Research on the Application of Reading Recommendation System in High Medical College Library Based on the Local Data

This paper summarizes the feasibility of constructing the recommended reading system in the library of high medical college, andanalyzes the core technology-recommendation algorithm in the recommendation system. At the same time, it introduces the innovative design ofthe recommendation model of the recommendation system of high medical institutions. Based on the local data to promote the implementation ofthe model, the domestic library to provide recommended services to the future made a prospect.

Elevated degradation of di-n-butyl phthalate by activating peroxymonosulfate over GO-CoFe_(2)O_(4)composites:Synergistic effects and mechanisms

Rational design of heterogeneous catalysts with high activity and stability is crucial in peroxymonosulfate(PMS)-based oxidation treatment of wastewater.Herein,the graphite oxide-cobalt ferrite(GOCoFe_(2)O_(4))composite was constructed,and its morphological,component and structural characteristics were thoroughly examined,respectively.GO-CoFe_(2)O_(4)obviously boosted PMS catalytic performance on di-n-butyl phthalate removal(DBP,RpBp=90%,Roc=37%),which indicated by the first-order kinetic constant(kpBp=0.060 min^(-1))being roughly 4 times than pure CoFe_(2)O_(4)(kpBp=0.015 min-1).The fabrication of GO-CoFe_(2)O_(4)brought the favorable stability and repeatability up to six cycles.Moreover,the method of batch dosing catalyst was creatively proposed to improve the PMS utilization efficiency.The coupling of GO enhanced the dispersion of CoFe_(2)O_(4)particles to obtain sufficient active sites,additionally,the plentiful C=O groups and free-flowing electrons on GO promoted GO-CoFe_(2)O_(4)to coordinate a redox process during PMS activation.With the aid of theoretical calculations,GO-CoFe_(2)O_(4)was revealed to exhibit a strong affinity toward PMS adsorption,where PMS spontaneously dissociated into sulfate radical(SO_(4)^(·-)),hydroxyl radical(^(·)OH)and singlet oxygen(^(1)O_(2)),acting as the reactive oxygen species(ROSs).Electrons cycling between Co,Fe and O species ensured continuous ROSs generation and excellent catalytic performance.

Neuroprotective effects of Ginkgo biloba extract and GinkgoUde B against oxygen-glucose deprivation/reoxygenation and glucose injury in a new in vitro multicellular network model

Acute ischemic stroke （AIS）, as the third leading cause of death worldwide, is characterized by its high incidence, mortality rate, high incurred disability rate, and frequent reoccurrence. The neuroprotective effects of Ginkgo biloba extract （GBE） against several cerebral diseases have been reported in previous studies, but the underlying mechanisms of action are still unclear. Using a novel in vitro rat cortical capillary endothelial cell- astrocyte-neuron network model, we investigated the neuroprotective effects of GBE and one of its important constituents, Ginkgolide B （GB）, against oxygenglucose deprivation/reoxygenation and glucose （OGD/R） injury. In this model, rat cortical capillary endothelial cells, astrocytes, and neurons were cocultured so that they could be synchronously observed in the same system. Pretreatment with GBE or GB increased the neuron cell viability, ameliorated cell injury, and inhibited the cell apoptotic rate through Bax and Bcl-2 expression regulation after OGD/R injury. Furthermore, GBE or GB pretreatment enhanced the transendothelial electrical resistance of capillary endothelial monolayers, reduced the endothelial permeability coefficients for sodium fluorescein （Na-F）, and increased the expression levels of tight junction proteins, namely, ZO-1 and occludin, in endothelial cells. Results demonstrated the preventive effects of GBE on neuronal cell death and enhancement of the function of brain capillary endothelial monolayers after OGD/R injury in vitro; thus, GBE could be used as an effective neuroprotective agent for AIS/reperfusion, with GB as one of its significant constituents.

WIP1 Phosphatase Plays a Critical Neuroprotective Role in Brain Injury Induced by High-Altitude Hypoxic Inflammation

The hypobaric hypoxic environment in highaltitude areas often aggravates the severity of inflammation and induces brain injury as a consequence. However, the critical genes regulating this process remain largely unknown. The phosphatase wild-type p53-induced phosphatase 1（WIP1） plays important roles in various physiological and pathological processes, including the regulation of inflammation in normoxia, but its functions in hypoxic inflammation-induced brain injury remain unclear.Here, we established a mouse model of this type of injury and found that WIP1 deficiency augmented the release of inflammatory cytokines in the peripheral circulation and brain tissue, increased the numbers of activated microglia/macrophages in the brain, aggravated cerebral histological lesions, and exacerbated the impairment of motor and cognitive abilities. Collectively, these results provide the first in vivo evidence that WIP1 is a critical neuroprotector against hypoxic inflammation-induced brain injury.

Capsaicin restores sodium iodine symportermediated radioiodine uptake through bypassing canonical TSH–TSHR pathway in anaplastic thyroid carcinoma cells

Anaplastic thyroid cancer(ATC)is a rare but highly lethal disease.ATCs are resistant to standard therapies and are extremely difficult to manage.The stepwise cell dedifferentiation results in the impairment of the iodine-metabolizing machinery and the infeasibility of radioiodine treatment in ATC.Hence,reinducing iodine-metabolizing gene expression to restore radioiodine avidity is considered as a promising strategy to fight against ATC.In the present study,capsaicin(CAP),a natural potent transient receptor potential vanilloid type 1(TRPV1)agonist,was discovered to reinduce ATC cell differentiation and to increase the expression of thyroid transcription factors(TTFs including TTF-1,TTF-2,and PAX8)and iodine-metabolizing proteins,including thyroidstimulating hormone receptor(TSHR),thyroid peroxidase,and sodium iodine symporter(NIS),in two ATC cell lines,8505C and FRO.Strikingly,CAP treatment promoted NIS glycosylation and its membrane trafficking,resulting in a significant enhancement of radioiodine uptake of ATC cells in vitro.Mechanistically,CAP-activated TRPV1 channel and subsequently triggered Ca2þinflux,cyclic adenosine monophosphate(cAMP)generation,and cAMP-responsive element-binding protein(CREB)signal activation.Next,CREB recognized and bound to the promoter of SLC5A5 to facilitate its transcription.Moreover,the TRPV1 antagonist CPZ,the calcium chelator BAPTA,and the PKA inhibitor H-89 effectively alleviated the redifferentiation exerted by CAP,demonstrating that CAP might improve radioiodine avidity through the activation of the TRPV1–Ca2þ/cAMP/PKA/CREB signaling pathway.In addition,our study indicated that CAP might trigger a novel cascade to redifferentiate ATC cells and provide unprecedented opportunities for radioiodine therapy in ATC,bypassing canonical TSH–TSHR pathway.