Detection of the mRNA expression of human angiotensin-converting enzyme 2 as a SARS coronavirus functional receptor in human femoral head / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the mRNA expression of severe acute respiratory syndrome-associated coronavirus (SARS-COV) functional receptor, angiotensin-converting enzyme 2 (ACE2), in human femoral head and conjunctiva, and explore the possible entry route of SARS-COV in human femoral head.</p><p><b>METHODS</b>ACE2 mRNA in human femoral head was detected by nested RT-PCR with human beta actin gene as the positive control.</p><p><b>RESULTS</b>The mRNA of human beta actin gene could be amplified efficiently in all the tissue samples. The mRNA of human ACE2 was expressed efficiently in the normal lung tissue, but not in the cartilage and cancellous bone under the weight-bearing area of the femoral head.</p><p><b>CONCLUSION</b>SARS-COV can not infect the femoral head tissue and lead to avascular necrosis of the femoral head directly by the spike glycoprotein, and mechanism of the virus for causing avascular necrosis needs further investigation.</p>

Effects of iontophoretic etorphine and naloxone, and electroacupuncture on nociceptive responses from thalamic neurones in rabbits.

A total of 88 somatosensory neurones were recorded from n. anterodorsalis, n. anteroventralis, n. lateralis dorsalis, n. lateralis posterior and n. centralis lateralis of rabbit thalamus. Among the 88 neurones, 50 were noxious-excited (convergent, n = 36; non-convergent with long latency responses, n = 14), 23 noxious-inhibited and 15 non-convergent neurones with short latency responses that were activated by innocuous stimuli only. Iontophoresis of etorphine predominantly depressed the late burst of the response to strong sural nerve stimulation in convergent neurones (25/26), the depression being readily blocked by iontophoresis of naloxone (16/16). After naloxone, the late burst was occasionally larger than that before etorphine. Etorphine depressed non-convergent neurones with long latency responses (13/13), but had no marked effects on non-convergent neurones with short latency responses. On the noxious-inhibited neurones, etorphine could enhance the inhibitory response when it was weak prior to drug administration (12/12). Contrary to etorphine, naloxone could block the inhibitory response when it was administered either iontophoretically (15/15) or intravenously (4/4). Naloxone could enhance the weak late burst of the evoked response in convergent neurones (2/2). Similarly to etorphine, electroacupuncture depressed noxious-excited neurones, convergent (18/18) and non-convergent neurones with long latency responses (6/6), the depression being blocked by naloxone (16/16). The results suggest that noxious inputs may activate the release of opioid peptides onto opiate receptors, the interaction of which mediates the modulation of thalamic nociceptive transmission.