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BACKGROUND:Hard palate mucosa serves as a main donor material in periodontal plastic surgery and its thickness is crucial for the surgical outcomes. OBJECTIVE: To analyze the thickness of hard palate mucosa in Han population, and analyze the consistency between cone-beam CT image analysis and trans-gingival probing method. METHODS: A total of 30 Han volunteers (300 teeth) were recruited, and the thickness of hard palate mucosa was measured using cone-beam CT image analysis or trans-gingival probing method, to analyze their consistency. RESULTS AND CONCLUSION: The two methods showed a higher consistency in the thickness of hard palate mucosa at the cuspid, first and second premolars as well as first and second molars. The thickness of the hard palate mucosa related to the distance from the gingival margin and tooth position, the thickness from the canine region to the second premolar region thickening gradually, and became the thickest at the second molar, and the thinnest at the cuspid. This study for the first time analyzed the thickness of hard palate mucosa in Chinese Han population, and confirmed there is a high consistency between cone-beam CT image analysis and trans-gingival probing method.
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@#Objective To explore the effect of electroacupuncture and transcutaneous electrical acupoint stimulation (TEAS) on somatosensory evoked potential (SEP) of the upper extremity in healthy subjects. Methods From October, 2015 to April, 2016, ten healthy young volunteers were selected. Each of the subjects was randomly treated with electroacupuncture and TEAS. Before and after treatment, the latency and amplitude of N20 and N9 of SEP were detected. Results After electroacupuncture, the latency of N20 prolonged in the stimulated side (Z=-2.620, P<0.01); the latency of N9 prolonged (Z=-2.454, P<0.05), and the amplitude of N9 decreased (Z=-2.330, P<0.05) in the non-stimulated side. After TEAS, the latencies of N9 both in the stimulated side and the non-stimulated side prolonged (Z>2.695, P<0.01). There was no significant difference in the D-value of latency and amplitude of N20 and N9 in both two sides between two treatments (Z<1.817, P>0.05). Conclusion Both electroacupuncture and TEAS could affect the latency and amplitude of N20 and N9, and no difference was found between two treatments.
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<p><b>OBJECTIVE</b>To observe the effects of low molecular weight heparin (LMWH) on the inflammatory response and vascular injury in rat after electric burn.</p><p><b>METHODS</b>A homemade regulator and transformer apparatus was used to reproduce the model of electric burn (0.5 cm×0.5 cm in size) with depth from full-thickness to full-thickness skin plus muscle and bone on the middle of the inside of right hind limb in 60 Wistar rats. The open wounds were covered with 20 g/L sulfadiazine silver paste immediately after injury. The wound condition was observed every day. The injured rats were divided into group LMWH and control group (C) according to the random number table, with 30 rats in each group. Rats in group LMWH were given subcutaneous injection of LMWH (1 U/g) in abdominal wall, 2 times a day. No other treatment was given in rats in group C. On post burn day (PBD) 3, 5, and 10, 10 rats respectively of two groups were sacrificed. The damaged tissue of wound and that around the wound (1.0 cm×0.5 cm in size) were excised, and heart blood was obtained. The pathological changes and thrombosis in damaged tissue were observed with HE, Masson, and aldehyde fuchsin staining, and the thrombosis rate was calculated. Serum contents of TNF-α and endothelin-1 were determined with ELISA. The mRNA expression of TNF-α in damaged tissue was detected with RT-PCR. Data were processed with Levene homogeneity test, analysis of variance of factorial design, LSD- t test, SNK- q test, and Friedman M nonparametric test.</p><p><b>RESULTS</b>(1) The injured limb of rats was obviously swollen after electric burn, which reached deeply to the muscle and bone. Compared with those of group C, the swelling of rats subsided slightly faster and the inflammatory response was lighter in group LMWH at each time point. (2) The necrosis of damaged tissue and profuse infiltration of inflammatory cells were observed. Dilatation of blood vessels, congestion and thrombosis, and swelling, necrosis, and desquamation of vascular endothelial cells were observed in the damaged tissue. Damaged blood vessel wall, ruptured elastic fiber, loss of internal elastic membrane, and other pathological changes were observed in the damaged tissue of rats in the two groups. Above lesions were improved gradually along with the passage of time, and the improvement was more obvious in rats of group LMWH compared with that of group C on PBD 5 and 10. (3) The thrombosis rates of rats in group LMWH were obviously lower than those of rats in group C (F = 4.921, P < 0.05). The thrombosis rates of rats in group LMWH on PBD 3 and 10 were respectively (0.07 ± 0.11)% and (0.03 ± 0.05)%, which were significantly lower than those of rats in group C [(0.16 ± 0.15)% and (0.13 ± 0.18)%, with t values respectively 2.17 and 2.07, P values below 0.05]. In group LMWH, the thrombosis rate of rats on PBD 10 was obviously lower than that on PBD 3 (t = 3.61, P < 0.05). (4) The serum contents of TNF-α and endothelin-1 of rats in group LMWH were significantly lower than those of rats in group C (F = 47.161, χ(2) = 81.46, P values below 0.01). In group LMWH, TNF-α contents were respectively (71 ± 24), (74 ± 14), (72 ± 20) pg/mL, and endothelin-1 contents were respectively (20.9 ± 3.2), (19.8 ± 5.2), (18.6 ± 1.1) ng/mL on PBD 3, 5, and 10, and they were significantly lower than those of rats in group C [(195 ± 148), (96 ± 20), (159 ± 46) pg/mL and (38.8 ± 15.4), (27.9 ± 3.6), (25.6 ± 7.6) ng/mL, with t values from 3.81 to 8.05, q values from 4.41 to 7.85, P < 0.05 or P < 0.01]. (5) The mRNA expression levels of TNF-α in damaged tissue of rats in group LMWH were significantly lower than those of rats in group C (F = 199.113, P < 0.01). The mRNA expression levels of TNF-α of rats in group LMWH were respectively 0.93 ± 0.10, 1.15 ± 0.12, 1.21 ± 0.11 on PBD 3, 5, and 10, and they were significantly lower than those of group C (1.68 ± 0.15, 1.43 ± 0.12, 1.50 ± 0.13, with t values from 3.75 to 6.12, P < 0.05 or P < 0.01). In group LMWH, the mRNA expression level of TNF-α of rats on PBD 10 was obviously higher than that on PBD 3 (t = 3.61, P < 0.05).</p><p><b>CONCLUSIONS</b>LMWH intervention can ameliorate vascular injury and inflammatory response of electrically burned wounds in rats, and it decreases thrombosis rate in the vessels of injured limb.</p>
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Animals , Male , Rats , Anticoagulants , Burns, Electric , Blood , Therapeutics , Endothelin-1 , Heparin, Low-Molecular-Weight , Rats, Wistar , Serum , Metabolism , Treatment Outcome , Tumor Necrosis Factor-alpha , Blood , Vascular System Injuries , TherapeuticsABSTRACT
Objective To study the effects of functional electric stimulation(FES) on neural function recovery and expression of nestin around cerebral infract area of rats with acute stroke.Methods The model of middle cerebral artery occlusion(MCAO) of male adult SD rats was established with the method of modified intraluminal filament occlusion.Sixty successfully established model rats were randomly allocated into FES group, placebo group and control group(20/group).Three days after MCAO' s surgery, rats in FES group were treated with FES device while the ones in placebo stimulation group were treated with the same FES device but without electrical output.Rats in control group had no treatment.All groups were randomly assigned into 4 subgroups according to treatment time:1 d,3 d ,7 d and 14 d (5/subgroup).The modified neurological severity score(mNSS) was adopted to evaluate neural function recovery before and after treatment in 4 time points as mentioned above.Meanwhile,the nestin expression in various time points was detected by immunohistochemistry stain in distant area of ipsilateral cortex of infarction.Results The mNSS sours in FES group is lower than that in placebo simulation group and control group at the 7 thd and 14thd (P < 0.05 ) ;The expression of nestin-positive cells in distant area of ipsilateral cortex of infarction of rats in FES group is higher than that in placebo stimulation group and control group ( P < 0.05 ).Conclusions FES may improve the recovery of neural function in the earlier stage of cerebral infarction.FES treatment could improve the expression of nesitin around cerebral infarct area and it could be one of the mechanisms of FES' s effect.
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Objective To observe the effects of low frequency electrical stimulation (LFES) on the proliferation of endogenous brain neural stem cells (NSCs) and on the expression of basic fibroblast growth factor (bFGF)and epidermal growth factor (EGF) in rats with acute cerebral infarction; to explore the therapeutic mechanism of LFES in improving neural function. Methods Fifty-four rats were randomly divided into a LFES group, a placebo stimulation group and a sham-operated group. Each group was further divided into 3rd day, 7th day and 14th day subgroups, with 6 rats in each subgroup. An acute cerebral infarction model was induced in the rats of the LFES and placebo stimulation groups by middle cerebral artery occlusion (MCAO). Three days after the operation, rats in the LFES group began LFES treatment (frequency 30 Hz, pulse width 250 μs, current intensity 3 mA, 10 min/d) ,while the placebo stimulation group was treated identically but without electricity. The rats in the sham-operated group had no special treatment. The expression of nestin positive cells in the subgranular zone of the hippocampus and the subventricular zone was detected by immunohistochemical staining. The expression of bFGF, EGF proteins and mRNA in the ischemic hemisphere was detected by Western blotting and RT-PCR analysis. A screen test was applied to evaluate motor function. Results Nestin-positive cells in the subgranular and subventricular zones of rats in the LFES group increased significantly more than in the placebo stimulation group at the 7th and 14th day. The expression of bFGF, EGF proteins and mRNA in the ischemic hemisphere was up-regulated compared to the placebo stimulation group at the 7th and 14th day. At the 14th day a difference in motor function was observed in rats in the LFES group compared with the placebo stimulation group. Conclusion LFES can promote the proliferation of endogenous brain NSCs and the expression of bFGF and EGF in rats with acute cerebral infarction. It can also improve motor function and enhance neural plasticity in the brain.
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Objective To study the effects of low-frequency electrical stimulation(LFES)on motor function and the expression of glia fibrillary acidic protein(GFAP)around cerebral infarction sites in rats.Methods Fifty-four male adult Sprague-Dawley rats were randomly divided into a LFES group,a placebo group and a sham operation group(18/group).All groups were randomly divided into 3 treatment groups.A rat model of middle cerebral artery occlusion(MCAO)was established using intraluminal filament occlusion.Treatment was carried out 3 d after the operation.Rats in the LFES treatment groups were stimulated with LFES for 3,7 or 14 days (10 min/d);the placebo groups were treated in the same way without electric stimulation;the sham operation subgroups didn't receive any therapy.Scores on a beam-walking test,a rotating pole test and a screen test were assessed at each time point mentioned above.Expression of GFAP was also assessed using immunohistochemcal techniques.Results The paralysed limbs recovered motor function better in the LFES groups than in the control groups.GFAP-positive cells were more numerous at the margins of the infarction area in the treated groups than in the control groups.Conclusions LFES might increase the expression of GFAP,which might be an important mechanism in improving brain plasticity after cerebral ischemia,aiding the recovery of the central nervous system and rebuilding its functioning.
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Objective To study changes in synaptic plasticity in the contralesional mirror area of the cortexes of rats with cerebral infarction treated by low-frequency electrical stimulation(LFES)and to explore the therapeutic mechanism of LFES on the molecular level.Methods Forty-eight Sprague-Dawley rats were randomly allocated into a LFES group,a placebo group and a sham-operation group.Following middle cerebral artery occlusion(MCAO),rats in the LFES group were treated with LFES for 7 d(20 min/d),while the ones in placebo group were connected with the same LFES device but without electricity.Rats in the sham-operation group were subjected to a MCAO operation without occlusion and then received no special treatment.Synaptic ultra-structures and the expression levels of glia fibrillary acidic protein(CFAP)and synaptophysin in the contralesional mirror area of the cortexes of the rats in each group were measured with electron-microscopy and Western blotting.Results Compared with the placebo group or the rats before treatment,rats treated with LFES exhibited ultra-structural changes in the form of larger curvature of synaptic interfaces and narrower synaptic clefts.GFAP expression levels did not fluctuate significantly,but the expression of synaptophysin was significantly up-regulated.Conclusion LFES treatment can induce active changes in synaptic plasticity in the contralesional mirror area of the cortex of rats after cerebral infarction.
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Objective To systematically review the effectiveness and safety of transcutaneous electricalnerve stimulation (TENS) on symptomatic diabetic neuropathy (DNP). Methods Electronic databases such asPUBMED, EMBASE, Cochrane Central Register of Controlled Trials, and Chinese Biomedical Database weresearched by using such mesh and text keywords as "TENS" and "diabetic neuropathy". Randomized controlled trials(RCTs) on the effect of TENS on symptomatic diabetic neuropathy were included. Studies were selected and availa-ble data was extracted independently by two reviewers. Meta-analysis was performed using RevMan 4.2.8 software.Results Three RCTs involving 78 patients were included in this study. Compared with sham-stimulation, TENStherapy significantly reduced the score in pain (SMD -2.35, 95% CI [-4.24, -0.46 ] ) and the score in numb-ness (WMD -0.18, 95% CI [-0.32, -0.05 ] ). Subgroup analysis shows that TENS therapy was associated with a significant reduction in the score of pain in both 4-week treatment duration ( SMD - 5.37, 95% CI [ - 6.97,- 3.77 ] ) and 6-week treatment duration ( SMD - 1.01, 95% CI [ - 2.01, - 0.01 ] ), but not 12-week treatmentduration (SMD - 1.65, 95% CI [ -4.02, 0.73 ] ). Conclusion TENS therapy is a promising and safe strategyfor treatment of symptomatic diabetic neuropathy. More studies are still warranted to accumulate the evidence of theeffect of TENS therapy on DNP.
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AIM: To investigate the effect of peroxisome proliferator-activated receptor ? (PPAR?) activator rosiglitazone on myocardial ischemic-reperfusion injury in rats. METHODS: Forty-two SD rats were randomly divided into three groups: sham group (n=14), I/R group (n=14) and I/R+rosiglitazone group (n=14). Myocardial infarct size was assessed by NBT staining. Plasma and myocardial angiotensin and aldosterone as well as plasma renin activity were detected by radioimmunoassay. RESULTS: Compared with I/R group, myocardial infarct size was reduced by 23.9% (P