An attempt to reduce the loss of pain and touch sensations in leprosy patients

An attempt was made to improve the perception of pain and touch sensations at the leprosy lesions. The loss of pain and touch sensations in a lesion was graded using Pain/Touch-Sensation-Testing-and-Grading devices. Application of a solution containing 1 mg of histamine per ml of DMSO, at the affected area decreased the grades of the loss of pain sensation in 11 (31.4%) patients and of touch sensation in 8 (22.8%) patients, out of the 35 patients tested, indicating an improvement in the perception at the lesion. This effect, however, did not persist even for 5 minutes. A higher concentration (2 mg/ml) of histamine produced reduction in the sensory loss in a larger percentage (47% for pain and 35.3% for touch) of patients, though the duration of this effect was still not prolonged.     

Circulating immune complexes in sera of patients with oral cancer

Circulating immune complexes (IC) in the sera of patients with oral cancer have been measured by using polyethylene glycol (PEG) precipitation assay. At least 60% of patients with carcinomatous buccal mucosa were found to have markedly higher amounts of IC. Results have been discussed in view of other types of cancer and the various methods used for the assay of IC.     

Hepatitis C virus NS5A anchor peptide disrupts human immunodeficiency virus

In the absence of an effective vaccine, there is an urgent need for safe and effective antiviral agents to prevent transmission of HIV. Here, we report that an amphipathic alpha-helical peptide derived from the hepatitis C virus NS5A anchor domain (designated C5A in this article) that has been shown to be virocidal for the hepatitis C virus (HCV) also has potent antiviral activity against HIV. C5A exhibits a broad range of antiviral activity against HIV isolates, and it prevents infection of the three in vivo targets of HIV: CD4(+) T lymphocytes, macrophages, and dendritic cells by disrupting the integrity of the viral membrane and capsid core while preserving the integrity of host membranes. C5A can interrupt an ongoing T cell infection, and it can prevent transmigration of HIV through primary genital epithelial cells, infection of mucosal target cells and transfer from dendritic cells to T cells ex vivo, justifying future experiments to determine whether C5A can prevent HIV transmission in vivo.     

Proteasome Inhibitor MG132 Inhibits Angiogenesis in Pancreatic Cancer by Blocking NF-κB Activity

Since angiogenesis enables solid tumors, including pancreatic cancer (PaCa), to grow and metastasize, the development of anti-angiogenic agents is currently one of the urgent issues. Proteasome inhibitors are well known for inhibiting nuclear factor-kappa B (NF-κB) activity in various cancer cells, but little is known about their biologic mechanisms against angiogenesis in PaCa. We divided human PaCa cell lines into high-angiogenic (BxPC-3 and SW 1990) and low-angiogenic (MIA PaCa-2 and Capan-2) groups. The high-angiogenic PaCa cell lines constitutively expressed high NF-κB activity and produced high levels of vascular endothelial growth factor (VEGF) and interleukin 8 (IL-8). The conditioned media from BxPC-3 significantly enhanced both proliferation of and tube formation by human umbilical vein endothelial cells (HUVECs) and these enhancements were significantly inhibited by the proteasome inhibitor MG132 treatment. Collectively, MG132 blocked PaCa-derived VEGF and IL-8 production through inhibition of NF-κB activity. Thus, proteasome inhibitors may prove beneficial as anti-angiogenic therapy for PaCa. Our studies show that MG132, a proteasome inhibitor, significantly blocked pancreatic-cancer-associated angiogenesis through inhibition of NF-κB and NF-κB-dependent proangiogenic gene products VEGF and IL-8.     

Revascularization Options in Patients with Chronic Kidney Disease

Cardiovascular disease is the leading cause of death in patients who have chronic kidney disease or end-stage renal disease and are undergoing hemodialysis. Chronic kidney disease is a recognized risk factor for premature atherosclerosis. Unfortunately, most major randomized clinical trials that form the basis for evidence-based use of revascularization procedures exclude patients who have renal insufficiency. Retrospective, observational studies suggest that patients with end-stage renal disease and severe coronary occlusive disease have a lower risk of death if they undergo coronary revascularization rather than medical therapy alone. Due to a lack of prospective studies, however, the relative merits of percutaneous versus surgical revascularization are merely a matter of opinion. Several small, retrospective studies have shown that coronary artery bypass grafting is associated with higher procedural death but better long-term survival than is percutaneous coronary intervention. This difference appears to result from poor long-term results of percutaneous coronary intervention in patients who have chronic kidney disease or end-stage renal disease.Because randomized trials comparing percutaneous coronary intervention and coronary artery bypass grafting have included patients undergoing balloon angioplasty and placement of bare-metal stents, their conclusions are suspect in the era of drug-eluting stents. In this review, we discuss different revascularization options for patients with chronic kidney disease, the outcomes of revascularization procedures, and the risk factors for adverse outcomes.Key words: Angioplasty, transluminal, percutanous coronary; coronary artery bypass; coronary artery bypass, off-pump; creatinine/blood/metabolism; drug-eluting stents; extracorporeal circulation; glomerular filtration rate; kidney failure, chronic; renal dialysis; stents; treatment outcomeThe prevalence of end-stage renal disease (ESRD), defined as renal dysfunction requiring chronic renal replacement therapy, is increasing. In 2007, there were about 341,000 patients with ESRD on hemodialysis and 143,000 patients with transplanted kidneys in the United States.¹ An additional 8% of adults in the U.S. have chronic kidney disease stages 3 and 4 (characterized by a glomerular filtration rate [GFR] between 15 and 60 mL/min/1.73 m²).² The United States Renal Data System (USRDS) projects that, at the current growth rate, the number of patients with ESRD will increase to 534,000 by the year 2020.¹ Within 18 to 24 months of beginning renal replacement therapy, 12% of patients will have an acute myocardial infarction, more than 60% will receive a diagnosis of congestive heart failure, and, by 3 years, 38% will die suddenly, presumably of cardiovascular causes.¹ In chronic kidney disease patients who are not hemodialysis dependent, the risk of dying of cardiovascular disease is greater than the risk of developing ESRD.³ In addition to the traditional risk factors for atherosclerosis,⁴ an abnormal GFR contributes independently to the risk of atherosclerosis-related events in patients with kidney disease.⁵