Monitoring ocean currents during the passage of Typhoon Muifa using optical-fiber distributed acoustic sensing.

In situ observations under typhoon conditions are sparse and limited. Distributed acoustic sensing (DAS) is an emerging technology that uses submarine optical-fiber (OF) cables to monitor the sea state. Here, we present DAS-based ocean current observations when a super typhoon passed overhead. The microseismic noise induced by ocean surface gravity waves (OSGWs) during Typhoon Muifa (2022) is observed in the ~0.08-0.38 Hz frequency band, with high-frequency (>0.3 Hz) component being tidally modulated. The OSGW propagation along the entire cable is successfully revealed via frequency-wavenumber analysis. Further, a method based on the current-induced Doppler shifts of DAS-recorded OSGW dispersions is proposed to calculate both speeds and directions of horizontal ocean currents. The measured current is consistent with the tidally induced sea-level fluctuations and sea-surface winds observed at a nearby ocean buoy. These observations demonstrate the feasibility of monitoring the ocean current under typhoon conditions using DAS-instrumented cables.

Improved Cardiac Function in Postischemic Rats Using an Optimized Cardiac Reprogramming Cocktail Delivered in a Single Novel Adeno-Associated Virus.

BACKGROUND: Cardiac reprogramming is a technique to directly convert nonmyocytes into myocardial cells using genes or small molecules. This intervention provides functional benefit to the rodent heart when delivered at the time of myocardial infarction or activated transgenically up to 4 weeks after myocardial infarction. Yet, several hurdles have prevented the advancement of cardiac reprogramming for clinical use. METHODS: Through a combination of screening and rational design, we identified a cardiac reprogramming cocktail that can be encoded in a single adeno-associated virus. We also created a novel adeno-associated virus capsid that can transduce cardiac fibroblasts more efficiently than available parental serotypes by mutating posttranslationally modified capsid residues. Because a constitutive promoter was needed to drive high expression of these cell fate-altering reprogramming factors, we included binding sites to a cardiomyocyte-restricted microRNA within the 3' untranslated region of the expression cassette that limits expression to nonmyocytes. After optimizing this expression cassette to reprogram human cardiac fibroblasts into induced cardiomyocyte-like cells in vitro, we also tested the ability of this capsid/cassette combination to confer functional benefit in acute mouse myocardial infarction and chronic rat myocardial infarction models. RESULTS: We demonstrated sustained, dose-dependent improvement in cardiac function when treating a rat model 2 weeks after myocardial infarction, showing that cardiac reprogramming, when delivered in a single, clinically relevant adeno-associated virus vector, can support functional improvement in the postremodeled heart. This benefit was not observed with GFP (green fluorescent protein) or a hepatocyte reprogramming cocktail and was achieved even in the presence of immunosuppression, supporting myocyte formation as the underlying mechanism. CONCLUSIONS: Collectively, these results advance the application of cardiac reprogramming gene therapy as a viable therapeutic approach to treat chronic heart failure resulting from ischemic injury.

Prevalence and risk factors of diabetic retinopathy among Chinese adults with type 2 diabetes in a suburb of Shanghai, China.

BACKGROUND: To investigate the prevalence and risk factors of diabetic retinopathy (DR) in a Chinese population with type 2 diabetes mellitus (T2DM) in a suburb (Qingpu) of Shanghai, China. METHODS: A population-based cross-sectional study. A total of 7462 residents with T2DM in Qingpu were enrolled according to the resident health archives from January 2020 to December 2020. Blood and urine samples of the subjects were collected. Disc- and macula-centred retinal images were taken to assess DR. SPSS was used to analyse and investigate the prevalence and risk factors of DR. RESULTS: The fundus images of 6380 (85.5%) subjects were of sufficiently good quality for grading. The average (range) age of 6380 subjects was 63.46±7.77 (28-92) years. Six hundred forty-four subjects were diagnosed with DR. The prevalence of DR was 10.1% (95% CI 9.4%-10.8%), with mild, moderate, and severe non-proliferative retinopathy and proliferative retinopathy being 2.1%, 6.3%, 1.3% and 0.4%, respectively. The prevalence of bilateral DR was 6.5%. Higher T2DM duration (OR, 1.057), fasting plasma glucose (OR, 1.063), glycated hemoglobinA1c (OR, 1.269), urea nitrogen (OR, 1.059), and urinary albumin (OR, 1.001) were associated with the higher DR prevalence. CONCLUSION: The prevalence of DR among Chinese adults with T2DM in Qingpu was 10.1%, in which non-proliferative DR was more common. Higher fasting plasma glucose and glycated hemoglobinA1c are well-known risk factors of DR, consistent with the findings in our study. Our study didn't find the risk between lipid indicators and DR. However, several renal function indicators, like higher urea nitrogen and urinary albumin, were risk factors for DR in this study. Appropriate diagnosis and intervention should be taken in time to prevent and control DR development.

Icariin promotes mouse Leydig cell testosterone synthesis via the Esr1/Src/Akt/Creb/Sf-1 pathway.

Icariin (ICA), extracted from Epimedium, is a flavonoid used in traditional Chinese medicine. Di(2-ethylhexyl) phthalate (DEHP) is a phthalate used in commercial products as a plasticizer that can influence the human endocrine and reproduction system. We previously found that ICA reversed DEHP-induced damage through the prevention of reactive oxygen species accumulation and promotion of testosterone secretion. Here we investigated the mechanisms of ICA in promoting testosterone secretion from murine Leydig cells. We used ICA, DEHP, the Akt agonist SC-79, the Akt inhibitor MK2206, and the Creb inhibitor KG501 to determine the effect of these treatments on the expression levels of the steroidogenic enzymes, Cyp11a1 and Hsd3b, which play critical roles in androgen production, in Leydig cells. Bioinformatic analysis was used to search for ICA-targeted proteins and their associated pathways. We found that icariin interacted with estrogen receptor on the cell membrane, leading to increased phosphorylation levels of Akt and Creb proteins and enhanced transcription of genes encoding steroidogenic enzymes and testosterone synthesis. We further investigated ICA activity in vivo using male mice pretreated with 100 mg/kg ICA and then treated with 750 mg/kg DEHP. ICA pretreatment reversed the reduced protein expression levels of Cyp11a1 and Hsd3b induced by DEHP in Leydig cells in vivo. Furthermore, while the phosphorylation levels of Akt and Creb were decreased in testes of mice exposed to DEHP alone, these effects were reversed by ICA pretreatment. These findings indicate that ICA promotes testosterone synthesis via the Esr1/Src/Akt/Creb/Sf-1 signaling pathway.

Nuclear-localized eukaryotic translation initiation factor 1A is involved in mouse preimplantation embryo development.

Preimplantation embryo development is characterized by drastic nuclear reprogramming and dynamic stage-specific gene expression. Key regulators of this earliest developmental stage have not been revealed. In the present study, a "non-classical" nuclear-localization pattern of eIF1A was observed during early developmental stages of mouse preimplantation embryo before late-morula. In particular, eIF1A is most highly expressed in the nuclear of 2-cell embryo. Knockdown eIF1A by siRNA microinjection affected the development of mouse preimplantation embryo, resulted in decreased blastocyst formation rate. CDX2 protein expression level significantly down-regulated after eIF1A knockdown in morula stage. In addition, the mRNA expression level of Hsp70.1 was also decreased in 2-cell embryo. The results indicate an indispensable role of eIF1A in mouse preimplantation embryos.

Trps1 targets Ccnd1 to regulate mouse Leydig cell proliferation.

BACKGROUND: The tricho-rhino-phalangeal syndrome-1 gene (Trps1) is an atypical GATA family member. Although current studies of Trps1 mainly focus on tumors, whether Trps1 plays a role in the male reproductive system remains unknown. OBJECTIVES: The purpose of this study was to elucidate the function of Trps1 in Leydig cells, indicating its regulatory mechanism on the cell cycle. METHODS: Gene-silencing technology, RNA-seq, RT-qPCR, and western blotting were used to evaluate the function of Trps1 in mouse primary Leydig cells and MLTC-1 cells. In addition, ChIP-base sets and ChIP-qPCR were employed to further assess the regulatory mechanism of Trps1 in MLTC-1 cells. RESULTS: Knockdown of Trps1 in Leydig cells significantly suppressed phosphorylation of Src and Akt and expression of Ccnd1, which was accompanied by impairment of cell proliferative ability. Trps1 may affect the cell cycle through the Src/Akt/Ccnd1 signaling pathway. In addition, Trps1 may bind to the promoter of Srcin1 to regulate its transcription, thus influencing Src phosphorylation levels and the proliferation of Leydig cells. DISCUSSION AND CONCLUSION: Src increases in Leydig cells during pubertal development, suggesting its functional involvement in differentiated adult Leydig cells. Inhibition of the Src/Akt pathway would reduce Ccnd1 expression. In the present study, we found that Trps1 may regulate the phosphorylation level of Src and Akt through Srcin1, targeting Ccnd1 to influence mouse Leydig cell proliferation. These findings shed light on the regulation of Trps1 on cell proliferation and differentiation of mouse Leydig cells.

Upregulation of microRNA-181a-5p increases the sensitivity of HS578T breast cancer cells to cisplatin by inducing vitamin D receptor-mediated cell autophagy.

Breast cancer (BC) is the leading cause of death in females worldwide. Although cisplatin is a strong-effect and broad-spectrum chemotherapy drug, resistance to cisplatin remains a significant factor effecting clinical efficacy. The underlying mechanism of cancer cell resistance to cisplatin is not fully understood. MicroRNAs (miRs/miRNAs), as a regulator, are involved in regulating chemosensitivity to numerous chemotherapeutic drugs. The present study aimed to investigate the function of miR-181a-5p as a potential tumor suppressor in improving the efficiency of cisplatin in BC. The IC50 of cisplatin and miR-181a-5p expression were determined in five BC cell lines, and HS578T was selected as an appropriate cell line for subsequent experiments. The sensitivity of HS578T cells to cisplatin was assessed using cell proliferation, migration and apoptosis assays. Western blotting was performed to detect the expression of vitamin D receptor (VDR) and autophagy in HS578T cells. It was found that the increase in autophagy resulted in increased apoptosis and sensitivity to cisplatin in HS578T cells. miR-181a-5p transfection also inhibited the proliferation and migration ability of HS578T cells and induced apoptosis. Meanwhile, HS578T cells have increased sensitivity to cisplatin. VDR, as a target gene and autophagy regulator of miR-181a-5p, was negatively regulated by miR-181a-5p. Upon the decrease in VDR expression, the autophagy in HS578T cells was increased. These results indicate that the increase in autophagy enhanced the chemosensitivity of cisplatin by inducing apoptosis of HS578T cells and by inhibiting proliferation and migration. The present study showed that miR-181a-5p increased the chemical sensitivity of HS578T cells to cisplatin by inhibiting VDR to promote autophagy. The use of miR-181a-5p/autophagy/VDR-based treatment strategies may be a potential method to overcome cisplatin resistance in BC.

Improving seismic remote sensing of typhoon with a three-dimensional Earth model.

Typhoon-induced P-wave microseisms can be observed using seismological arrays and analyzed for the seismic monitoring of ocean storms. This paper presents a frequency-domain beamforming (FB) method that integrates a three-dimensional (3-D) Earth model to better capture the heterogeneities in the subsurface structure, and therefore yield more accurate ray-tracing and travel-time predictions. This method is applied to the Super Typhoon Lupit (2009) using seismological array observations from the Northeast China Extended Seismic Array (NECESSArray) and high-sensitivity seismograph network in Japan (Hi-net). The results show that the localized P-wave microseism source regions based on the 3-D model are in better agreement with the theoretical source regions and typhoon centers than those based on a conventional one-dimensional (1-D) model. The significance of using a 3-D model instead of a 1-D model in the FB method is further investigated by comparing the consistency of the localization results for the two different arrays, with the localized source regions being more mutually concordant when using the 3-D model. The results demonstrate that integrating the 3-D model into the FB method improves the accuracy of locating the typhoon-induced P-wave microseism source regions.

Chloroplast genome of silverleaf nightshade (Solanum elaeagnifolium Cav.), a Weed of National Significance in Australia.

Solanum elaeagnifolium Cav. is a widely distributed weed and recognized as a Weed of National Significance in Australia. This study sequenced the chloroplast (cp) genome of S. elaeagnifolium, which is 155,049 bp in length, including a large single-copy region at 85, 426 bp, a small single-copy region at 18,419 bp and two inverted repeats at 25,602 bp. A total of 130 genes were annotated. The phylogeny among the S. elaeagnifolium and 42 Solanum chloroplast genomes suggested S. elaeagnifolium is closely related to Solanum species from the section of Melongena.

Akt plays indispensable roles during the first cell lineage differentiation of mouse.

The first cell lineage differentiation occurs during the development of mouse 8-cell embryo to blastocyst. Akt is a potent kinase whose role during blastocyst formation has not been elucidated. In the present study, immunofluorescence results showed that the Akt protein was specifically localized to the outer cells of the morula. Akt-specific inhibitor MK2206 significantly inhibited mouse blastocyst formation and resulted in decreased expression of the trophectoderm marker Cdx2 and led to granular distribution of ERα in the cytoplasm. Furthermore, knockdown of ERα by siRNA microinjection can also lead to a decrease in the development rate of mouse blastocysts, accompanied by a decrease in the expression level of Yap protein. We conclude that Akt may be indispensable for the first cell lineage differentiation of mouse.

Icariin protects mouse Leydig cell testosterone synthesis from the adverse effects of di(2-ethylhexyl) phthalate.

Infertility caused by environmental pollution is becoming a global problem, but an effective prevention or treatment is lacking. Icariin (ICA) is a flavonoid used in traditional Chinese medicine. The present study investigated the possible roles of ICA in preventing testicular dysfunction caused by di(2-ethylhexyl) phthalate (DEHP), one of the most studied environmental endocrine disruptors. Cultured mouse Leydig cells were pretreated with ICA and exposed to DEHP to determine ICA effects upon cell proliferation, reactive oxygen species (ROS) levels, mitochondrial membrane potential (Δψm), testosterone levels and the expression of transcription factor SF-1 and steroidogenic enzymes (CYP11, 3ß-HSD and 17ß-HSD), which play critical roles in androgen production. Our results showed that ICA reversed the adverse effect of DEHP on Leydig cell proliferation, and decreased ROS levels and elevated Δψm levels. Also, ICA promoted testosterone production and up-regulated the expression of SF-1 and steroidogenic enzymes. We investigated ICA actions in vivo, using male mice administrated DEHP followed by ICA. Exposure to DEHP decreased epididymal sperm counts and disrupted seminiferous tubules, and both of these effects were reversed by ICA treatment. These results showed that the mechanisms of ICA in protecting mouse testes against DEHP-induced damage involves the prevention of ROS accumulation and promotion of testosterone secretion.

Species Identification of Conyza bonariensis Assisted by Chloroplast Genome Sequencing.

Flaxleaf fleabane (Conyza bonariensis [L.] Cronquist) is one of the most difficult weeds to control worldwide. There are more than 150 Conyza species in the world and eight species in Australia. Correct identification of these species can be problematic due to their morphological similarities especially at seedling stage. Developing a robust genetics - based species identification method to distinguish C. bonariensis from other closely related species is important for early control of weeds. We thus examined the chloroplast (cp) genome of C. bonariensis, aiming to identify novel DNA barcodes from the genome sequences, and use the entire cp genome as a super-barcode for molecular identification. The C. bonariensis chloroplast genome is 152,076 bp in size, encodes 133 genes including 88 protein-coding genes, 37 tRNA genes and 8 ribosomal RNA genes. A total of 151 intergenic regions and 19 simple sequence repeats were identified in the cp genome of C. bonariensis, which provides a useful genetic resource to develop robust markers for the genetic diversity studies of Conyza species. The sequence information was used to design a robust DNA barcode rps16 and trnQ-UUG which successfully separated three predominant Conyza species (C. bonariensis, C. canadensis, and C. sumatrensis). Phylogenetic analyses based on the cp genomes of C. bonariensis, C. canadensis and 18 other Asteraceae species revealed the potential of using entire cp genome as a plant super-barcode to distinguish closely-related weed species.

Targeting endosialin/CD248 through antibody-mediated internalization results in impaired pericyte maturation and dysfunctional tumor microvasculature.

Over-expression of endosialin/CD248 (herein referred to as CD248) has been associated with increased tumor microvasculature in various tissue origins which makes it an attractive anti-angiogenic target. In an effort to target CD248, we have generated a human CD248 knock-in mouse line and MORAb-004, the humanized version of the mouse anti-human CD248 antibody Fb5. Here, we report that MORAb-004 treatment significantly impacted syngeneic tumor growth and tumor metastasis in the human CD248 knock-in mice. In comparison with untreated tumors, MORAb-004 treated tumors displayed overall shortened and distorted blood vessels. Immunofluorescent staining of tumor sections revealed drastically more small and dysfunctional vessels in the treated tumors. The CD248 levels on cell surfaces of neovasculature pericytes were significantly reduced due to its internalization. This reduction of CD248 was also accompanied by reduced α-SMA expression, depolarization of pericytes and endothelium, and ultimately dysfunctional microvessels. These results suggest that MORAb-004 reduced CD248 on pericytes, impaired tumor microvasculature maturation and ultimately suppressed tumor development.

The antitumor activity of the human FOLR1-specific monoclonal antibody, farletuzumab, in an ovarian cancer mouse model is mediated by antibody-dependent cellular cytotoxicity.

Because of its high mortality rate, ovarian cancer is a leading cause of death among women and a highly unmet medical need. New therapeutic agents that are effective and well tolerated are needed and cancer antigen-specific monoclonal antibodies that have direct pharmacologic effects or can stimulate immunological responses represent a promising class of agents for the treatment of this disease. The human folate receptor α (FOLR1), which is overexpressed in ovarian cancer but largely absent in normal tissues, appears to play a role in the transformed phenotype in ovarian cancer, cisplatin sensitivity, and growth in depleted folate conditions and therefore has potential as a target for passive immunotherapy. The anti-FOLR1 monoclonal antibody MORAb-003 (farletuzumab) was previously shown to elicit antibody dependent cellular cytotoxicity (ADCC) and inhibit tumor growth of human tumor xenografts in nude mice. Because of its promising preclinical profile, farletuzumab has been evaluated in clinical trials as a potential therapeutic agent for ovarian cancer. In this report, we demonstrated that farletuzumab's antitumor effect against an experimental model of ovarian cancer is mediated by its ADCC activity.

A novel mutation in the myeloperoxidase gene in a Chinese female with complete myeloperoxidase deficiency: the role of nonsense-mediated mRNA decay.

Myeloperoxidase (MPO) is an important enzyme in innate immunity. Here, we describe the first identified Chinese individual with complete MPO deficiency. The proband was ascertained through routine automated complete blood analysis. Analysis of MPO function and immunogenicity revealed that MPO levels in neutrophils were significantly decreased. Mutational analysis revealed a novel premature termination codon p.(Trp602*) in exon 11 of the MPO gene, which was inherited in an autosomal recessive manner. We demonstrated that nonsense-mediated mRNA decay is involved in the molecular pathology of MPO deficiency in this case. The study of MPO deficiency can be helpful in understanding the function and biosynthesis mechanisms of MPO.

Fabrication and photocatalytic property of Pt-intercalated layered perovskite niobates H(1-x)LaNb(2-x)Mo(x)O(7) (x=0-0.15).

H(1-x)LaNb(2-x)Mo(x)O(7) was prepared by solid-state reaction followed by an ion-exchange reaction. Pt was incorporated in the interlayer of H(1-x)LaNb(2-x)Mo(x)O(7) by the stepwise intercalation reaction. The H(1-x)LaNb(2-x)Mo(x)O(7) showed hydrogen production activity and the activities were greatly enhanced by Pt co-incorporating. The x value in H(1-x)LaNb(2-x)Mo(x)O(7) had an important effect on the photocatalytic activity of the catalyst. When the x=0.05, the H(1-x)LaNb(2-x)Mo(x)O(7)/Pt showed a photocatalytic activity of 80 cm(3)h(-1)g(-1) hydrogen evolution rate in 10 vol.% methanol solution under irradiation from a 100 W mercury lamp at 333K.

Established B16 tumors are rejected following treatment with GM-CSF-secreting tumor cell immunotherapy in combination with anti-4-1BB mAb.

Immunization with irradiated tumor cells engineered to secrete granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulates potent, specific and long lasting anti-tumor immunity in clinical and preclinical settings. Efforts to further increase immunotherapy efficacy with immune-modulatory agents are under evaluation. Based on the immune-modulatory properties of 4-1BB (CD137), it has been postulated that agonistic 4-1BB antibodies may add additional anti-tumor efficacy to GM-CSF-secreting tumor cell immunotherapy. The combination of GM-CSF-secreting tumor cell immunotherapy and anti-4-1BB monoclonal antibody (mAb) treatment resulted in rejection of established tumors in the B16 melanoma model. These anti-tumor effects correlated with persistent tumor-specific CD8(+) T cell responses. In addition, early tumor infiltration of functional CD8(+) T cells and a greater expansion of antigen-specific memory T cells were found in mice treated with the combination therapy. In summary, an agonistic anti-4-1BB mAb combined with GM-CSF-secreting tumor cell immunotherapy may provide a novel and potent treatment strategy for patients with cancer.

Inhibition of lymphogenous metastasis using adeno-associated virus-mediated gene transfer of a soluble VEGFR-3 decoy receptor.

The presence of metastases in regional lymph nodes is a strong indicator of poor patient survival in many types of cancer. It has recently been shown that the lymphangiogenic growth factor, vascular endothelial growth factor-C (VEGF-C), and its receptor, VEGF receptor-3 (VEGFR3), may play a pivotal role in the promotion of metastasis to regional lymph nodes. In this study, human prostate and melanoma tumor models that preferentially metastasize to the lymph nodes following s.c. tumor cell implantation were established from lymph node metastases via in vivo selection. Melanoma tumor cell sublines established from lymph node metastasis express higher amounts of VEGF-C than the parental tumor cells. The inhibition of tumor-derived VEGF-C with a soluble VEGFR3 decoy receptor, sVEGFR3-Fc, expressed via a recombinant adeno-associated viral vector, potently blocks tumor-associated lymphangiogenesis and tumor metastasis to the lymph nodes, when the treatment was initiated before the tumor implantation. In addition, sVEGFR3-Fc serum levels required for efficient blockade of lymph node metastases are strictly dependent on the VEGF-C levels generated by the primary tumor. Recombinant adeno-associated virus-mediated gene transfer of sVEGFR3-Fc may represent a feasible therapeutic strategy for blockade of lymphogenous metastasis.

Anti-tumor efficacy of human angiostatin using liver-mediated adeno-associated virus gene therapy.

Angiostatin is a potent endogenous inhibitor of angiogenesis and tumor growth in vivo. The therapeutic potential of adeno-associated viral (AAV) gene delivery of angiostatin in modulating tumor growth in vivo was evaluated. Sustained levels of angiostatin were detected in the sera of mice for up to 6 months after they received a single injection of AAV-angiostatin. AAV-mediated stable expression of angiostatin inhibited tumor burden in the highly aggressive B16F10 melanoma and Lewis lung carcinoma (LLC) models of experimental metastasis. Moreover, AAV-angiostatin prolonged survival in B16F10 and LLC tumor-bearing mice compared to control groups. Anti-tumor efficacy was consistently observed when angiostatin serum levels of 15-50 ng/ml were detected following gene transfer, but the effect was minimal when the levels were lower or higher than this range. The combination of AAV-angiostatin gene therapy with chemotherapy was also shown to extend marginally the survival of mice bearing preestablished human tumors; however, the effect was evident only within a narrow dose of circulating angiostatin. These studies demonstrate the feasibility of using AAV anti-angiogenic gene therapy as a cancer treatment modality and suggest that the optimal anti-tumor efficacy of angiostatin following gene transfer may be limited to a narrow dose range.

[Study on a test of screening to predict stroke-using cerebral vascular hemodynamic indexes].

OBJECTIVE: To evaluate efficacy and optimal cut-off-point through cerebral vascular hemodynamic indexes (CVHI) examination to predict stroke. METHODS: A number of 20,333 people at 35 years old and over were checked by CVHI and accumulative score was calculated according to the value of detected indexes. Risk factors of stroke were investigated simultaneously. One hundred and sixty-eight patients with stroke occurred during 4-year following up. Typical syndromes and signs stroke were used as golden standard to evaluate screening efficacy of CVHI. RESULTS: Score of optimal cut-off-point of cerebral vascular hemodynamic indexes was under 75 in ROC curve analyses. Sensitivity, specificity, accuracy, positive and negative predictive values, positive and negative likelihood ratios as well as Youden's index for predicting stroke within 4 years after examination were found to be 87.50%, 67.70%, 67.86%, 2.21%, 99.85%, 2.71, 0.18 and 0.55 respectively. Sensitivity and positive predict values for predicting cerebral vascular thrombosis were superior to predicting cerebral hemorrhage. Positive predicting value in risk exposure population was higher than that of overall population. Coefficiency of variation of cerebral vascular hemodynamic examination was 4.03%. The agreement rate of examination between two physicians was 97.62% and Kappa value was 0.94. CONCLUSION: The score of optimal cut-off-point of cerebral vascular hemodynamic indexes examination was 75. Both Efficacy and reliability for predicting stroke seemed to be good, especially for predicting cerebral vascular thrombosis.