Optimized Design of a Pump Laser System for a Spin Exchange Relaxation Free Inertial Measurement Device.

In order to improve the precision and beam quality of a pump laser for a spin exchange relaxation free inertial measurement device, we applied one scheme to achieve the square wave modulation and power stability control of the pump laser and another one to obtain the uniform intensity distribution of the laser beam, in which the acousto-optic modulator (AOM) and proportion integration differentiation (PID) controller were used to achieve the former, and the freeform surface lens was designed and optimized to achieve the latter based on the TracePro software. In experiments, the first-order diffraction light beam coming through the AOM had a spot size of about 1.1×0.7 mm2, and a spherical vapor cell with a radius of 7 mm was placed behind the freeform surface lens. Results show that the uniformity of the reshaped intensity distribution is higher than 90% within the target area with a radius of 7 mm both in the simulation and the experiment, which ensure that the uniform laser beam covers the area of cell. On the other hand, the power stability of the pump laser is controlled to be less than 0.05%. Compared with traditional methods, the complicated calculation process in optical design is better solved, and a higher uniformity with slight energy loss is achieved.

Arctigenin enhances the sensitivity of cisplatin resistant colorectal cancer cell by activating autophagy.

Arctigenin is the active content of arctium lappa that present anti-cancer abilities in various carcinomas. However, its role and underlying mechanism in drug-resistant colorectal cancer cells has not been addressed. The present study used SW480 and SW620 to established cisplatin-resistant colorectal cancer cell lines, and explored the impact of arctigenin on these cells. Arctigenin at 100 µM significantly inhibited cell proliferation of cisplatin treated R-SW480 and R-SW620 cells as compared with cells treated with cisplatin alone. Arctigenin elevates cell apoptosis, up-regulated pro-apoptotic protein cleaved-caspase-3 and caspase-9 expression level in cisplatin treated R-SW480 and R-SW620 cells. Additionally, arctigenin triggered autophagy and promoted LC3-Ⅱ and p65 expression, while inhibited LC3-Ⅰexpression. Arctigenin impeded the IC50 of not only cisplatin but also oxaliplatin, doxorubicin and Paclitaxel of R-SW480 and R-SW620 cells. More importantly, the mRNA expression of multi drug resistance 1 (MDR1) and protein expression of pgp were significantly inhibited by arctigenin administration. Taken together, arctigenin has the potential in sensitize colorectal cancer cells by activating autophagy, which induced cell apoptosis and inhibited cell growth. Our study revealed that arctigenin has the potential for colorectal cancer treatment and may be useful in adjuvant chemotherapy.

Glioma malignancy is linked to interdependent and inverse AMOG and L1 adhesion molecule expression.

BACKGROUND: Gliomas account for the majority of primary human brain tumors and remain a challenging neoplasm for cure due to limited therapeutic options. Cell adhesion molecules play pivotal roles in the growth and progression of glial tumors. Roles of the adhesion molecules on glia (AMOG) and L1CAM (L1) in glioma cells have been shown to correlate with tumorigenesis: Increased expression of L1 and decreased expression of AMOG correlate with degree of malignancy. METHODS: We evaluated the interdependence in expression of these molecules by investigating the role of AMOG in vitro via modulation of L1 expression and analyzing apoptosis and cell senescence of glioma cells. RESULTS: Immunohistochemical staining of normal human cortical and glioma tissue microarrays demonstrated that AMOG expression was lower in human gliomas compared to normal tissue and is inversely correlated with the degree of malignancy. Moreover, reduction of AMOG expression in human glioblastoma cells elevated L1 expression, which is accompanied by decreased cell apoptosis as well as senescence. CONCLUSION: AMOG and L1 interdependently regulate their expression levels not only in U-87 MG cells but also in U251 and SHG44 human glioma cell lines. The capacity of AMOG to reduce L1 expression suggests that methods for increasing AMOG expression may provide a therapeutic choice for the management of glial tumors with high expression of L1.

Effect of Shuanglu Tongnao Formula on Neuronal Ferroptosis in Ischemic Stroke Rats by Regulating the SIRT1/Nrf2/GPx4 Signaling Pathway / 医药导报

Objective To explore the effect of Shuanglu Tongnao Formula on neuronal ferroptosis in ischemic stroke rats and its regulatory mechanism on the silent information regulator 2 homolog 1(SIRT1)/nuclear factor erythroid 2-related fac-tor 2(Nrf2)/glutathione peroxidase 4(GPx4)signaling pathways.Methods Twenty rats were selected as sham operation group by the random number table method,and the remaining seventy rats were made ischemic stroke rat models by the middle cerebral artery occlusion method.The rats that had been successfully modeled were randomly divided into the model control group,Shuanglu Tongnao formula group,Shuanglu Tongnao formula+SIRT1 inhibitor group(Shuanglu Tongnao formula+EX527 group),with 20 rats in each group.After 14 days,the rats were scored for neurological injury;TTC staining was applied to detect the area of cerebral infarction in rats;HE staining was applied to detect pathological changes in rat brain tissue;Nissl staining was applied to detect the number of neurons in rat brain tissue;the kit was applied to detect the levels of ferri ion(Fe2+),superoxide dismutase(SOD),glutathione(GSH),and malonaldehyde(MDA)in rat brain tissue;immunohistochemistry was applied to de-tect the positive expression of acyl-CoA synthetase long-chain family member 4(ACSL4),transferrin receptor(TFR),and ferritin heavy polypeptide 1(FTH1)proteins in rat brain tissue;Western blotting method was applied to detect the expression of SIRT1,Nrf2,GPx4,and cystine/glutamate antiporter solute carrier family 7 member 11(SLC7A11)proteins in rat brain tissue.Results Compared with the sham operation group,the neurological deficit score,cerebral infarction area,the contents of Fe2+and MDA,and the protein expressions of ACSL4 and TFR in model control group were increased(P<0.05);the number of neurons,the con-tents of SOD and GSH,the protein expression of FTH1,SIRT1,Nrf2,GPx4,and SLC7A11 were all reduced(P<0.05).Compared with the model control group,the neurological deficit score,cerebral infarction area,the contents of Fe2+and MDA,and the protein expression of ACSL4 and TFR in the Shuanglu Tongnao formula group were reduced(P<0.05),and the number of neurons,the contents of SOD and GSH,the protein expressions of FTH1,SIRT1,Nrf2,GPx4,and SLC7A11 are all increased(P<0.05).The results of the SIRT1 inhibitor supplementation experiment showed that the SIRT1 inhibitor reversed the inhibitory effect of Shuan-glu Tongnao formula on neuronal ferroptosis,while also inhibited the expression of Nrf2 and GPx4(P<0.05).Conclusion The Shuanglu Tongnao formula may inhibit neuronal ferroptosis in ischemic stroke rats by activating the SIRT1/Nrf2/GPx4 signa-ling pathway.

Effects of Zhuangyao Shuanglu Tongnao Formula on neuronal apoptosis of rats with ischemia-reperfusion induced injury / 中成药

AIM To investigate the effects of Zhuangyao Shuanglu Tongnao Formula on neuronal apoptosis in rats with cerebral ischemia-reperfusion injury based on the study of oxidative stress and inflammatory response.METHODS The rats were randomly divided into the sham operation group,the model group,the edaravone group(3.0 mg/kg),the low,medium and high dose groups(9.0,18.0,36.0 g/kg)of Zhuangyao Shuanglu Tongnao Formula,with 18 rats in each group.The middle cerebral artery occlusion/reperfusion was conducted by thread embolism method to simulate cerebral ischemia reperfusion injury in rats followed by 6 days corresponding drugs administration.Subsequently,the rats had their neurological function deficit scored by Zeal Longa scoring method;their sizes of cerebral infarction areas measured by TTC staining;their pathological damage and apoptosis of neurons in hippocampal CA1 area of ischemic penumbra of the brain tissue detected by HE staining and TUNEL staining;their SOD activity and levels of GSH,MDA,IL-6,IL-1β,TNF-α in brain tissue detected by kits;and their protein expressions of Bax,Bcl-2,caspase-3,cleaved-capase-3,TLR4,NF-κB p65,Nrf2,HO-1 in rat brain tissue determined by Western blot.RESULTS Compared with the model group,the groups intervened with edaravone,medium and high dose of Zhuangyao Shuanglu Tongnao Formula displayed improvements in the scores of nerve function defects,the rate of cerebral infarction,the rate of neuronal apoptosis,the levels of IL-6,IL-1β,TNF-α and MDA in the ischemic penumbra of brain tissues,the protein expressions of Bax and TLR4,the ratio of cleaved-capase-3/caspase-3 and p-NF-κB p65/NF-κB p65(P＜0.05),the levels of GSH,the activity of SOD and the protein expressions of Bcl-2,Nrf2 and HO-1(P＜0.05).CONCLUSION Being an inhibitor of oxidative stress and inflammatory response,Zhuangyao Shuanglu Tongnao Formula can alleviate brain injury in rats with cerebral ischemia reperfusion injury through the inhibition of neuronal apoptosis and improvement of neural function mediated by the inhibition of TLR4/NF-κB signal pathway and activation of Nrf2/HO-1 signal pathway.

CHL1 Is Expressed and Functions as a Malignancy Promoter in Glioma Cells.

The cell adhesion molecule with homology to L1CAM (close homolog of L1) (CHL1) is a member of the cell adhesion molecule L1 (L1CAM) gene family. Although CHL1 expression and function have been reported in several tumors, the roles of CHL1 in the development of glioma remain unclear. In the present study, we investigated the effects of CHL1 on proliferation indexes and activation of Akt1 and Erk signaling by siRNA in U-87 MG human glioblastoma and human U251 and SHG-44 glioma cells. We found that siRNA targeting CHL1 significantly down-regulated the expression of CHL1 mRNA and protein accompanied by reduced cell proliferation and transmigration invasion in all three cell lines. Down-regulating CHL1 expression also reduced cell survival, as measured by the Bax/Bcl-2 ratio, and increased activation of caspase-3. In subcutaneous U-87 MG cell xenograft tumors in nude mice, intratumoral administration of siRNA targeting CHL1 treatment significantly down-regulated CHL1 expression in vivo, accompanied by increased levels of activated caspase-3. Our combined results confirmed for the first time that in contrast to findings about CHL1 in most other cancer types, CHL1 functions in promoting cell proliferation, metastasis and migration in human glioma cells both in vitro and in vivo. These results indicate that CHL1 is a therapeutic target in the clinical management of glioma/glioblastoma.

Differential changes in Neuregulin-1 signaling in major brain regions in a lipopolysaccharide-induced neuroinflammation mouse model.

Neuregulin 1 (Nrg1) is involved in multiple biological processes in the nervous system. The present study investigated changes in Nrg1 signaling in the major brain regions of mice subjected to lipopolysaccharide (LPS)-induced neuroinflammation. At 24 h post­intraperitoneal injection of LPS, mouse brain tissues, including tissues from the cortex, striatum, hippocampus and hypothalamus, were collected. Reverse transcription­polymerase chain reaction was used to determine the expression of Nrg1 and its receptors, Neu and ErbB4, at the mRNA level. Western blotting was performed to determine the levels of these proteins and the protein levels of phosphorylated extracellular signal-regulated kinases (Erk)1/2 and Akt1. Immunohistochemical staining was utilized to detect the levels of pNeu and pErbB4 in these regions. LPS successfully induced sites of neuroinflammation in these regions, in which changes in Nrg1, Neu and ErbB4 at the mRNA and protein levels were identified compared with controls. LPS induced a reduction in pNeu and pErbB4 in the striatum and hypothalamus, although marginally increased pErbB4 levels were found in the hippocampus. LPS increased the overall phosphorylation of Src but this effect was reduced in the hypothalamus. Moreover, increased phosphorylation of Akt1 was found in the striatum and hippocampus. These data suggest diverse roles for Nrg1 signaling in these regions during the process of neuroinflammation.

Down-regulation of HOTAIR Reverses the Resistance of Gefitinib in HCC827 Cells by Increasing the Expression of PTEN / 中国肺癌杂志

BACKGROUND@#Lung cancer is the most common cancer worldwide with the highest morbidity and mortality, in which the non-small cell lung cancer accounts for 80% of all cases. The expression of (HOX transcript antisense RNA) HOTAIR were abnormal in a variety of tumor tissues and is involved in the regulation of the occurrence and development of lung cancer. The purpose of this study is to investigate the effect and mechanism of down-regulation of HOTAIR on gefitinib resistance of lung adenocarcinoma HCC827 cells by targeting PTEN.@*METHODS@#The HOTAIR downstream target gene was predicted by bioinformatics database. The small interfering RNAs (siRNA) which is corresponding to HOTAIR was transfected using Lipofectamine™ 2000. Quantitative real-time PCR (RT-qPCR) and Western blot were used to detect the expression of HOTAIR, PTEN, PI3K and AKT in HCC827 and HCC827GR cells. MTT assay was used to detect the changes in drug resistance of HCC827GR cells. Flow cytometry analysis were used to test the cell proliferation and the rate of apoptosis.@*RESULTS@#The expression of HOTAIR increased in HCC827GR and the serum of NSCLC patients with gefitinib resistance (P<0.05). Transfection of HOTAIR siRNA decreased the expression of HOTAIR (P<0.05), and increased the expressions of PTEN (P<0.05), while the expression of PI3K and AKT were decreased (P<0.05). Compared with the blank control group, down-regulation of HOTAIR increased the sensitivity of HCC827GR cells to gefitinib. The cell proliferation ability was decreased and the apoptosis was promoted apparently (P<0.05).@*CONCLUSIONS@#Down-regulation of HOTAIR can suppress the cell growth and promote the apoptosis, and it can reverse the resistance of HCC827GR cells to gefitinib. Its potential mechanism may be related with the targeting of PTEN/PI3K/AKT pathway.

Down-regulation of HOTAIR Reverses the Resistance of Gefitinib in HCC827 Cells by Increasing the Expression of PTEN / 中国肺癌杂志

BACKGROUND@#Lung cancer is the most common cancer worldwide with the highest morbidity and mortality, in which the non-small cell lung cancer accounts for 80% of all cases. The expression of (HOX transcript antisense RNA) HOTAIR were abnormal in a variety of tumor tissues and is involved in the regulation of the occurrence and development of lung cancer. The purpose of this study is to investigate the effect and mechanism of down-regulation of HOTAIR on gefitinib resistance of lung adenocarcinoma HCC827 cells by targeting PTEN.@*METHODS@#The HOTAIR downstream target gene was predicted by bioinformatics database. The small interfering RNAs (siRNA) which is corresponding to HOTAIR was transfected using Lipofectamine™ 2000. Quantitative real-time PCR (RT-qPCR) and Western blot were used to detect the expression of HOTAIR, PTEN, PI3K and AKT in HCC827 and HCC827GR cells. MTT assay was used to detect the changes in drug resistance of HCC827GR cells. Flow cytometry analysis were used to test the cell proliferation and the rate of apoptosis.@*RESULTS@#The expression of HOTAIR increased in HCC827GR and the serum of NSCLC patients with gefitinib resistance (P<0.05). Transfection of HOTAIR siRNA decreased the expression of HOTAIR (P<0.05), and increased the expressions of PTEN (P<0.05), while the expression of PI3K and AKT were decreased (P<0.05). Compared with the blank control group, down-regulation of HOTAIR increased the sensitivity of HCC827GR cells to gefitinib. The cell proliferation ability was decreased and the apoptosis was promoted apparently (P<0.05).@*CONCLUSIONS@#Down-regulation of HOTAIR can suppress the cell growth and promote the apoptosis, and it can reverse the resistance of HCC827GR cells to gefitinib. Its potential mechanism may be related with the targeting of PTEN/PI3K/AKT pathway.

Finite-element analysis of mandibular first molar with two marginal designs of endocrown for the repair of different defects / 华西口腔医学杂志

OBJECTIVE@#This study aimed to evaluate the stress distribution of the mandibular first molar with different thicknesses and heights of the axial wall restored by the endocrown with two marginal designs and thus provide a theoretical basis for selecting clinical preparation through the finite-element method.@*METHODS@#Two marginal endocrowns of the mandibular first molar with different axial-wall thicknesses (t=1, 2, 3 mm) and heights (h=2, 3, 4 mm) were established. Group A was the butt-joint design, whereas group B was the shoulder-surrounded design. After applying vertical and oblique loads , the size and distribution of the maximum principal stress and equivalent stress of residual tooth tissue were recorded.@*RESULTS@#The maximum principal stress and equivalent stress distribution of residual tooth tissue were similar among different models. Group A showed a lower maximum principal stress and equivalent stress than group B at the same thickness and height under vertical load. Meanwhile, under oblique load, the maximum principal stress values of groups A and B decreased with increased thickness at constant height. Group A showed lower equivalent stress than group B at the same thickness and height of 2 and 
3 mm. However, when the height was 4 mm, the trend was reversed.@*CONCLUSIONS@#In mastication, when bearing the vertical force, the retention of the butt-joint marginal endocrown preferred to the shoulder-surrounded one. Given the higher axial wall of the shoulder-surrounded marginal endocrown, it showed better ability to bear the oblique force than the butt-joint one.

Association of different sleep characteristics and cardiometabolic risk in college students / 中国学校卫生

Objective@#To describe the association of different sleep characteristics and cardiometabolic risk among college students, so as to provide reference for health promotion of college students.@*Methods@#By random cluster sampling method, a questionnaire survey and physical examination including blood pressure, waist circumference and blood lipid indicators, which were conducted in April and May of 2019 among a total of 1 179 college students from the first grade in two universities in Hefei City of Anhui Province and Shangrao City of Jiangxi Province. A total of 729 college students with valid questionnaires were included into analysis. The Pittsburgh Sleep Quality Index (PSQI) and Insomnia Severity Index (ISI) were used to investigate sleep behavior, and the Morning And Evening Questionnaire-5 (MEQ-5) was used to investigate sleep characteristics. The cardiometabolic risk score was derived using the sum of the standardized sex specific Z scores of waist circumference, mean arterial pressure, HDL cholesterol (multiplied by -1), triglycerides, and insulin resistance index. The rank sum tests were used to compare differences in cardiometabolic risk scores across demographic characteristics. Generalized linear models were used to compare the association of different sleep characteristics with cardiometabolic risk scores among college students.@*Results@#The average cardiovascular metabolic risk score of college students was -0.32(-2.03, 1.58). There were statistically significant differences in cardiovascular metabolic risk scores among college students in variables such as smoking, health status, and physical activity levels ( t/F=-3.41, 12.88, 51.07, P <0.01). The results of the generalized linear model showed that nighttime preference ( B=1.89, 95%CI =1.02-3.49), insomnia symptoms ( B=3.25, 95%CI =1.79-5.90), and short or long sleep duration ( B=1.92, 95%CI =1.21-3.05) were positively correlated with the cardiovascular metabolic risk score of college students ( P <0.05).@*Conclusions@#Poor sleep patterns among college students are positively correlated with the risk of cardiovascular metabolism. The sleep behavior of college students should be actively changed to reduce the risk of cardiovascular disease.

Quantitative Study on Articular Cartilage By Fourier Transform Infrared Spectroscopic Imaging and Support Vector Machine / 分析化学

Fourier transform infrared spectroscopic imaging (FTIRSI) technology can simultaneously obtain microstructure information and infrared spectral information of the samples. The method of FTIRSI combined with chemometric algorithms can be used for quantitative analysis of sample spectral information and tissue discrimination research. Based on this, FTIRSI and support vector machine classification (SVC) for the first time were used in this work to discriminate healthy and degenerated articular cartilage, with high accuracies of 100％ and 95. 4％ , respectively, and sum accuracy of 97. 7％ . The support vector regression (SVR) model was used to quantitatively study the contents and distribution of two biomacromolecules, collagen and proteoglycan, in articular cartilage. The proteoglycan loss occurred in the degenerated articular cartilage, especially in the superficial area. This study indicates that the combination of FTIRSI and support vector machine (SVM) is expected to become a new diagnostic tool for osteoarthritis, which is of great significance for the early diagnosis and research of osteoarthritis.