ObjectiveTo investigate the diagnosis and operative procedure for spontaneous perforation of congenital choledochal cyst in children. MethodsThe clinical data of 16 cases with spontaneous perforation of congenital choledochal cyst were analysed retrospectively.ResultsAll cases were under 4 years old with a mean age of 23 months. Abdominal distension, pain, vomiting, fever and diffuse tenderness were present in all patients. The preoperative diagnosis was established by paracentesis in ten patients. Abdominal sonography and CT found a cyst in 5 of the 10 cases reviewed. In 11 cases (68.7%), the site of perforation was found on the confluence of common bile duct and gallbladder cystic duct. T-tube drainage was used as a transition measure. All patients recovered uneventfully. Radical resection was performed in about three months after the initial operation. ConclusionsThe obstruction of the bile duct and poor blood supply to the choledochal cyst are major causes leading to perforation. Routine abdominal paracentesis should be carried out for a small child with peritonitis and general abdominal tenderness, especially on the right upper quadrant.T-tube drainage should be adopted as an emergent procedure to tide the patient over the crisis followed by elective choledochal cyst resection and bile duct reconstruction.

Objective To provide an optimal working process for crossmatching by full-automatic blood typing instrument.Methods Two workflows were applied to crossmatch test by full-automatic blood typing instrument.One was diluting red blood cells of donor samples to concentrate of 1%,the other was detecting directly the donor′s packed red blood cells.Compared consistency and processing time of the two different workflows.Results Cross match results of two workflows were consistent well(U=0,P>0.05).The average processing times before testing and undergoing testing were not significantly different(t=0.692,t=0.562,P>0.05),whereas the average processing times after testing and throughout testing were significantly different(t=146.485,t=67.053,P<0.05).Conclusion The workflow of diluting donor′s sample before testing saved processing time and better suits hospital having a large quantity of specimens.

Objective To establish a method for the dissolution determination of ambroxol hydrochloride orally disinegreting tablets. Methods The UV spectrophotometry was used. The detecting wavelength was at 244 nm. The liquid of dissolution was hydrochloride(0.1 mol·L -1). Rotational speed was 50 r·min-1. Results The linearity range was 3.16-28.44 μg·mL-1.The regression equation was Y＝0.024 2X+0.018 3(r＝0.999 3).The RSD of repeatable test was 0.28%.The average recovery of methodology was 100.4% and RSD was 0.77%. Conclusion The method is simple and reliable, and can be used for the dissolution determination of ambroxol hydrochloride orally disinegreting tablets.

Child ; Colon ; abnormalities ; surgery ; Humans ; Male ; Treatment Outcome ; Urethra ; abnormalities ; Urinary Bladder ; abnormalities

As one of the most common malignant tumors, lung cancer poses a serious threat to human life and health. The platinum-based drug cisplatin (DDP) is used as the first-line treatment for lung cancer. The poor prognosis of lung cancer is mostly due to developed resistance to cisplatin, which poses a serious treatment challenge. The mechanism of cisplatin resistance is complex and unclear. Numerous studies have shown that DNA methylation plays a crucial role in the emergence of lung cancer cisplatin resistance. DNA hypermethylation results in the deactivation of numerous drug resistance genes and tumor suppressor genes through a change in chromatin conformation. Finding new therapeutic targets and indicators to predict the therapeutic effect can be aided by elucidating the complex mechanism. In order to discover novel strategies to overcome cisplatin resistance in lung cancer, this paper discusses DNA methylation-mediated cisplatin resistance and offers an overview of current demethylation procedures.
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Humans ; Antineoplastic Agents/therapeutic use* ; Cell Line, Tumor ; Cisplatin/therapeutic use* ; DNA Methylation ; Drug Resistance, Neoplasm/genetics* ; Gene Expression Regulation, Neoplastic ; Lung Neoplasms/pathology*

Colorectal cancer (CRC) is one of the leading causes of death worldwide. Thus, the development of new therapeutic targets for CRC treatment is urgently needed. SGK1 is involved in various cellular activities, and its dysregulation can result in multiple cancers. However, little is known about its roles and associated molecular mechanisms in CRC. In present study, we found that SGK1 was highly expressed in tumor tissues compared with peri-tumor samples from CRC patients. In vitro experiments revealed that SGK1 overexpression promoted colonic tumor cell proliferation and migration and inhibited cell apoptosis induced by 5-fluorouracil (5-FU), while SGK1 shRNA and inhibitors showed the inverse effects. Using CRC xenograft mice models, we demonstrated that knockdown or therapeutic inhibition of SGK1 repressed tumor cell proliferation and tumor growth. Moreover, SGK1 inhibitors increased p27 expression and promoted p27 nuclear accumulation in colorectal cancer cells, and p27 siRNAs could attenuate the repression of CRC cell proliferation induced by SGK1 inhibitors. Collectively, SGK1 promotes colorectal cancer development via regulation of CRC cell proliferation, migration and survival. Inhibition of SGK1 represents a novel strategy for the treatment of CRC.
Animals ; Apoptosis ; Cause of Death ; Cell Proliferation ; Colon ; Colorectal Neoplasms* ; Fluorouracil ; Heterografts ; Humans ; In Vitro Techniques ; Mice ; Repression, Psychology ; RNA, Small Interfering