[The feasibility study of objective evaluation of the severity of motion sickness by quantitative analysis of the facial skin color].

Objective: To explore the feasibility of applying quantitative analysis of the facial skin color to evaluate the severity of motion sickness objectively and to seek objective indicators that can reflect the severity of motion sickness. Methods: Motion sickness was induced in 51 male adult subjects recruited at the Air Force Medical University by Coriolis acceleration stimulation, and facial skin colorimetric values were acquired using a portable spectrophotometer at five time points: before stimulation and at 0 min, 10 min, 20 min and 30 min after the end of stimulation. The Graybiel rating scales were applied to assess the severity of motion sickness in subjects at each time point after stimulation, and the correlation between the magnitude of change in each colorimetric value and the maximum Graybiel's score was analyzed. The ROC curves were used to compare the evaluation performance of colorimetric value indicators which could reflect the severity of motion sickness. Results: Each colorimetric value in the CIE-L*a*b* color system changed significantly after exposure to provocative motion stimuli, and the trend was consistent with the typical sign of pallor in motion sickness. The magnitudes of the increase in the colorimetric value CIE-L*, the decrease in CIE-a*, and the increase in CIE-b* were all significantly and positively correlated with the maximum of Graybiel's scores (r=0.490 0, P=0.000 3; r=0.549 3, P<0.000 1; r=0.540 9, P<0.000 1). Comparing the performance of three colorimetric indicators to assess the severity of motion sickness, CIE-a* had an area under the ROC curve of 0.875 0, a sensitivity of 85.71%, and a specificity of 87.50%, which was better than CIE-L* and CIE-b*. Conclusions: The CIE-L*a*b* colorimeter values can be considered as objective indicators of the severity of motion sickness, among which the colorimetric indicator CIE-a* has the most diagnostic significance, and the method of quantitative analysis of the facial skin color can provide a new reference for the objective evaluation of the severity of motion sickness.

[The study of the rational use of antibiotics after nasal surgery].

Objective:To study whether the antibiotics should be used in the patients with or without chronic nasal sinusitis after the nasal surgery,and how to rationally use it.Method：Study design:prospective stratified randomized controlled study.Patients with sinusitis were divided into three groups.A group was without antibiotics,B group was with standard antibiotics using ,and C group was with prolonged antibiotics using.Patients without sinusitis were divided into D group without antibiotics,E group with standard antibiotics using,and F group with prolonged antibiotics using. Observe the postoperative infection rate in each group and compare them.Result：The infection rates were 3.53%,2.67%,0.00% in A,B and C group, and there was no significant differences between three groups. The infection rates were 1.22%,0.00%,1.39% in D,E and F group,and there was no significant differences between them.Conclusion： There was no influence in patients with or without using antibiotics,standard or prolonged using antibiotics after nasal surgery. Recommend not to use antibiotics after nasal surgery,and appropriately use antibioctics within 48 hours.Prolonged using is not recommended.

Up-regulation of miR-190b promoted growth, invasion, migration and inhibited apoptosis of Wilms' tumor cells by repressing the PTEN expression.

OBJECTIVE: Wilms' tumor (WT) is the most common malignant tumor in the children's urogenital system. MiR-190b was found to participate in the development and progression of several cancers. However, the molecular mechanism of miR-190b in WT is still unclear. PATIENTS AND METHODS: We detected the miR-190b in WT tissue samples compared to adjacent normal samples as well as in WT patients' blood sample compared to normal volunteers using qRT-PCR. With over-expression and knockdown of miR-190b in WT-derived cell line SK-NEP-1, we next studied cell proliferation, cell circle, apoptosis, invasion and migration abilities change caused by miR-190b ectopic expression. Dual-luciferase assay and Western-blot analysis were used to explain the mechanism of miR-190b in WT. RESULTS: MiR-190b was over-expressed in WT tissue and blood samples compared to normal group, relatively. Up-regulation of miR-190b in SK-NEP-1 cells significantly increased the growth and decreased the apoptosis of cells, while its down-regulation reduced cell proliferation and promoted cell apoptosis of SK-NEP-1. Also, cell invasion and migration abilities were significantly improved after miR-190b over-expression. Moreover, PTEN was proved to be a direct target of miR-190b and its protein level was remarkably decreased after miR-190b up-regulation. CONCLUSIONS: miR-190b over-expressed in WT and promoted cell proliferation, invasion and migration while reduced cell apoptosis of WT cells by repressing PTEN repression, which might provide a potential target for WT diagnosis and therapy.

Expression of autophagy in different stages of neurogenic bladder after spinal cord injury in rats.

STUDY DESIGN: Experimental study. OBJECTIVES: To investigate the expression of autophagy in different stages of the neurogenic bladder after spinal cord injury (SCI) in rats. SETTING: Second Hospital of Shandong University, Jinan, China. METHODS: A total of 36 Wistar rats were divided into the SCI and control groups. In total, six animals were killed and sampled from each group at 1, 4 and 14 days after surgery of T10-T11 level. BBB scale, residual urine volume and urinary bladder function score were estimated at each time point. The expression of microtubule-associated protein 1 light chain 3 (LC3) and P62 was detected using western blot analysis, immunofluorescence staining or real-time PCR (RT-PCR). RESULTS: The locomotor functions of the hindlimbs and the bladder function of the SCI group rats were lost after surgery, but gradually recovered from 1 day. Western blot showed that the LC3-II/actin was higher in the SCI than in the control group. Immunofluorescence staining revealed that LC3 and P62 were expressed in bladder smooth muscle cell. RT-PCR showed a remarkably increased LC3 mRNA expression at 1, 4 and 14 days in the SCI than in the control group. The P62 mRNA level of the SCI bladder tissues did not differ from that of the control group at 1 day but decreased at 4 and 14 days after surgery. CONCLUSIONS: Autophagy is activated during the recovery of the bladder after SCI and sustained. Autophagy may play an important role in bladder neurogenesis and may represent one of the mechanisms of bladder self-repair.

Leptin promotes apoptosis and inhibits autophagy of chondrocytes through upregulating lysyl oxidase-like 3 during osteoarthritis pathogenesis.

OBJECTIVE: Leptin has been found highly expressed in human osteoarthritis. We aimed to explore the possible effects and mechanisms of leptin on the apoptosis and autophagy of chondrocytes during osteoarthritis pathogenesis. METHODS: Gene expression profile from osteoarthritis affected and preserved cartilage were downloaded from NCBI's Gene Expression Omnibus database (GSE57218). Lysyl oxidase-like 3 (LOXL3) mRNA expression in cartilage tissues and leptin concentration in joint synovial fluid (SF) was measured in samples from 45 osteoarthritis patients and 25 healthy donors by real-time PCR and radioimmunoassay, respectively. Rat osteoarthritis model was induced by anterior cruciate ligament transection (ACLT). The expression of apoptosis regulators and autophagy markers were detected by Western blot. Cell survival and cell apoptosis were identified by CCK-8 and flow cytometry, respectively. RESULTS: Re-analysis on GSE57218 indicated that LOXL3 mRNA was upregulated in osteoarthritis affected cartilage. LOXL3 mRNA was upregulated in osteoarthritis patients, which was positively correlated with SF leptin concentration. Similar results were obtained in rat osteoarthritis model. Moreover, ACLT surgery led to a significant increase in the protein levels of cleaved caspase 3, and a notable decrease in the protein levels of Bcl-2, LC3 II/LC3 I and Beclin1. Silencing of LOXL3 in ACLT and leptin treated primary chondrocytes significantly inhibited cell apoptosis, and promoted cell proliferation and autophagy. Moreover, overexpression of LOXL3 remarkably inhibited autophagy of chondrocytes via activating mTORC1. CONCLUSIONS: LOXL3, a downstream of leptin, stimulated the apoptosis, but inhibited the autophagy of chondrocytes. LOXL3 is a potential therapy target for osteoarthritis.

Protective effects of bifidobacteria on intestines in newborn rats with necrotizing enterocolitis and its regulation on TLR2 and TLR4.

We established a necrotizing enterocolitis (NEC) rat model and explored the role of bifidobacteria in the intestines of the rats and its regulation on intestinal Toll-like receptors (TLRs). Seventy-five newborn Sprague-Dawley rats were randomly divided into 5 groups (15 rats/group): group A, artificial feeding group (formula-fed); group B, NEC model (LPS + formula-fed); group C, bifidobacterium (LPS + formula-fed + bifidobacterium microcapsules, intragastric administration); group D, artificial feeding + bifidobacterium (formula-fed + bifidobacterium microcapsules gavage); group E, rat breast-feeding group (rat breast-feeding). After 3 days of feeding, rats were placed in incubators, fasted for 12 h, and killed by decapitation. The ileocecal proximal segment ileum was fixed and sliced; pathological examination was conducted, and TLR2, TLR4, and nuclear factor-kB p65 protein expression in the intestinal tissue was detected by immunohistochemistry. There was a statistically significant difference in pathological scores between groups C and B (H = 21.789, P = 0.000), and the former was lower than the latter. TLR2, TLR4, and nuclear factor-kB p65 expression in intestinal tissue was determined in groups A-E. There were statistically significant differences between groups C and B (P = 0.001; P = 0.000; P = 0.000). Bifidobacteria had a protective effect on the intestines of newborn rats with NEC, which showed reduced NEC and intestinal damage severity. This observation may be related to the reduced levels of TLR2, TLR4, and nuclear factor-kB P65 observed during the inflammatory response.

Effect of Bifidobacterium on the mRNA expression levels of TRAF6, GSK-3ß, and microRNA-146a in LPS-stimulated rat intestinal epithelial cells.

We investigated the effect of inactivated Bifidobacterium on the mRNA expression of TRAF6, GSK-3ß, and microRNA-146a in lipopolysaccharide (LPS)-stimulated rat small intestinal epithelial cells (IEC-6s). IEC-6s were randomly divided into an LPS group, a culture supernatant group, and an inactivated bacteria group. After stimulation with LPS for 5 h, the three groups were treated as follows: the LPS group was cultured for 24 h with sterile saline; the culture supernatant group was cultured with Bifidobacterium (infantis strain) culture supernatant for 24 h; and the inactivated bacteria group was cultured with inactivated infantis Bifidobacterium for 24 h. Reverse transcription polymerase chain reaction was used to determine mRNA expression levels. The mRNA expression levels of TRAF-6 and GSK-3ß in the culture supernatant group were lower, and microRNA-146a expression was higher, compared with the LPS group (t = 5.278, P = 0.000; t = 6.316, P = 0.000; t = 13.218, P = 0.000, respectively). GSK-3ß mRNA expression in the inactivated bacteria group was lower than in the LPS group (t = 4.837, P = 0.000). There was no difference in the mRNA expression levels of TRAF-6 and microRNA-146a between the two groups (t = 0.732, P = 0.472 and t = 1.463, P = 0.164). Both the culture supernatant and the inactivated Bifidobacterium had a protective effect on LPS-stimulated IEC-6s. The protective effect of Bifidobacterium may be achieved through increased microRNA-146a by reducing levels of TRAF6 and GSK-3ß; the protective effect of inactivated Bifidobacterium may be achieved by reducing levels of GSK-3ß.

Zinc finger protein 637 protects cells against oxidative stress-induced premature senescence by mTERT-mediated telomerase activity and telomere maintenance.

Oxidative stress is believed to be an important inducer of cellular senescence and aging. Zinc finger protein 637 (Zfp637), which belongs to the Krüppel-like protein family, has been hypothesized to play a role in oxidative stress. Nevertheless, the precise function of Zfp637 has seldom been reported, and it remains unclear whether Zfp637 is involved in oxidative stress-induced premature senescence. In this study, we show that the endogenous expression levels of Zfp637 and mouse telomerase reverse transcriptase (mTERT) are downregulated during oxidative stress-induced premature senescence and in senescent tissues from naturally aged mice. The overexpression of Zfp637 markedly increases mTERT expression and telomerase activity, maintains telomere length, and inhibits both H2O2 and D-galactose-induced senescence accompanied by a reduction in the production of reactive oxygen species (ROS). In contrast, the knockdown of Zfp637 significantly aggravates cellular senescence by downregulating mTERT and telomerase activity, accelerating telomere shortening, and increasing ROS accumulation. In addition, the protective effect of Zfp637 against premature senescence is abrogated in the absence of mTERT. We further confirm that Zfp637 binds to and transactivates the mTERT promoter (-535/-502) specifically. As a result, the mTERT-mediated telomerase activity and telomere maintenance are responsible for the protective effect of Zfp637 against oxidative stress-induced senescence. We therefore propose that Zfp637 prevents oxidative stress-induced premature senescence in an mTERT-dependent manner, and these results provide a new foundation for the investigation of cellular senescence and aging.

The GSTP1 A1578G polymorphism and the risk of childhood acute lymphoblastic leukemia: results from an updated meta-analysis.

Studies investigating the association between the glutathione S-transferase P1 (GSTP1) A1578G polymorphism and the risk of childhood acute lymphoblastic leukemia (ALL) report conflicting results. The aim of this study was to quantitatively summarize the evidence for such a relationship. Two investigators independently searched the Medline, Embase, China National Knowledge Infrastructure, and Wangfang databases for studies of the polymorphism and ALL. Summary odds ratios (ORs) and 95% confidence intervals (CIs) for the GSTP1 polymorphism and childhood ALL were calculated in a fixed-effect model. Pooled ORs were calculated for a co-dominant model (GG vs AA, AG vs AA), a dominant model (GG + AG vs AA), and a recessive model (GG vs AA + AG). Analyses were also performed in subgroups stratified by race, study design, genotyping methods, and study sample size. This meta-analysis included 8 case-control studies with 1384 childhood ALL cases and 1755 controls. Overall, the variant genotypes (GG and AG) of A1578G were not associated with childhood ALL risk, when compared with the wild-type homozygote AA genotype (GG vs AA, OR = 1.09, 95%CI = 0.84-1.43; AG vs AA, OR = 1.05, 95%CI = 0.91-1.23). Similarly, no associations were found in the dominant and recessive models (dominant model, OR = 1.06, 95%CI = 0.92-1.23; recessive model, OR = 1.09, 95%CI = 0.84-1.43). Stratified analyses did not detect significant association in any subgroup. No heterogeneity or publication bias was observed in the present study. This updated meta-analysis indicates that the GSTP1 A1578G polymorphism is not associated with the risk of childhood ALL. In the future, additional studies in Asian and African-American patients should be performed to re-evaluate the association in these populations.

Calcium function in affective disorders and healthy controls.

Calcium metabolism has been reported to be disturbed in some forms of affective disorder. We studied concurrently a battery of calcium measures in 29 unipolar, 14 bipolar depressed, 11 manic, and 10 healthy control subjects. In addition to measures of extracellular calcium, we studied intracellular calcium concentration in platelets and measures that reflect cellular capability to maintain a low intracellular Ca++ concentration in red blood cells (RBCs) and platelets. Plasma calcium was lower in unipolar and manic patients than in control subjects. Platelet calcium concentration was lower in unipolar than bipolar depressed patients. RBC Ca++ adenosine triphosphatase (ATPase) was lower in unipolar and control subjects than in bipolar depressed and manic patients. Platelet Ca++ ATPase and Ca++ uptake were inversely correlated with severity of illness in unipolar patients. In bipolar depressed patients, RBC Ca++ ATPase and platelet Ca++ uptake were inversely correlated with severity. In addition to indicating abnormalities in calcium activity in affective disorders, the data suggest that unipolar and bipolar patients differ in several measures and may have different pathophysiological disturbances in calcium metabolism.

Platelet monoamine oxidase response to lithium treatment in psychiatric patients.

Platelet monoamine oxidase (MAO) activity was studied in bipolar and schizophrenic patients treated with lithium and was found to be increased as a nonspecific drug effect. Greater MAO increase in manic patients was correlated with lesser clinical improvement. There was no correlation of MAO activity with short-term outcome in schizophrenic patients. Change in MAO was not correlated with lithium dosage or plasma levels. Patients with baseline MAO values below the median had the largest activity increases. Platelet MAO might thus be characterized as a state variable, increased by lithium as a nonspecific pharmacologic effect, with the increase associated with poor clinical outcome in manic patients.