Current Issue : July - September Volume : 2013 Issue Number : 3 Articles : 5 Articles
Background: Mycoplasma fermentans has been associated with respiratory, genitourinary tract infections and\r\nrheumatoid diseases but its role as pathogen is controversial. The purpose of this study was to probe that\r\nMycoplasma fermentans is able to produce respiratory tract infection and migrate to several organs on an\r\nexperimental infection model in hamsters. One hundred and twenty six hamsters were divided in six groups (A-F)\r\nof 21 hamsters each. Animals of groups A, B, C were intratracheally injected with one of the mycoplasma strains:\r\nMycoplasma fermentans P 140 (wild strain), Mycoplasma fermentans PG 18 (type strain) or Mycoplasma pneumoniae\r\nEaton strain. Groups D, E, F were the negative, media, and sham controls. Fragments of trachea, lungs, kidney, heart,\r\nbrain and spleen were cultured and used for the histopathological study. U frequency test was used to compare\r\nrecovery of mycoplasmas from organs.\r\nResults: Mycoplasmas were detected by culture and PCR. The three mycoplasma strains induced an interstitial\r\npneumonia; they also migrated to several organs and persisted there for at least 50 days. Mycoplasma fermentans\r\nP 140 induced a more severe damage in lungs than Mycoplasma fermentans PG 18. Mycoplasma pneumoniae\r\nproduced severe damage in lungs and renal damage.\r\nConclusions: Mycoplasma fermentans induced a respiratory tract infection and persisted in different organs for\r\nseveral weeks in hamsters. This finding may help to explain the ability of Mycoplasma fermentans to induce\r\npneumonia and chronic infectious diseases in humans....
Background: Causes of neuropathic pain following nerve injury remain unclear, limiting the development of\r\nmechanism-based therapeutic approaches. Animal models have provided some directions, but little is known\r\nabout the specific sensory neurons that undergo changes in such a way as to induce and maintain activation of\r\nsensory pain pathways. Our previous studies implicated changes in the Ab, normally non-nociceptive neurons in\r\nactivating spinal nociceptive neurons in a cuff-induced animal model of neuropathic pain and the present study\r\nwas directed specifically at determining any change in excitability of these neurons. Thus, the present study aimed\r\nat recording intracellularly from Ab-fiber dorsal root ganglion (DRG) neurons and determining excitability of the\r\nperipheral receptive field, of the cell body and of the dorsal roots.\r\nMethods: A peripheral neuropathy was induced in Sprague Dawley rats by inserting two thin polyethylene cuffs\r\naround the right sciatic nerve. All animals were confirmed to exhibit tactile hypersensitivity to von Frey filaments\r\nthree weeks later, before the acute electrophysiological experiments. Under stable intracellular recording conditions\r\nneurons were classified functionally on the basis of their response to natural activation of their peripheral receptive\r\nfield. In addition, conduction velocity of the dorsal roots, configuration of the action potential and rate of\r\nadaptation to stimulation were also criteria for classification. Excitability was measured as the threshold to\r\nactivation of the peripheral receptive field, the response to intracellular injection of depolarizing current into the\r\nsoma and the response to electrical stimulation of the dorsal roots.\r\nResults: In control animals mechanical thresholds of all neurons were within normal ranges. Ab DRG neurons in\r\nneuropathic rats demonstrated a mean mechanical threshold to receptive field stimulation that were significantly\r\nlower than in control rats, a prolonged discharge following this stimulation, a decreased activation threshold and a\r\ngreater response to depolarizing current injection into the soma, as well as a longer refractory interval and delayed\r\nresponse to paired pulse electrical stimulation of the dorsal roots.\r\nConclusions: The present study has demonstrated changes in functionally classified Ab low threshold and high\r\nthreshold DRG neurons in a nerve intact animal model of peripheral neuropathy that demonstrates nociceptive\r\nresponses to normally innocuous cutaneous stimuli, much the same as is observed in humans with neuropathic\r\npain. We demonstrate further that the peripheral receptive fields of these neurons are more excitable, as are the\r\nsomata. However, the dorsal roots exhibit a decrease in excitability. Thus, if these neurons participate in\r\nneuropathic pain this differential change in excitability may have implications in the peripheral drive that induces\r\ncentral sensitization, at least in animal models of peripheral neuropathic pain, and Ab sensory neurons may thus\r\ncontribute to allodynia and spontaneous pain following peripheral nerve injury in humans....
Muscle injury and inflammation (myositis) in a rabbit model of an unilateral muscle overuse were examined. It is unknown if the\r\ntachykinin system has a functional role in this situation. In this study, therefore, the neurokinin-1 receptor (NK-1R) expression\r\npatterns were evaluated. White blood cells, nerve fascicles, fine nerve fibers, and blood vessel walls in myositis areas showed NK-\r\n1R immunoreaction. NK-1R mRNA reactions were observable for white blood cells and blood vessel walls of these areas. NK-1R\r\nimmunoreaction and NK-1R mRNA reactions were also seen for muscle fibers showing degenerative and regenerative features.\r\nThere were almost no NK-1R immunoreactions in normal muscle tissue. Interestingly, marked NK-1R expressions were seen for\r\nmyositis areas of both the experimental side and the contralateral nonexperimental side. EIAanalyses showed that the concentration\r\nof substance P in the muscle tissue was clearly increased bilaterally at the experimental end stage, as compared to the situation\r\nfor normal muscle tissue. These observations show that the tachykinin system is very much involved in the processes that occur\r\nin muscle injury/myositis. The effects can be related to proinflammatory effects and/or tissue repair. The fact that there are also\r\nmarked NK-1R expressions contralaterally indicate that the tachykinin system has crossover effects....
Human lifespan is positively correlated with childhood intelligence, as measured by psychometric (IQ) tests. The\r\nstrength of this correlation is similar to the negative effect that smoking has on the life course. This result suggests\r\nthat people who perform well on psychometric tests in childhood may remain healthier and live longer. The\r\ncorrelation, however, is debated: is it caused exclusively by social-environmental factors or could it also have a\r\nbiological component? Biological traits of systems integrity that might result in correlations between brain function\r\nand lifespan have been suggested but are not well-established, and it is questioned what useful knowledge can\r\ncome from understanding such mechanisms. In a recent study, we found a positive correlation between brain\r\nfunction and longevity in honey bees. Honey bees are highly social, but relevant social-environmental factors that\r\ncontribute to cognition-survival correlations in humans are largely absent from insect colonies. Our results,\r\ntherefore, suggest a biological explanation for the correlation in the bee. Here, we argue that individual differences\r\nin stress handling (coping) mechanisms, which both affect the bees� performance in tests of brain function and\r\ntheir survival could be a trait of systems integrity. Individual differences in coping are much studied in vertebrates,\r\nand several species provide attractive models. Here, we discuss how pigs are an interesting model for studying\r\nbehavioural, physiological and molecular mechanisms that are recruited during stress and that can drive\r\ncorrelations between health, cognition and longevity traits. By revealing biological factors that make individuals\r\nsusceptible to stress, it might be possible to alleviate health and longevity disparities in people....
The Spontaneously Diabetic Torii (SDT) rat is an inbred strain of Sprague-Dawley rat and recently is established as a nonobese model of type 2 diabetes (T2D). Male SDT rats show high plasma glucose levels (over 700?mg/dL) by 20 weeks. Male SDT rats show pancreatic islet histopathology, including hemorrhage in pancreatic islets and inflammatory cell infiltration with fibroblasts. Prior to the onset of diabetes, glucose intolerance with hypoinsulinemia is also observed. As a result of chronic severe hyperglycemia, the SDT rats develop profound complications. In eyes, retinopathy, cataract, and neovascular glaucoma are observed. Proliferative retinopathy, especially, resulting from retinal neovascular vessels is a unique characteristic of this model. In kidney, mesangial proliferation and nodular lesion are observed. Both peripheral neuropathy such as decreased nerve conduction velocity and thermal hypoalgesia and autonomic neuropathy such as diabetic diarrhea and voiding dysfunction have been reported. Osteoporosis is another complication characterized in SDT rat. Decreased bone density and low-turnover bone lesions are observed. Taking advantage of these features, SDT rat has been used for evaluating antidiabetic drugs and drugs/gene therapy for diabetic complications. In conclusion, the SDT rat is potentially a useful T2D model for studies on pathogenesis and treatment of diabetic complications in humans....
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