistochemical technique as well. The results indicated: (1) 44.8% (13/29) cases of HCC presented higher level of PIN1 gene expression than non-cancerous tissues (x2 =32.63, P＜0.05), especially in cytoplasm and nucleus, while there was lower level of PIN1 expression in non-cancerous tissues; (2) 58.6% (17/29) HCC tissues showed β-catenin protein accumulation in cytoplasm and nucleus. 46.2% (6/13) HCC tissues indicated β-catenin protein accumulation with higher level of PIN1 expression, while 53.8% (7/13) HCC tissues indicated β-catenin protein accumulation with lower level or trace of PIN1 expression (x2 =0.00, P＞0.05); (3) 24.1% (7/29) of primary tumor lesions carried gene mutations in exon 3 of β-catenin, and accompanied by β-catenin protein accumulation. There was no mutation in non-cancerous tissues. All the mutation presented in tissues with low level of PIN1 expression. There was no mutation of β-catenin gene in tissues with high PIN1 expression level (x2=58.12, P＜0.05). So it was postulated that the increase of PIN1 gene expression could promote hepatocellular carcinogenesis via a way different from β- catenin gene mutation.