Acute esophageal obstruction caused by reverse migration of gastric bezoars: A case report.

BACKGROUND: Bezoars can be found anywhere in the gastrointestinal tract. Esophageal bezoars are rare. Esophageal bezoars are classified as either primary or secondary. It is rarely reported that secondary esophageal bezoars caused by reverse migration from the stomach lead to acute esophageal obstruction. Guidelines recommend urgent upper endoscopy (within 24 h) for these impactions without complete esophageal obstruction and emergency endoscopy (within 6 h) for those with complete esophageal obstruction. Gastroscopy is regarded as the mainstay for the diagnosis and treatment of esophageal bezoars. CASE SUMMARY: A 59-year-old man was hospitalized due to nausea, vomiting and diarrhea for 2 d and sudden retrosternal pain and dysphagia for 10 h. He had a history of type 2 diabetes mellitus for 9 years. Computed tomography revealed dilated lower esophagus, thickening of the esophageal wall, a mass-like lesion with a flocculent high-density shadow and gas bubbles in the esophageal lumen. On gastroscopy, immovable brown bezoars were found in the lower esophagus, which led to esophageal obstruction. Endoscopic fragmentation was successful, and there were no complications. The symptoms of retrosternal pain and dysphagia disappeared after treatment. Mucosal superficial ulcers were observed in the lower esophagus. Multiple biopsy specimens from the lower esophagus revealed nonspecific findings. The patient remained asymptomatic, and follow-up gastroscopy 1 wk after endoscopic fragmentation showed no evidence of bezoars in the esophagus or the stomach. CONCLUSION: Acute esophageal obstruction caused by bezoars reversed migration from the stomach is rare. Endoscopic fragmentation is safe, effective and minimally invasive and should be considered as the first-line therapeutic modality.

The -250G/A and -514C/T Polymorphisms in Hepatic Lipase Gene Promoter Confers an Increased Risk of Hepatocellular Carcinoma in a Chinese Population.

INTRODUCTION AND AIM: Hepatocellular carcinoma (HCC) is a lethal malignancy, but the molecular mechanisms of hepatocarcinogenesis remain undefined. The present study aims to investigate the relationship between polymorphisms of the hepatic lipase (HL) gene promoters and risk of HCC. MATERIAL AND METHODS: Totally, 279 HCC patients and 200 healthy individuals were enrolled. Polymerase chain reaction-restriction fragment length polymorphisms (PCR-RFLP) was used to analyze the genotypes of HL gene. Logistic regression analysis was conducted to identify risk factors of HCC. RESULTS: There was significant difference in the distribution of smoking history, drinking history, and family history of subjects between the case and control groups (all p < 0.05). Difference in the -250G/A (p = 0.011; OR = 1.61; 95%CI: 1.11-2.34) and -514C/T (p = 0.007; OR = 1.65; 95%CI: 1.14-2.38) genotypes and allele frequencies between two groups was significant. A higher risk of HCC was identified in those with polymorphisms in the - 250G/A (p = 0.007; OR = 1.45; 95%CI: 1.11-1.89) and -514C/T (p = 0.003; OR = 1.51; 95%CI: 1.15-2.00). Polymorphisms at - 250G/A (GA + AA) (p = 0.025; OR = 1.55; 95%CI: 1.06-2.28), -514C/T (CT + TT) (p = 0.021; OR = 1.57; 95%CI: 1.07-2.29), smoking history (p = 0.017; OR = 1.70; 95%CI: 1.10-2.63) and drinking history (p = 0.003; OR = 2.04; 95%CI: 1.27-3.27) were significantly related to the risk of HCC (all p < 0.05). CONCLUSION: The results obtained from this study indicated that polymorphisms of -250G/A and -514C/T in HL gene promoters were associated with the risk of HCC.

[Expression and Significance of PD-L1, HSP90 and HSP90α in Serum of Patients with Acute Leukemia].

OBJECTIVE: To explore the expression and clinical significance of PD-L1, heat shock protein 90 (HSP90) and HSP90α in the serum of patients with acute leukemia (AL) of different types and disease stages. METHODS: A total of 84 AL patients from January 2013 to October 2016 in our hospital and 20 healthy persons as controls were selected. All the samples of serum or bone marrow were separated. The protein expression levels of serum HSP90, HSP90α were detected by ELISA. The flow cytometry was used to detect PD-L1 expression. The relationship of the expression level of PD-L1, HSP 90, and HSP90α with clinical outcome was analyzed. RESULTS: The expression levels of serum HSP90, HSP90α and PD-L1 positive rate in AL patients were significantly higher those that in control group (P<0.05), the expression levels of serum HSP90, HSP90α and PD-L1 positive rate of Al patients in remission were lower than those in newly diagnosed patients (P<0.05). The expression level of HSP90, HSP90α and PD-L1 positive rate in the relapsed AL patients were higher than those in newly diagnosed AL patients and patients in remission (P<0.05). There was no significant difference of HSP90 protein level and PD-L1 positive rate between newly diagnosed AML patients and ALL patients(P>0.05). HSP90α level of newly diagnosed AML patients was lower than that in newly diagnosed ALL (P<0.05). HSP90α and HSP90 levels and PD-L1 positive rate in no remission patients were significantly higher than those in complete remission patients (P<0.05). The HSP90α level in patients without recurrence decreased during chemotherapy. The HSP90α protein level was the lowest after the hematopoietic stem cell transplantation, but increased after relapse. CONCLUSION: The PD-L1,HSP90 and HSP90α play an important role in the developmental process of acute leukemia, which can be used as reference indications to assess clinical efficacy and prognosis.

Role of osteopontin in the regulation of human bladder cancer proliferation and migration in T24 cells.

Osteopontin (OPN), a secreted acid glycoprotein with a variety of functions, promotes tumor proliferation, differentiation, invasion and metastasis. The aim of the current study was to investigate whether OPN may serve as a potential therapeutic target for human bladder cancer. RNA interference (RNAi) was performed to downregulate the expression of the OPN gene in T24 human bladder cancer cells. The mRNA and protein expression levels of OPN following RNAi were determined using reverse transcription­quantitative polymerase chain reaction and western blot analysis, respectively. In addition, the cell cycle progression, apoptosis and proliferation were investigated using by flow cytometric analysis and MTT assay. The cell invasion ability was measured using a Matrigel transwell assay. The mRNA and protein expression levels of OPN were found to be significantly downregulated following RNAi. The proliferation and invasion of T24 cells were significantly inhibited in vitro. In conclusion, RNAi­targeting OPN may inhibit the proliferation, invasion and tumorigenicity of human bladder cancer cells. Therefore, OPN may serve as a potential therapeutic target for human bladder cancer.

Lipopolysaccharide (LPS) induces the apoptosis and inhibits osteoblast differentiation through JNK pathway in MC3T3-E1 cells.

Bone degradation is a serious complication of chronic inflammatory diseases such as septic arthritis, osteomyelitis, and infected orthopedic implant failure. Up to date, effective therapeutic treatments for bacteria-caused bone destruction are limited. In our previous study, we found that LPS promoted osteoclast differentiation and activity through activation of mitogen-activated protein kinases (MAPKs) pathway such as c-Jun N-terminal kinases (JNK) and extracellular signal regulated kinase (ERK1/2). The current study was to evaluate the mechanism of LPS on the apoptosis and osteoblast differentiation in MC3T3-E1 cells. MC3T3-E1 osteoblasts were non-treated, treated with LPS. After treatment, the cell viability, the activity of alkaline phosphatase (ALP) and caspase-3 were measured. The expressions of osteoblast-specific genes and Bax, Bcl-2, and caspase-3 were determined by real-time quantitative polymerase chain reaction (qPCR). Protein levels of Bax, Bcl-2, caspase-3, and phosphorylation of MAPKs were measured using Western blotting assays. The MAPK signaling pathway was blocked by pretreatment with JNK inhibitor SP600125. LPS treatment induced a significant decrease in cell metabolism, viability, and ALP activity in MC3T3-E1 cells. LPS also significantly decreased mRNA expressions of osteoblast-related genes in MC3T3-E1 cells. On the other hand, LPS significantly upregulated mRNA expressions and protein levels of Bax and caspase-3 as well as activation of caspase-3, whereas decreased Bcl-2 expression in MC3T3-E1 cells. Furthermore, LPS significantly promoted MAPK pathway including the phosphorylation of JNK and the phosphorylation of ERK1/2; moreover, pretreatment with JNK inhibitor not only attenuated both of phosphorylation-JNK and ERK1/2 enhanced by LPS in MC3T3-E1 cells, but also reversed the downregulated expressions of osteoblast-specific genes including ALP and BSP induced by LPS. In conclusion, LPS could induce osteoblast apoptosis and inhibit osteoblast differentiation via activation of JNK pathway.

The effect of imatinib therapy on the outcome of allogeneic stem cell transplantation in adults with Philadelphia chromosome-positive acute lymphoblastic leukemia.

OBJECTIVE: To evaluate the efficacy of imatinib administration before and/or after allogeneic hematopoietic stem cell transplantation (allo-HSCT) for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). METHOD: Patients with imatinib therapy time exceeding 30 days pre-/post-transplant were screened in our data. Imatinib was used in induced or consolidated chemotherapy pre-transplant, or maintenance therapy after 60 days post-transplant (therapy time was less than 180 days) regardless of the molecular status of the disease. RESULTS: Sixty-nine patients with Ph+ ALL were enrolled in the retrospective analysis. Forty-four patients received imatinib therapy, including 24 pre-transplant, 9 post-transplant, and 11 both pre- and post-transplant. With a median follow-up time of 395 days (range, 55-2762 days) post-transplant, 3-year estimated overall survival was 62.3 ± 16.6, 40.0 ± 21.9, 41.7 ± 22.2, and 25.9 ± 11.4%, respectively (P = 0.221), and disease-free survival (DFS) was 53.6 ± 17.9, 20.0 ± 17.9, 33.3 ± 25.5% and 23.6 ± 11.4%, respectively (P = 0.421), in patients with imatinib therapy pre-transplant, post-transplant, both pre- and post-transplant, neither pre- nor post-transplant. The incidence of relapse at 3 year for patients with imatinib therapy post-transplant (n = 20) was 63.6%, comparing with 24.2% (P = 0.018) in patients without imatinib therapy post-transplant (n = 49). The ratio of CD4+CD25+Foxp3+ cells in blood was significantly higher at 30 and 60 days after imatinib therapy than that at the time of pre-imatinib in 20 patients (P = 0.019 and 0.001, respectively). CONCLUSIONS: Application of imatinib pre-transplant might have benefited for patients with Ph+ ALL. Whether administration of imatinib, regardless of the molecular status of the disease post-transplant increases relapse, is a worthy goal for further study.

[Shaping ability of two nickel-titanium rotary systems in simulated S-shaped canals].

OBJECTIVE: To evaluate the shaping ability of two nickel-titanium rotary systems (ProTaper and Hero642) in simulated S-shaped canals. METHODS: Thirty simulated S-shaped canals were randomly divided into three groups and prepared by ProTaper, Hero642, ProTaper combined with Hero642 respectively. All the canals were scanned before and after instrumentation, and the amount of material removed in the inner and outer wall and the canal width after instrumentation were measured with a computer image analysis program. RESULTS: There was significant difference in the amount of material removed at the inner side of apical curvature and outer side of apex between ProTaper combined with Hero642 and ProTaper files (P < 0.05) at the same tip size. The inner and outer wall of the canals were evenly prepared by ProTaper combined with Hero642, and the taper of canals were better than those prepared by Hero642. CONCLUSIONS: ProTaper combined with Hero 642 had better shaping ability to maintain the original shape and could create good taper canals in the simulated S-shaped canal model.

[Expression of cyclooxygenase-2 and urokinase plasminogen activator in gastric carcinoma and the clinical significance thereof].

OBJECTIVE: To investigate expression of cyclooxygenase-2 (COX-2) and urokinase plasminogen activator (uPA) in gastric carcinoma and the clinical significance thereof. METHODS: Strepavidin-peroxidase method was used to detect the expression of COX-2 and uPA in 192 specimens of gastric carcinoma, 56 specimens of paracancer tissues obtained during operation. Immunohistochemical double staining was used to detect the microvessel density (MVD) and microlymphatic density (MLD). Thirty specimens of normal gastric mucosa obtained during gastroscopy were used as controls. RESULTS: The positive rates of COX-2 in the gastric carcinoma and paracancer tissues were 67.7% and 62.5% respectively, both significantly higher than that of the control group (40.0%, both P < 0.05). The positive expression of COX-2 in gastric carcinoma was significantly related with the depth of invasion and MVD (both P < 0.05). The positive rates of uPA in the gastric carcinoma, paracancer tissue were 78.1% and 44.6% respectively, both significantly higher than that of the control tissues (6.7%, both P < 0.01) and there was a significant difference in the positive rates of uPA between the first 2 groups too (P < 0.01). The positive expression of uPA in gastric carcinoma was significantly related with lymph node metastasis, depth of invasion, Lauren typing, differentiation, MVD, and MLD (P < 0.05, P < 0.01). COX-2 expression was positively linked with uPA expression (r = 0.167, P = 0.021). The survival time of the uPA positive group was (38 +/- 4) months, significantly shorter than that of the negative group [(54 +/- 6) months, P < 0.05]. The survival time of the group positive in both COX-2 and uPA was (27 +/- 3) months, significantly shorter than that of the single positive or double negative groups [both (58 +/- 4) months, both P < 0.01). CONCLUSION: COX-2 and uPA are highly expressed in gastric carcinoma. COX-2 expression is positively linked with uPA expression. COX-2 and uPA in the gastric carcinoma participate in the development of gastric cancer in the early process. uPA is significantly related with the survival time.