The vulnerability assessment and obstacle factor analysis of urban agglomeration along the Yellow River in China from the perspective of production-living-ecological space.

Urban agglomerations are sophisticated territorial systems at the mature stage of city development that are concentrated areas of production and economic activity. Therefore, the study of vulnerability from the perspective of production-living-ecological space is crucial for the sustainable development of the Yellow River Basin and global urban agglomerations. The relationship between productivity, living conditions, and ecological spatial quality is fully considered in this research. By constructing a vulnerability evaluation index system based on the perspectives of production, ecology, and living space, and adopting the entropy value method, comprehensive vulnerability index model, and obstacle factor diagnostic model, the study comprehensively assesses the vulnerability of the urban agglomerations along the Yellow River from 2001 to 2020. The results reveal that the spatial differentiation characteristics of urban agglomeration vulnerability are significant. A clear three-level gradient distribution of high, medium, and low degrees is seen in the overall vulnerability; these correspond to the lower, middle, and upper reaches of the Yellow River Basin, respectively. The percentage of cities with higher and moderate levels of vulnerability did not vary from 2001 to 2020, while the percentage of cities with high levels of vulnerability did. The four dimensions of economic development, leisure and tourism, resource availability, and ecological pressure are the primary determinants of the urban agglomeration's vulnerability along the Yellow River. And the vulnerability factors of various urban agglomerations showed a significant evolutionary trend; the obstacle degree values have declined, and the importance of tourism and leisure functions has gradually increased. Based on the above conclusions, we propose several suggestions to enhance the quality of urban development along the Yellow River urban agglomeration. Including formulating a three-level development strategy, paying attention to ecological and environmental protection, developing domestic and foreign trade, and properly planning and managing the tourism industry.

Relations between antinuclear, antineutrophil cytoplasmic, anticardiolipin antibodies and degree of neurological deficit, cerebrovascular stenosis in cerebral infarction patients.

Objective: To investigate the correlation of antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA) and anticardiolipin antibody (ACA) with the degree of the neurological defect and cerebrovascular stenosis in patients with cerebral infarction. Methods: Clinical data of 99 patients with acute cerebral infarction (ACI) admitted to the Department of Neurology of Baoding First Central Hospital from June 2020 to December 2021 were retrospectively analyzed, and their ANA, ACA, ANCA, neurological deficit (NIHSS) scores as well as cerebrovascular stenosis were detected and assessed. Moreover, the correlation between the positive expression rates of ANA, ANCA, ACA and the degree of the neurological deficit, as well as the location and degree of cerebrovascular stenosis, were analyzed. Results: All patients had ANA, ACA, ANCA antibodies with positive rates of 68.69%, 70.71%, 69.70%, and mild, moderate, and severe cerebrovascular stenosis with incidence rates of 28.28%, 32.32%, and 39.39% respectively; Moreover, their incidence of mild, moderate, and severe neurological deficits were 15.15%, 44.44%, and 40.40%, respectively. Statistically significant differences could be observed in the degree of cerebrovascular stenosis and neurological deficit between the ANA, ACA and ANCA antibody positive group and the negative group (p<0.05). ANA, ACA, ANCA antibody positive was moderately positively correlated with cerebrovascular stenosis rate and NIHSS score (0.40

Graphene Oxide-Gold Star Construct on Triangular Electrodes for Alzheimer's Disease Identification.

Nanotechnology is playing a major role in the field of medical diagnosis, in particular with the biosensor and bioimaging. It improves the performance of the desired system dramatically by displaying higher selectivity and sensitivity. Carbon nanomaterial, gold nanostructure, magnetite nanoparticle, and silica substrate are the most popular nanomaterials greatly contributed to make the affordable and effective biosensor at low-cost. This research work is introducing a new sensing strategy with graphene oxide-constructed triangular electrodes to diagnose Alzheimer's disease (AD). MicroRNA-137 (miRNA-137) was found as a suitable biomarker for AD, and the sensing method was established here to detect miRNA-137 on the complementary sequence. To enhance the immobilization of capture miRNA-137, gold nanostar (GNS) was conjugated with capture miRNA and immobilized on the GO-modified surface through an amine linker. This immobilization process enhanced the hybridization of the target and reaches the detection limit at 10 fM with the sensitivity of 1 fM on the linear curve with a regression coefficient of 0.9038. Further control sequences of miRNA-21 and single and triple base mismatched miRNA-137 did not show a significant response in current changes, indicating the specific miRNA-137 detection for diagnosing AD.

Graphene oxide-gold nanoparticle-aptamer complexed probe for detecting amyloid beta oligomer by ELISA-based immunoassay.

Highly sensitive and easy detection method for Alzheimer's disease (AD) with a suitable biomarker is mandatory for preventing the factors resulting from AD. This research reports a modified ELISA with graphene for the detection of AD biomarker amyloid beta (Aß) oligomer. Gold nanoparticle (AuNP) conjugated aptamer was used as the capture probe and attached on ELISA-graphene oxide surface through the amine linker. Antibody was used as the detection molecule to reach the maximum detection of Aß oligomer. Suitable level of APTMS (2%), size of AuNP (30 nm) and aptamer concentration (2 µM) were optimized. This sandwich pattern of aptamer-Aß oligomer-antibody helps to reach the detection at 50 pM on the optimized ELISA surface and the control experiments in the absence of Aß oligomer or anti-Aß oligomer antibody did not show the significant optical detection at 492 nm, indicting the specific detection. Further, Aß oligomer spiked artificial cerebrospinal fluid did not interfere the detection of Aß oligomer, confirming the selective detection. This new and modified ELISA surface helps to reach the lower detection of Aß oligomer and diagnose AD.

Neuroprotective Effects of D-(-)-Quinic Acid on Aluminum Chloride-Induced Dementia in Rats.

OBJECTIVE: The present study was designed to evaluate the neuroprotective effects of D-(-)-quinic acid on aluminum chloride- (AlCl3-) induced neurobehavioral and biochemical changes in rats. This study showed the behavioral and biochemical effects of D-(-)-quinic acid on rats with particular emphasis on the hippocampus and frontal cortex which are associated with memory. MATERIALS AND METHODS: Chronic administration of aluminum chloride at a dose of 175 mg/kg, p.o. for a period of 25 days markedly increased the level of acetylcholinesterase (AChE) activity and reduced the levels of antioxidant enzymes in the brain. Two doses of D-(-)-quinic acid (200 mg/kg and 400 mg/kg) were selected based on previous safety/toxicity studies and administered orally from the 26th day to the 36th day of the trial. Behavioral parameters were assessed using the Morris water maze test and an actophotometer in rats. Biochemical parameter content and histology of brain tissue were assessed on the final day of the experiment. RESULTS: D-(-)-Quinic acid (200 mg/kg and 400 mg/kg) orally administered alongside AlCl3 rescued AChE activity and the behavioral impairments caused by aluminum. There was significant inhibition of MAO-B in D-(-)-quinic acid-treated rats. Histopathological studies in the hippocampus and cortex of the rat brain also supported that D-(-)-quinic acid markedly reduced the toxicity of AlCl3 and preserved the normal histoarchitecture pattern of the hippocampus and cortex. These results indicate that D-(-)-quinic acid can reverse memory loss caused by aluminum intoxication by attenuating AChE activity and rescuing the deleterious effect of AlCl3.