Objective To predict the occurrence of hypoparathyroidism following total thyroidectomy. Methods In this study, 124 patients underwent total thyroidectomy, 46 for thyroid cancer and 78 for multinodular goiter, additional neck dissection was performed on cancer patients. Serum calcium and parathyroid hormone (PTH) levels were examined preoperatively and at 1 h, 1 d and 2 d postoperatively. The occurrence of postoperative hypoparathyroidism was observed. Receiver operating characteristic curve analysis was employed to identify the best indicator to early predict the occurrence of clinical hypocalcemic symptoms. Results Fifty-eight (46.8%) patients suffered from postoperative transient hypoparathyroidism, with 22 ( 47. 8% ) cases in thyroid cancer group and 36 ( 46. 2% ) in multinodular goiter group ( λ2 = 0. 033, P = 0. 857). One (0.8%) patient in cancer group had permanent hypoparathyroidism. 90 patients (72.6%) had postoperative hypocalcaemia, 58 (46. 8% ) had subnormal serum PTH levels, 40 (32. 3% ) had hypocalcaemia symptoms. Postoperative serum calcium (F=21. 358,P =0. 000) and PTH ( F = 18.253, P =0.000) levels decreased more in cancer group than in goiter group.Receiver operating characteristic curve analysis demonstrated that the percentage of serum PTH level decline at 1 h postoperatively was most predictive and 76. 6% decline was the best cut-off value for the occurrence of clinical hypocalcaemia symptoms ( area under the curve being 0.933 ) with a sensitivity of 89. 7% and a specificity of 87.9%. Conclusions Neck dissection added to total thyroidectomy can decrease the postoperative serum calcium and PTH levels more seriously, but may not increase the incidence of postoperative transient hyperparathyroidism. The percentage of serum PTH level decline at 1 h postoperatively predicts the occurrence of clinical hypocalcaemia symptoms.

Objective To investigate the characteristics in sleep architecture of sub-healthy people with in-somnia,and to study the relationship between the sleep architecture and the degree of insomnia.Methods Sleep ar-chitecmre and Pittsburg sleep quality index(PSQI)value and PSQI scale were detected respectively.Results Sleep architecture of 46 subjects was abnormal-including shortened total-sleep-time(26.1%),excessive superficial-sleep stage(100%).inadequate deep-sleep stage(87.0%),insufficient rapid eye movement sleep(REM) (60.9%),longer sleep latency(65.2%)-more wakening times(47.8%)and longer wakeful time(43.5%).PSQI value of each insomniac exceeded 7,and the valtie of most objects was between 12 and 16(73.9%).The in-gredients of sleep architecture were not significantly correlated with the values of PSQI (P>0.05).Conclusion The sleep architecture of sub-healthy people with insomnia is mainly characterized with difficulty in falling asleep,light sleep and festless sleep,but the characteristics of sleep architecture is not inevitablly related with the degree of insomnia.

AIM: To elucidate the role of mitochondrial DNA (mtDNA) deletion in the pathogenesis of viral myocarditis in mice. METHODS: 50 BALB/c mice were divided into two groups randomly. 40 were experimental group, each of them was injected 0.1 mL Eagle liquids with CVB_3 (TCID_ 50=108) intraperitoneally. Another 10 mice were given equal volume Eagle liquids as control group. Cardiac functions in vivo and mtDNA 3867 deletion rate in myocytes were detected separately at the day 3, 11 and 24 after injection. The correlation of mtDNA 3867 deletion rate to cardiac functions was analyzed using Spearman method. RESULTS: At the day 3 after injection, mtDNA 3867 deletion rate in experimental group was 8.3 times higher than that in control group [(0.01970?0.00118)% vs (0.00211?0.00032)%,P

Objective To discuss the operation style of filling,film-style,three-dimensional double-layer mesh tension-free for hernia and the repair materials,the selectlon of surgical operation style for reducing recurrence.Methods We used the style of plug-and-chip,two-dimensional mesh tension-free hernia repair for the treatment of 130 cases of inguinal hernia patients.Results In 130 cases of patients with 1~5 years of follow-up,there was no recurrence.Conclusion A reasonable choice of repair materials and improving the surgical operation can be effective in reducing recurrence.

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA(3867) (mtDNA(3867)) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3(TCID50=10(8)), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA(3867) deletion rate was significantly higher in experimental group than in control group (P<0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P>0.05). At day 11 after injection, the mtDNA(3867) deletion rate of both cells in experimental group was increased to the peak level (P<0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P>0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P<0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA(3867) deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P<0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocarditis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.

Objective To establish a scald-induced pain model using a constant-temperature electrical scald instrument in rats.Methods Thirty-six pathogen-free male Sprague-Dawley rats, weighing 200-250 g, were randomly divided into 4 groups (n =9 each) using a random number table: control group (group C), scald for 5 s group (group S5), scald for 10 s group (group S10), and scald for 15 s group (group S15).The rats were anesthetized with intraperitoneal chloral hydrate.In S5, S10 and S15 groups, the plantar surface of the left hindpaw of rats were exposed to a constant-temperature electrical scald instrument (85 ℃) for 5, 10 and 15 s, respectively.The plantar surface of the left hindpaw of rats was exposed to an electrical scald instrument (room temperature) for 10 s in group C.At 1 day before treatment (T0),and 1, 3, 5, 7 and 14 days after treatment (T1-5), the mechanical and thermal pain thresholds were measured.Immediately after treatment, and at 24 h after treatment, the total body condition, wound color, and shape of the margin of the wound were observed and recorded.At 24 h after treatment, 3 rats were randomly sacrificed, and the skin from the plantar surface of the left hindpaw was removed for microscopic examination.Results Compared with group C, the thermal pain threshold at T1-2, and the mechanical pain threshold at T1-3 were significantly decreased in group S5, and the thermal pain threshold,and mechanical pain threshold were significantly decreased at T1-4 in group S10 (P＜0.05).The thermal pain threshold ＞ 25 s, and the mechanical pain threshold ＞30 g at T1-5 in group S15.The swelling in foot was bovious, burn blister appeared, and the degree of damage was aggravated in group S10 compared with S5 and S15 groups.Conclusion The scald-induced pain model is successfully established using a constant-temperature electrical scald instrument in rats.

Objective To investigate the application of MRI in evaluation of the traumatic temporomandibular joint (TMJ) injury induced by type Ⅵ condylar fracture. MethodsMRI was performed in TMJs in 18 patients with type Ⅵ condylar fractures at days 3-14 post-injury and the MRI findings were analyzed. ResultsMRI findings of 18 patients with traumatic TMJ injury with 19 sides of type Ⅵ condylar fractures showed 15 sides of TMJ disk displacement,nine sides of capsule tear,16 sides of retrodiscal tissue tear (double-plate area) and 19 sides of joint effusion change. Conclusions MRI is very important in the diagnosis and evaluation of traumatic TMJ injury,since it can clearly display the TMJ injuries in type Ⅵ condylar fractures.Therefore,the clinical application of MRI is beneficial for selection of the therapeutic schedules.

Objective To explore the protective mechanism of HSP70 protein in traumatic brain injury (TBI)‐related acute gastric mucosal lesions in mice .Methods Forty adult male Balb/c mice were randomly divided into sham (A) ,TBI (B) ,TBI+ geranylgeranylacetone (GGA) (C) ,and TBI+saline (D) groups .TBI was induced via the Feeney impact model .GGA (800 mg/kg) was administered via oral tube beginning before the model was built in group C .The expressions of HSP70 protein in brain and gastric mucosa were determined by immunohistochemistry , and the apoptotic index was detected by TUNEL method .Results The injury area in mouse brain and gastric mucosa was greater in group B than in groups A and C (P<0 .05) .After model induction ,the content of HSP70 protein in group B was markedly higher in the brain and gastric mucosa ,which was notably higher than in group A (P<0 .05) .Obviously apoptotic cells were observed in groups B and D ,which were significantly higher than in groups A and C .GGA pretreatment enhanced the up‐regulated expression of HSP70 and decreased the apoptotic index distinctly ;HSP70 expression was higher in group C than in groups B and D ,but the apoptotic index was lower (P<0 .05) .Conclusion GGA can induce HSP70 protein expression in mouse brain and gastric mucosa .HSP70 is involved in the process of apoptosis inhibition .GGA can be used in the prevention and therapy of TBI‐related acute gastic mucosal lesions .

Objective To investigate the capability of 99 Tcm?tricine?EDDA/HYNIC?SFSIIHTPILPL ( SP94) as a specific probe for HCC imaging. Methods HYNIC?SP94 peptide was prepared by solid phase synthesis, followed by 99 Tcm labeling with tricine?EDDA as the coligand. After determination of radiochemical purity and stability, cell binding study was carried out by incubating Huh?7 cells with 99 Tcm?tricine?EDDA/HYNIC?SP94 at different specific activities (2.5, 4.0 and 30.0 GBq/μmol). The biodistribution studies and microSPECT/CT imaging were performed in Huh?7 tumor?bearing mice ( study group) and Hela tumor?bear?ing mice ( control group ) . Statistical analysis was by two?sample t test. Results 99 Tcm?tricine?EDDA/HYNIC?SP94 was synthesized with over 95% of labeling yield, which remained stable in saline and FBS up to 12 h. With increasing concentrations of 99 Tcm?tricine?EDDA/HYNIC?SP94, Huh?7 cell binding increased but became gradually saturated. In biodistribution studies, (1.02±0.26) %ID/g of tracer was accumulated in Huh?7 tumors at 0.5 h after injection of 99 Tcm?tricine?EDDA/HYNIC?SP94, higher than that in the HYNIC?SP94 blocking group ((0.34±0.09) %ID/g;t=3.537, P<0.05). Compared to Hela tumors, Huh?7 tumors were clearly visualized by microSPECT/CT, with which better imaging quality could be achieved with higher specific radioactivity. Conclusion 99 Tcm?tricine?EDDA/HYNIC?SP94 could achieve a high labeling effi?ciency and good in vitro stability as a potential diagnostic tracer specifically targeted for HCC.

In order to investigate the impairment of mitochondrial membrane phospholipid localization and DNA3867 (mtDNA3867) deletion and the correlation between cardiac and skeletal muscle cells in mice with viral myocarditis, 50 BALB/c mice were divided into two groups randomly. In experimental group (n=40), the mice were intraperitoneally injected with 0.1 mL Eagle liquid with CVB3 (TCID50=108), while in the control group (n=10), the mice were subjected to equal volume of Eagle liquid. The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate of cardiac and skeletal muscle were detected separately at day 3, 11 and 24 after injection. The correlation of mitochondrial membrane phospholipid localization and mtDNA3867 deletion rate between cardiac and skeletal muscle cells cells was analyzed using Spearman method. At the day 3 after injection, in both cardiac and skeletal muscle cells, mtDNA3867 deletion rate was significantly higher in experimental group than in control group (P＜0.05), but the localization of mitochondrial membrane phospholipid showed no difference between two groups (P＞0.05). At day 11 after injection, the mtDNA3867 deletion rate of both cells in experimental group was increased to the peak level (P＜0.05), and the impairment of mitochondrial membrane phospholipid localization of both cells also increased markedly in experimental group as compared with control group (P＞0.05). At the day 24 after injection, the impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion of both cells showed a recovery tendency, but still severer than those at the day 3 after injection (P＜0.05). The impairment of mitochondrial membrane phospholipid localization and mtDNA3867 deletion were consistent and synchronistic between cardiac and skeletal muscle cells, and showed good correlations (P＜0.05). The impairment of mitochondria plays an important role in the pathogenesis of viral myocardifis, and the skeletal muscle cells might act as a peripheral "window" to reflect the mitochondrial damage of cardiac myocytes.