BACKGROUND: The minimally invasive axial lumbar interbody approach (AxiaLIF) for L4–S1 fusion has been applied in America and Europe, and has obtained satisfactory curative efficacy. Because of significant anatomical differences between Chinese and Europeans and Americans, whether AxiaLIF is appropriate for Chinese remains unclear. Moreover,there are some problems in the application of AxiaLIF, so how to optimize AxiaLIF is a key to its promotion in China.OBJECTIVE: To provide anatomical data for the design of axial screws suitable for Chinese through measuring the mid axial line of the lateral lumbar radiograph and cross sections of L5 and S1 on lumbar CT in normal Chinese population.METHODS: The lateral lumbar radiographs from Chinese healthy population were selected, including 35 males and 30 females, the axial height of S1, the disc distance between L5 and S1, and the axial height of L5 were measured so as to provide anatomical data for designing the length of the axial screw. The transverse and sagittal diameters of L5 and S1 in the lumbar CT of 26 adult healthy males and 24 healthy females were measured to provide anatomical data for designing the diameter of the axial screw.RESULTS AND CONCLUSION: (1) The axial height of S1 in males and females was (26.76±3.94) mm and (22.91±2.91) mm, respectively (P < 0.05). The disc distance between L5 and S1 was (12.62±1.90) mm for males and (11.92±1.78) mm for females (P > 0.05). The axial height of L5 was (29.12±2.18) mm for males and (26.91±2.47) mm for females (P <0.05). (2) The transverse diameter of S1 was (49.14±4.14) mm for males and (46.11±4.44) mm for females (P < 0.05).The transverse diameter of L5 was (41.34±4.31) mm for males and (43.12±3.71) mm for females (P < 0.05). The sagittal diameter of L5 was (34.48±2.32) mm for males and (33.03±3.48) mm for females, and the sagittal diameter of S1 was (35.65±4.28) mm for males and (33.53±3.26) for females, (both P > 0.05). (3) That is to say, this study provides the anatomical data for designing the axial screws suitable for the lumbar fusion of Chinese by measuring the mid axial line of the lateral lumbar radiographs and the cross sections of L5 and S1 on lumbar CT. The image measurement method can be used to analyze the preoperative images of the patients to predict the feasibility of the surgical approach and pre-select the internal fixation model for personalized screw positioning.

Objective To investigate the alteration of serotonin-producing gastric enterochromaffin (EC)cell in patients with functional dyspepsia(FD).Methods Fifteen healthy volunteers and 33 patients with FD were enrolled.Proximal gastric mucosal EC cells were countered after immunohisto- chemistry staining.The ultrastructure of EC cell was observed by electromicroscope.Results The EC cells in proximal gastric mucosa in patients with FD were significant higher than that in controls(12.5?2.1 vs 8.3?1.4,t=2.353,P＜0.05),and the staining intensity of EC cell in patients with FD was also stronger than that in controls(3.72?0.42 vs 2.61?0.57,t=2.078,P＜0.05).The more sever the gastric mucosal inflammation was,the more number of EC cells and the stronger staining intensity were.Under the electromicroscopy,more Golgi apparatus,mitochondria and endoplasmic reticulum were found in EC cells.Special secreting particles were also found in cytoplasm.Conclusions EC cells may be involved in the pathogenesis of FD.The number of EC cell is related with the severity of gastric mucosal inflammation.

OsRacD is a critical molecular switch involved in photoperiod fertility conversion of photoperiod sensitive genic male sterile rice.Taking OsRacD as bait,a new rice myosin heavy chain partial cDNA was isolated from the rice panicle by yeast two-hybrid,and designated OsMY1.The interaction between OsMY1 and OsRacD had been testified by yeast two-hybrid and pull down assay,it showed that OsMY1 could bind with OsRacD,suggested that OsMY1 maybe the target of OsRacD.The important evidence for further study on the functional relationship between OsMY1 and OsRacD in vivo are also provided.

Objective To investigate the mechanisms of the protective effects of dexmedetomidine against the propofol-induced neuroapoptosis in primary cultured cortical neurons.Methods The neurons were cultured 7days and then divided into four groups: vehicle-control group (treated with equal volume of intralipid), propofoltreated group (treated with 500 μmol/L propofol), propofol plus dexmedetomidine treated group (treated with 500 μmol/L propofol and 0.1 μmol/L dexmedetomidine), and LY294002 pretreated group (treated with 500 μmol/L propofol ,0.1 μ mol/L dexmedetomidine and 10 μmol/L LY294002).12 hours after different treatments, neuron viability was measured by MTT assay,neuroapoptosis was detected by Hoechst33258 staining, and the levels of pAkt and Bcl-2 protein were detected by Western blot.Results Compared with the vehicle-reduced group,propofol reduced neuron viability greatly((53.4±4.2)％ vs (99.9±6.3)％;P＜0.01), but increased neuroapoptosis greatly((44.6±4.3)％ vs (5.8±0.4)％;P＜0.01).The levels of pAkt((0.41±0.03) vs (0.86±0.07))and Bcl-2 ((0.15±0.02) vs (0.72±0.03)) were decreased greatly (both P＜0.01).Compared with propofol treatment group, the neuron viability of propofol plus dexmedetomidine group were increased greatly((86.4±5.3) ％ , P＜0.01) ,the neu roapoptosis was decreased greatly ((23.1 ± 3.5) ％, P＜ 0.01), and the levels of pA kt (0.8 ± 0.03) and Bc1-2 (0.52 ±0.05) were increased greatly (both P＜0.01).Compared with propofol plus dexmedetomidine treated group,LY294002 inhibited the protective effects of dexmedetomidine, decreased neuron viability greatly ((64.3±5.1) ％ ,P＜0.01), increased the number of apoptotic neurons((38.8±4.9) ％, P＜0.01), and reduced the levels of pAkt (0.52±0.04) and Bcl-2(0.31±0.02) significantly (P＜0.01).Conclusion Dexmedetomidine exerts the neuroprotective effects against propofol-induced neuroapoptosis by activating the PI3K-Akt-Bcl-2 signalling pathway.

Craniofacial pain is a common disease and it is complicated in its diagnosis and treatment.Some common kinds of craniofacial pain are introduced according to the criteria of headache classification of International Headache Society(IHS)2004.Trigeminal neuralgia,glossopharyngeal neuralgia,nervus intermedius neuralgia,supra-orbital neuralgia,occipital neuralgia,acute zoster and postherpetic neuraigia and Tolosa-Hunt syndrome are included with their key points of clinical diagnosis and treatment.

Objective To investigate the protective effects and the mechanisms of 17β-estradiol on the propofol-induced neuroapoptosis in primary cultured rat cortical neurons.Methods The neurons were cultured for 7 days and then divided into three groups: vehicle-control group ( treated with equal volume of 20% intralipid ) , propofol-treated group ( treated with 500μmol/L propofol) , and propofol plus 17β-estradiol treated group ( treated with 500μmol/L propofol and 0.1 μmol/L 17β-estradiol).12 hours after the treatment, neuroapoptosis was detected by Hoechst 33258 staining and TUNEL assay, and the levels of Bcl-2, Bax and cleaved caspase-3 proteins were detected by Western blot.Results Compared with the vehicle-control group, the neuroapoptosis increased greatly ( P<0.01 ) , Bcl-2 level reduced ( P <0.01), Bax and cleaved caspase-3 levels increased greatly (P<0.01), and Bcl-2/Bax ratio reduced significantly (P<0.01).Compared with the propofol-treatment group, the neuroapoptosis decreased greatly ( P <0.01), Bcl-2 level increased ( P<0.01 ) , Bax and cleaved caspase-3 levels reduced greatly ( P <0.01 ) , and Bcl-2/Bax ratio increased greatly ( P <0.01 ) . Conclusions 17β-estradiol can protect cortical neurons against propofol-induced cortical neuroapoptosis by regulating the expression of Bcl-2 and Bax.

Objective To investigate the effect of propofol exposure on neuroapoptosis in pri-mary cultured cortical neurons and its mechanisms.Methods Cortical neurons were primarily cultured for seven days,then divided into two groups:control group (treated with equal volume of 20% in-tralipid),propofol-treated group (treated with 500 μmol/L propofol).The neurons were treated for 12 h.The neuron viability was determined by MTT.Neuroapoptosis was identified by Hoechest 33 258 dying.Mitochondrial membrane potential was measured by the fluorescent dye rhodamine 123 (Rh123).Western blot was performed to detect the level of cyt-c and cleaved-caspase-3.Results Neu-rons survival rate (54.4%±6.4%)in the propofol group was significantly lower than that of control group (99.8% ± 4.1%) (P < 0.05 ), the rate of neuronal apoptosis (46.5% ± 5.3%) was significantly higher than that of control group (7.2%±0.9%)(P <0.05),mitochondrial membrane potential (59.6%±4.3%)was significantly lower than that of the control group (99.9% ± 5.7%) (P <0.05 ),cyt-C protein level (0.38 ± 0.03 )was significantly higher than that of control group (0.1 5±0.02)(P < 0.05 ),level of cleaved-caspase-3 protein level (0.46 ± 0.04)was significantly higher than that of control group (0.13±0.02)(P <0.05).Conclusion Propofol induces neuroapo-tosis in primary cultured cortical neurons,which is associated with the decreased level of MPP and the increase levels of cyt-c and cleaved-caspase-3.

Objective To investigate the protective effect and the mechanisms of 17β-estradiol on ketamine-induced apoptosis on primary cultured rat cortical neurons. Methods Cortical neurons were primarily cultured for seven days,then divided into four groups :control group ( treated with equal valume of DMSO ),estradiol-treated group ( treated with 0.1 μmol·L-1 17β-estradiol),ketamine-treated group(treated with 100 μmol·L-1 ketamine),ketamine plus 17β-estradiol-treated group( treated with 0. 1 μmol·L-1 17β-estradiol+100μmol·L-1 ketamine). The neurons were treated for 24 hours. The neuron viability was determined by MTT. Neuroapoptosis was measured by nuclear morphometry after Hoechest 33258 dying. Western blotting was performed to detect the expression levels of cleaved-caspase-3 and Bcl-2protein. Results The neuron viability in the ketamine group was(54. 02±7. 78)%,significantly decreased from the control group,whereas ketamine plus 17β-estradiol increased the cell viability to(88. 09±6. 54)%,significantly higher than the ketamine group. The neuroapoptosis rate in the ketamine group was(49. 50±4. 34)%,significantly increased from the control group,while that in the drug combination group was(15. 74 ± 3. 40)%,significantly lower compared with the ketamine group. Meanwhile,the cleaved-caspase-3 expression increased,and Bcl-2 expression decreased remarkably after ketamine treatment,while which was reversed in the drug combination group. Conclusion 17β-estradiol can protect against ketamine-induced injury by inhibiting neuron apoptosis.

Objective To compare the effects of no-rinse skin cleanser and warm water with paraffin oil in first brush bath of the new-born. Methods About 42 newborns who were born from January to March 2016 were set as control group and used warm water with paraffin oil in first brush bath. About 43 newborns who were born from April to June 2016 were set as observation group and used no-rinse skin cleanser in first brush bath. The cleaning time and effect ,the rectal temperature before and after sponge and dermatitis were compared. Results Both groups did not develop dermatitis. But the observation group had better cleaning satisfaction , less cleaning time, faster rewarming than those of the control group with statistical significance (all p<0.05). Conclusion No-rinse skin cleanser used in the first brush for the new-born can reduce cleaning time and difference of temperature, which is safe for clinical application.

In order to assess the feasibility of subcutaneous administration of Triptorelin with 6-week intervals for the suppression of pituitary-gonadal axis and changes of clinical signs in girls with idiopathic central precocious puberty (ICPP), 46 girls with ICPP were treated with GnRHa. Triptorelin (Decapeptyl, 3.75 mg) was administered subcutaneously (SC) at 6-weeks intervals or intramuscularly (IM) at 4-weeks intervals randomly for more than 12 months consecutively. During GnRHa therapy, clinical parameters and laboratory data, including height, weight, pubertal stage, bone age, uterine volume and ovarian size, serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH) and estradiol (E2), were monitored and analyzed. It was found that both treatment regimes led to regression of precocious puberty and reversal of secondary sexual characteristics. Breast developments regressed. Uterine volume was decreased after treatment, but there was no statistically significant difference. Mean ovarian volume did not change significantly during treatment. The height velocity was decreased significantly from 6.3+/-1.4 cm/year to 5.8+/-1.2 cm/year in group SC and 6.7+/-1.3 cm/year to 5.4+/-1.0 cm/year in group IM, respectively. The rate of bone maturation was reduced significantly during treatment. The ratio of deltaBA/deltaCA was 1.2+/-0.2 or 1.3+/-0.3 at the onset of therapy and decreased significantly after the treatment to 0.7+/-0.2 or 0.9+/-0.1, respectively. The predicted adult height was increased significantly and progressively during therapy. The levels of serum LH, FSH and E2 returned to the prepubertal condition. No significant side effects of therapy were noted. The most common side effect during SC treatment was that a non-irritating, 1 cm in diameter mass was palpated at the site of subcutaneous injection in the abdominal wall of patients, which disappeared after 6-12 weeks. Two girls had minimal withdrawal vaginal bleeding episodes after the first injection. It was concluded that both IM and SC triptorelin administrations were clinically effective. They induce profound suppression of hypothalamic-pituitary-gonadal axis while stabilizing height velocity, slowing bone maturation and increasing predicted adult height. These results suggest that subcutaneous injection of triptorelin in 6-weeks intervals at a dosage of 3.75 mg be a safe and acceptable regimen for ICPP