A method of gastric conduit elevation via the posterior mediastinal pathway in thoracoscopic subtotal esophagectomy

<p>Abstract</p> <p>Background</p> <p>Despite efforts to improve surgical techniques, serious complications still sometimes occur. Use of a physiological posterior mediastinal pathway has increased given advances such as automated anastomotic devices and a reduction in the incidence of anastomotic sufficiency. Until now the gastric conduit created has been protected by an echo probe cover and, sown to the ventral side of polyester tape placed through the abdomen to the neck, and then blindly elevated to the neck. We report on a new method of gastric conduit elevation.</p> <p>Methods</p> <p>Two 60-cm lengths polyester tape are ligated at both ends to form a loop. An echo probe cover of 10 cm in diameter and 50 cm in length is prepared and the tip cut off, forming a cylinder. The knots in the previously looped polyester tape are inserted into the echo probe cover. The looped polyester tape and echo probe cover is ligated with silk approximately 5 cm in front of the knots on both sides.</p> <p>After dissection is carried out according to practice, the previously crafted polyester tape is inserted into the chest cavity. One end of polyester tape is fixed to the distal esophageal stump with the clips, with the opposite end fixed to the proximal esophageal stump. The echo probe cover that connects the proximal esophagus and distal esophagus is monitored for the presence of creases along the long axis to ensure there are no twists in the echo probe cover.</p> <p>We carry out a laparoscopic-assisted perigastric lymph node dissection, make a small skin incision, and guide part of the thoracic esophagus and stomach outside the body.</p> <p>Either one of the two lengths of polyester tape is connected to the gastric conduit. By pulling up this length of polyester tape from the neck, the gastric conduit can pass through the echo probe cover and be elevated to the neck.</p> <p>Results</p> <p>No perioperative complications such as bleeding or difficulty of the gastric conduit elevation were recognized with this method.</p> <p>Conclusions</p> <p>This method is considered to serve as a useful technique for gastric conduit elevation.</p

Variations of the cephalic vein anterior to the clavicle in humans

Background: Clinicians should understand that jugulocephalic vein (JCV) variants may be occasionally found. This study aims to classify JCV variants and obtain their frequency.   Materials and methods: We investigated anatomical variants of the cephalic vein in 55 human cadavers during a gross anatomy course at our medical school.   Results: The percentage of JCVs that pass through the anterior part of the clavicle and anastomose to the jugular vein as per previous studies and our study was 2–5%. Five cases with anastomosis between the cephalic and external jugular veins that pass through the anterior part of the clavicle were found. The courses were classified into 1A, 1B, 2A, and 2B. Type 1 extends beyond the clavicle and anastomoses with the external jugular vein. Type 2 follows the same course as type 1, but anastomoses with the subclavian vein. Subtype A does not have a branch that anastomoses with the axillary vein, whereas subtype B does. We encountered two cases of type 1A and three of type 1B.   Conclusions: Four anatomical variants of the cephalic vein around the clavicle were identified. Clinicians’ knowledge of these variants is expected to decrease possible complications if venous access via the cephalic vein is needed

Sorafenib as a secondary treatment

Background and Aim: Currently, there is no molecular‐targeted agent that has demonstrated evidence of efficacy in patients with unresectable hepatocellular carcinoma (u‐HCC) who have developed resistance to treatment with lenvatinib (LEN). In this real‐world study, we aimed to investigate the therapeutic effect and safety of sorafenib (SOR) in patients with u‐HCC after progression on treatment with LEN. Methods (Patients) and Results: A total of 13 patients with u‐HCC (12 males and 1 female), who were treated with SOR after progression on LEN, were enrolled in this retrospective study. Therapeutic efficacy was evaluated via contrast‐enhanced computerized tomography at 8 weeks after the initiation of SOR therapy according to modified response evaluation criteria in solid tumors (mRECIST) and RECIST. According to mRECIST, the objective response rate (ORR) and disease control rate (DCR) were 15.3% (2/13) and 69.2% (9/13), respectively. According to RECIST, the ORR and DCR were 0% (0/13) and 69.2% (9/13), respectively. The median progression‐free survival was 4.1 months. The median albumin‐bilirubin scores did not deteriorate significantly at 4, 6, and 8 weeks after initiation of SOR, compared with the scores at the baseline. The most frequent grade 1 or 2 adverse events (AEs) were palmar–plantar erythrodysesthesia, fatigue, diarrhea, and hypertension. There was no incidence of grade 3 AEs. Conclusion: Treatment with SOR may be effective for u‐HCC after failure on LEN and may not worsen the liver reserve

Establishment of a monoclonal antibody for human LXRα: Detection of LXRα protein expression in human macrophages

Liver X activated receptor alpha (LXRα) forms a functional dimeric nuclear receptor with RXR that regulates the metabolism of several important lipids, including cholesterol and bile acids. As compared with RXR, the LXRα protein level in the cell is low and the LXRα protein itself is very hard to detect. We have previously reported that the mRNA for LXRα is highly expressed in human cultured macrophages. In order to confirm the presence of the LXRα protein in the human macrophage, we have established a monoclonal antibody against LXRα, K-8607. The binding of mAb K-8607 to the human LXRα protein was confirmed by a wide variety of different techniques, including immunoblotting, immunohistochemistry, and electrophoretic mobility shift assay (EMSA). By immunoblotting with this antibody, the presence of native LXR protein in primary cultured human macrophage was demonstrated, as was its absence in human monocytes. This monoclonal anti-LXRα antibody should prove to be a useful tool in the analysis of the human LXRα protein

Influence of light alcohol consumption on lifestyle-related diseases : a predictor of fatty liver with liver enzyme elevation in Japanese females with metabolic syndrome

Background Although heavy drinking is known to lead to liver injury, some recent studies have reported that light alcohol consumption (LAC) may play a protective role against fatty liver in the general population, and may even play a protective role against non-alcoholic fatty liver disease (NAFLD) in males with metabolic syndrome (MS). However, the association between LAC and fatty liver with liver enzyme elevation in females with MS is unclear. Methods Participants of this study were 20,853 females who underwent a regular health check-up between April 2008 and March 2012 at our hospital. Enrolled subjects were 1141 females with MS, who underwent all necessary tests and drank less than 20 g/day of alcohol. We investigated the presence of fatty liver with liver enzyme elevation, defined in this study as alanine aminotransferase (ALT) levels ≧31 IU/I, and the association between LAC and fatty liver with ALT elevation. Results There was no significant difference in the prevalence of fatty liver and ALT between light drinkers and non-drinkers. The prevalence of individuals receiving a treatment for dyslipidemia and impaired glucose tolerance (IGT) was significantly lower in light drinkers than in non-drinkers. Body mass index (BMI), waist circumference (WC), diastolic blood pressure (DBP), triglyceride (TG), uric acid (UA), IGT, and visceral fat type MS (V-type MS) were significant predictors of the prevalence of fatty liver with ALT elevation in logistic regression analysis. The odds ratio [OR] (95 % confidence interval [CI], p value) for fatty liver with ALT elevation were as follows: BMI, 2.181 (1.445–3.293, p <0.001); WC, 1.853 (1.280–2.684, p <0.01); DBP, 1.604 (1.120–2.298, p <0.05); TG, 2.202 (1.562–3.105, p <0.001); UA, 2.959 (1.537–5.698, p <0.01); IGT, 1.692 (1.143–2.506, p <0.01); and V-type MS, 3.708 (2.529–5.437, p <0.001). Conclusions There was no significant difference in the prevalence of fatty liver with ALT elevation in females with MS between light drinkers and non-drinkers, suggesting that other factors such as BMI, WC, V-type MS, and lifestyle-related disease may be more important than LAC for the prevalence of fatty liver with ALT elevation

lenvatinib in nonviral hepatocarcinoma

Aim: To investigate the therapeutic effect of lenvatinib (LEN) in liver disease etiology, especially nonviral hepatocellular carcinoma (HCC). Methods and Results: Sixty-seven patients with unresectable advanced HCC (u-HCC) treated with LEN and consisting of 26 hepatitis C virus (HCV), 19 hepatitis B virus (HBV), 11 alcohol, and 11 nonalcoholic steatohepatitis (NASH) cases were retrospectively recruited. Univariate and multivariate Cox proportional hazard models were used to determine predictive factors for survival. The objective response rate in the nonviral (alcohol and NASH) group was higher than that in the viral group (59.1% [13/22] vs. 46.7% [21/45]). Progression-free survival was significantly longer in the nonviral group than in the viral group (13.7 vs. 6.6 months; hazard ratio [HR] 0.324; 95% confidence interval [CI] 0.174–0.602; P < 0.01). Similarly, median overall survival (OS) was significantly longer in the nonviral group than in the viral group (not evaluable vs. 15.9 months; HR = 0.277; 95% CI = 0.116–0.662; P < 0.01). Multivariate analysis revealed that portal vein invasion (HR = 5.327, P = 0.0025), treatment line (HR = 0.455, P = 0.023), and etiology (HR = 0.180, P = 0.00055) were significant independent factors associated with OS in u-HCC patients treated with LEN. Conclusion: Our results suggest that LEN is more effective against nonviral u-HCC than against viral u-HCC