The cGAS-STING-interferon regulatory factor 7 pathway regulates neuroinflammation in Parkinson's disease

Interferon regulatory factor 7 plays a crucial role in the innate immune response.However,whether interferon regulatory factor 7-mediated signaling contributes to Parkinson's disease remains unknown.Here we report that interferon regulatory factor 7 is markedly up-regulated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease and co-localizes with microglial cells.Both the selective cyclic guanosine monophosphate adenosine monophosphate synthase inhibitor RU.521 and the stimulator of interferon genes inhibitor H151 effectively suppressed interferon regulatory factor 7 activation in BV2 microglia exposed to 1-methyl-4-phenylpyridinium and inhibited transformation of mouse BV2 microglia into the neurotoxic M1 phenotype.In addition,si RNA-mediated knockdown of interferon regulatory factor 7 expression in BV2 microglia reduced the expression of inducible nitric oxide synthase,tumor necrosis factorα,CD16,CD32,and CD86 and increased the expression of the anti-inflammatory markers ARG1 and YM1.Taken together,our findings indicate that the cyclic guanosine monophosphate adenosine monophosphate synthase-stimulator of interferon genes-interferon regulatory factor 7 pathway plays a crucial role in the pathogenesis of Parkinson's disease.

Evaluation and Analysis of Hospital Disaster Preparedness in Jeddah

Introduction: Disaster damage to health systems is a human and health tragedy, results in huge economic losses, deals devastating blows to development goals, and shakes social confidence. Hospital disaster preparedness presents complex clinical operation. It is difficult philosophical challenge. It is difficult to determine how much time, money, and effort should be spent in preparing for an event that may not occur. Health facilities whether hospitals or rural health clinics, should be a source of strength during emergencies and disasters. They should be ready to save lives and to continue providing essential emergencies and disasters. Jeddah has relatively a level of disaster risk which is attributable to its geographical location, climate variability, topography, etc. This study investigates the hospital disaster preparedness (HDP) in Jeddah. Methods: Questionnaire was designed according to five Likert scales. It was divided into eight fields of 33 indicators: structure, architectural and furnishings, lifeline facilities’ safety, hospital location, utilities maintenance, surge capacity, emergency and disaster plan, and control of communication and coordination. Sample of six hospitals participated in the study and rated to the extent of disaster preparedness for each hospital disaster preparedness indicators. Two hazard tools were used to find out the hazards for each hospital. An assessment tool was designed to monitor progress and effectiveness of the hospitals’ improvement. Weakness was found in HDP level in the surveyed hospitals. Disaster mitigation needs more action including: risk assessment, structural and non-structural prevention, and preparedness for contingency planning and warning and evacuation. Conclusion: The finding shows that hospitals included in this study have tools and indicators in hospital preparedness but with lack of training and management during disaster. So the research shed light on hospital disaster preparedness. Considering the importance of preparedness in disaster, it is necessary for hospitals to understand that most of hospital disaster preparedness is built in the hospital system.

Significance of dormant forms of Helicobacter pylori in ulcerogenesis

Nearly half of the global population are carriers of Helicobacter pylori(H. pylori),a Gram-negative bacterium that persists in the healthy human stomach. H. pylori can be a pathogen and causes development of peptic ulcer disease in a certain state of the macroorganism. It is well established that H. pylori infection is the main cause of chronic gastritis and peptic ulcer disease(PUD). Decontamination of the gastric mucosa with various antibiotics leads to H. pylori elimination and longer remission in this disease. However,the reasons for repeated detection of H. pylori in recurrent PUD after its successful eradication remain unclear. The reason for the redetection of H. pylori in recurrent PUD can be either reinfection or ineffective anti-Helicobacter therapy. The administration of antibacterial drugs can lead not only to the emergence of resistant strains of microorganisms,but also contribute to the conversion of H. pylori into the resting(dormant) state. The dormant forms of H. pylori have been shown to play a potential role in the development of relapses of PUD. The paper discusses morphological H. pylori forms,such as S-shaped,C-shaped,U-shaped,and coccoid ones. The authors proposes the classification of H. pylori according to its morphological forms and viability.

The miR-9-5p/CXCL11 pathway is a key target of hydrogen sulfide-mediated inhibition of neuroinflammation in hypoxic ischemic brain injury

We previously showed that hydrogen sulfide(H2S)has a neuroprotective effect in the context of hypoxic ischemic brain injury in neonatal mice.However,the precise mechanism underlying the role of H2S in this situation remains unclear.In this study,we used a neonatal mouse model of hypoxic ischemic brain injury and a lipopolysaccharide-stimulated BV2 cell model and found that treatment with L-cysteine,a H2S precursor,attenuated the cerebral infarction and cerebral atrophy induced by hypoxia and ischemia and increased the expression of miR-9-5p and cystathionineβsynthase(a major H2S synthetase in the brain)in the prefrontal cortex.We also found that an miR-9-5p inhibitor blocked the expression of cystathionineβsynthase in the prefrontal cortex in mice with brain injury caused by hypoxia and ischemia.Furthermore,miR-9-5p overexpression increased cystathionine-β-synthase and H2S expression in the injured prefrontal cortex of mice with hypoxic ischemic brain injury.L-cysteine decreased the expression of CXCL11,an miR-9-5p target gene,in the prefrontal cortex of the mouse model and in lipopolysaccharide-stimulated BV-2 cells and increased the levels of proinflammatory cytokines BNIP3,FSTL1,SOCS2 and SOCS5,while treatment with an miR-9-5p inhibitor reversed these changes.These findings suggest that H2S can reduce neuroinflammation in a neonatal mouse model of hypoxic ischemic brain injury through regulating the miR-9-5p/CXCL11 axis and restoringβ-synthase expression,thereby playing a role in reducing neuroinflammation in hypoxic ischemic brain injury.

Spontaneous and Bleomycin-Induced <i>&gamma;</i>H2AX Signals in CHO9 Metaphase Chromosomes

In eukaryotes, a cascade of events named DNA damage response (DDR) has evolved to handle DNA lesions. DDR engages the recruitment of signaling, checkpoint control, repair and chromatin remodeling protein complexes, allowing cell cycle delay, DNA repair or induction of apoptosis. An early DDR event involves the phosphorylation of the histone variant γH2AX on serine 139 (H2AX139 phosphorylation) originating the so-called γH2AX. DDR-related H2AX139 phosphorylation have been extensively studied in interphase nuclei. More recently, γH2AX signals on mitotic chromosomes of asynchronously growing cell cultures were observed. We performed a quantitative analysis of γH2AX signals on γH2AX immunolabeled cytocentrifuged metaphase spreads, analyzing the γH2AX signal distributions of CHO9 chromosomes harboring homologous regions both in control and bleomycin (BLM)-treated cultures. We detected γH2AX signals in CHO9 chromosomes of controls which significantly increase after BLM-exposure. γH2AX signals were uniformly distributed in chromosomes of controls. However, the γH2AX signal distribution in BLM exposed cells was significantly different between chromosomes and among chromosome regions, with few signals near the centromeres and a tendency to increase towards the telomeres. Interestingly, both basal and BLM-induced γH2AX signal distribution were statistically equal between CHO9 homologous chromosome regions. Our results suggest that BLM exerts an effect on H2AX139 phosphorylation, prevailing towards acetylated and gene-rich distal chromosome segments. The comparable H2AX139 phosphorylation of homologous regions puts forward its dependence on chromatin structure or function and its independence of the position in the karyotype.

3,4-二氢-2(1H)喹啉酮衍生物的合成研究

对3,4-二氢-2(1H)喹啉酮衍生物1,2,3(R= NO2,NH2,OH;R= H,NO2,NH2)的合成进行了研究。以苯胺和3-氯丙酰氯为原料,制得N-苯基-3-氯丙酰胺,然后经环合得到3,4-二氢-2(1H)喹啉酮,再经由硝化、还原、重氮化水解合成了一系列3,4-二氢-2(1H)喹啉酮衍生物:6-硝基-3,4-二氢-2(1H)喹啉酮(1a),6,8-二硝基-3,4-二氢-2(1H)喹啉酮(1b),6-氨基-3,4-二氢-2(1H)喹啉酮(2a),6,8-二氨基-3,4-二氢-2(1H)喹啉酮(2b),6-氨基-8-硝基-3,4-二氢-2(1H)喹啉酮(2c),6-羟基-3,4-二氢-2(1H)喹啉酮(3a)和6-羟基-8-硝基-3,4-二氢-2(1H)喹啉酮(3b),其中化合物(2c)及(3b)为新化合物。单步产率均在86%以上,路线简单,操作简便,反应条件温和。采用MS,1HNMR对产品进行了定性及结构表征。

抗纤维化与促“H”型血管核壳结构生物支架修复临界骨缺损

背景:在骨组织愈合过程中,促进新生骨的血管化是加速骨组织修复的常用策略,然而骨缺损修复过程中过快的纤维化进程常常被忽略。目的:设计并制备一种具有调节新生骨痂内纤维化及血管化进程的核壳结构仿生支架,表征其物理学特征,验证其体内外抗纤维化与促成骨性能。方法:制备具有调节新生骨痂内纤维化及血管化进程的核壳结构仿生支架,外层壳结构由聚己内酯静电纺丝纳米纤维负载成纤维细胞活化蛋白抑制剂组成,内层核结构由甲基丙烯酸酐明胶水凝胶负载去铁胺组成,表征静电纺丝和水凝胶的物理学特征,利用活死染色与CCK-8实验验证材料的生物相容性。通过成纤维细胞体外实验分析支架壳结构的抗纤维化作用,通过MC3T3-E1细胞体外实验分析支架壳结构中成纤维细胞活化蛋白抑制剂的促成骨作用,通过人脐静脉内皮细胞分析支架核结构中去铁胺的促血管形成作用。通过大鼠临界骨缺损实验评估核壳结构仿生支架的骨修复作用。结果与结论:①核壳结构仿生支架具有良好的生物相容性,静电纺丝技术制备的聚己内酯电纺纤维具有疏水性,在物理层面上有效阻隔外源性纤维组织长入,电纺纤维膜在2周内可有效释放抗纤维化药物成纤维细胞活化蛋白抑制剂,释放的抗纤维化药物可以抑制骨缺损周围成纤维细胞的生长、黏附,有效降低成纤维相关蛋白的表达,同时可促进MC3T3-E1细胞成骨蛋白的表达,加快其矿化速度;支架核结构中的去铁胺可促进人脐静脉内皮细胞的迁移、成管能力,并促进其强烈表达“H”血管特征性蛋白。②在SD大鼠的股骨制造临界骨缺损模型中,相较于聚己内酯膜,核壳结构仿生支架实现了骨缺损的有效修复。③结果表明,核壳结构仿生支架在预防骨痂过度纤维化的同时促进新生骨痂内“H”血管形成,能有效避免骨不连的发生,加速临界骨缺损修复进程。

温肾通络止痛方对小鼠H型骨微血管内皮细胞/骨髓间充质干细胞共培养体系的影响

背景:骨骼依赖血管与骨细胞之间的密切连接来维持完整性,骨骼处在生理低氧环境中,因此在低氧环境下研究血管生成与骨生成具有重要意义。目的:探究在低氧环境下温肾通络止痛方对H型骨微血管内皮细胞/骨髓间充质干细胞共培养体系的影响及相关机制。方法:运用酶消化法及流式分选技术,分选小鼠H型血管特异型骨微血管内皮细胞;应用骨髓贴壁法分离获取小鼠骨髓间充质干细胞;采用Transwell小室以及缺氧培养工作站建立两种细胞低氧共培养体系,使用50,100μg/m L质量浓度温肾通络止痛方冻干粉进行干预;通过划痕迁移实验与管形成实验评估共培养体系内H型骨微血管内皮细胞的成血管功能;通过碱性磷酸酶染色与茜素红染色评估共培养体系内骨髓间充质干细胞的成骨分化能力;使用Western Blotting与q-PCR检测共培养体系内H型骨微血管内皮细胞中PDGF/PI3K/AKT信号轴相关分子的蛋白表达及mRNA表达。结果与结论:(1)与常氧组相比,低氧组H型骨微血管内皮细胞划痕迁移率及新生血管长度均显著升高(P<0.05),骨髓间充质干细胞成骨分化能力增强(P<0.05);PDGF/PI3K/AKT信号轴相关分子的蛋白、mRNA表达升高(P<0.05);(2)与低氧组相比,经不同质量浓度温肾通络止痛方干预后H型骨微血管内皮细胞划痕迁移率及新生血管长度进一步提高(P<0.05),骨髓间充质干细胞成骨分化能力更强(P<0.05),PDGF/PI3K/AKT信号轴相关分子的蛋白、mRNA表达也进一步升高(P<0.05)。结果表明:低氧条件下H型血管生成及骨生成可能与PDGF/PI3K/AKT信号轴有关,而温肾通络止痛方可能通过激活PDGF/PI3K/AKT信号轴促进“H型血管生成-骨生成”作用从而防治骨质疏松症。

The MADS-box gene RhAGL6 plays a master role in regulating the receptacle malformation in rose at low temperature

Low temperature usually results in the developmental deformity of flower organs,immensely affecting the quality of rose flowers.However,it's largely unknown about the regulatory mechanisms activated by low temperature.Here,we used a low temperature-sensitive Rosa hybrida cv.‘Peach Avalanche’to screen a MADS-box gene RhAGL6 via conjoint analysis between RNA sequencing(RNA-seq)and whole-genome bisulfite sequencing(WGBS).Furthermore,we found that low temperature induced the hypermethylation and elevated histone 3 lys-27 trimethylation(H3K27me3)level on the RhAGL6 promoter,leading to decreased RhAGL6 expression.In addition,RhAGL6 silencing resulted in the formation of abnormal receptacles.We also found that the levels of gibberellins(GA3)and abscisic acid(ABA)in the receptacle under low temperature were lower and higher,respectively,than under normal temperature.Promoter activity analysis revealed that GA3 significantly activated RhAGL6 promoter activity,whereas ABA inhibited it.Thus,we propose that RhAGL6 regulates rose receptacle development by integrating epigenetic regulation and phytohormones signaling at low temperature.

Evaluation of Technical Education by Using a Modern Structured MOODLE Laboratory Course, in Relation to Recent Data

E-learning platforms support education systems worldwide, transferring theoretical knowledge as well as soft skills. In the present study high-school pupils’, and adult students’ opinions were evaluated through a modern structured MOODLE interactive course, designed for the needs of the laboratory course “Automotive Systems”. The study concerns Greek secondary vocational education pupils aged 18 and vocational training adult students aged 20 to 50 years. The multistage, equal size simple random cluster sample was used as a sampling method. Pupils and adult students of each cluster completed structured 10-question questionnaires both before and after attending the course. A total of 120 questionnaires were collected. In general, our findings disclosed that the majority of pupils and adult students had significantly improved their knowledge and skills from using MOODLE. They reported strengthening conventional teaching, using the new MOODLE technology. The satisfaction indices improved quite, with the differences in their mean values being statistically significant.

Loss of LBP triggers lipid metabolic disorder through H3K27 acetylation-mediated C/EBPβ-SCD activation in non-alcoholic fatty liver disease

Non-alcoholic fatty liver disease(NAFLD)is associated with mutations in lipopolysaccharide-binding protein(LBP),but the underlying epigenetic mechanisms remain understudied.Herein,LBP^(-/-)rats with NAFLD were established and used to conduct integrative targetingactive enhancer histone H3 lysine 27 acetylation(H3K27ac)chromatin immunoprecipitation coupled with high-throughput and transcriptomic sequencing analysis to explore the potential epigenetic pathomechanisms of active enhancers of NAFLD exacerbation upon LBP deficiency.Notably,LBP^(-/-)reduced the inflammatory response but markedly aggravated high-fat diet(HFD)-induced NAFLD in rats,with pronounced alterations in the histone acetylome and regulatory transcriptome.In total,1128 differential enhancer-target genes significantly enriched in cholesterol and fatty acid metabolism were identified between wild-type(WT)and LBP^(-/-)NAFLD rats.Based on integrative analysis,CCAAT/enhancer-binding proteinβ(C/EBPβ)was identified as a pivotal transcription factor(TF)and contributor to dysregulated histone acetylome H3K27ac,and the lipid metabolism gene SCD was identified as a downstream effector exacerbating NAFLD.This study not only broadens our understanding of the essential role of LBP in the pathogenesis of NAFLD from an epigenetics perspective but also identifies key TF C/EBPβand functional gene SCD as potential regulators and therapeutic targets.

4-(3-吲哚基)-3-丁烯-2-酮苯甲酰腙Schiff碱过渡金属配合物的合成、表征及生物活性研究

A Schiff base ligand 4-[indol-3-yl]-but-3-en-2-one benzoyl hydrazone (HL), and its four transition metal complexes (ML2,M=Cu(, Ni(, Zn( and Co() have been prepared and characterized by means of elemental analysis, EI-MS, molar conductivity, IR, UV-Vis and 1H NMR. The results showed that HL as a bidentate ligand coordinated with transition metal ions to form four-coordination complexes. The antibacterial activity was studied by using the filter scraps diffusion method, and the results indicated that the ligand and the complexes had a low bacteriostatic activity against S. Aureu, P. Aeruginosa and E. Coli. The low in vitro antitumor activity of the title complexes was also observed by using MTT method against KB, A2780, Bel7402 and HELF.

免疫性血小板输注无效患者HLA/HPA抗体特性分析及其对血小板输注效果的影响

目的 探讨免疫性血小板输注无效(PTR)患者HLA/HPA抗体特异性分布特征及其对血小板输注效果的影响。方法 本研究以86例免疫性PTR患者为研究对象,收集其性别、年龄、身高、体重、配血次数、疾病类型、输注前后血小板计数等临床资料,通过微珠法进行HLA特异性抗体的检测,并分析抗体特性对血小板输注效果的影响。结果 86例PTR患者中,单独HLA抗体、单独HPA抗体、HLA+HPA抗体阳性的患者分别为72例(83.72%)、8例(9.30%)、6例(6.98%)。HLA抗体在各位点中检出频率最高的抗体对应等位基因分别为A*25:01、B*15:12、C*02:02(和C*17:01),检出率分别为81.48%、87.04%、48.15%;而对应抗原表位出现频率最高的前三位为163LG、97V、71ATD,检出率分别为87.04%、77.78%、74.07%。仅存在HLA抗体的患者,输注交叉配型相合血小板的24 h血小板计数纠正增加指数(CCI)及输注有效情况均明显优于随机血小板(P<0.01)。在血小板交叉配型阴性结果的患者中,HLA抗体强度与交叉配型相合血小板的24 h CCI值及输注有效情况呈负相关关系,强度越高,输注效果越差(P<0.01)。HLA抗体强度为中、低等水平的患者,输注交叉配型相合血小板的24 h CCI值及输注有效情况均优于输注随机血小板(P<0.05)。结论 本研究所得到的PTR患者HLA/HPA抗体特性及其对血小板输注效果影响的结果,可为血小板库建立时供者的选择提供指导,同时对临床PTR患者的治疗方式选择有一定的参考价值。

Durable hierarchical phosphorus‐doped biphase MoS_(2)electrocatalysts with enhanced H^(*)adsorption

Phase engineering is an efficient strategy for enhancing the kinetics of electrocatalytic reactions.Herein,phase engineering was employed to prepare high‐performance phosphorous‐doped biphase(1T/2H)MoS_(2)(P‐BMS)nanoflakes for hydrogen evolution reaction(HER).The doping of MoS_(2)with P atoms modifies its electronic structure and optimizes its electrocatalytic reaction kinetics,which significantly enhances its electrical conductivity and structural stability,which are verified by various characterization tools,including X‐ray photoelectron spectroscopy,high‐resolution transmission electron microscopy,X‐ray absorption near‐edge spectroscopy,and extended X‐ray absorption fine structure.Moreover,the hierarchically formed flakes of P‐BMS provide numerous catalytic surface‐active sites,which remarkably enhance its HER activity.The optimized P‐BMS electrocatalysts exhibit low overpotentials(60 and 72 mV at 10 mA cm^(−2))in H_(2)SO_(4)(0.5 M)and KOH(1.0 M),respectively.The mechanism of improving the HER activity of the material was systematically studied using density functional theory calculations and various electrochemical characterization techniques.This study has shown that phase engineering is a promising strategy for enhancing the H*adsorption of metal sulfides.

Chlorogenic acid ameliorates heart failure by attenuating cardiomyocyte ferroptosis

Objective:To elucidate the effects of chlorogenic acid(CGA),a bioactive polyphenol compound prevalent in traditional Chinese medicine and various foods,including Lonicera japonica Thunb.(Jin Yin Hua),Eucommia ulmoides Oliv.(Du Zhong Ye),tea,and coffee,on cardiomyocyte ferroptosis and heart failure.Methods: We assessed the effect of CGA on cardiac function using a mouse model of heart failure induced by transverse aortic constriction(TAC).These indicators included the left ventricular ejection fraction(LVEF),fractional shortening(LVFS),end-systolic volume(LVESV),end-diastolic volume(LVEDV),end-systolic diameter(LVESD),and end-diastolic diameter(LVEDD).An isoprenaline hydrochloride(ISO)-induced H9c2 cardiomyocyte cell model was also established,and the cells were treated with various concentrations of CGA.To assess the effect of CGA on ferroptosis in cardiomyocytes,we measured cell viability and evaluated the levels of intracellular reactive oxygen species(ROS),ferrous ions(Fe^(2+)),and lipid peroxidation using fluorescent staining.To clarify the ferroptosis signaling pathway regulated by CGA,western blotting was used to examine the expression of ferroptosis biomarkers,specifically solute carrier family 7 member 11(SLC7A11)and glutathione peroxidase 4(GPX4),in H9c2 cardiomyocytes and mouse myocardial tissues.Results: CGA significantly enhanced cardiac performance indices such as LVEF,LVFS,LVESV,LVEDV,LVESD,and LVEDD.H9c2 cardiomyocytes exposed to ISO showed decreased cell viability and increased ROS levels,Fe^(2+)content,and lipid peroxidation levels.However,CGA treatment significantly ameliorated these changes.Additionally,in both H9c2 cardiomyocytes and myocardial tissue obtained from mice with TAC,CGA increased the expression of ferroptosis-related proteins,including SLC7A11 and GPX4.Conclusion: CGA has the potential to enhance cardiac function and diminish lipid peroxidation and ROS levels in cardiomyocytes via the SLC7A11/GPX4 signaling pathway.This process alleviates ferroptosis in cardiomyocytes.These results provide new insights into the clinical use of CGA and the management of heart failure.

Microstructure and martensitic transformation in quaternary NiTiHfV alloy

The effect of age hardening on the microstructure,martensitic transformation behavior,and shape memory properties of the(Ni_(50)Ti_(30)Hf_(20))_(95)V_(5)alloy was investigated by scanning electron microscopy,transmission electron microscopy,X-ray diffraction,differential scanning calorimetry,microhardness,and bending tests.The results demonstrate a significant influence of V addition on the microstructure of the alloy.V addition leads to the formation of a(Ni,V)_(2)(Ti,Hf)-type Laves phase,which coexists with B19'martensite at room temperature.Aging at 550℃results in precipitation hardening due to the formation of nano-scale orthorhombic H-phase,with the peak hardness observed after 3 h of aging.The alloy at peak hardness state exhibits higher transformation strain and lower unrecovered strain compared to the solution-treated sample.The aged sample achieves a maximum transformation strain of 1.56%under 500 MPa.

第Ⅴ类两态叠加多模叠加态光场的等阶N次方H压缩特性研究

本文构造了由多模真空态 |{ 0 j}〉q和多模虚相干态的相反态 |{ - i Zj}〉q这两者的线性叠加所组成的第 类两态叠加多模叠加态光场 |ψ( 2 )5〉q,利用多模压缩态理论详细研究了态|ψ( 2 )5〉q的广义非线性等阶 N次方 H压缩特性 .结果发现 :1 )态 |ψ( 2 )5〉q是一种典型的多模非经典光场 ;无论腔模总数 q与压缩阶数 N这两者之积 q· N取奇还是取偶 ,只要各模的初始相位之和 qj =1φj、态间的初始相位之差 (θ( I)nq- θ( o)0 q )等满足一定的量子化条件 ,态 |ψ( 2 )5〉q 总可分别呈现出周期性变化的、任意的奇数模 -奇数阶、奇数模 -偶数阶、偶数模 -偶数阶和偶数模 -奇数阶这四种不同形式的等阶 N次方 H压缩效应 .2 )上述四种不同形式的等阶 N次方 H压缩效应 ,其态间压缩条件完全相同 ,但模间压缩条件完全不同 ,结果使其压缩幅度、压缩结果和压缩特性等各不相同 .3 )无论 q· N取奇还是取偶 ,态 |ψ( 2 )5〉q的第一和第二这两个正交分量的等阶 N次方

HB-Continuous Mappings in L-Topological Space

In this paper, we introduce and study the notion of HB-closed sets in L-topological space. Then, HB-convergence theory for L-molecular nets and L-ideals is established in terms of HB-closedness. Finally, we give a new definition of fuzzy H-continuous [1] which is called HB-continuity on the basis of the notion of H-bounded L-subsets in L-topological space. Then we give characterizations and properties by making use of HB-converges theory of L-molecular nets and L-ideals.

An Explanation of the Temperature-Dependent Upper Critical Field Data of H3S on the Basis of the Thermodynamics of a Superconductor in a Magnetic Field

Excellent fits to a couple of the data-sets on the temperature (T)-dependent upper critical field (Hc2) of H3S (critical temperature, Tc ≈ 200 K at pressure ≈ 150 GPa) reported by Mozaffari, et al. (2019) were obtained by Talantsev (2019) in an approach based on an ingenious mix of the Ginzberg-Landau (GL), the Werthamer, Helfand and Hohenberg (WHH), and the Gor’kov, etc., theories which have individually been employed for the same purpose for a long time. Up to the lowest temperature (TL) in each of these data-sets, similarly accurate fits have also been obtained by Malik and Varma (2023) in a radically different approach based on the Bethe-Salpeter equation (BSE) supplemented by the Matsubara and the Landau quantization prescriptions. For T TL, however, while the (GL, WHH, etc.)-based approach leads to Hc2(0) ≈ 100 T, the BSE-based approach leads to about twice this value even at 1 K. In this paper, a fit to one of the said data-sets is obtained for the first time via a thermodynamic approach which, up to TL, is as good as those obtained via the earlier approaches. While this is interesting per se, another significant result of this paper is that for T TL it corroborates the result of the BSE-based approach.

h-Said-Ball基与h-Said-Ball曲线

h-Bezier曲线是Bezier曲线基于h-微积分意义下的推广模型.为增强Said-Ball曲线的造型能力,提高h-Bezier曲线递归求值速度,该文提出任意次的h-Said-Ball基函数,构造了h-Said-Ball曲线.通过分析Said-Ball曲线递归求值算法与Bezier曲线的转化关系,结合h-Bezier曲线的递归求值算法和h-Bernstein基函数的构造方式,得到任意次h-Said-Ball基函数的表达式.h-Said-Ball基具有非负,单位分解,端点插值等优良性质,和h-Bernstein基之间存在显式转换矩阵.进一步,定义h-Said-Ball曲线并分析其基本性质,推导递归求值算法和包络表示,h-Said-Ball曲线的求值计算量是h-Bezier曲线的一半.借助从h-Said-Ball曲线到h-Bezier曲线的割角算法,证明了h-Said-Ball基是全正基,从而h-Said-Ball曲线具有变差缩减性和保凸性.数值实例显示了h-Said-Ball曲线相比Said-Ball曲线的造型优势和灵活性.