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Transporter associated with antigen processing 1 (TAP1) and TAP2 serve pivotal roles in adaptive immunity. Tumor cells often show reduced antigen presentation on their surface as one mechanism to escape immune recognition. Whether downregulation of TAPs is a common mechanism of tumor immune evasion in squamous cell carcinoma of the oral tongue (SCCOT) is unclear. In the present study, samples from 78 patients with SCCOT and 17 patients with benign hyperplastic tongue lesions were analyzed for TAP1 and TAP2 expression by immunohistochemistry. The percentage of positive cells and staining intensity were scored. Associations with clinicopathological variables and survival outcome were also investigated. The results demonstrated that TAP1 and TAP2 levels were highly associated with each other in individual samples and were upregulated in SCCOT compared with benign lesions (P80% in all but two of the tumors, whereas 25.6 and 23.0% of the tumors showed weak intensity of TAP1 and TAP2, respectively. There were no significant associations with clinicopathological variables or survival outcomes between TAP‐intermediate/strong and TAP‐weak tumors. However, in patients

We report on a patient whose type 2 diabetes mellitus resolved during IFN-alpha therapy for hepatitis C virus (HCV). A 40-year-old man was diagnosed with type II diabetes in year 2000. His body mass index (BMI) was 30.8 kg/m and glycosylated haemoglobin (HbA1c) was 10.7%. He was treated with metformin. Later, his glycaemic control deteriorated despite additional dietary and lifestyle advice and the addition of glibenclamide. He was started on subcutaneous insulin in 2002 with the continuation of metformin. In 2003 he was diagnosed with chronic hepatitis caused by HCV. In September 2003 he was started on IFN-alpha and ribavirin. After 24 weeks of treatment his HCV polymerase chain reaction remained positive and treatment was stopped as per guidelines. At the commencement of antiviral therapy, HbA1c was 7.7%. In April 2004 his BMI of 29.38 kg/m had reduced and he then stopped insulin therapy because of repeated hypoglycaemia. After stopping insulin his HbA1c was 4.7%. Fasting plasma glucose of 6.2 mmol/l and anti-glutamic acid decarboxylase antibodies were negative. Urea and creatinine levels were normal. Most of the earlier literature describes diabetes developing in the course of IFN-alpha therapy for a variety of diseases. More recent research has described a relationship between hepatitis C infection and the development of diabetes and insulin resistance. Responders to IFN-alpha treatment manifest an improvement in insulin sensitivity compared with non-responders after the completion of IFN-alpha therapy. Our case shows the resolution of pre-existing diabetes in a patient with chronic HCV infection, which did not respond to IFN-alpha therapy. Whether this occurred as a direct result of IFN-alpha on insulin sensitivity or indirectly as a result of weight loss because the therapy for HCV precipitated additional lifestyle changes in the patient is as yet unclear.

Real-time diagnostics of ceramic powder injection molding using a commercial micromolding machine was performed using ultrasound. Miniature ultrasonic sensors were integrated onto the mold insert. Melt front, solidification, temperature variation and part detachment of the feedstock inside the mold cavity were observed. It has been demonstrated that ultrasonic velocity in feedstock inside the mold cavity, the ultrasonic contact duration during which the part and mold are in contact, and holding pressure can be used to assist with optimization of injection and cooling parameters to minimize energy consumption and maximize process efficiency.

A healthy 20-year-old man presented with a bony lump above the left clavicle associated with upper limb pain, numbness, and tingling. Examination in the surrender position elicited left hand weakness and pain with loss of the radial pulse. The patient had paresthesia of the ulnar border of the left hand but no interossei wasting. A lateral neck radiograph identified an unusual bony contour anteriorly at C7/T1 suggesting a cervical rib (A). Duplex ultrasound scan showed widely patent left axillary and subclavian arteries with the arm adducted but severe compression of the subclavian artery on abducting the arm to 90°. A subsequent computed tomography angiogram confirmed bilateral cervical ribs; the left articulating with an extended left transverse process of the seventh cervical vertebra, extending inferiorly to fuse with the first rib (B and C/Cover). The left subclavian artery passed immediately superior to this bony extension whereas the left vertebral artery lay immediately anterior to the origin of the cervical rib at C7. The right cervical rib was much smaller and not in proximity to the vessels. Intraoperatively, the left cervical rib was found to extend from the C7 transverse process to form a true joint with a hypertrophied scalene tubercle on the first rib; both the cervical rib and hypertrophied scalene tubercle were excised via the supraclavicular incision (D). A T1 sensory and motor neuropraxia was noted day 1 postsurgery which, together with his preoperative symptoms, completely resolved within 5 days and continued at 5-month follow-up. Cervical ribs are a known cause of arterial and neurogenic thoracic outlet syndrome. These congenital abnormalities occur in 1% of the population but are bilateral in 50%. Ninety percent are asymptomatic and do not require resection. Complete cervical ribs occur in approximately 25% of patients, most commonly attached to the first rib by a fibrous band, or more rarely, as in this case, via a true joint, often with the scalene tubercle. Surgical management involves removal of the cervical rib; if this does not provide adequate decompression of the subclavian artery and the brachial plexus, removal of the first rib should be done.

The present study was undertaken to investigate whether Epstein-Barr virus-(EBV) encoded latent membrane protein (LMP) induces the expression of BCL-2 in Hodgkin and Reed-Sternberg (HRS) cells of Hodgkin's disease (HD) and thereby provide a possible mechanism for the role of EBV in the pathogenesis of this disease. Fifty-three cases of HD were studied for the presence of EBV using EBV-encoded RNA in situ hybridization and LMP immunohistochemistry. Immunostaining for BCL-2 on paraffin material was performed using microwave treatment of tissue sections before the application of the primary monoclonal antibody. EBV was located in HRS cells in 16 cases (30%). All cases that were EBV-encoded RNA in situ hybridization positive, also expressed LMP. BCL-2 expression in HRS cells was detected in 16 cases (30%), but only two of these were also EBV-positive. In both of these cases, only occasional HRS cells expressed BCL-2, in contrast to LMP, which was detected in nearly all such cells. BCL-2 staining was predominantly cytoplasmic with some membrane pattern. These results demonstrate that BCL-2 expression can be detected in HRS cells in routinely processed HD tissue and that whereas EBV does not induce the expression of BCL-2 in HD, BCL-2 may have a role in the pathogenesis of EBV-negative cases of HD.