The effects of massage therapy on the human immune response in healthy adults

Little scientific investigation has been conducted to examine objectively the belief that massage therapy can effect the immune system of healthy people. If there are any links between massage therapy and improved immune function, the mechanisms by which they operate are not known. This study evaluated the effects of massage therapy on immune functions of two healthy females.Using a single-case experimental ABAB design, two subjects received a relaxing massage during the experimental phases (B) and no massage during baseline phases (A). Assays were conducted for T and B lymphocyte mitogen-induced proliferation, enumeration of T and B lymphocyte subsets, quantification of immunoglobulins A, G and M (IgA, IgG, IgM) and cortisol levels. Trait and state anxiety levels were also examined.The results indicated a consistent and significant trend of increased activity of both T and B lymphocytes and levels of serum IgG for both subjects during the B phases compared to the A phases. There were no other significant differences between experimental and control conditions for the remaining measures, although serum IgM levels approached significance (P=0.06). Both subjects demonstrated a reduction in trait anxiety over the period of massage therapy.Further studies with larger sample sizes in control and experimental groups, over a longer experimental period are necessary. The study of the effects of massage therapy poses an exciting challenge in psychoneuroimmunology.     

Systematic Isolation of Genes Differentially Expressed in Normal and Cancerous Tissue of the Pancreas

Background: There is increasing knowledge about the genetic basis of pancreatic cancer (PaCa). Tumor suppressor genes (TSGs; e.g. p53 and DPC4) and oncogenes (e.g. K-ras) have been shown to be involved in the development of PaCa. However, the extent of chromosomal changes (gains and losses) implicates that many more genes may be involved in the multistep progression of PaCa. Identification of these genes is essential for understanding the molecular events in the development of PaCa. Methods: We assembled public and proprietary libraries of more than 4 million expressed sequence tags using newly developed software tools. Results: We identified a total of 249 genes with specific expression patterns in normal and cancerous tissue of the pancreas. Of these, 27 genes were found to be preferentially expressed in normal tissue of the pancreas, while 222 genes showed significant upregulation of expression in PaCa. Of the 249 genes, 232 (93.2%) were found to represent known human genes or putative human homologues of genes characterized previously in other species, while 17 (6.8%) represent putative new genes. Conclusion: These genes may represent a valuable source to identify novel TSGs and oncogenes involved in the carcinogenesis of PaCa.     

Treatment of cardiovascular implantable electronic device infection with daptomycin

We describe a case of 83-year-old man who was admitted to our department for treatment of recurrent device-pocket infections. Our report shows that in a case of high-risk patient with a complicated cardiac implantable electric devices infection involving multidrug-resistent gram-positive pathogen, the application of daptomycin in combination with staged surgical therapy can be efficient and safe.     

Survey of 548 oncogenic fusion transcripts in thyroid tumors supports the importance of the already established thyroid fusions genes

Neoplasms frequently present structural chromosomal aberrations that can alter the level of expression of a protein or to the expression of an aberrant chimeric protein. In the thyroid, the PAX8‐PPARG fusion is present in the neoplastic lesions that have a follicular architecture—follicular thyroid carcinoma (FTC) and follicular variant of papillary thyroid carcinoma (FVPTC), and less frequently in follicular thyroid adenoma (FTA), while the presence of RET/PTC fusions are largely restricted to papillary thyroid carcinoma (PTC). The ability to detect fusion genes is relevant for a correct diagnosis and for therapy. We have developed a new fusion gene microarray‐based approach for simultaneous analysis of all known and predicted fusion gene variants. We did a comprehensive screen for 548 known and putative fusion genes in 27 samples of thyroid tumors and three positive controls—one thyroid cancer cell line (TPC‐1) and two PTCs with known CCDC6‐RET (alias RET/PTC1) fusion gene, using this microarray. Within the thyroid tumors tested, only well known, previously reported fusion genes in thyroid oncology were identified. Our results reinforce the pathogenic role played by RET/PTC1, RET/PTC3, and PAX8‐PPARG fusion genes in thyroid tumorigenesis. © 2012 Wiley Periodicals, Inc.     

Altered melusin pathways involved in cardiac remodeling following acute myocardial infarction

BackgroundMelusin, a muscle-specific integrin-linked protein, has been reported to be a biomechanical sensor and to protect the heart from pressure overload. In the present study, we investigated the possible role that melusin plays during cardiac remodeling after myocardial infarction (MI).MethodsWe constructed a heart failure model of rats induced by left anterior descending coronary artery ligation. At different time points (1, 2, 3, 4, 6, and 8 weeks) following the operation, cardiac function was monitored by echocardiography and hemodynamic assessment; cardiac morphology was measured using hematoxylin–eosin-stained sections. Melusin expression, as well as p-Akt, Akt, and one of the Rho small GTPase family members, CDC42, was determined dynamically by Western blotting analysis during the postinfarction cardiac remodeling.ResultsProgressive increase in left ventricular (LV) end-systolic dimension and LV end-diastolic dimension and decrease in percent LV fractional shortening (%FS) and LVdp/dt_max demonstrated gradually deteriorated cardiac function in rats following MI operation. Morphological analysis revealed cardiac remodeling in MI animals, including increased LV diameter and decreased border zone thickness. We also showed a dynamic change in melusin during heart failure progression; it had an initial decline which was evident at 3 weeks and increased subsequently, reaching peak levels at 6 weeks. This dynamic change in melusin was significantly correlated with %FS and LVdp/dt_max. p-Akt/Akt and CDC42 protein expression was correlated with melusin content.ConclusionsThe altered melusin pathways and CDC42 parallel the cardiac function progression during cardiac remodeling post-MI. The dynamic change of them during this procedure may represent an important molecular mechanism underlying postinfarction cardiac remodeling and provide potential therapeutic targets.