[Impact of portal vein thrombosis on the efficacy of endoscopic treatment in preventing re-bleeding from ruptured gastroesophageal varices in hepatitis B-related liver cirrhosis].

Objective: To explore whether portal vein thrombosis affects the efficacy of endoscopic treatment in preventing re-bleeding from ruptured gastroesophageal varices in hepatitis B-related liver cirrhosis. Methods: Hospitalized patients who received endoscopic therapy to prevent re-bleeding from ruptured gastroesophageal varices due to hepatitis B-related liver cirrhosis during 2013 to 2017 were selected, and followed up for 1 year after treatment for re-bleeding and survival status. Patients were divided into thrombotic and non-thrombotic group according to whether they were combined with portal vein thrombosis at the time of initial admission. The baseline data characteristics of the two groups were analyzed. The 1-year re-bleeding rate and survival rate of the two groups were compared by Kaplan-Meier survival analysis. The other risk factors for re-bleeding after endoscopic variceal therapy were evaluated by univariate and multivariate regression. Results: A total of 124 cases with re-bleeding from ruptured gastroesophageal varices due to hepatitis B-related liver cirrhosis were included. The average age was 50.7 years old. 81.5% (101 cases) were male, and 24.2% (30 cases) were combined with portal vein thrombosis. There were no statistically significant differences between the thrombotic and the non-thrombotic group in the average age, gender, liver function classification, transjugular portal pressure gradient, antiviral treatment, and non-selective ß-blockers. Kaplan-Meier analysis of the re-bleeding rate after endoscopic treatment indicated that the incidence of non-bleeding in patients with thrombotic group at 60 days, 180 days and 1 year was significantly lower than that in the non-thrombotic group [86.7%, 80.0%, 56.7% vs. 95.7%, 93.6%, 87.2% (P = 0.000 1)]. Analysis of the location of portal vein thrombosis showed that the bleeding rate in the main portal trunk, left and right branches and superior mesenteric vein had increased significantly after endoscopic treatment, while the splenic vein had no effect on the bleeding after endoscopic treatment. Univariate and multivariate regression analysis indicated that age (HR 1.05, 95% CI: 1.01-1.09, P = 0.02) and thrombosis in the main portal trunk, left and right branches (HR 4.95, 95% CI: 2.05-11.95, P < 0.01) were independent risk factors for re-bleeding at 1 year after endoscopic treatment. Conclusion: Portal vein thrombosis is an independent risk factor that affects the efficacy of endoscopic treatment in preventing re-bleeding from ruptured gastroesophageal varices in hepatitis B-related liver cirrhosis and the risk of re-bleeding increases significantly after endoscopic treatment in patients with thrombosis.

MicroRNA-30c suppressed giant-cell tumor of bone cell metastasis and growth via targeting HOXA1.

OBJECTIVE: To dissect the functioning mode of miR-30c on giant cell tumor of bone cell metastasis and growth and provide therapeutic targets for giant cell tumor of bone. PATIENTS AND METHODS: By quantitative Real-time polymerase chain reaction (qRT-PCR), miR-30c expression level in 62 pairs of giant cell tumor of bone cells tissue samples and five breast cancer-derived cell lines. Using miR-30c mimics and inhibitors, we analyzed the effects of miR-30c over-expression and knockdown on cell proliferation, invasion, and migration. Dual-luciferase activity assay was recruited to examine the potential target gene HOXA1, which predicted by several databases. Protein level was studied using Western blot. RESULTS: MiR-30c expressed significantly lower in giant cell tumor of bone tissue samples and cell lines. Over-expression miR-30c in giant cell tumor of bone cells decreased the cell proliferation, invasion, and migration abilities while down-regulation miR-30c in giant cell tumor of bone cells increased these abilities oppositely. Dual-luciferase and Western blot confirmed HOXA1 as a target gene of miR-30c. Furthermore, up-regulation of HOXA1 reserved the suppressive effect of miR-30c over-expression on cell growth and progression. CONCLUSIONS: miR-30c could suppress giant cell tumor of bone cell proliferation and progression via HOXA1, which might provide a new target for giant cell tumor of bone diagnosis and therapy.

[Diagnosis and treatment of traumatic optic neuropathy with internal carotid artery trauma].

Objective: To summarize our experience in the diagnosis of internal carotid artery trauma in patients with traumatic optic neuropathy, and to make recommendations for the treatment. Methods: The clinic data of 6 cases who had traumatic optic neuropathy with internal carotid artery trauma and who were admited in Department of Otorhinolaryngology, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University from Jan. 2013 to Dec. 2015 were analyzed retrospectively. Results: All 6 cases were monocular blindness. Four cases did not undergo nasal endoscopic optic nerve decompression because of the diagnoses of internal carotid artery trauma. One case was diagnosed after nasal endoscopic optic nerve decompression because of fatal bleeding during the operation. One case was diagnosed because of late-onset recurrent epistaxis. Among the 6 cases with internal carotid artery trauma, 3 cases were successfully treated with endovascular interventional treatment (stent embolization was used in one case, Coil embolization was used in two cases), and 3 patients refused treatment. Conclusions: The patients with traumatic optic neuropathy have the possibility of severe carotid artery trauma. Endoscopic optic nerve decompression is not suitable for these cases. It should pay more attention to patients with traumatic optic neuropathy. For suspected cases, vascular-enhanced computed tomography screening and digital subtraction angiography should be recommended and patients should be treated by endovascular intervention in a timely manner.

The route of incorporation of nitrogen atom into rifamycin during its biosynthesis.

In this paper, it was first shown that under various conditions of nitrogen supply the rifamycin yield was positively correlated with the mycelial specific activity of glutamine synthetase (GS), then the enhancing effect of glutamine, the product of GS, on rifamycin biosynthesis was demonstrated with resting cell system. The stimulatory effect of glutamine was more pronounced than that of glutamate, and not reduced by a GS specific inhibitor, DON. However, the increase in yield brought about by glutamate, and by asparagine was strongly inhibited by this inhibitor. Glutamine-CO15NH2 amd glutamate-alpha-15NH2 were synthesized and compared for the incorporation of 15N into rifamycin. It was found that the amide nitrogen was incorporated to a much greater extent than the alpha-amino nitrogen, showing that glutamine was a direct precursor of the nitrogen atom in rifamycin. In addition, synthesis of A-32 (C7N), an intermediate secreted by an inactive mutant rif 1, was also greatly stimulated by glutamine, and the synthetic C7N was found to be able to stimulate the biosynthesis of rifamycin. Based upon the above results, the route of incorporation of nitrogen atom into rifamycin is summarized as follows: (Formula: see text).

Studies of donors who transmit posttransfusion hepatitis.

Sera and questionnaires were evaluated retrospectively from 128 volunteer blood donors whose blood had been implicated in cases of clinically recognized post-transfusion hepatitis in recipients of one- or two-unit blood transfusion between 1971 and 1977. Serologic markers of hepatitis B virus (HBV) infection were found in 23 percent, compared to 9.7 percent of 3,230 prospective blood donors. The prevalence of antibody to hepatitis A virus was similar among implicated donors (44%), prospective donors (58%), and among those implicated donors with (41%) and without (44%) HBV markers. Among implicated donors, none had a history at the time of donation of having had clinically recognizable hepatitis, 93 percent had no history of prior blood transfusion, and 80 percent had normal hepatic enzymes. Data from this study confirm that non-A, non-B hepatitis has been a common form of posttransfusion hepatitis in recent years, since 77 percent of these implicated donors had no HBV serologic markers. In addition, these donors could not be distinguished by age, race, sex, history of clinical hepatitis or of prior blood transfusion, or in most cases by hepatic enzyme levels.

The solid phase radioimmunoassay technique for hepatitis B (surface) antigen: effects of progressive modification.

Serum specimens submitted for confirmation of hepatitis B antigen (HBsAg) reactivity were tested by counterelectrophoresis (CEP) and by three modifications of the solid phase radioimmunoassay "sandwich" technique (SPRIA). In addition, the specificity of each reaction was determined for two of the SPRIA test methods. One hundred seventy-five of the 688 specimens were reactive by all techniques and a further 60 ere specifically reactive by two of modifications of SPRIA. An additional five specimens were positive by a third SPRIA modification. The primary SPRIA technique, using a homologous guinea pig antibody sandwich, detected 184 nonspecific reactive samples. With the same test done at 45C with a reduced incubation time, there were only 37 nonspecific reactive samples. None of the nonspecific samples was detected when the SPRIA technique used a heterologous guinea pig-human antibody sandwich. The results provide a basis for estimating the effectiveness of the SPRIA technique for HBsAg testing.

Hepatitis B (surface) antigen testing by radioimmunoassaymexperience in a very large volunteer donor population.

The results of hepatitis B surface antigen (HBs-Ag) testing in a large volunteer blood donor population are described. Counterelectrophoresis and three versions of solid-phase radioimmunoassay technic are compared and evaluated. Initial results suggested that the radioimmunoassay technic are compared and evaluated. Initial results suggested that the radioimmunoassay technic detected more than five times as many reactive donors as did counterelectrophoresis. The specificity of the radioimmunoassay technic has been increased by successive modifications, and recent results show that the technic detects 73 percent more reactive donors than does counterelectrophoresis. Not all of these reactions are specific, and it is estimated that the true gain in detection of HBsAg carriers is 49 percent of the value found by counterelectroesis. The incidence of HBsAg carriers in the America Red Cross donor population is about 1.25 per 1,000.

American National Red Cross experience with hepatitis-B antibody (HBAb or anti-HBAg) testing.

Blood collected by 11 Red Cross Regional Blood Centers were screened by the method of agar gel diffusion (AGD) for the presence of hepatitis-B antibody. Of the 185,134 units tested, 114 were found to be positive for HBAb by the Regional Centers and were forwarded to National Special Projects Laboratory for confirmation. Only five out of 114 samples revealed lines of identity with a control anti-HBAg when reacted with a pool of plasma positive for hepatitis-B antigen that was different from that which was provided to the Centers. Apparently, the precipitation reactions observed by the Centers were largely due to the antithrombin antibodies in the donors' sera reacting with the residual thrombin used by the manufacturer to convert HBAg positive plasma to serum. We conclude that the incidence of hepatitis-B antibody as measured by agar gel diffusion in the Red Cross Blood donor population was extremely low.