ABSTRACT
BACKGROUND@#Gastric cancer (GC) is one of the most globally prevalent cancers in the world. The pathogenesis of GC has not been fully elucidated, and there still lacks effective targeted therapeutics. The influence of altered kinesin superfamily protein 22 (KIF22) expression in GC progression is still unclearly. The aim of this study was to investigate the KIF22 effects on GC and related mechanisms.@*METHODS@#Gastric carcinoma tissues and matching non-cancerous tissues were collected from patients with GC who have accepted a radical gastrectomy in Lanzhou University Second Hospital from May 2013 to December 2014. The expression of KIF22 was examined in GC of 67 patients and 20 para-carcinoma tissues by immunochemical staining. The relationship between the expression of KIF22 and clinicopathologic characteristics was next investigated in the remaining 52 patients except for 15 patients who did not complete follow-up for 5 years. Cell viability was performed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) test and colony formation assay in the MGC-803 and BGC-823 GC cells. Cell scratch and trans-well invasion assay was performed to assess migration ability in the MGC-803 and BGC-823 GC cells. Gene set enrichment analysis (GSEA) pathway enrichment analysis was performed to explore the potential functions. Cell cycle was detected by flow cytometry. In addition, the two GC cell lines were used to elucidate the underlying mechanism of KIF22 in GC in vitro via assessing the effects on mitogen-activated protein kinase and extracellular regulated protein kinases (MAPK/ERK) signal transduction pathway-related expressions by Western blotting assays. The differences were compared by t tests, one-way analysis of variance, and Chi-squared tests.@*RESULTS@#The study showed that KIF22 was up-regulated in GC, and KIF22 high expression was significantly related to differentiation degree (χ = 12.842, P = 0.002) and poorly overall survivals. GSEA pathway enrichment analysis showed that KIF22 was correlated with the cell cycle. Silence of KIF22 decreased the ability of the proliferation and migration in gastric cells, induced G1/S phase cell cycle arrest via regulating the MAPK-ERK pathways.@*CONCLUSIONS@#KIF22 protein level was negatively correlated with prognosis. KIF22 knockdown might inhibit proliferation and metastasis of GC cells via the MAPK-ERK signaling pathway.
ABSTRACT
Small intestinal hemangioma is a rare condition that can be divided histologically into capillary, cavernous or mixed types, among which the cavernous type is the most common. Here we report a case of small intestinal cavernous hemangioma with chronic hemorrhage in 44-year-old man. The patient complained of weakness and dizziness for 2 years that aggravated 1 month before admission accompanied by intermittent melena. Laboratory tests suggest severe anemia, and computed tomography, gastroscopy and colonoscopy all revealed signs of anemia. Capsule endoscopy detected small intestinal erosions, bleeding lesions and prominent neoplasms. An exploratory laparotomy was performed, in which the segment of the jejunum with lesions was resected. Pathological examination of the resected jejunum identified the neoplasm as cavernous hemangioma of the small intestine, which was the cause of severe anemia.
ABSTRACT
<p><b>OBJECTIVE</b>The aim of this study was designed to evaluate the outcomes of liver transplant recipients with chronic hepatitis B (CHB) receiving either lamivudine monotherapy or lamivudine combined with individualized low-dose hepatitis B immunoglobulin (HBIG) therapy.</p><p><b>METHODS</b>A total of 111 liver transplant recipients with CHB were divided not randomly into two groups according to the availability of HBIG before liver transplantation (LT). Thirty-two patients received lamivudine monotherapy (100 mg/d) and 79 patients received lamivudine (100 mg/d) combined with individualized low-dose HBIG (intramuscular administration) to maintain the titer of antibody to hepatitis B virus (HBV) surface antigen (anti-HBs) not less than 100 U/L. The patients were followed-up for a median time of 32 months (1 to 88 months).</p><p><b>RESULTS</b>In the lamivudine monotherapy group, 5 patients hepatitis B relapsed (3/5 developed YMDD mutants of HBV), with 1-, 2-, and 3-year cumulative recurrence rates of 7.1%, 14.3% and 17.9% and survival rates of 87.5%, 84.4% and 74.6%. In the lamivudine and HBIG combination therapy group, 2 patients hepatitis B relapsed (2/2 developed YMDD mutants of HBV), with 1-, 2-, and 3-year cumulative recurrence rates of 0, 1.8% and 5.7% (P < 0.01) and survival rates of 83.5%, 80.9% and 77.6% (P > 0.05).</p><p><b>CONCLUSIONS</b>Compared with lamivudine monotherapy, lamivudine combined with individualized low-dose HBIG can further reduce the recurrence risk of hepatitis B in liver transplant recipients. This combined therapy could be used as a rational strategy for prophylaxis of hepatitis B recurrence in such patients.</p>