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1.
Sensors (Basel) ; 20(24)2020 Dec 17.
Article in English | MEDLINE | ID: mdl-33348777

ABSTRACT

The study of visible light indoor position has received considerable attention. The visible light indoor position has problems such as deployment difficulty and high cost. In our system, we propose a new fingerprint construction algorithm to simplify visible light indoor position. This method can realize the rapid construction of a visible fingerprint database and prove that the fingerprint database can be used repeatedly in different environments. We proved the theoretical feasibility of this method through theoretical derivation. We carried out extensive experiments in two classic real indoor environments. Experimental results show that reverse fingerprinting can be achieved. In 95% of cases, the positioning accuracy can be guaranteed to be less than 10 cm.

2.
J Cell Physiol ; 234(7): 11240-11246, 2019 07.
Article in English | MEDLINE | ID: mdl-30537069

ABSTRACT

OBJECTIVE: To study the mechanism of collapsin response mediator protein-2 (CRMP-2) phosphorylation changes and cyclin-dependent kinase 5 (CDK5) expression after optic nerve injury. METHODS: Optic nerve injury rat models were constructed, the messenger RNA (mRNA) level of CRMP-2 in optic nerve tissues was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR) after building models 0, 3, 7, and 14 days. The protein expression of CRMP-2, phospho-CRMP-2 (p-CRMP-2), and CDK5 were also determined by western blot analysis. Lentivirus overexpressing CRMP-2 and CRMP-2 small interfering RNA (siRNA) plasmid were designed and transfected to retina ganglion cells (RGCs), and then the neurites outgrowth of RGCs were cultured with CDK5 inhibitor or CDK5 activator was determined by tubulin staining. Inhibition on CDK5 promotes injured optic nerve by using carrying CDK5 siRNA inject into vitreous chamber. RESULTS: There was no significant change in CRMP-2 expression in optic nerve injury rat, while p-CRMP-2 expression was evidently increased compared with sham operation group. The expression level of CDK5 in optic nerve tissue was upregulated after optic nerve injury in rat, and the upward trend of p-CRMP-2 and CDK5 was consistent with the time after the injury was prolonged. Inhibition on CDK5 evidently decreased the expression of p-CRMP-2. CDK5 siRNA had an obvious repair effect on the injured optic nerve. CONCLUSION: The increase of CDK5 activity can lead to CRMP-2 hyperphosphorylation, which results in the difficult repair of damaged optic nerve. Therefore, inhibition on CDK5 could promote the repair of damaged optic nerve.


Subject(s)
Cyclin-Dependent Kinase 5/metabolism , Intercellular Signaling Peptides and Proteins/metabolism , Nerve Tissue Proteins/metabolism , Optic Nerve Injuries/pathology , Optic Nerve/pathology , Animals , Cell Line , Disease Models, Animal , Intercellular Signaling Peptides and Proteins/genetics , Nerve Tissue Proteins/genetics , Optic Nerve Injuries/therapy , Phosphorylation , RNA Interference , RNA, Messenger/genetics , RNA, Small Interfering/genetics , Rats , Rats, Sprague-Dawley , Retina/cytology
3.
J Cell Biochem ; 120(10): 17912-17925, 2019 10.
Article in English | MEDLINE | ID: mdl-31135072

ABSTRACT

OBJECTIVE: To investigate the regulation of special protein 1 (SP1) and hypoxia-inducible factor-1α (HIF1α) on human microvascular endothelial cells (HMEC-1) under hypoxic conditions. METHODS: The expression of SP1 and HIF1α under normoxia and hypoxic conditions were assessed by Western blot. SP1 and HIF1α were knocked down by small interfering RNA (siRNA) under hypoxic conditions. The proliferation, migration, and invasion of HMEC-1 were measured by cell counting kit 8, 5-ethynyl-2'-deoxyuridine and Transwell coculture system. Western blot analysis and Immunofluorescence were carried out to study the mechanisms of simultaneously inhibiting the adenosine triphosphatase (CD39), 5'-nucleotidase (CD73), adenosine, and vascular endothelial growth factor (VEGF). We compared the inhibitory effects between groups concurrently interfering SP1, HIF-1α, and ranibizumab under hypoxic conditions. RESULTS: Under hypoxic conditions, the protein expression of SP1 and HIF1α was increased in HMEC-1, contrarily, SP1 siRNA and HIF1α siRNA downregulated the expression. Simultaneous inhibition of SP1 and HIF1α demonstrated a much greater restraint of proliferation, migration, and invasion characteristics on HMEC-1 than respectively knocking down SP1 or HIF1α and anti-VEGF drugs (0.5 mg/mL ranibizumab) (siRNA and the VEGF inhibitor were applied separately in different groups). Meanwhile, simultaneous inhibition of SP1 and HIF1α effectively reduced the expression of CD39, CD73, adenosine, and VEGF on HMEC-1 under hypoxic conditions. CONCLUSIONS: Our study demonstrated that both SP1 and HIF1α played important roles in HMEC-1 under hypoxia condition. Simultaneous inhibition of SP1 and HIF1α effectively decreased the activity of HMEC-1 under hypoxic conditions through the CD39-CD73-adenosine and VEGF angiogenesis pathways. Our study may provide a new approach to the treatment of retinal neovascular diseases.


Subject(s)
Cell Movement , Endothelial Cells/pathology , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Microvessels/pathology , Sp1 Transcription Factor/metabolism , Adenosine/pharmacology , Antigens, CD/metabolism , Cell Hypoxia/drug effects , Cell Movement/drug effects , Cell Proliferation/drug effects , Endothelial Cells/drug effects , Endothelial Cells/metabolism , Gene Silencing/drug effects , Humans , RNA, Small Interfering/metabolism , Ranibizumab/pharmacology , Up-Regulation/drug effects
4.
Sci Total Environ ; 580: 550-555, 2017 Feb 15.
Article in English | MEDLINE | ID: mdl-27988189

ABSTRACT

BACKGROUND: Previous studies have shown increased precipitation to be associated with higher frequency of traffic collisions. However, data regarding how extreme weather events, projected to grow in frequency, intensity, and duration in response to a changing climate, might affect the risk of motor vehicle collisions is particularly limited. We investigated the association between frequency of extreme heat and precipitation events and risk of motor vehicle collision in Maryland between 2000 and 2012. METHODS: Motor vehicle collision data was obtained from the Maryland Automated Accident Reporting System. Each observation in the data set corresponded to a unique collision event. This data was linked to extreme heat and precipitation events that were calculated using location and calendar day specific thresholds. A time-stratified case-crossover analysis was utilized to assess the association between exposure to extreme heat and precipitation events and risk of motor vehicle collision. Additional stratified analyses examined risk by road condition, season, and collisions involving only one vehicle. RESULTS: Overall, there were over 1.28 million motor vehicle collisions recorded in Maryland between 2000 and 2012, of which 461,009 involved injuries or death. There was a 23% increase in risk of collision for every 1-day increase in extreme precipitation event (Odds Ratios (OR) 1.23, 95% Confidence Interval (CI): 1.22, 1.27). This risk was considerably higher for collisions on roads with a defect or obstruction (OR: 1.46, 95% CI: 1.40, 1.52) and those involving a single vehicle (OR: 1.41, 95% CI: 1.39, 1.43). Change in risk associated with extreme heat events was marginal at best. CONCLUSION: Extreme precipitation events are associated with an increased risk of motor vehicle collisions in Maryland.


Subject(s)
Accidents, Traffic , Weather , Humans , Maryland , Motor Vehicles , Risk
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