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Tissue Resistance (tissue + resistance)
Selected AbstractsThyroid hormone resistance: the role of mutational analysisINTERNAL MEDICINE JOURNAL, Issue 11 2006C. M. Florkowski Abstract The finding of increased thyroxine (T4) and tri-iodothyronine (T3) levels in a patient with normal or increased thyroid-stimulating hormone is unexpected and presents a differential diagnosis between a thyroid-stimulating hormone-secreting pituitary adenoma, generalized resistance to thyroid hormone (RTH) and laboratory artefact. Without careful clinical and biochemical evaluation, errors may occur in patient diagnosis and treatment. In the case of RTH, mutation of the thyroid hormone receptor beta gene results in generalized tissue resistance to thyroid hormone. As the pituitary gland shares in this tissue resistance, euthyroidism with a normal thyroid-stimulating hormone is usually maintained by increased thyroid hormones. To date, we have identified eight pedigrees in New Zealand with mutations in the thyroid hormone receptor beta gene, including two novel mutations. Mutational analysis of the thyroid hormone receptor beta gene allows definitive diagnosis of RTH, potentially avoiding the need for protracted and expensive pituitary function testing and imaging. Mutational analysis also enables family screening and may help to avoid potential misdiagnosis and inappropriate treatment. [source] Pressures generated in vitro during Stabident intraosseous injectionsINTERNATIONAL ENDODONTIC JOURNAL, Issue 5 2005J. M. Whitworth Abstract Aim, To test the hypothesis that the Stabident intraosseous injection is a potentially high-pressure technique, which carries serious risks of anaesthetic cartridge failure. Methodology, A standard Astra dental syringe was modified to measure the internal pressure of local anaesthetic cartridges during injection. Intra-cartridge pressures were measured at 1 s intervals during slow (approximately 15 s) and rapid (<10 s) injections of 2% Xylocaine with 1 : 80 000 adrenaline (0.25 cartridge volumes) into air (no tissue resistance), or into freshly prepared Stabident perforation sites in the anterior mandible of freshly culled young and old sheep (against tissue resistance). Each injection was repeated 10 times over 3 days. Absolute maximum pressures generated by each category of injection, mean pressures at 1 s intervals in each series of injections, and standard deviations were calculated. Curves of mean maximum intra-cartridge pressure development with time were plotted for slow and rapid injections, and one-way anova (P < 0.05) conducted to determine significant differences between categories of injection. Results, Pressures created when injecting into air were less than those needed to inject into tissue (P < 0.001). Fast injection produced greater intra-cartridge pressures than slow delivery (P < 0.05). Injection pressures rose more quickly and to higher levels in small, young sheep mandibles than in larger, old sheep mandibles. The absolute maximum intra-cartridge pressure developed during the study was 3.31 MPa which is less than that needed to fracture glass cartridges. Conclusions, Stabident intraosseous injection conducted in accordance with the manufacturer's instructions does not present a serious risk of dangerous pressure build-up in local anaesthetic cartridges. [source] Deficiency of the ,-Subunit of the Stimulatory G Protein and Severe Extraskeletal Ossification,JOURNAL OF BONE AND MINERAL RESEARCH, Issue 11 2000Mark C. Eddy Abstract Progressive osseous heteroplasia (POH) is a rare disorder characterized by dermal ossification beginning in infancy followed by increasing and extensive bone formation in deep muscle and fascia. We describe two unrelated girls with typical clinical, radiographic, and histological features of POH who also have findings of another uncommon heritable disorder, Albright hereditary osteodystrophy (AHO). One patient has mild brachydactyly but no endocrinopathy, whereas the other manifests brachydactyly, obesity, and target tissue resistance to thyrotropin and parathyroid hormone (PTH). Levels of the ,-subunit of the G protein (Gs,) were reduced in erythrocyte membranes from both girls and a nonsense mutation (Q12X) in exon 1 of the GNAS1 gene was identified in genomic DNA from the mildly affected patient. Features of POH and AHO in two individuals suggest that these conditions share a similar molecular basis and pathogenesis and that isolated severe extraskeletal ossification may be another manifestation of Gs, deficiency. [source] An islet in distress: , cell failure in type 2 diabetesJOURNAL OF DIABETES INVESTIGATION, Issue 4 2010Takeshi Ogihara Abstract Over 200 million people worldwide suffer from diabetes, a disorder of glucose homeostasis. The majority of these individuals are diagnosed with type 2 diabetes. It has traditionally been thought that tissue resistance to the action of insulin is the primary defect in type 2 diabetes. However, recent longitudinal and genome-wide association studies have shown that insulin resistance is more likely to be a precondition, and that the failure of the pancreatic , cell to meet the increased insulin requirements is the triggering factor in the development of type 2 diabetes. A major emphasis in diabetes research has therefore shifted to understanding the causes of , cell failure. Collectively, these studies have implicated a complex network of triggers, which activate intersecting execution pathways leading to , cell dysfunction and death. In the present review, we discuss these triggers (glucotoxicity, lipotoxicity, amyloid and cytokines) with respect to the pathways they activate (oxidative stress, inflammation and endoplasmic reticulum stress) and propose a model for understanding , cell failure in type 2 diabetes. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2010.00021.x, 2010) [source] Regulation of restitution after superficial injury in isolated guinea pig gastric mucosaAPMIS, Issue 4-5 2004ARUN BHOWMIK The immediate response of the gastrointestinal epithelium to superficial (i.e. microscopic) injury is primarily directed towards restoring the disturbed epithelial continuity. Both structural (i.e. cytoskeleton) and humoral (i.e. growth factors and cytokines) involvement in the process has recently been documented. Yet it is unclear whether humoral signaling regulating mucosal recovery after superficial injury is associated with tyrosine phosphorylation, and whether there are other signs of downstream activation of the signaling pathway. To evaluate the effects of exogenous genistein and phorbol-myristate acetate in the assessment of the role of tyrosine receptor-mediated signaling in the immediate repair of gastric mucosa after superficial injury. Guinea pig gastric mucosa was mounted in a Ussing chamber, injured with 1.25 M NaCl, and perfused for 4 h. Simultaneously, potential difference and tissue resistance were recorded. In some sets of experiments the tissue was exposed bilaterally either to genistein in order to inhibit tyrosine receptor-mediated signaling or to 4-phorbol-myristate 13-acetate (PMA) in order to enhance PKC signaling during the 4 h recovery. Phosphotyrosine (PTYR) and protein kinase C (PKC) immunoreactivity were assessed by immunoblotting and by immunohistochemistry. Proliferative activity was determined morphometrically after staining of the tissue for Ki-67 nuclear antigen and expressed as proliferative index (PI). The inhibition of tyrosine kinases with exogenous genistein resulted in a significant decrease of the PTYR and the stimulation of PKC with PMA increased the PTYR. Nevertheless, no change in the PTYR was observed by immunoblotting after superficial injury alone. Several PKC isoenzymes were found in the guinea pig gastric mucosa, including PKC-,, -,, -, and -,. They were unaffected either by the injury or the PMA treatment. The mean PI of tissues subjected to NaCl-injury was higher than that of uninjured control tissues (p<0.05) (n=7). Exposure of tissue to genistein during recovery decreased the PI, while stimulation with PMA increased it (p<0.05 for both) (n=6). Both electrophysiologic and morphologic restitution were sensitive to genistein, but not to PMA. Superficial injury alone does not influence tyrosine phosphorylation to a degree which could be assessed by immunoblotting. Nevertheless, exogenous modulation of tyrosine receptor-mediated signaling results in downstream signaling effects. The injury-associated induction of proliferation is sensitive to modulation of tyrosine phosphorylation and PKC, suggesting that superficial epithelial injury results in endogenous activation of the epithelium, presumably after paracrine stimulation of the neighboring cells. [source] | ||||||||||