Characteristics of Atrial Fibrillation Patients Suffering Esophageal Injury Caused by Ablation for Atrial Fibrillation.

The close proximity of esophagus to the left atrial posterior wall predisposes esophagus to thermal injury during catheter ablation for atrial fibrillation (AF). In this retrospective study, we aimed to investigate risk factors of esophageal injury (EI) caused by catheter ablation for AF. Patients who underwent first-time AF ablation from July 2013 to June 2018 were included. The esophagus was visualized by oral soluble contrast during ablation for all patients and a subset of patients were selected to undergo endoscopic ultrasonography (EUS) to estimate EI post ablation. Degree of EI was categorized as Kansas City classification: type 1: erythema; type 2: ulcers (2a: superficial ulcers; 2b: deep ulcers); type 3: perforation (3a: perforation without communication with the atria; 3b: atrioesophageal fistula [AEF]). Of 3,852 patients, 236 patients (61.5 ± 9.7 years; male, 69%) received EUS (EUS group) and 3616 (63.2 ± 10.9 years; male, 61.1%) without EUS (No-EUS group). In EUS group, EI occurred in 63 patients (type 1 EI in 35 and type 2 EI in 28), and no type 3 EI was observed during follow up. In a multivariable logistic regression analysis, an overlap between the ablation lesion and esophagus was an independent predictor of EI (odds ratio, 21.2; 95% CI: 6.23-72.0; P < 0.001). In No-EUS group, esophagopericardial fistula (EPF; n = 3,0.08%) or AEF (n = 2,0.06%) was diagnosed 4-37 days after ablation. In 3 EPF patients, 2 completely recovered with conservative management and 1 died. Two AEF patients died. Ablation at the vicinity of the esophagus predicts risk of EI. EUS post ablation may prevent the progression of EI and should be considered in management of EI. It remains challenging to identify patients with high risk of EI.

Endoscopic submucosal dissection for localised gastric amyloidosis mimicking malignancy / Disección submucosa endoscópica para la amiloidosis localizada gástrica que simula una malignidad

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Pancreatic solid cystic desmoid tumor: case report and literature review.

Desmoid tumors (DTs) are nonmetastatic, locally aggressive neoplasms with a high rate of postoperative recurrence. Pancreatic DTs are especially rare; only a few cases have been reported to date. This paper describes a case of a sporadic cystic DT of the pancreas managed successfully with central pancreatectomy, with no signs of recurrence 40 mo after surgery. According to the literature, this is the first reported case in China of a pancreatic DT presenting as a solid cystic lesion, as well as the first pancreatic DT managed with central pancreatectomy and pancreaticogastrostomy. We report the case for its rarity and emphasize disease management by concerted application of clinical, pathological, radiological and immunohistochemical analyses.

Curcumin reverses chemoresistance of human gastric cancer cells by downregulating the NF-κB transcription factor.

Gastric cancer remains one of the major health problems worldwide. Chemotherapy is an important therapeutic modality for gastric cancer, but the success rate of this treatment is limited because of chemoresistance. The ubiquitously expressed transcription factor NF-κB has been suggested to be associated with chemoresistance of gastric cancer. Agents that can either enhance the effects of chemotherapeutics or overcome chemoresistance to chemotherapeutics are needed for the treatment of gastric cancer. Curcumin, a component of turmeric, is one such agent that has been shown to suppress NF-κB and increase the efficacy of chemotherapy. In this study, we investigated whether curcumin can reverse chemoresistance by downregulating NF-κB in human gastric cancer cells. SGC-7901 human gastric cancer cells was treated with chemotherapeutics (etoposide and doxorubicin) or by combined application of curcumin and chemotherapeutics. The viability of SGC-7901 cells was measured by MTT assay. Apoptosis of SGC-7901 cells was detected using the TUNEL and Annexin V/PI methods. The protein levels of NF-κB were analyzed by immunocytochemical staining. EMSA was used to confirm the increased nuclear translocation of RelA. The protein levels of p-IκBα, Bcl-2 and Bcl-xL were analyzed by Western blotting. The chemotherapeutics (etoposide and doxorubicin) suppressed the growth of SGC-7901 cells, in a time-dose-dependent manner. Use of curcumin in addition to these agents can suppress cell growth further (inhibitory rate: doxorubicin vs. doxorubicin + curcumin, 33% vs. 45%, p<0.05; etoposide vs. etoposide + curcumin, 35% vs. 48%, p<0.05). Furthermore, chemotherapeutics induced apoptosis of SGC-7901 cells and activated NF-κB. The combination of curcumin and chemotherapeutics induced apoptosis of SGC-7901 cells further, attenuated the activation of NF-κB, and reduced expression of the NF-κB-regulated anti-apoptotic gene products Bcl-2 and Bcl-xL. Curcumin potentiates the antitumor effects of chemotherapeutics in gastric cancer by suppressing NF-κB and NF-κB-regulated anti-apoptotic genes.

[Effect of Luteolin and its combination with chemotherapeutic drugs on cytotoxicity of cancer cells].

OBJECTIVE: To investigate the effect of Luteolin alone or combination with chemotherapentic drugs on the cytoxicity of cancer cells. METHODS: Cultured A549, Hela, MCF-7, AGS, MGC-803, Caco2 and HepG2 cells were treated with Luteolin or the combination of Luteolin with other chemotherapeutic agents (Bexarotene, Cisplatin and Bleomycin). Cell viability was measured by MTS assay and IC(50) was calculated. RESULTS: The IC(50) of Bexarotene to Hela cells was 2 micromol/L, but with the combination of 5 micromol/L of Luteolin that reduced to 0.2 micromol/L. However, the combination of Bexarotene and Luteolin did not show significant benefit in MGC-803, HepG2 cells, Caco2 and MCF-7 cells. The IC(50) of Cisplatin to Hela cells was over 30 micromol/L,but it decreased to 3 micromol/L in the presence of 5 micromol/L Luteolin; Luteolin also sensitized Cisplatin in MGC-803, HepG2 and A549 cells studied. The IC(50) of Bleomycin to Hela cells was over 100 micromol/L, but it was about 1 micromol/L in the presence of 5 micromol/L Luteolin. A549 cells were resistant to Bleomycin with an IC(50) of 100 micromol/L, 10 micromol/L Luteolin greatly enhanced the cytotoxicity of Bleomycin to the cells with the IC(50) of about 10 micromol/L. The inhibitions of MGC-803, HepG2, A549 and AGS cells didn't change by combination of Luteolin. CONCLUSION: Low concentration of Luteolin has little toxic effect on the cancer cell lines tested in the study, but it can sensitize chemotherapeutic drugs in various cancer cell lines.

Therapeutic effects of rectal administration of muscovite on experimental colitis in rats.

BACKGROUND AND AIMS: The aim of this study was to investigate whether rectal administration of muscovite can ameliorate colonic inflammation in a rat model of experimental colitis, and its possible mechanism. METHODS: Female Sprague-Dawley (SD) rats with trinitrobenzene sulfonic acid (TNBS)-induced colitis were treated with rectal administration of muscovite or 5-aminosalicylic acid (5-ASA) daily for 14 days. The changes in body weight, macroscopic damage and histologic scores were subsequently evaluated. Gene expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), mucin2 (MUC2) and trefoil factor 3 (TFF3) in the colonic tissues was assessed by semiquantitative reverse transcription polymerase chain reaction (RT-PCR) while protein levels of TNF-alpha and IL-1beta were detected by ELISA. Mucin2 expression in colonic mucosa was detected by immunohistochemistry. The capacity of muscovite to adsorb cytokines in vitro was determined by the changes in the amount of TNF-alpha, IL-1beta secreted by lipopolysaccharide (LPS)-stimulated THP-1 cells and IL-8 secreted by LPS-stimulated HT-29 cells. RESULTS: Rectal administration of muscovite improved the loss of body weight, macroscopic and histologic scores of TNBS-induced colitis in a dose-dependent manner. Trinitrobenzene sulfonic acid-induced expression of TNF-alpha and IL-1beta was reduced by muscovite and 5-ASA treatment. Reduction of MUC2 expression in colitis rats was reversed by muscovite and 5-ASA treatment. However, the expression of TFF3 mRNA in colonic mucosa was not affected. In addition, we found muscovite inhibited the expression of TNF-alpha, IL-1beta secreted by THP-1 and IL-8 secreted by HT-29 cells in a dose-dependent manner. CONCLUSIONS: Our study demonstrated for the first time that rectal administration of muscovite can ameliorate colonic inflammation of TNBS-induced colitis. Further confirmatory studies are needed to prove that muscovite might be a potential therapeutic agent for the treatment of ulcerative colitis.

[Laparoscopic splenectomy and pericardial devascularization for treatment of portal hypertension due to liver cirrhosis].

OBJECTIVE: To evaluate the safety and efficacy of laparoscopic splenectomy (LS) and pericardial devascularization in treatment of portal hypertension due to liver cirrhosis. METHODS: Twenty three cases with hepatitis B and schistosoma cirrhosis and portal hypertension underwent LS and paraesophagogastric devascularization performed by one treatment team. Follow-up was conducted for 9 months. RESULTS: LS combined with pericardial devascularization was successfully performed on these 20 cases. Three cases were converted to open surgery due to intra-operative bleeding. The mean operative time was 235 min (180 - 350), and mean intra-operative blood loss was 520 ml (200 - 1600 ml). All patients were treated with plasma transfusion, antibiotics, and abdominal drainage post-operatively. Peristalsis of stomach and intestine recovered 24 - 72 hours after operation. The mean hospitalization time was 8.5 days (6 - 17 days). The peri-operative complication included plural effusion in 3 cases and subphrenic abscess in one case, .mild ascites in two cases, and wound dehiscence in one case. No mortality occurred. Rebleeding rare was 0%. CONCLUSION: LS combined with pericardial devascularization is relatively safe and effective in treatment of portal hypertension due to liver cirrhosis. The keys to success include experienced laparoscopic skills, use of harmonic scalpel and careful manipulation.

A primary intestinal lymphangiectasia patient diagnosed by capsule endoscopy and confirmed at surgery: a case report.

Intestinal lymphangiectasia (IL) is a rare disease characterized by dilated lymphatic vessles in the intestinal wall and small bowel mesentery which induce loss of protein and lymphocytes into bowel lumen. Because it most often occurs in the intestine and cannot be detected by upper gastroendoscopy or colonoscopy, and the value of common image examinations such as X-ray and computerized tomography (CT) are limited, the diagnosis of IL is difficult, usually needing the help of surgery. Capsule endoscopy is useful in diagnosing intestinal diseases, such as IL. We here report a case of IL in a female patient who was admitted for the complaint of recurrent edema accompanied with diarrhea and abdominal pain over the last twenty years, and aggravated ten days ago. She was diagnosed by M2A capsule endoscopy as a primary IL and confirmed by surgical and pathological examination.

Gynura root induces hepatic veno-occlusive disease: a case report and review of the literature.

Gynura root has been used extensively in Chinese folk medicine and plays a role in promoting microcirculation and relieving pain. However, its hepatic toxicity should not be neglected. Recently, we admitted a 62-year old female who developed hepatic veno-occlusive disease (HVOD) after ingestion of Gynura root. Only a few articles on HVOD induced by Gynura root have been reported in the literature. It is suspected that pyrrolizidine alkaloids in Gynura root might be responsible for HVOD. In this paper, we report a case of HVOD and review the literature.

[Effect of mucosal protective on the quality of gastric ulcer healing].

OBJECTIVE: To explore the mucosal protective effect on the quality of gastric ulcer healing. METHODS: Gastric ulcers were induced in male rats by serosal application of acetic acid. Rats were gavaged for 14 days with saline, omeprazole (OME), teprenone (TEP) and TEP plus OME starting 3 days after ulcer induction. Then the tissues and blood samples were obtained and measured. RESULT: The lower ulcer index (UI) and increased ulcer inhibition rate were observed in OME and OME+TEP groups. In TEP and OME+TEP groups, restored mucosa thickness increased, cystically dilated glands decreased, microvessels in connective tissue increased, the secretion of mucus, hexosamine, PGE(2), bFGF were enhanced, the expression of EGFR was increased. CONCLUSION: TEP can improve the quality of gastric ulcer healing, when combined with OME,the effect is more marked.

[The effect of muscovite on the quality of gastric ulcer healing].

OBJECTIVE: To explore the effect of muscovite on the quality of gastric ulcer healing. METHOD: Gastric ulcers were produced in male rats by serosal application of acetic acid. Rats were gavaged for 14 days with saline, omeprazole and muscovite starting 3 days after ulcer induction. Then the tissue and blood samples were obtained and measured. RESULT: In the muscovite group, restored mucosa thickness increased, cystically dilated glands decreased, microvessels in connective tissue increased, the secretion of mucus, hexosamine, PGE2, EGF, bFGF were enhanced, and the express of EGFR was stronger. CONCLUSION: Muscovite can promote the gastric ulcer healing and improve the quality of gastric ulcer healing.

Quality of gastric ulcer healing evaluated by endoscopic ultrasonography.

AIM: To evaluate the quality of gastric ulcer healing after different antiulcer treatment by endoscopic ultrasonography (EUS). METHODS: The patients were divided into three groups, and received lansoprazole, amoxicillin and clarithromycin for 1 wk. Then group A took lansoprazole combined with tepreton for 5 wk, group B took lansoprazole and group C took tepreton for 5 wk. Endoscopy and EUS were performed before and 6 wk after medication. RESULTS: There was no significant difference in cumulative healing rate to S stage between the groups (89%, 82% vs 83%, P>0.05). The rate of white scar formation was significantly higher in group A than in groups B and C (67%, 36%, 50%, P<0.05). The average contraction rates of the width of ulcer crater, length of disrupted muscularis propria layer and hypoechoic area were higher in group A than in groups B and C (0.792+/-0.090, 0.660+/-0.105 vs 0.668+/-0.143, P<0.05). The hypoechoic area disappeared in four cases of group A, one of group B and two of group C. The percentage of hypoechoic area disappearance was higher in group A than in the other two groups (44%, 9% vs 17%, P<0.05). Gastric ulcer healing was better in group A. CONCLUSION: The combined administration of proton-pump inhibitors and mucosal protective agent can improve gastric ulcer healing.

[Mechanism of isinglass in prevention and treatment of chronic atrophic gastritis in rats].

OBJECTIVE: To investigate the mechanism of isinglass in the prevention and treatment of chronic atrophic gastritis (CAG) in rats. METHOD: Animal models of SD rats with CAG were made in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while CAG rat model was being made. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed. Then the length of the proliferation zone of the gastric mucosa and serum epidermal growth factors (EGF) and growth hormones (GH)level were studied. RESULT: In isinglass prevention groups and high dose isinglass reverse group, the length of the proliferation zone of the gastric mucosa was very close to that in normal control group (P > 0.05), much better than model control group (P < 0.01). In low dose isinglass reverse group, it was lower than that in normal control group (P < 0.01), but much better than model control group (P < 0.01). In both prevention and reverse groups, serum EGF level was higher than that in normal (P < 0.01) and model control group (P < 0.05). Serum GH level was the same in every group (P > 0.05). CONCLUSION: The mechanism of isinglass in the prevention and treatment of CAG rats lies in revitalizing and proliferating gastric mucosal cells by stimulating endogenous EGF secretion.

[Prevention and treatment of chronic atrophic gastritis in rats with isinglass].

OBJECTIVE: To evaluate the effect of isinglass on the prevention and treatment of chronic atrophic gastritis in rats. METHOD: Animal model of SD rats with CAG was established in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while we were establishing CAG rat model. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed and pathologic changes of the gastric mucosa were studied by gross appearance and microscopy. RESULT: In isinglass prevention groups and reverse groups, inflammation grades of gastric antrum were less than these in model control group (P < 0.01) while the means of ratios of the thickness of gastric mucosal gland and muscularis mucos (L1/L2), the number of gastric glands in 1-mm lengths of mucosal layer were much better than those in model control group (P < 0.01). They were very close to normal control group (P > 0.05). CONCLUSION: Isinglass can prevent the gastric mucosal atrophy in the CAG model and can improve and cure the gastric mucosal atrophy of the SD rats with GAG.

[Effects of EGF/EGFR expression on atrophic gastritis in rats].

OBJECTIVE: To investigate the epidermal growth factor(EGF) and epidermal growth factor receptor(EGFR) expression in atrophic gastritis in rats to explore the relationship between EGF and chronic atrophic gastritis(CAG). METHODS: The serum EGF and gastric mucosal, EGFR level were measured in 20 rats with CAG and 20 normal controls. RESULTS: The average EGF level (0.149+/-0.020) microg/L and 80% positive rate of EGFR expression observed in CAG group were significantly higher than those in control group[(0.043+/-0.003) microg/L and 0%,P<0.01]. CONCLUSION: The study demonstrates an association of high levels of EGF and positive EGFR expression in CAG rats. Further studies are necessary to clarify whether EGF/EGFR play a significant role in the pathogenesis of CAG.