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/Objective: Laparoscopic distal gastrectomy for early gastric cancer is described as a treatment option in general practice. However, the oncological efficacy and technical safety of laparoscopic gastrectomy with D2 lymphadenectomy in locally advanced gastric cancer are controversial, and clinical trials are ongoing. This study aimed to evaluate the short-term and surgical outcomes between laparoscopic and open gastrectomy procedures in locally advanced gastric cancer.We retrospectively analyzed data from 134 patients who underwent subtotal D2 gastrectomy for locally advanced gastric cancer in our hospital between January 2011 and December 2018. Clinicopathological characteristics, surgical outcome, postoperative recovery, disease-free survival, and overall survival were compared between those who underwent laparoscopic and open gastrectomies.Baseline characteristics were similar between patients who underwent open and laparoscopic surgeries. Less surgical time (250.8 vs. 347.6 min in laparoscopic vs. open surgery, respectively; P 0.05) and lower blood loss (83.7 vs. 333 mL in laparoscopic vs. open surgery, respectively; P 0.05) were noted in patients who underwent laparoscopic surgery than in those who underwent open gastrectomy. The time of starting oral intake was earlier and the length of postoperative hospital stay was shorter in the laparoscopic group than in the open group. Surgical morbidity and mortality rates, as well as disease-free survival and overall survival rates, did not differ between the two groups.Laparoscopic gastrectomy is feasible and safe for locally advanced gastric cancer. Based on the perioperative results and short-term outcomes, laparoscopic gastrectomy is non-inferior to open gastrectomy.

Background: The prognosis of HCC patients with main portal vein invasion (Vp4) is poor. We retrospectively reviewed the therapeutic outcomes with our new HAIC regimen in treating Vp4 HCC patients. Patients and Methods: Seventy-one patients received the new regimen of combining HAIC (daily infusion of cisplatin (10 mg/m2), mitomycin-C (2 mg/m2) and Leucovorin (15 mg/m2) plus 100 mg/m2 of 5-fluorouracil (5-FU) using an infusion pump for 5 consecutive days) with Lipiodol embolization between 2002 and 2018. Twenty-two patients (31.0%) also received sorafenib. The Kaplan–Meier curve was used to calculate progression-free survival (PFS) and overall survival (OS). The OS of patients with or without additional sorafenib use or extrahepatic spread (EHS) was also compared. Results: Fifty-six patients (78.9%) had Child-Pugh A liver function. The mean maximal tumor size was 10.3 cm. Twenty patients (28.2%) had EHS at their initial diagnosis. The objective response rate according to the Modified Response Evaluation Criteria in Solid Tumors (mRECIST) and median OS were 64.8% and 13 months. The 1-, 2- and 3-year survival rates were 53.1%, 21.5% and 18.7%, respectively. In the subgroup analysis, there were no significant survival difference between patients with HAIC only vs. HAIC plus sorafenib (14 vs. 13 months) and between patients with vs. without EHS (12 vs. 13 months). Conclusions: Our new HAIC regimen is effective in treating Vp4 HCC patients. Additional sorafenib use with our new HAIC regimen provided no survival benefit.

Background: Vacuum-assisted breast biopsy (VABB) for benign breast tumor excision is a developing trend in breast surgery. The most common complication of VABB is hematoma. We assessed the efficiency of the thrombin-gelatin matrix (TGM) for hemostasis after VABB. Methods: From December 2013 to June 2017, 147 patients with breast tumors > 2 cm in size were treated with a 7-gauge ultrasound-guided EnCor EnSpire® breast biopsy system. After VABB, the TGM was applied using an iron-tube device. After injection, brief external compression for 15 min and postoperative bandage compression for approximately 12 h were applied. The medical records were reviewed and analyzed for hematoma and acute bleeding at 1 and 3 months after VABB. Results: A total of 72 patients received hemostasis via TGM, and 75 patients received hemostasis by compression. The rates of postoperative acute bleeding in the TGM group were significantly lower than those in the non-TGM group (5.5% vs. 22.7%, p = 0.003). Among patients with hematoma, there was no statistically significant difference between the two groups (25% vs. 26.7%, p = 0.85). Conclusions: This is the first cohort study to apply the TGM hemostatic matrix for post-VABB hemostasis. The TGM hemostatic matrix could be an option for patients with large breast tumors.

The occurrence of hiatal hernia after total gastrectomy with Roux-en-Y reconstruction is rare. We report the case of a 76-year-old man who presented with dyspnea, vomiting, and fever around 8 days after total gastrectomy with Roux-en-Y reconstruction. Abdominal computed tomography revealed a hiatal hernia containing part of the small intestine in the left thoracic cavity. Emergent reduction and repair of the hiatal hernia were performed later. Operative findings revealed that the Roux limb was incarcerated in the left pleural cavity. Esophagojejunostomy leakage, perforation of the small intestine with transient ischemic change, and pyothorax were also found. Thus, feeding jejunostomy, thoracoscopic decortication, and diversion T-tube esophagostomy were performed. Considering that the main cause of hiatal hernia is blunt dissection with division of the phrenoesophageal membrane, approximating the crus with 1 or 2 figure-8 sutures, according to the size of the defect, to prevent the incidence of hiatal hernia after total gastrectomy may be performed.

Indocyanine green (ICG) angiography, a real-time intraoperative imaging technique, is associated with better parathyroid identification and functional evaluation during open thyroidectomy. However, the benefits of ICG fluorescence imaging application in transoral endoscopic thyroidectomy are not well-documented. Consecutive patients who underwent transoral endoscopic thyroidectomy were retrospectively reviewed. Parathyroid glands were assessed with visual inspection followed by ICG angiography. The fluorescence intensity of all parathyroid glands was recorded. In total, 158 parathyroid glands from 60 patients (41 underwent lobectomy and 19 underwent total thyroidectomy) were eligible for evaluation. A total of 135 parathyroid glands (85.4%) were identified, including nine glands (5.7%) that were solely localized because of ICG angiography. Incidental parathyroidectomy occurred in 12 patients with predominant inferior gland (83.3%) and associated with central neck dissection (66.7%). Among patients receiving total thyroidectomy, patients who retained at least one well-perfused parathyroid gland had higher parathyroid hormone (PTH) level and were less likely to develop hypoparathyroidism on postoperative day one than those without any well-perfused ICG-enhanced parathyroid gland (p = 0.038). In addition, the duration of calcium supplementation to maintain normocalcemia was also shorter. ICG angiography is a feasible adjunct procedure for parathyroid identification and postoperative functional prediction in transoral endoscopic thyroidectomy.

Yu-Chia Chen,1,* I-shu Chen,1,* Guan-Jin Huang,2 Chi-hsiang Kang,1 Kuo-Chiang Wang,1 Min-Jen Tsao,3 Hung-Wei Pan4,5 1Department of Surgery, Division of General Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan; 2Department of Pathology, National Chung Kung University Hospital, Tainan, Taiwan; 3Department of General Surgery, Zuoying Branch of Kaohsiung Armed Forces General Hospital, Kaohsiung, Taiwan; 4Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan; 5Department of Applied Chemistry, National Pingtung University, Pingtung, Taiwan *These authors contributed equally to this work Background: Hepatocellular carcinoma (HCC) has an increasing incidence and high mortality. Surgical operation is not a comprehensive strategy for liver cancer. Moreover, tolerating systemic chemotherapy is difficult for patients with HCC because hepatic function is often impaired due to underlying cirrhosis. Therefore, a comprehensive strategy for cancer treatment should be developed. DTL (Cdc10-dependent transcript 2) is a critical regulator of cell cycle progression and genomic stability. In our previous study, the upregulation of DTL expression in aggressive HCC correlated positively with tumor grade and poor patient survival. We hypothesize that targeting DTL may provide a novel therapeutic strategy for liver cancer. DTL small interference RNAs were used to knock down DTL protein expression.Methods: A clonogenic assay, immunostaining, double thymidine block, imaging flow cytometry analysis, and a tumor spheroid formation assay were used to analyze the role of DTL in tumor cell growth, cell cycle progression, micronucleation, ploidy, and tumorigenicity.Results: Our results demonstrated that targeting DTL reduced cell cycle regulators and chromosome segregation genes, resulting in increased cell micronucleation. DTL depletion inhibited liver cancer cell growth, increased senescence, and reduced tumorigenesis. DTL depletion resulted in the disruption of the mitotic proteins cyclin B, CDK1, securin, seprase, Aurora A, and Aurora B as well as the upregulation of the cell cycle arrest gene p21. A rescue assay indicated that DTL should be targeted through TPX2 downregulation for cancer cell growth inhibition. Moreover, DTL silencing inhibited the growth of patient-derived primary cultured HCC cells.Conclusion: Our study results indicate that DTL is a potential novel target gene for treating liver cancer through liver cancer cell senescence induction. Furthermore, our results provide insights into molecular mechanisms for targeting DTL in liver cancer cells. The results also indicate several other starting points for future preclinical and clinical studies on liver cancer treatment. Keywords: DTL, cell cycle, senescence, TPX2, hepatocellular carcinoma

Transoral thyroidectomy is a novel technique that uses three small incisions hidden in the oral vestibule to remove the thyroid gland. It provides excellent cosmetic results and outcomes comparable to the open approach. One of the main obstacles for this technique is the creation of a working space from the lip and chin to the neck. The anatomy of the perioral region and the top-down surgical view are both unfamiliar to general surgeons. As a result, inadequate manipulation might easily occur and would lead to several unconventional complications, such as mental nerve injury, carbon dioxide embolism, and skin perforation, which are rarely observed in open surgery. Herein, we summarize the basic concepts, techniques, and rationales behind working space creation in transoral thyroidectomy to assist surgeons in obtaining an adequate surgical field while eliminating preventable complications.

The incidence rate of newly developed gallstone disease after gastrectomy for gastric cancer is thought to be higher than that in the general population. However, the presentation and management of these gallstones remain under debate, and the role of prophylactic cholecystectomy remains questionable.Data on adult patients who were diagnosed with gastric cancer and received gastrectomy between 2000 and 2011 were extracted from the Taiwan National Health Insurance Research Database. A patient was excluded if he or she had gallstone disease or received cholecystectomy before the index date. The incidence of newly developed gallstone disease and its subsequent management were recorded. Data were analyzed to evaluate the factors associated with gallstone development and treatment options.A total of 17,325 gastric cancer patients who underwent gastrectomy were eligible for analysis. During the follow-up period (mean 4.1 years; median, 2.9 years), 1280 (7.4%) patients developed gallstone disease and 560 (3.2%) patients subsequently underwent cholecystectomy. The in-hospital mortality for cholecystectomy was 1.8% (10/560). Development of gallstone disease was associated with older age, total gastrectomy, duodenal exclusion, diabetes, cirrhosis, and more comorbidities. Factors associated with the use of cholecystectomy to treat gallstone disease included younger age, fewer comorbidities, medical center admission, and presentation as cholecystitis.Although few patients required further gallbladder removal after gastrectomy for gastric malignancy, the increased mortality rate for subsequent cholecystectomy was worth noting. The decision to undergo prophylactic cholecystectomy might be individualized based upon patient characteristics and the surgeon's discretion.

Cytochalasin B, a cell-permeable mycotoxin isolated from the fungus Phoma spp., shows a wide range of biological effects, among which its potent antitumor activity has raised great interests in different models. However, the cytotoxic activity of cytochalasin B and its underlying mechanisms have not been elucidated in breast cells. This study examined the effect of cytochalasin B on MCF 10A human breast epithelial cells and ZR-75-1 human breast cancer cells. Cytochalasin B (10–20 μM) concentration-dependently induced cytotoxicity, cell cycle arrest, and [Ca2+]i rises in ZR-75-1 cells but not in MCF 10A cells. In ZR-75-1 cells, cytochalasin B triggered G2/M phase arrest through the modulation of CDK1, cyclin B1, p53, p27 and p21 expressions. The Ca2+ signal response induced by cytochalasin B was reduced by removing extracellular Ca2+ and was inhibited by the store-operated Ca2+ channel blocker 2-APB and SKF96365. In Ca2+-free medium, cytochalasin B induced Ca2+ release through thapsigargin-sensitive endoplasmic reticulum stores. Moreover, cytochalasin B increased H2O2 levels but reduced GSH levels. The apoptotic effects evoked by cytochalasin B were partially inhibited by prechelating cytosolic Ca2+ with BAPTA-AM and the antioxidant NAC. Together, in ZR-75-1 cells but not in MCF 10A cells, cytochalasin B activated Ca2+-associated mitochondrial apoptotic pathways that involved G2/M phase arrest and ROS signaling. Furthermore, cytochalasin B induced [Ca2+]i rises by releasing Ca2+ from the endoplasmic reticulum and causing Ca2+ influx through 2-APB or SKF96365-sensitive store-operated Ca2+ entry. Our findings provide new insights into the possible application of cytochalasin B in human breast cancer therapy.

The effect of protriptyline on Ca2+ physiology in human hepatoma is unclear. This study explored the effect of protriptyline on [Ca2+ ]i and cytotoxicity in HepG2 human hepatoma cells. Protriptyline (50-150 μM) evoked [Ca2+ ]i rises. The Ca2+ entry was inhibited by removal of Ca2+ . Protriptyline-induced Ca2+ entry was confirmed by Mn2+ -induced quench of fura-2 fluorescence. Except nifedipine, econazole, SKF96365, GF109203X, and phorbol 12-myristate 13 acetate did not inhibit Ca2+ entry. Treatment with the endoplasmic reticulum Ca2+ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) inhibited 40% of protriptyline-induced response. Treatment with protriptyline abolished BHQ-induced response. Inhibition of phospholipase C (PLC) suppressed protriptyline-evoked response by 70%. At 20-40 μM, protriptyline killed cells which was not reversed by the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM). Together, in HepG2 cells, protriptyline induced [Ca2+ ]i rises that involved Ca2+ entry through nifedipine-sensitive Ca2+ channels and PLC-dependent Ca2+ release from endoplasmic reticulum. Protriptyline induced Ca2+ -independent cell death.

Background: Hepatic steatosis is defined as excessive amounts of triglyceride and other fats inside liver cells and has become an emergent liver disease in developed and developing countries. Methods: Deep seawater (DSW)300, DSW900, and DSW1500 drinking waters were formulated via a combination of reverse osmosis and electrodialysis. Hamsters on a high-fat diet were assigned to drink the following solutions: (1) normal distilled water, (2) DSW300, (3) DSW900, or (4) DSW1500. Serum, liver, and fecal biochemical values, expression of hepatic genes related to fatty-acid homeostasis, as well as liver antioxidative levels were measured after a 6-week feeding period. Additionally, hematoxylin and eosin staining was used to investigate the liver histopathology. Results: Serum/liver lipids, liver sizes, liver malondialdehyde content, and serum aspartate aminotransferase and alanine aminotransferase of high-fat diet hamsters were reduced (p 0.05) altered, DSW drinking water upregulated (p

Inflammation and hepatic stellate cell (HSC) activation are the most crucial steps in the formation of hepatic fibrosis. Hepatocytes damaged by viral or bacterial infection, alcohol or toxic chemicals initiate an inflammatory response that activates collagen production by HSCs. Recent studies indicate curcumin has liver-protective effects due to its anti-inflammatory, antioxidant and anticancer activities; however, the mechanisms are not well understood. In this study, we show that curcumin protected against hepatic fibrosis in BALB/c mice in vivo by inhibiting HSC activation, inflammatory responses and inducing apoptosis of damaged hepatocytes. Using the thioacetamide (TAA)-induced hepatic fibrosis animal model, we found that curcumin treatment up-regulated P53 protein expression and Bax messenger RNA (mRNA) expression and down-regulated Bcl-2 mRNA expression. Together, these responses increased hepatocyte sensitivity to TAA-induced cytotoxicity and forced the damaged cells to undergo apoptosis. Enhancing the tendency of damaged hepatocytes to undergo apoptosis may be the protective mechanism whereby curcumin suppresses inflammatory responses and hepatic fibrogenesis. These results provide a novel insight into the cause of hepatic fibrosis and the cytoprotective effects curcumin has on hepatic fibrosis suppression.

1. Short-wave diathermy (SWD) is a form of radiofrequency radiation that is used therapeutically by physiotherapists. The cellular mechanisms of SWD are unclear. The present study was performed to explore the effect of different conditions of short-wave exposure on the proliferation of cultured human chondrocytes. 2. Cells exposed to short waves once per day for seven consecutive days exhibited a significant increase in proliferation by 42% compared with the control cells. In cells that were treated with short waves twice per day for seven consecutive days, or only once on Day 1 and then examined for proliferation on Day 7, cell proliferation was greater than the control cells by 40% and 30%, respectively. 3. Given the importance of mitogen-activated protein kinases (MAPK) in the proliferation of different cell types, efforts were extended to explore the role of three major types of MAPK; that is, extracellular signal-regulated kinase (ERK), c-Jun NH(2)-terminal protein kinase (JNK) and p38. 4. It was found that the level of phosphorylated ERK (phospho-ERK 1 and ERK 2) increased significantly within 5-120 min following consecutive exposure to short waves for 7 days. Exposure to short waves failed to alter the intensity of phosphorylated JNK and p38 within 0-240 min. 5. Cells were exposed to short waves once for seven consecutive days in the presence of 0, 10 micromol/L, 20 micromol/L or 50 micromol/L PD98059 (an ERK inhibitor). PD98059 totally inhibited short waves-induced enhancement of proliferation without altering normal control viability. In the presence of short waves and PD98059, the cell viability was lower than the normal control. Together, the data suggest that short waves could increase proliferation in human chondrocytes through activation of the ERK pathway, which is also involved in maintaining normal cell proliferation under physiological conditions.

Hepatic resection for huge hepatocellular carcinoma (HCC) is challenging. The role of multimodality nonsurgical therapy for HCC larger than 10 cm is unclear.We retrospectively investigated 131 HCC patients with main tumors larger than 10 cm in diameter seen between October 1990 and October 2001. Fifty-six patients (group A) underwent hepatectomy and 75 patients (group B) underwent nonsurgical multidisciplinary therapy including hepatic arterial infusion, transcatheter arterial embolization, and percutaneous acetic acid injection.Patients in group B were older, had lower serum albumin levels, and there were more patients with liver cirrhosis and great vessel invasion. Median survivals of group A and B patients were 17 months and 7 months, respectively (p0.001). But the 1-, 3-, 5-year survival rates in group B using 38 patients undergoing 3 or more sessions of nonsurgical treatment were not significantly worse than those for group A using 53 patients with followup (57.1%, 19.0%, 16.3% versus 60.7%, 24.5%, 24.5%, respectively). Group A patients had 37.7% and 71.7% recurrence rates at 6 and 12 months, respectively, after operation, and they had a significantly higher frequency of overall extrahepatic recurrence compared with group B patients (43.4% versus 18.7%, p = 0.005). In group B, only 3 of 35 patients younger than 60 years had tumor shrinkage after nonsurgical treatment modalities in comparison to 17 of 40 patients in the elderly group (p = 0.003). Younger patients had a significantly higher prevalence of hepatitis B surface antigen positivity (85.7% versus 47.5%) and infiltrating tumor growth pattern (74.3% versus 45.0%) compared with older patients.Our study suggests that the advantage of hepatic resection in patients with huge HCC is marginal. An effective adjuvant therapy is needed to improve outcomes after hepatic resection. The experience in using nonsurgical treatment shows that the result is poor in young patients compared with that in elderly patients.

To assess the risk factors that influence mortality from perforated peptic ulcer.Retrospective study.General hospital, Taiwan.179 patients who had their perforated peptic ulcers operated on and who had minimum follow-up of one year.Mortality.The overall mortality was 15% (26/179). Of the 26 patients who died, the cause of death was uncontrolled systemic infection in 21 (81%), hypovolaemic shock in 2, and fatal arrhythmia and heart failure in 1 each. 15 of the patients who died of sepsis did not have fulminant abdominal sepsis. Most deaths occurred early after operation, (range 1-96 days). Old age, preoperative shock, and type of operation seemed to be related to these deaths on univariate analysis, but multivariate analysis showed that coexisting medical illness, delayed treatment, and low albumin concentration were independent risk factors for mortality.To improve the result of treatment of perforated peptic ulcer, the diagnosis and treatment should not be delayed, the associated medical illnesses should be treated, and nutritional support should be given.

A 46-year-old nonsmoking female was diagnosed with pulmonary lymphoepithelioma-like carcinoma (LELC). She simultaneously had a rare skin manifestation, erythema elevatum diutinum (EED), which did not respond to topical treatment. The patient underwent platinum-based chemotherapy and thoracic radiotherapy and had shown complete remission in both LELC and EED. EED is therefore considered as a paraneoplastic syndrome of pulmonary LELC in this case. Literature on LELC and EED were also reviewed.

Effect of the carcinogen thapsigargin on human prostate cancer cells is unclear. This study examined if thapsigargin altered basal [Ca²⁺](i) levels in suspended PC3 human prostate cancer cells by using fura-2 as a Ca²⁺-sensitive fluorescent probe. Thapsigargin at concentrations between 10 nM and 10 µM increased [Ca²⁺](i) in a concentration-dependent fashion. The Ca²⁺ signal was reduced partly by removing extracellular Ca²⁺ indicating that Ca²⁺ entry and release both contributed to the [Ca²⁺](i) rise. This Ca²⁺ influx was inhibited by suppression of phospholipase A2, but not by inhibition of store-operated Ca²⁺ channels or by modulation of protein kinase C activity. In Ca²⁺-free medium, pretreatment with the endoplasmic reticulum Ca²⁺ pump inhibitor 2,5-di-(t-butyl)-1,4-hydroquinone (BHQ) nearly abolished thapsigargin-induced Ca²⁺ release. Conversely, pretreatment with thapsigargin greatly reduced BHQ-induced [Ca²⁺](i) rise, suggesting that thapsigargin released Ca²⁺ from the endoplasmic reticulum. Inhibition of phospholipase C did not change thapsigargin-induced [Ca²⁺](i) rise. At concentrations of 1-10 µM, thapsigargin induced cell death that was partly reversed by chelation of Ca²⁺ with BAPTA/AM. Annexin V/propidium iodide staining data suggest that apoptosis was partly responsible for thapsigargin-induced cell death. Together, in PC3 human prostate cancer cells, thapsigargin induced [Ca²⁺](i) rises by causing phospholipase C-independent Ca²⁺ release from the endoplasmic reticulum and Ca²⁺ influx via phospholipase A2-sensitive Ca²⁺ channels. Thapsigargin also induced cell death via Ca²⁺-dependent pathways and Ca²⁺-independent apoptotic pathways.

The effect of sertraline, an antidepressant, on cytosolic-free Ca(2+) levels ([Ca(2+) ](i) ) in human cancer cells is unclear. This study examined whether sertraline altered basal [Ca(2+) ](i) levels in suspended PC3 human prostate cancer cells by using fura-2 as a Ca(2+) -sensitive fluorescent probe. At concentrations of 10-150 μM, sertraline induced a [Ca(2+) ](i) rise in a concentration-dependent fashion. The Ca(2+) signal was reduced partly by removing extracellular Ca(2+) indicating that Ca(2+) entry and release both contributed to the [Ca(2+) ](i) rise. Sertraline induced Mn(2+) influx, leading to quench of fura-2 fluorescence suggesting Ca(2+) influx. This Ca(2+) influx was inhibited by the suppression of store-operated Ca(2+) channels or by the modulation of protein kinase C activity. In Ca(2+) -free medium, pre-treatment with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin or 2,5-di-(t-butyl)-1,4-hydroquinone nearly abolished sertraline-induced Ca(2+) release. Conversely, pre-treatment with sertraline greatly reduced the inhibitor-induced [Ca(2+) ](i) rise, suggesting that sertraline released Ca(2+) from the endoplasmic reticulum. Inhibition of phospholipase C inhibited sertraline-induced [Ca(2+) ](i) rise. At 20-30 μM, sertraline killed cells in a concentration-dependent manner. The cytotoxic effect of sertraline was enhanced by chelating cytosolic Ca(2+) with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/AM. Annexin V-FITC data suggest that sertraline (20 and 30 μM) evoked apoptosis in a concentration-dependent manner. Together, in PC3 human prostate cancer cells, sertraline induced [Ca(2+) ](i) rises by causing phospholipase C-dependent Ca(2+) release from the endoplasmic reticulum and via multiple Ca(2+) influx pathways that involve store-operated Ca(2+) channels. Sertraline also induced apoptosis that was not triggered by [Ca(2+) ](i) rise.

Adenomyoma of the small intestine is rare. It occurs mostly in the periampullary region or ileum. The common presentations are intussusception and intestinal or biliary obstruction, depending on the location. To our knowledge, gastrointestinal (GI) bleeding from a jejunal adenomyoma has not been reported previously. We present a 74-year-old female patient who suffered intermittent tarry stool passage for 1 month. Initial upper GI endoscopy, colonoscopy and computed tomography failed to find the bleeder. A papilla-like tumor with central depression and active bleeding in the proximal jejunum was found by push enteroscopy. Exploratory laparotomy showed a submucosal nodule about 1.5 cm in size located about 20 cm distal to the Treitz ligament. Wedge resection was carried out. Pathologic examination revealed that the tumor was composed of some cystic exocrine-type ducts and bundles of smooth muscle, indicating adenomyoma. The patient was symptom-free following operation.

Background To evaluate hyperthermic intraperitoneal chemotherapy (HIPEC) as an adjuvant chemotherapy in advanced gastric cancer (AGC) patients with serosal invasion. Methods Patients who received radical surgery and palliative surgery between January 2002 and December 2010 were retrospectively examined. Patients were divided into two groups, namely, one group that underwent surgery and another group that underwent surgery with HIPEC. All patients who received HIPEC had suspected serosal invasion on an abdominal computed tomography or by the surgeon's assessment during the operation. Results The prophylactic groups included 83 patients who underwent gastrectomy alone. A total of 29 patients underwent gastrectomy with HIPEC. The 5-year survival rates were 10.7% and 43.9%, respectively. The 5-year mean survival times were 22.66 (17.55–25.78) and 34.81 (24.97–44.66) months ( p = 0.029), respectively. There were 52 patients who had a recurrence of carcinomatosis among 133 patients who had resections (52/133, 39.1%). The 3-year disease-free survival rate for carcinomatosis was 28.87% in the group that received surgery alone, whereas it was 66.03% in the group that received HIPEC. There was no significant difference in the rate of complication between the two groups in the prophylactic group ( p = 0.542). Thus, curative surgery with HIPEC had a better prognosis for AGC with serosal invasion. The carcinomatosis recurrence time was longer in patients who underwent gastrectomy with HIPEC and received R0 resection. Conclusion The survival benefit of HIPEC as an adjuvant therapy for gastric cancer patients with serosal invasion should be validated in a large cohort.