Retrospective analysis of the changes in the surgical treatment of benign prostatic hyperplasia during an 11-year period: a single-center experience / 亚洲男科学杂志(英文版)

The present study aimed to determine whether the number of patients with symptomatic benign prostatic hyperplasia (BPH) who preferred surgery decreased during the past 11 years at our center (West China Hospital, Chengdu, China), and whether this change affected the timing of surgery and the physical condition of surgical patients. This retrospective study included 57 557 patients with BPH treated from January 2008 to December 2018. Of these, 5427 patients were treated surgically. Surgical patients were divided into two groups based on the time of treatment (groups 8-13 and groups 13-18). The collected data comprised the percentage of all patients with BPH who underwent surgery, baseline characteristics of surgical patients, rehabilitation time, adverse events, and hospitalization costs. The surgery rates in groups 8-13 and groups 13-18 were 10.5% and 8.5% (P < 0.001), respectively. The two groups did not clinically differ regarding patient age and prostate volume. The rates of acute urinary retention and renal failure decreased from 15.0% to 10.6% (P < 0.001) and from 5.2% to 3.1% (P < 0.001), respectively. In groups 8-13 and groups 13-18, the mean catheterization times were 4.0 ± 1.7 days and 3.3 ± 1.6 days (P < 0.001), respectively, and the mean postoperative hospitalization times were 5.1 ± 2.4 days and 4.2 ± 1.8 days (P < 0.001), respectively. The incidences of unplanned second surgery and death reduced during the study period. The surgery rate decreased over time, which suggests that medication was chosen over surgery. However, the percentage of late complications of BPH also decreased over time, which indicates that the timing of surgery was not delayed.

Pathogenesis of liver fibrosis in patients with chronic hepatitis B / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To explore the role of sinusoidal endothelial cell in the development of liver fibrosis, and to dissect the relationship among hepatic microcirculation disorders, hepatic sinusoidal capilarization and liver fibrosis.</p><p><b>METHODS</b>Liver biopsy was performed in fifty-six patients with chronic hepatitis B. The liver tissues were observed under light microscope and transmitted electronic microscope.</p><p><b>RESULTS</b>Of 56 cases, 39 cases were mild hepatitis, 10 were moderate hepatitis, and 7 were severe hepatitis. The morphology of hepatic stellate cells (HSCs) was similar to that of fibroblasts in the tissues of the patients with chronic hepatitis B. Collagenous fibers were deposited around the hepatic stellate cells. Electron-dense materials were deposited between sinusoidal endothelial cell and hepatic stellate cell. The size and amount of fenestraes of sinusoidal endothelial cells were reduced in 53 of 56 cases. The consecutive or inconsecutive membrane-like materials were observed along sinusoidal endothelial cells in 20 cases. Collagen fibers were observed in the space of Disse in 15 cases. Even in the patients with normal hepatic functions, red blood cells aggregation and microthrombi could be observed in the liver tissues.</p><p><b>CONCLUSION</b>Sinusoidal endothelial cells are involved in development of liver fibrosis by interacting with hepatic stellate cells. Hepatic microcirculation disorders and sinusoidal capillarization are important changes in the early stage of liver fibrosis.</p>

Produce of marker-free transgenic tobacco plants by FLP/frt recombination system / 生物工程学报

Selectable marker genes that usually encode antibiotic or herbicide resistances are widely used for the selection of the transgenic plants, but they become unnecessary and undesirable after transformation selection. An important strategy to improve the transgenic plants' biosafety is to eliminate the marker genes after successful selection. In the FLP/frt site-specific system of the 2 microm plasmid of Saccharomyces cerevisiae, the FLP enzyme efficiently catalyzes recombination between two directly repeated FLP recombination target (frt) sites, eliminating the sequence between them. By controlled expression of the FLP recombinase and specific allocation of the frt sites within transgenic constructs, the system can be applied to eliminate the marker genes after selection. Through a series of procedures, the plant FLP/frt site-specific recombination system was constructed, which included the frt containing vector pCAMBIA1300-betA-frt-als-frt and the FLP expression vector pCAMBIA1300-hsp-FLP-hpt. The FLP recombinase gene was introduced into transgenic (betA-frt-als-frt) tobacco plants by re-transformation. In re-transgenic plants, after heat shock treatment, the marker gene als flanked by two identical orientation frt sites could be excised by the inducible expression of FLP recombinase under the control of hsp promoter. Excision of the als gene was found in 41% re-transgenic tobacco plants, which indicated that this systerm could make a great contribution to obtain the marker free transgenic plants.

Progress of research on non-small cell lung cancer stem cell / 北京大学学报(医学版)

Non-small cell lung cancer(NSCLC)is now regarded as the most common cause of cancer-related mortality in China.Despite continuous efforts to improve the therapeutic response,the overall five-year survival rate for NSCLC is still less than 15%.Now we have known that the growth of neoplastic tumors is maintained exclusively by a small subpopulation called "cancer stem cells" which posseses ability of self-renew and differentiation.It has been widely accepted that cancer stem cells are chemoresistant and radioresistant.Therefore,a major challenge in treating this and other cancers is the intrinsic resistance to conventional therapies demonstrated by the stem/progenitor cell that is responsible for the sustained growth,survival,and invasion of the tumor.Identifying these stem cells in non-small cell lung cancer and defining the biologic processes necessary for their existence are paramount in developing new clinical approaches with the goal of preventing disease recurrence.This review summarizes our update understandings of the cellular and molecular mechanisms operating within the putative cancer-initiating cells at the core of non-small cell lung cancer.