The congenital esophageal atresia with proximal tracheoesophageal fistula is a developmental defect with incomplete septation of the foregut of embryonic period and is often associated with other congenital anomaly. We experienced a case of the esophageal atresia with proximal tracheoesophageal fistula in a 1-day old male patient who was transferred from an obstetric clinic due to respiratory distress soon after birth. The baby was treated not by primary anastomosis but by operation of ligation of proximal part of fistula and gastrostomy because of too long distance of 4cm between proximal and distal pouches of esophageal atresia. His weight gain has been good in the treatment of reverse gastric tube interposition for 9 months after birth. We presented the case with brief review of the related literatures.
Esophageal Atresia* ; Fistula ; Gastrostomy ; Humans ; Ligation ; Male ; Parturition ; Tracheoesophageal Fistula* ; Weight Gain

In vascular smooth muscle cells (VSMCs), induction of the heme oxygenase-1 (HO-1) confers vascular protection against cellular proliferation mainly via its up-regulation of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1) that is involved in negative regulation of cellular proliferation. In the present study, we investigated whether the phytochemical curcumin and its metabolite tetrahydrocurcumin could induce HO-1 expression and growth inhibition in rat VSMCs and, if so, whether their antiproliferative effect could be mediated via HO-1 expression. At non-toxic concentrations, curcumin possessing two Michael-reaction acceptors induced HO-1 expression by activating antioxidant response element (ARE) through translocation of the nuclear transcription factor E2-related factor-2 (Nrf2) into the nucleus and also inhibited VSMC growth triggered by 5% FBS in a dose-dependent manner. In contrast, tetrahydrocurcumin lacking Michael-reaction acceptor showed no effect on HO-1 expression, ARE activation and VSMC growth inhibition. The antiproliferative effect of curcumin in VSMCs was accompanied by the increased expression of p21(WAF1/CIP1). Inhibition of VSMC growth and expression of p21(WAF1/CIP1) by curcumin were partially, but not completely, abolished when the cells were co- incubated with the HO inhibitor tin protoporphyrin. In human aortic smooth muscle cells (HASMCs), curcumin also inhibited growth triggered by TNF-alpha and increased p21(WAF1/CIP1) expression via HO-1-dependent manner. Our findings suggest that curcumin has an ability to induce HO-1 expression, presumably through Nrf2-dependent ARE activation, in rat VSMCs and HASMCs, and provide evidence that the antiproliferative effect of curcumin is considerably linked to its ability to induce HO-1 expression.
Active Transport, Cell Nucleus ; Animals ; Aorta/cytology ; Cell Nucleus/metabolism ; Cell Proliferation/*drug effects ; Cells, Cultured ; Curcumin/analogs & derivatives/*pharmacology ; Cyclin-Dependent Kinase Inhibitor p21/biosynthesis/metabolism ; Gene Expression Regulation ; Heme Oxygenase (Decyclizing)/biosynthesis/genetics/*physiology ; Heme Oxygenase-1/biosynthesis/genetics/*physiology ; Humans ; Metalloporphyrins/pharmacology ; Muscle, Smooth, Vascular/drug effects/*physiology ; Myocytes, Smooth Muscle/drug effects/*physiology ; NF-E2-Related Factor 2/metabolism ; Protoporphyrins/pharmacology ; Rats ; Regulatory Sequences, Nucleic Acid ; Response Elements ; Tumor Necrosis Factor-alpha/pharmacology

Behcet's disease is an important cause of fatal vasculitis in young adult males and vascular involvement has been reported in more than 25% of patients. Pulmonary vascular involvement has been found in 1~7.7% of patients and is known to be related to poor prognosis. A incidence of fatal hemoptysis is high in patients whose Behcet`s disease is complicated by pulmonary artery aneurysm (PAA). The recurrence of hemoptysis in PAA of Behcet's disease may result from inadequate medical therapy and complications of surgical treatment. We report a case with Behcet's disease whose fatal hemoptysis has been successfully treated with bronchial artery embolization.
Aneurysm ; Bronchial Arteries* ; Hemoptysis* ; Humans ; Incidence ; Male ; Prognosis ; Pulmonary Artery ; Recurrence ; Vasculitis ; Young Adult

The abscess is a common complication of Crohn’s disease (CD), with the perianal form more frequent than gluteal or presacral which is relatively rare. There are few case reports of gluteal abscess combined with presacral abscess caused by CD and the treatment has not been established. A 21-year-old male was admitted with right buttock and lower back pain with a duration of 3 months. He had a history of CD in the small intestine diagnosed 10 months previously. He had poor compliance and had not returned for follow-up care during the previous 6 months. Abdominopelvic CT indicated newly developed multiple abscess pockets in right gluteal region, including piriformis muscle and presacral space. Additionally, fistula tracts between small bowel loops and presacral space were observed. Patient’s CD was moderate activity (273.12 on the Crohn’s Disease Activity Index [CDAI]). Treatment was started with piperacillin/tazobactam antibiotic but patient developed a fever and abscess extent was aggravated. Therefore, surgical incision and drainage was performed and 4 Penrose drains were inserted. Patient’s pain and fever were resolved following surgery. Infliximab was then administered for the remaining fistulas. After the induction regimen, multiple fistula tracts improved and patient went into remission (CDAI was -0.12).

Synaptotagmin is a Ca2+ sensing protein, which triggers a fusion of synaptic vesicles in neuronal transmission. Little is known regarding the expression of Ca2+ - dependent synaptotagmin isoforms and their contribution to the release of secretory vesicles in mouse and rat parotid acinar cells. We investigated a type of Ca2+ - dependent synaptotagmin and Ca2+ signaling in both rat and mouse parotid acinar cells using RT-PCR, microfluorometry, and amylase assay. Mouse parotid acinar cells exhibited much more sensitive amylase release in response to muscarinic stimulation than did rat parotid acinar cells. However, transient [Ca2+]i increases and Ca2+ influx in response to muscarinic stimulation in both cells were identical, suggesting that the expression or activity of the Ca2+ sensing proteins is different. Seven Ca2+ - dependent synaptotagmins, from 1 to 7, were expressed in the mouse parotid acinar cells. However, in the rat parotid acinar cells, only synaptotagmins 1, 3, 4 and 7 were expressed. These results indicate that the expression of Ca2+ - dependent synaptotagmins may contribute to the release of secretory vesicles in parotid acinar cells.
Synaptotagmins/*metabolism ; Signal Transduction ; Rats ; Protein Isoforms/metabolism ; Parotid Gland/cytology/*metabolism ; Muscarinic Agonists/pharmacology ; Mice ; Exocytosis/drug effects/physiology ; Carbachol/pharmacology ; Calcium/metabolism/*physiology ; Animals ; Amylases/secretion