Removal of a large foreign body in the rectosigmoid colon by colonoscopy using gastrolith forceps.

Rectal foreign bodies are man-made injury that occurs occasionally. The management depends on its depth and the consequence it caused. We here report a case of rectal foreign body (a glass bottle measuring about 38 mm × 75 mm) which was located 13-15 cm from the anus. The patient had no sign of perforation, and we managed to remove it using endoscopy with gastrolith forceps.

Upregulation of PREX2 promotes the proliferation and migration of hepatocellular carcinoma cells via PTEN-AKT signaling.

Phosphatidylinositol-3,4,5-trisphosphate Rac exchanger 2 (PREX2), a regulator of the small guanosine triphosphatase Rac, demonstrates an inhibitory effect on the activity of phosphatase and tensin homolog (PTEN). Previously, PREX2 was implicated in the regulation of cell invasion in hepatocellular carcinoma (HCC). However, the exact role of PREX2 in the regulation of HCC cell proliferation and migration, as well as the underlying mechanisms, remains unclear. In the present study, reverse transcription-quantitative polymerase chain reaction revealed that PREX2 was upregulated in HCC tissue compared with matched adjacent non-tumorous tissue. In addition, the present study demonstrated that the messenger RNA and protein levels of PREX2 increased in human HCC HepG2, LH86, LMH and PLHC-1 cell lines compared with normal human liver THLE-3 cells. Overexpression of PREX2 significantly enhanced the proliferation and migration of HCC cells, and knockdown of PREX2 expression significantly suppressed the proliferation and migration of HCC cells. Additional investigation revealed that overexpression of PREX2 suppressed the activity of PTEN, leading to an enhancement in the activity of protein kinase B (AKT). By contrast, knockdown of PREX2 expression upregulated the activity of PTEN and suppressed the activity of AKT. Overall, the present study suggests that PREX2 promotes the proliferation and migration of HCC cells by inhibiting PTEN-AKT signaling.

Lower gastrointestinal tract bleeding caused by dieulafoy-like lesion synchronous meckel diverticulum: A rare case report.

Meckel diverticulum is an embryonic remnant of the Gastrointestinal duct which causes symptoms < 5% in the 2% population. Painless bleeding and abdominal pain are the most often reported symptoms. Dieulafoy lesion/dieulafoy-like lesion often cause upper gastrointestinal (GI) tract bleeding, but massive lower gastrointestinal bleeding is rare. We reported a 19-year-old male presented massive lower GI tract bleeding caused by Meckel diverticulum synchronous dieulafoy-like lesion.

Unsedation colonoscopy can be not that painful: Evaluation of the effect of "Lamaze method of colonoscopy".

AIM: To evaluate the pain relieving effect of intervention with "Lamaze method of colonoscopy" in the process of colonoscopy. METHODS: Five hundred and eighty-five patients underwent colonoscopy were randomly divided into three groups, Lamaze group, anesthetic group and control group. Two hundred and twenty-four patients of Lamaze group, the "Lamaze method of colonoscopy" were practiced in the process of colonoscopy. The Lamaze method of colonoscopy is modified from the Lamaze method of childbirth, which helped patients to relieve pain through effective breathing control. One hundred and seventy-eight patients in anesthetic group accepted sedation colonoscopy. For 183 patients in control group, colonoscopy was performed without any intervention. The satisfactory of colon cleaning, intestinal lesions, intubation time, success ratio, pain grading and complications were recorded. All data were statistically analyzed. RESULTS: There were no significant differences at base line of the three groups (P > 0.05). Anesthetic group shows advantage in intubation time than the other two groups (P < 0.05). Lamaze group shows no advantage in intubation time than that in control group (P > 0.05). The anesthetic group showed an apparent advantage in relieving pain (P < 0.01). Therefore, the "Lamaze method of colonoscopy" performed in colonoscopy could relieve pain effectively comparing with control group (P < 0.05). The patients in anesthetic group had the highest incidence of complications (P < 0.05). CONCLUSION: The performance of the "Lamaze method of colonoscopy" in the process of colonoscopy could relieve patients' pain, minimize the incidence of complications, and is worthy promotion in clinical practice.

Shenfu Injection suppresses inflammation by targeting haptoglobin and pentraxin 3 in rats with chronic ischemic heart failure.

OBJECTIVE: To investigate the regulatory effects of Shenfu Injection (SFI, ) on hemodynamic parameters and serum proteins in rats with post-infarction chronic heart failure (CHF). METHODS: Forty-five healthy Wistar rats were randomized into three groups: sham, heart failure (model) and SFI group. The CHF was induced by left coronary artery ligation. Seven days after the surgical operation, animals in the sham group and the model group received saline (6.2 mL/kg/d), while animals in the SFI group received SFI (6.2 mL/kg d) intraperitoneally. Four weeks later, cardiac hemodynamic parameters were measured via the carotid route. The expression of serum proteins was analyzed by two-dimensional electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometer (MALDI-TOF MS). RESULTS: Recording of hemodynamic parameters showed that left ventricular systolic pressure (LVSP), maximum rate of left ventricular pressure (+dp/dtmax) rise, and maximum rate of left ventricular pressure (-dp/dtmax) decrease, while the left ventricular end diastolic pressure (LVEDP) rose in the model group compared to those in the sham group (P <0.05). The results of the MALDI-TOF MS indicated that haptoglobin (HP), pentraxin 3 (PTX3) and alpha-1-antitrypsin were up-regulated, while serum albumin and 40S ribosomal protein were down-regulated in the model group (P <0.05). Compared with the model group, LVSP, +dp/dtmax and -dp/dtmax were higher, while LVEDP was lower in the SFI group (P<0.05). Expression levels of HP and PTX3 were lower than in the model group (P<0.05). CONCLUSION: SFI could improve hemodynamic function and decrease inflammatory reactions in the pathophysiology of CHF. The serum proteins HP and PTX3 could be potential biomarkers for chronic ischemic heart failure, and they could also be the serum protein targets of SFI.

Application of blunt dissection in ESD of a gastric submucosal tumor.

We performed endoscopic submucosal dissection of a gastric fundus tumor. It was difficult to strip the tumor completely due to space limitation, and we used blunt dissection to remove the tumor quickly and safely. Firstly, the basal area of the 2.5 cm submucosal tumor located in the gastric fundus was cut open, and the mucosa was dissected. The tumor was difficult to peel, therefore, a snare was used and the tumor was pulled and tightened slightly. Short electronic coagulation was used during the procedure. The tumor was then bluntly dissected. This method ensured rapid and complete removal of the tumor.

Promoter hypermethylation of death-associated protein kinase gene in cholangiocarcinoma.

BACKGROUND: Death-associated protein kinase (DAPK) is a Ca2+/calmodulin-regulated Ser/Thr kinase which is involved in apoptosis. The aberrant methylation of its promoter region CpG islands may be one of the important mechanisms of carcinogenesis. We studied the relationship of methylation status and expression of the DAPK gene with the clinical findings in cholangiocarcinoma. METHODS: Target DNA was modified by sodium bisulfite, coverting all unmethylated, but not methylated, cytosines to uracil, and subsequently detected by methylation-specific PCR. Moreover, mRNA expression of the DAPK gene was assessed by RT-PCR. RESULTS: Aberrant methylation of the DAPK gene was detected in 11 (30.6%) of 36 tissue specimens of cholangiocarcinoma, and in 2 (5.6%) of 36 specimens of adjacent normal tissues. DAPK mRNA was not expressed in tumor and adjacent tissues with hypermethylation of the DAPK promoter. There were no statistical differences in the extent of differentiation and invasion, lymph node metastasis or pathologic type between the methylated and unmethylated tissues. CONCLUSIONS: The frequency of DAPK gene methylation in cholangiocarcinoma is high and it may offer an effective means for earlier auxiliary diagnosis of the malignancy. The DAPK gene is probably suppressed by methylation, and it could become resistant to apoptosis and immunological surveillance. The DAPK gene epigenetically affected by methylation may be associated with the carcinogenesis of cholangiocarcinoma.

[Relationship between Helicobacter pylori infection and expression of c-myc, Bcl-2, and Bax protein in different gastric mucosa lesions].

BACKGROUND & OBJECTIVE: Helicobacter pylori (HP) has been believed to be a carcinogen of gastric carcinoma. However, its mechanism was yet not clearly understood. This study was designed to investigate the relationship between HP infection and gastric epithelial cell proliferation as well as apoptosis in different gastric mucosa lesions and elucidate the probable mechanism of gastric carcinogenesis relating with HP infection. METHODS: A total of 272 cases were available for the study including 42 cases of chronic gastritis (CG), 46 cases of intestinal metaplasia I or II (IM I- II), 25 cases of intestinal metaplasia III (IM III), 21 cases of mild dysplasia (Dys I), 54 cases of modest or severe dysplasia (Dys II- III), and 84 cases of gastric cancer (GC). HP infection was detected by Warthin-Starry bacterium staining method and streptavidin-peroxidase (SP) immunohistochemical method. HID-AB(pH2.5)- PAS method was used to define the quality of mucus. The expression of c-myc, Bcl-2, and Bax were detected using SP immunohistochemical method. The chi-square test and the Fisher's exact probability test were used to compare the frequencies. RESULTS: (1)The expression of c-myc and Bcl-2 increased as gastric mucosa lesions developed from CG,IM,Dys to GC,but the expression of Bax decreased. The expression of c-myc was significantly higher in GC than that in Dys II- III and IM III(all P< 0.01), but the expression of Bax was significantly lower in GC than that in Dys II- III and IM III(P< 0.05 or P< 0.01). (2)The expression of c-myc in IM III and Dys II- III with HP infection was 62.50% and 66.67%,respectively, significantly higher than that without infection(11.11%,27.78%,all P< 0.05). The expression of Bax in CG, IM I- II and IM III with HP infection were 87.10%, 81.25%, and 62.50%, respectively, significantly higher than those without infection (54.55%, 42.86%, 11.11%, all P< 0.05). Furthermore HP infection was associated with the expression of Bcl-2 in IM III, Dys II- III and GC (P< 0.05 or P< 0.01). CONCLUSION: HP infection can cause serious imbalance between cell proliferation and apoptosis in the precancerous lesions (IM III and Dys II- III), giving chances for gastric carcinogenesis.

[Multidrug resistance and its relationship with neuroendocrine differentiation in non-small cell lung carcinoma].

OBJECTIVE: To study the multidrug resistance (MDR) of non-small lung cancer (NSCLC) and its relationship with neuroendocrine (NE) differentiation. METHODS: NSCLC samples from 113 untreated patients were analyzed immunohistochemically with antibodies to glutathion-s-transferase-pi (GST-pi), multidrug resistance associated protein (MRP), lung resistance associated protein (LRP), neuro-specific enolase (NSE), synaptophysin (SYN) and chromogranin (CgA). RESULTS: (1) The expression of the three proteins was significantly associated with the type of lung carcinoma (P < 0.05), but not with the differentiation and lymph node metastasis. The expression of GST-pi was significantly related with MRP, MRP and LRP (P < 0.05). (2) The positive rates of the NE markers were: NSE, 53.1%; SYN, 26.6%; CgA, 6.2%; and 21.2% for at least two markers. The expression of at least 2 markers was associated with the degree of differentiation (P < 0.05), but not with the type of lung cancer and lymph node metastasis. (3) The expression of the three multidrug resistance related proteins in the positive group for at least 2 markers was significantly lower than that in the negative group (P < 0.05). CONCLUSIONS: The over-expressions of GST-pi, MRP and LRP are important causes of primary multidrug resistance in NSCLC. The differentiation of NE may be one of the factors involved in multidrug resistance.

[The expression of DNA-PKcs in non-small cell lung cancer and its relationship with apoptosis associated proteins].

BACKGROUND: To study the expression of catalylic subunit of DNA-dependent protein kinase (DNA-PKcs) in non-small cell lung cancer (NSCLC) and its relationship with apoptosis. METHODS: NSCLC tissues from 113 untreated patients were analyzed immnohistochemically with antibodies to DNA-PKcs, p53 and bcl-2. RESULTS: There were expressions of DNA-PKcs, p53 and bcl-2 in NSCLC at different levels. The positive rate of DNA-PKcs, p53 and bcl-2 was 89.38%(101/113), 61.95%(70/113) and 59.29%(67/113) respectively. The expression of DNA-PKcs was significantly related with the histological types. Its expression in squamous carcinoma was significantly lower than that in adenocarcinoma and bronchioloalveolar carcinoma. The expression of DNA-PKcs increased with the increasing differentiated degree of NSCLC ( P < 0.05), but had no relationship with lymph node metastasis. There was no significant relation between the expression of p53 and the pathological type of NSCLC. A significant difference of bcl-2 expression existed in the histological types of lung cancer ( P < 0.01). Its expression in squamous carcinoma was significantly higher than that in adenocarcinoma, bronchioloalveolar carcinoma and adenosquamous carcinoma, but had no relationship with the differentiated degree of lung cancer and lymph node metastasis. The expressions were significantly related between DNA-PKcs and p53 ( P < 0.01), p53 and bcl-2 ( P < 0.05). CONCLUSIONS: The expression of DNA-PKcs is fairly high in NSCLC. The high expression of DNA-PKcs and overexpressions of mutated p53 and bcl-2 may be important causes of radioresistance in NSCLC.

[Relationship between Helicobacter pylori infection and expressions of tumor suppressor genes in gastric carcinoma and related lesions].

BACKGROUND & OBJECTIVE: Helicobacter pylori (Hp) are believed to be a carcinogen of gastric carcinoma. However, its mechanism was yet not clearly understood. p53, p21WAF1, and p16 are main negative regulator genes of cell cycle. This study was designed to investigate the relationship between these 3 genes and Hp infection. METHODS: The authors examined the expression of these 3 tumor suppressor genes and Hp infection in 65 cases with chronic atrophic gastritis (CAG), 93 cases with intestinal metaplasia(IM), 94 cases with gastric epithelial dysplasia (GED) and 60 cases with gastric carcinoma (GC) using HID-AB (pH 2.5)-PAS, SP immunohistochemistry staining, and Warthin-Starry staining. RESULTS: For CAC, IM stage I-II, IM stage III, GED stage I, GED stage II-III, and GC, the positive expression rates of p53 were 0, 1.64%, 6.25%, 5.45%, 23.08%, and 70.00%, respectively (increased with pathological process); the positive expression rates of p21WAF1 were 100%, 95.08%, 100%, 100%, 71.79%, and 45.00%, respectively; the positive expression rates of p16 were 83.08%, 81.97%, 78.13%, 89.09%, 69.23%, and 40.00%, respectively. All the expression of these 3 genes showed significant difference between GED stage II-III and GED stage I, GC and GED stage II-III. In the same pathological changes, the positive expression rate of these 3 genes was higher in Hp infection group than in no Hp infection group, while there was no significant difference (P > 0.05). CONCLUSION: The mutation of p53 and inactivation of p21WAF1 and p16 play an important role in carcinogenesis of stomach. However, Hp infection was not associated with the abnormal expression of these 3 genes.