CD34, vimentin, and vascular endothelial growth factor immunohistochemical analysis and electron microscopic tools were employed to record the initial appearance of telocytes (TCs) and stage-by-stage variations in TC localizations in the developing rabbit lung. TCs could not be identified in the primitive embryonic lung until day 18 of gestation. In the pseudoglandular lung, CD34+ TCs had been recorded under the cartilage of the main bronchus, in the wall of large-sized pulmonary vessels and large epithelial tubes. In the canalicular phase, TCs could be demonstrated in the smooth muscle layer of the bronchioles including the terminal ones. The strength of CD34 immunoreactive signals had been amplified by age until the day of parturition. Ultrastructurally, TCs consisted of a tiny body and exceptionally long telopodes (Tps). The Tp consisted of alternating thin segments (podomers) and dilated ones (podoms). The Tp sometimes branched with a dichotomous pattern. TCs interconnected in a network either by homocellular junctions with neighboring TCs or by heterocellular junctions with smooth muscle cells and alveolar cells. Collectively, early detection of TCs in pulmonary vessels suggests a potential role for TCs in their angiogenesis. For the lung tissue, TCs seem to be involved in the regulation of lung histogenesis.
Telocyte (TC) is an interesting unique interstitial cell demonstrated in many human and animal tissues and organs. This study verified, for the first time, the pattern of TC distribution in the testicular tissue of New Zealand White rabbits using histological, immunohistochemical, and electron microscopic tools. Rabbit testicular tissue samples were obtained from three pairs of adult healthy New Zealand white rabbit by surgical procedures. The testicular tissues were stained with hematoxyline-eosin, Crossmon's trichrome and Periodic acid Schiff. The immunohistochemistry was performed using three different antibodies CD34, CD117, and vimentin.
Background: There is a large variation in the magnitude of the response to asthma medications. Pharmacogenetics is responsible for a significant part of this variation. We aimed at studying the effect of the Glucocoricoid receptors NR3C1 BCLI single nucleotide polymorphism (SNP) on the susceptibility to bronchial asthma in children and to evaluate its effect on the response to inhaled corticosteroids (ICS). Method: Seventy five asthmatic children and a control group of 66 non asthmatic children were included in the study. The level of asthma symptom control and pulmonary function tests were measured initially and 3 months after treatment with inhaled corticosteroids. The genotypes were studied using PCR-RFLP method. Results: No statistically significant difference was found between asthmatic group and the control group as regard the studied genotype. Among asthmatic children, The CC genotype was statistically associated with controlled asthma symptoms 3 months after treatment and the GG genotype was associated with poor asthma symptom control. Also, FEV1% after 3 months of treatment was statistically lower in children with the GG genotype as compared to children with the CG and CC genotypes. Conclusion: glucocorticoid receptor NR3C1 SNP was not associated with asthma susceptibility in the studied group. However, the presence of the GG genotype was associated with decreased response to ICSs among asthmatic children as regards asthma symptom control and FEV1% response.
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