More than 7-year survival of a patient following repeat hepatectomy for total 20 colon cancer liver metastases

A 54-year-old man was transferred with sigmoid colon cancer combined with multiple bilobar liver metastases. Nine metastases were in the left lobe and 5 metastases were in the right lobe. After low anterior resection, all 9 lesions in the left lobe were completely removed by wedge resections. Because the remnant liver volume after multiple wedge resection of the left lobe was not sufficient to perform a right hepatectomy simultaneously, we planned a two-stage hepatectomy. Right portal vein embolization was performed one week after the first liver operation. A right hepatectomy was safely performed 22 days after the first hepatectomy. A recurrent mass developed in the segment III 18 months after the right hepatectomy. Radiofrequency ablation (RFA) was performed to remove that lesion. Five other metastases developed 18 months after RFA whereby multiple wedge resections were performed. The patient has survived for more than 7 years after the first liver operation

Staged Surgery for Chronic Primary Aortoduodenal Fistula in a Septic Patient

Aortoenteric fistula is one of the most challenging problems that confront the vascular surgeons. Controversy remains over the optimal treatment because of the continued publication of series with high mortality, amputation, and aortic disruption rates. A positive preoperative blood culture is the best predictor of mortality with increased amputation rates due to infection of the extra-anatomic bypass. Therefore, in selected cases with sepsis, a prudent management protocol is required. We report a 68-yr-old male presenting with a chronic primary aortoduodenal fistula extensively involving the duodenum and Gram-negative sepsis. We planned a staged operation. Initially, an emergency laparotomy and control of the aorta allowed stabilization of the patient, identification of the fistula, and direct in situ placement of the prosthetic graft followed by an en bloc resection of the aneurysm and the surrounding structures. After he recovered from sepsis and had been stabilized, a staged extra-anatomic bypass followed by transabdominal removal of the temporarily placed graft was done. This management plan will allow the highest success rate and may be a prudent management protocol for these difficult cases

Traumatic neuroma of the right posterior hepatic duct with an anatomic variation masquerading as malignancy: a case report

Traumatic neuroma (TN), also known as amputation neuroma, is a reactive hyperplasia of nerve fibers and connective tissue arising from Schwann cells after trauma or surgery. TN of the bile duct is usually asymptomatic, but rarely can lead to right upper quadrant pain, biliary obstruction, and acute cholangitis. It is very difficult to discriminate TN from malignancy before surgery, although doing so could avoid an unnecessary radical resection of the lesion. In the course of surgery, TN can be caused by unintentional injury of a nerve fiber near the common bile duct (CBD) and heat damage to an artery, complete ligation of an artery, and excessive manipulation of the CBD. Therefore, to prevent TN after cholecystectomy, surgery should be performed carefully with appropriate consideration of anatomic variations, and a cystic duct should not be resected too close to the CBD. The possibility of TN should be considered if a patient who has undergone CBD resection with hepaticojejunostomy or cholecystectomy long ago experiences symptoms of jaundice, cholangitis, or obliteration of the CBD. In this report, we present a case of TN mimicking cholangiocarcinoma that emerged from a cystic duct stump after cholecystectomy

Subchronic inhalation toxicity of gold nanoparticles

<p>Abstract</p> <p>Background</p> <p>Gold nanoparticles are widely used in consumer products, including cosmetics, food packaging, beverages, toothpaste, automobiles, and lubricants. With this increase in consumer products containing gold nanoparticles, the potential for worker exposure to gold nanoparticles will also increase. Only a few studies have produced data on the <it>in vivo </it>toxicology of gold nanoparticles, meaning that the absorption, distribution, metabolism, and excretion (ADME) of gold nanoparticles remain unclear.</p> <p>Results</p> <p>The toxicity of gold nanoparticles was studied in Sprague Dawley rats by inhalation. Seven-week-old rats, weighing approximately 200 g (males) and 145 g (females), were divided into 4 groups (10 rats in each group): fresh-air control, low-dose (2.36 × 10⁴particle/cm³, 0.04 μg/m³), middle-dose (2.36 × 10⁵particle/cm³, 0.38 μg/m³), and high-dose (1.85 × 10⁶particle/cm³, 20.02 μg/m³). The animals were exposed to gold nanoparticles (average diameter 4-5 nm) for 6 hours/day, 5 days/week, for 90-days in a whole-body inhalation chamber. In addition to mortality and clinical observations, body weight, food consumption, and lung function were recorded weekly. At the end of the study, the rats were subjected to a full necropsy, blood samples were collected for hematology and clinical chemistry tests, and organ weights were measured. Cellular differential counts and cytotoxicity measurements, such as albumin, lactate dehydrogenase (LDH), and total protein were also monitored in a cellular bronchoalveolar lavage (BAL) fluid. Among lung function test measurements, tidal volume and minute volume showed a tendency to decrease comparing control and dose groups during the 90-days of exposure. Although no statistically significant differences were found in cellular differential counts, histopathologic examination showed minimal alveoli, an inflammatory infiltrate with a mixed cell type, and increased macrophages in the high-dose rats. Tissue distribution of gold nanoparticles showed a dose-dependent accumulation of gold in only lungs and kidneys with a gender-related difference in gold nanoparticles content in kidneys.</p> <p>Conclusions</p> <p>Lungs were the only organ in which there were dose-related changes in both male and female rats. Changes observed in lung histopathology and function in high-dose animals indicate that the highest concentration (20 μg/m³) is a LOAEL and the middle concentration (0.38 μg/m³) is a NOAEL for this study.</p

Crotonis Fructus

Introduction. Crotonis fructus (CF) is the mature fruit of Croton tiglium L. and has been used for the treatment of gastrointestinal disturbance in Asia. It is well known that the main component of CF is croton oil (CO). The present study is to investigate the effects of CF extracts (CFE) and CO on lipolysis in OP9 adipocytes. Methods. Glycerol release to the culture supernatants was used as a marker of adipocyte lipolysis. Results. Treatment with various concentrations of CFE and CO stimulates glycerol release in a dose-dependent manner. The increase in glycerol release by CFE is more potent than isoproterenol, which is a β-adrenergic agonist as a positive control in our system. The increased lipolysis by CFE and CO was accompanied by an increase of phosphorylated hormone sensitive lipase (pHSL) but not nonphosphorylated HSL protein and mRNA. Pretreatment with H89, which is a protein kinase A inhibitor, significantly abolished the CFE- and CO-induced glycerol release in OP9 adipocytes. These results suggest that CFE and CO may be a candidate for the development of a lipolysis-stimulating agent in adipocytes

Atherosclerotic Progression Attenuates the Expression of Nogo-B in Autopsied Coronary Artery: Pathology and Virtual Histology Intravascular Ultrasound Analysis

The relation of Nogo-B to atherosclerotic plaque progression is not well understood. Thus, the purpose of this study was to assess the expression of Nogo-B in fibroatheromas (FA) of different stages, classified using virtual histology intravascular ultrasound (VH-IVUS) analysis in 19 autopsied cases of non-sudden cardiac death. VH-IVUS imaging analysis was performed 30 mm from the ostium of each coronary artery. VH-IVUS revealed 11 early FAs (34.5±8.3 yr), 12 late FAs (42.6±16.6 yr), 8 thick-cap FAs (TkCFAs) (46.4±11.1 yr), and 6 thin-cap FAs (TCFAs) (51.8±6.8 yr). TkCFAs and TCFAs were defined as advanced FA. FA progression advanced with age (P=0.04). VH-IVUS analysis of small, early FAs showed smaller necrotic cores and relatively less calcium compared to more advanced FAs with large necrotic cores (P<0.001). Histopathology and immunohistochemical stains demonstrated that early or late FAs had smaller necrotic cores, less empty space of decalcification, and greater Nogo-B expression compared to advanced FAs (vs. early FA, P=0.013; vs. late FA, P=0.008, respectively). These findings suggest that FA progression is inversely associated with Nogo-B expression. Local reduction of Nogo-B may contribute to plaque formation and/or instability

Roles of Exosome-Like Vesicles Released from Inflammatory C2C12 Myotubes: Regulation of Myocyte Differentiation and Myokine Expression

Background/Aims: The complicated differentiation processes of cells in skeletal muscle against inflammation that induce muscle atrophy are not fully elucidated. Given that skeletal muscle is a secretory organ, we evaluated the effects of inflammation on myogenic signals and myokine expression, and the roles of inflammatory exosomes released by myotubes in myogenic differentiation. Methods: Inflammation was induced by treatment of fully differentiated C2C12 myotubes with a cytokine mixture of TNF-α and INF-γ. Exosome-like vesicles (ELVs) were isolated from conditioned media of control or inflamed myotubes and incubated with myoblasts. The expression of molecular switches that contribute to myogenic differentiation, including several kinases, their downstream targets, and myokines, were evaluated using immunoblot analysis in inflamed myotubes and in myoblasts treated with ELVs. Results: Inflammation activated molecular mechanisms contributing to muscle atrophy, including AMPK, p-38 MAPK and JNK, while inhibiting Akt-mediated myogenic signals. In addition, inflammation induced myostatin expression with suppression of a myostatin-counteracting myokine, decorin. Well-characterized ELVs released from inflamed myotubes induced myoblast inflammation and inhibited myogenic mechanisms while stimulating atrophic signals. Conclusion: Inflammation of skeletal muscle induces muscle atrophy via multiple mechanisms, including the regulation of myokines and kinases. Inflammatory ELVs are likely to contribute to inflammation-induced muscle atrophy