Endoscopic submucosal dissection for treatment of gastric submucosal tumors originating from the muscularis propria layer.

BACKGROUND AND AIMS: We aimed to study the feasibility of endoscopic submucosal dissection (ESD) for the removal of gastric muscularis propria tumors and to evaluate the efficacy and safety of ESD for this treatment. METHODS: Eighteen patients with gastric SMTs originating from the muscularis propria were treated by ESD between July 2008 and July 2011. Tumor characteristics, complications, en bloc resection rate, and local recurrence rate were evaluated. RESULTS: Among the 18 patients, 11 were women (61.1 %). The median age was 65.3 ± 6.3 years old (range 30-71 years old). Seventeen tumors were resected completely by ESD (success rate 94.4 %). The mean tumor size as determined by endoscopic ultrasound was 2.6 ± 1.2 cm (range 1.0-3.5 cm). The histological diagnosis was gastrointestinal stromal tumor for 13 lesions and leiomyoma for four tumors. The mean operation time was 90 ± 38 min (range 50-120 min), and the average blood loss was 20 ml. Two patients developed perforation, which was closed by endoscopic methods with metallic clips. The tumor was closely adhered to the muscularis propria and was convex to the enterocoelia in one case. No single case had severe complications, such as GI bleeding, peritonitis, or abdominal abscess, and there were no other immediate post-procedure complications. CONCLUSIONS: ESD is a safe, effective, well-tolerated, and minimally invasive therapy for the intraluminal SMTs originating from gastric muscularis propria with relatively few complications. Although there is a risk of perforation which has become manageable endoscopically.

Expression and significance of nerve growth factor receptor p75 in rats' cathartic colonic wall.

OBJECTIVE: To investigate the expression of nerve growth factor receptor p75 in a normal and cathartic colon and its significance in the formation of the cathartic colon in rats. METHODS: Sixty Sprague-Dawley rats were equally divided into normal control group, rhubarb group and phenolphthalein group. A model of the cathartic colon was constructed by gastric infusion with rhubarb or phenolphthalein in rats. The first dose of rhubarb and phenolphthalein was both 200 mg/kg/d and was increased by 200 mg/kg/d with each passing day. The last dose of rhubarb and phenolphthalein was 3200 mg/kg/d and 4200 mg/kg/d, respectively. The transit function of colon was measured by the Chinese ink expulsion test; the p75 in colon wall was determined by the immunohistochemical method. RESULTS: The transit speed was much slower in the cathartic colon group than that in the control group. The imprinted Chinese ink length and the ratio of imprinted length/total colon length in the rhubarb-induced cathartic colon was significantly shorter than that of the control group (77.38 +/- 8.42 vs 94.25 +/- 7.07 cm, P < 0.01). Those in the phenolphthalein-induced group (83.38 +/- 9.75 cm) were also significantly shorter than those of the control group but to a lesser degree (P < 0.05). p75 was abundantly expressed in the submucosal nerve plexus and weakly expressed in the myenteric plexus. The expression of p75 was much higher in the rhubarb-induced group. The expression was strongly positive in the submucosal nerve plexus, significantly higher than that in the controls (P < 0.01). In the myenteric plexus, p75 was also highly expressed (P < 0.05). In the case of the phenolphthalein-induced group, the expression of p75 was positive in the submucosal nerve plexus but was positive in the myenteric plexus of three rats only. The remaining rats were negative or weakly positive. This was not significantly different from that of the control group. CONCLUSIONS: The abnormal expression of p75 in cathartic colon probably has some effect on the degeneration or apoptosis of neuronal cells in the enteric nerve plexus, with a subsequent pathological change of the enteric nervous system, and thus leads to abnormalities in colonic dynamics. The kind of lesion is probably associated with long-term use of irritative cathartics.

Right ventricular apical obstruction in a patient with hypereosinophilia: Löffler endocarditis.

Idiopathic hypereosinophilic syndrome (HES) is a rare leukoproliferative systemic disorder characterized by sustained overproduction of eosinophils and poor prognosis. A case that a 67-year-old man with persistent symptoms of heart failure due to cardiac involvement in idiopathic HES is concentrated on. Echocardiography revealed the marked endocardial thickening of both ventricles with an apical obstruction of the right ventricle. Medical therapy, including low dose dopamine and furosemidum, was initiated with corticosteroids, imatinib and hydroxycarbamide. Remission of symptoms had persisted for only 3 weeks. As the count of eosinophils rebounded, the patient suffered with refractory heart failure, severe hypoxemia and acute renal insufficiency, eventually died 62 days after his hospitalization. The rechecking of his last MRI showed thrombus both in right atrium and superior vena cava, which indicated that he might have died of pulmonary embolism, besides the refractory heart failure and multiple organ failure.

Evaluation of recombinant endostatin in the treatment of atherosclerotic plaques and neovascularization in rabbits.

OBJECTIVE: Atherosclerotic plaques and neovascularization play an important role in the course of coronary atherosclerosis. This study evaluated the effect of recombinant endostatin on experimental atherosclerotic plaques and neovascularization in rabbits. METHODS: Eighteen healthy male rabbits were divided into three groups: control group, atherosclerotic model group, and recombinant endostatin treated group. The atherosclerotic model was established via a high-cholesterol diet after balloon catheter injury. The subject weights, serum total cholesterol, creatine kinase-myocardial band fraction (CKMB), and matrix metalloproteinase-2 (MMP-2) were measured. Six weeks after treatment, the aortic roots were taken for pathological assay. The thickness ratio of the intima to media was measured by hematoxylin and eosin (HE) staining, and the number of neovessels was measured by immunohistochemistry via monoclonal antibody CD31 staining. RESULTS: The weight, plasma total cholesterol, and CKMB were not significantly different between the atherosclerotic model group and the recombinant endostatin treated group, but much higher than those of the control group (P<0.05). The thickness ratio of the intima to media in the recombinant endostatin treated group was distinctly less than that in the atherosclerotic model group (P<0.05). The number of neovessels decreased dramatically (P<0.05) and the content of MMP-2 decreased slightly without statistical difference (P>0.05) in the recombinant endostatin treated group, compared to the atherosclerotic model group. CONCLUSIONS: Recombinant endostatin is able to inhibit the growth of neovascularization in the atherosclerotic plaque and the development of plaque.