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Zhang H.-Y.,Chengdu Military General Hospital of PLA | Liu R.,Chongqing Medical University | Xing Y.-J.,Chengdu Military General Hospital of PLA | Xu P.,Chengdu Military General Hospital of PLA | And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2013

This study aimed to investigate the effects of hypoxia on the proliferation, mineralization and ultrastructure of human periodontal ligament fibroblasts (HPLFs) at various times in vitro in order to further study plateau-hypoxia-induced periodontal disease. HPLFs (fifth passage) cultured by the tissue culture method were assigned to the slight (5% O2), middle (2%O2)and severe hypoxia (1% O2) groups and the control (21%O2)group, respectively. At 12, 24, 48 and 72 h, the proliferation and alkaline phosphatase (ALP) activities were detected. The ultrastructure of the severe hypoxia group was observed. HPLFs grew more rapidly with an increase in the degree of hypoxia at 12 and 24 h, and significant levels of proliferation (P<0.05) were observed in the severe hypoxia group at 24 h. Cell growth was restrained with an increase in the degree of hypoxia at 48 and 72 h, and the restrictions were clear (P<0.05) in the middle and severe hypoxia groups. ALP activity was restrained with increasing hypoxia at each time point. The restrictions were marked (P<0.05) in the severe hypoxia group at 24 h and in the middle and severe hypoxia groups at 48 and 72 h. However, the restriction was more marked (P<0.05) in the severe hypoxia group at 72 h. An increase was observed in the number of mitochondria and rough endoplasmic reticula (RER), with slightly expanded but complete membrane structures, in the severe hypoxia group at 24 h. At 48 h, the number of mitochondria and RER decreased as the mitochondria increased in size. Furthermore, mitochondrial cristae appeared to be vague, and a RER structural disorder was observed. At 72 h, the number of mitochondria and RER decreased further when the mitochondrial cristae were broken, vacuolar degeneration occurred, and the RER particles were reduced while the number of lysosomes increased. HPLF proliferation and mineralization was restrained. Additionally, HPLF structure was broken for a relatively long period of time in the middle and severe hypoxia groups. This finding demonstrated that hypoxia was capable of damaging the metabolism, reconstruction and recovery of HPLFs. The poor state of HPLFs under hypoxic conditions may therefore initiate or aggravate periodontal disease. Source


Yong X.-L.,Chengdu Military General Hospital of PLA | Hu T.-T.,Chengdu Military General Hospital of PLA | Li N.,Chengdu Military General Hospital of PLA | Du X.-L.,Chengdu Military General Hospital of PLA | And 2 more authors.
Chinese Journal of New Drugs | Year: 2015

Objective: To observe effect of penehyclidine hydrochloride (PH) on heart rate and heart rate variability as well as its activity on autonomic nervous system in healthy volunteers. Methods: A total of 26 healthy volunteers were enrolled in a randomized, opened study. They were randomized to be divided into 5 groups and orally received PH 0.3~1.0 mg daily. Two healthy volunteers were selected from each group and monitored by dynamic electrocardiography recording 24-h average heart rate; parameters of time domain including SDNN, SDNN Idx, SDANN, rMSSD, pNN50 and TI were analyzed for evaluating heart rate variability. Other 16 healthy volunteers accepted routine electrocardiography to record heart rate. Data from average heart rate and parameters of heart rate variability befoe and after oral PH were analyzed by professional software. Results: Compared with baseline level, average heart rate of healthy subjects within 24 h was significantly retarded after PH administration (P<0.01), and SDNNs were significantly increased (P<0.01) in 5 PH dose groups. Other parameters including SDNN Idx, rMSSD, pNN50 and TI were slightly prolonged, and SDANN was shortened a little (P<0.05). Conclusion: PH retards heart rate, which may be mediated by the way of non-M2 receptor or strengthened vagal tone. © 2015, Chinese Journal of New Drugs Co. Ltd. All right reserved. Source

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