Current Issue : October - December Volume : 2015 Issue Number : 4 Articles : 6 Articles
Background: The surge in uptake of nasal continuous positive airway pressure (CPAP)\nfor respiratory support in preterm infants has occurred in the absence of an authentic\nanimal model. Such a model would allow investigation of research questions of\nphysiological and therapeutic importance. We therefore aimed to develop a preterm\nlamb model of the non-intubated very preterm infant on CPAP.\nMethods: After staged exteriorisation and instrumentation, preterm lambs were\ndelivered from anaesthetised ewes at 131 to 133 days gestation. Via a single nasal prong\n(4-mm internal diameter, 6- to 7-cm depth), positive pressure was delivered from the\noutset, with nasal intermittent positive pressure ventilation (NIPPV) used until transition\nto nasal CPAP was attempted, and periodically thereafter for hypoventilation. Caffeine\nand doxapram were used as respiratory stimulants. Gastric distension was prevented\nwith an oesophageal balloon. Cardiorespiratory parameters and results of arterial blood\ngas analyses were monitored throughout the study period, which continued for 150 min\nafter first transition to CPAP.\nResults: Ten preterm lambs were studied, at gestation 132 �± 1 days (mean �± SD)\nand birth weight 3.6 �± 0.45 kg. After stabilisation on NIPPV, transition to nasal CPAP\nwas first attempted at 28 �± 11 min. There was transient respiratory acidosis, with\ngradual resolution as spontaneous respiratory activity increased. In the final hour,\n79% �± 33% of time was spent on CPAP alone, with typical respiratory rates around\n60 breaths per minute. PaCO2 at end-experiment was 58 �± 36 mmHg.\nConclusions: Non-intubated preterm lambs can be effectively transitioned to nasal\nCPAP soon after birth. This animal model will be valuable for further research....
Hypertension and atherosclerosis are among the most common causes of mortality in both developed and developing countries.\nExperimental animalmodels of hypertension and atherosclerosis have becomea valuable tool for providing information on etiology,\npathophysiology, and complications of the disease and on the efficacy and mechanism of action of various drugs and compounds\nused in treatment. An animal model has been developed to study hypertension and atherosclerosis for several reasons. Compared\nto human models, an animal model is easily manageable, as compounding effects of dietary and environmental factors can be\ncontrolled. Blood vessels and cardiac tissue samples can be taken for detailed experimental and biomolecular examination. Choice\nof animal model is often determined by the research aim, as well as financial and technical factors. A thorough understanding of\nthe animal models used and complete analysis must be validated so that the data can be extrapolated to humans. In conclusion,\nanimal models for hypertension and atherosclerosis are invaluable in improving our understanding of cardiovascular disease and\ndeveloping new pharmacological therapies....
The activation of Translocator protein (18 kDa) (TSPO) has been demonstrated to mediate rapid anxiolytic efficacy in\nstress response and stress-related disorders. This protein is involved in the synthesis of endogenous neurosteroids\nthat promote ?-aminobutyric acid (GABA)-mediated neurotransmission in the central neural system. However, little\nis known about the functions and the underlying mechanisms of TSPO in chronic pain-induced anxiety-like behaviors.\nThe novel TSPO ligand N-benzyl-N-ethyl-2-(7,8-dihydro-7-benzyl-8-oxo-2-phenyl-9H-purin-9-yl) acetamide (ZBD-2) was\nused in the present study. We found that ZBD-2 (0.15 or 1.5 mg/kg) significantly attenuated anxiety-like behaviors in\nmice with chronic inflammatory pain induced by hindpaw injection of complete Freund�s adjuvant (CFA). However, the\ntreatment did not alter the nociceptive threshold or inflammation in the hindpaw. Hindpaw injection of CFA induced\nthe upregulation of TSPO, GluR1-containing ?-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors,\nand NR2B-containing N-methyl-D-aspartate (NMDA) receptors in the basolateral amygdala (BLA). ZBD-2 administration\nreversed the alterations of the abovementioned proteins in the BLA of the CFA-injected mice. Electrophysiological\nrecording revealed that ZBD-2 could prevent an imbalance between excitatory and inhibitory transmissions in the\nBLA synapses of CFA-injected mice. Therefore, as the novel ligand of TSPO, ZBD-2 induced anxiolytic effects, but did\nnot affect the nociceptive threshold of mice under chronic pain. The anxiolytic effects of ZBD-2 were related to the\nregulation of the balance between excitatory and inhibitory transmissions in the BLA....
Background: Dupuytren�s disease (DD) is a slow, progressive fibroproliferative disorder affecting the palms of the\nhands. The disease is characterized by the formation of collagen rich- cords which gradually shorten by the action\nof myofibroblasts resulting in finger contractures. It is a disease that is confined to humans, and a major limiting\nfactor in investigating this disorder has been the lack of a faithful animal model that can recapitulate its distinct\nbiology. The aim of this study was to develop such a model by determining if Dupuytren�s disease (DD)- and control\ncarpal tunnel (CT)-derived fibroblasts could survive in the forepaw of the nude rats and continue to exhibit the distinct\ncharacteristics they display in in vitro cultures.\nMethods: 1x107 fluorescently labeled DD- and CT-derived fibroblasts were transplanted into the left and right\nforepaws of nude rats respectively. Cells were tracked at regular intervals for a period of two months by quantifying\nemitted fluorescent signal using an IVIS imaging system. After a period of 62 days rat forepaw connective tissues were\nharvested for histology and total RNA was isolated. Human-specific probes were used to perform real time\nRT-PCR assays to examine the expression patterns of gene products associated with fibrosis in DD. Rat forepaw skin\nwas also harvested to serve as an internal control.\nResults: Both CT- and DD-derived fibroblasts survived for a period of 62 days, but DD-derived cells showed a significantly\ngreater level of persistent fluorescent signal at the end of this time than did CT-derived cells. mRNA expression levels of\n?-smooth muscle actin (?-SMA), type I- and type III- collagens were all significantly elevated in the forepaw receiving DD\ncord-derived fibroblasts in comparison to CT-derived fibroblasts. Masson�s trichrome stain confirmed increased collagen\ndeposition in the forepaw that was injected with DD cord-derived fibroblasts.\nConclusions: For the first time we describe an animal model for Dupuytren�s disease at the orthotopic anatomical\nlocation. We further show that gene expression differences between control (CT) and diseased (DD) derived fibroblasts\npersist when these cells are transplanted to the forepaw of the nude rat. These preliminary findings indicate that, with\nfurther refinements, this animal model holds promise as a baseline for investigating novel therapeutic regimens to\ndetermine an effective strategy in treating DD....
Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis,which occurs in the absence of alcohol abuse.NAFLD\ncan evolve into progressive liver injury and fibrosis in the formof nonalcoholic steatohepatitis (NASH). Several animal models have\nbeen developed to attempt to represent the morphological, biochemical, and clinical features of human NASH. The actual review\npresents a critical analysis of the most commonly used experimental models of NAFLD/NASH development. These models can\nbe classified into genetic, nutritional, and a combination of genetic and nutritional factors. The main genetic models are ob/ob\nand db/db mutant mice and Zucker rats. The principal nutritional models employ methionine- and choline-deficient, high-fat,\nhigh-cholesterol and high-cholate, cafeteria, and high-fructose diets. Currently, associations between high-fructose and various\ncompositions of high-fat diets have been widely studied. Previous studies have encountered significant difficulties in developing\nanimal models capable of reproducing human NASH. Some models produce consistent morphological findings, but the induction\nmethod differs significantly compared with the pathophysiology of human NASH. Other models precisely represent the clinical\nand etiological contexts of this disease but fail to provide accurate histopathological representations mainly in the progression from\nsteatosis to liver fibrosis...
Previous work has demonstrated that the hormone prolactin promotes oligodendrocyte precursor proliferation and\nremyelination following lysolecithin-induced demyelination of the mouse spinal cord. Prolactin, however, can elicit\npro-inflammatory responses, and its use in the prototypical demyelinating and inflammatory condition, multiple\nsclerosis (MS), should thus be approached cautiously. Here, we sought to determine whether recombinant prolactin\ncould alter the course of experimental autoimmune encephalomyelitis (EAE), an inflammatory animal model of MS.\nConsistent with previous literature, we found that prolactin activated leukocytes in vitro. Daily treatment with prolactin\nfrom around the time of onset of clinical signs, for 9 (days 9 to 17) or 25 (days 9 to 33) days did not increase clinical or\nhistological signs of EAE over that of vehicle-treated mice. Instead, the combination of prolactin and a suboptimal dose\nof recombinant murine interferon-? resulted in (days 9 to 17 group) or trended towards (days 9 to 33 group), a greater\namelioration of clinical signs of EAE, compared to either treatment alone or to vehicle controls. Histological analyses\ncorroborated the clinical EAE data. These results suggest that prolactin may be beneficial when administered in\ncombination with interferon-? in MS....
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