Left pneumonectomy for lung cancer after correction of contralateral partial anomalous pulmonary venous return

We report the successful treatment of a 48-year-old man with left lung cancer and contralateral partial anomalous pulmonary venous return (PAPVR). He was found to have an abnormal shadow on a regular checkup. Sputum cytology revealed squamous cell carcinoma. Chest computed tomography showed not only a left hilar mass but also showed that his right superior pulmonary vein was draining into the high portion of the superior vena cava. In the presence of the right partial anomalous pulmonary venous return, it was believed that left pneumonectomy would cause serious postoperative heart failure due to an increase in the left-to-right shunt. Therefore his partial anomalous pulmonary venous return was corrected first under cardiopulmonary bypass, and 3 weeks later he underwent successful radical left pneumonectomy.     

Excitatory amino acid transporters expressed by synovial fibroblasts in rats with collagen-induced arthritis

Although previous studies have demonstrated increased levels of the brain neurotransmitter glutamate (Glu) in the synovial fluid from patients with arthritis, not much attention has been paid to the possible role of Glu in joint synovial tissues to date. Constitutive expression of mRNA was for the first time shown with glutamate aspartate transporter, glutamate transporter-1 and excitatory amino acid carrier-1 (EAAC1), in addition to with particular ionotropic and metabotropic Glu receptors, in cultured synovial fibroblasts prepared from knee joints of male Lewis rats. Immunohistochemical analysis revealed high localization of immunoreactive EAAC1 at synovial tissues. The accumulation of [³H]Glu occurred in a temperature- and sodium-dependent manner in cultured synovial fibroblasts, with a K_m of 23.1 ± 1.1 μM and a V_max of 237.1 ± 31.1 pmol/(mg protein min), respectively. In rats with arthritis induced by immunization to type-II collagen, marked increases were seen in hind paw volume, cytokine mRNA expression and Glu levels in synovial tissues, in addition to histological erosion. In cultured synovial fibroblasts prepared from these arthritic rats, [³H]Glu accumulation was drastically increased with biochemical and pharmacological profiles similar to those seen in normal synovial fibroblasts. The exposure to Glu at 500 μM doubled the incorporation of 5-bromo-2′-deoxyuridine in cultured synovial fibroblasts of arthritic but not normal rats, without significantly affecting mRNA expression of different cytokines in both synovial fibroblasts. These results suggest that Glu may at least in part play a role in mechanisms associated with cellular proliferation through particular transporters functionally expressed by synovium in rheumatoid arthritis.     

Regeneration of osteonecrosis of canine scapho-lunate using bone marrow stromal cells: possible therapeutic approach for Kienböck disease

We evaluated the ability of canine bone marrow stromal cells (cBMSCs) to regenerate bone in a cavity of the scapholunate created by curretage and freeze-thawing with liquid nitrogen (LN). Autologous BMSCs were harvested from the iliac crest and expanded in vitro. Their potential to differentiate into osteo-, chondro-, and adipogenic lineages was confirmed using a standard differentiation induction assay. LN-treated scapholunates showed no regeneration of bone tissue when the cavity was left alone, demonstrating severe collapse and deformity as observed in human Kienb?ck disease. A combination of beta-tri-calcium phosphate and a vascularized bone graft with autologous fibroblasts failed to regenerate bone in the LN-treated cavity. When the same procedure was performed using BMSCs, however, LN-treated scapholunates showed no collapse and deformity, and the cavity was completely filled with normal cancerous bone within 4 weeks. These results suggested the potential of using BMSCs to treat Kienb?ck disease.     

alpha7 Nicotinic acetylcholine receptor stimulation inhibits lipopolysaccharide-induced interleukin-18 and -12 production in monocytes

Nicotine inhibited interleukin (IL)-18 and -12 production in lipopolysaccharide (LPS)-stimulated monocytes, and the action of nicotine was antagonized by a non-selective and a selective alpha7 nicotinic acetylcholine receptor (alpha7-nAChR) antagonist, suggesting that the stimulation of alpha7-nAChR may be involved in the action of nicotine. Nicotine is reported to induce prostaglandin E(2) (PGE(2)) production in monocytes through the up-regulation of cyclooxygenase (COX)-2 expression. PGE(2) is known to increase cAMP levels and to activate protein kinase A (PKA). COX-2 and PKA inhibitors prevented the action of nicotine, indicating that the mechanism of action of nicotine may be via endogenous PGE(2) production.     

A case of transitional cell carcinoma of the bladder in a juvenile patient

A 17-year-old male was referred to our hospital with the chief complaint of right back pain. Cystoscopic examination revealed a papillary tumor on the posterior wall following detection on screening ultrasound examination revealed a tumor in the bladder. Transurethral resection of the bladder tumor was performed. Histological examination of the excised tumor revealed transitional cell carcinoma, grade 1, pTa. No recurrence has been observed for about 1 year postoperatively.     

Fbxw7 contributes to tumor suppression by targeting multiple proteins for ubiquitin-dependent degradation

Fbxw7 (also known as Sel-10, hCdc4 or hAgo) is the F-box protein component of a Skp1-Cul1-F-box protein (SCF) ubiquitin ligase. Fbxw7 contributes to the ubiquitin-mediated degradation of cyclin E, c-Myc, Aurora-A, Notch and c-Jun, all of which appear to function as cell-cycle promoters and oncogenic proteins. Loss of Fbxw7 results in elevated expression of its substrates, which may lead to oncogenesis. However, it remains largely unclear which accumulating substrate is most related to cancer development in Fbxw7-mutant cancer cells. In the present study, we examined the abundance of cyclin E, c-Myc and Aurora-A in seven cancer cell lines, which harbor wild-type (three lines) or mutant (four lines) Fbxw7. Although these three substrates accumulated in the Fbxw7-mutant cells, the extent of increase in the expression of these proteins varied in each line. Forced expression of Fbxw7 reduced the levels of cyclin E, c-Myc and Aurora-A in the Fbxw7-mutant cells. In contrast, a decrease in the expression of cyclin E, c-Myc or Aurora-A by RNA interference significantly suppressed the rate of proliferation and anchorage-independent growth of the Fbxw7-mutant cells. These findings thus suggest that the loss of Fbxw7 results in accumulation of cyclin E, c-Myc and Aurora-A, all of which appear to be required for growth promotion of cancer cells. Fbxw7 seems to regulate the levels of multiple targets to suppress cancer development.     

Delayed development of hepatocellular carcinoma during long-term follow-up after eradication of hepatitis C virus by interferon therapy

A 42-year-old Japanese man with liver cirrhosis by hepatitis C virus (HCV) had successful interferon therapy in May 1991. Since then, serum HCV-RNA and liver function tests had been negative. He had continued to drink more than 100 g/d of alcohol as before. In June 2003, a 5-cm tumor was found in the posterior segment of the liver. The tumor was curatively resected and the surgical specimen showed a well-differentiated hepatocellular carcinoma (HCC). Non-cancerous lesions of the liver revealed fibrosis at stage F3 with minimal to mild inflammation of grade A1. Heavy drinking may retard the dissolution of fibrosis and accelerate HCC development in patients with sustained virological response.     

Sarcopenia is a risk factor for cardiovascular events experienced by patients with critical limb ischemia

Background

Prognosis is poor for patients with critical limb ischemia (CLI), and the most frequent cause of death is cardiovascular disease. Low grip strength is a risk factor for cardiovascular events, and sarcopenia may be associated as well. Thus, we hypothesized that sarcopenia is a risk factor for cardiovascular events experienced by patients with CLI. If this is true and appropriate therapy becomes available, the prognosis of patients with CLI will improve with appropriate risk management strategies to prevent cardiovascular events. Therefore, the aim of this study was to verify this hypothesis.

Posterior condylar offset influences the intraoperative soft tissue balance during posterior-stabilized total knee arthroplasty

Purpose

This study aimed to clarify the influence of the posterior condylar offset (PCO) on intraoperative soft tissue balance including the joint component gap and varus ligament balance measured by an offset-type tensor during posterior-stabilized (PS) total knee arthroplasty (TKA).