Association between baseline hemoglobin level and early neurological deterioration after intravenous thrombolysis in patients with acute ischemic stroke. / åŸºçº¿è¡€çº¢è›‹ç™½æ°´å¹³å¯¹æ€¥æ€§ç¼ºè¡€æ€§è„‘å’ä¸­æ‚£è€ é™è„‰æº¶æ “åŽæ—©æœŸç¥žç»åŠŸèƒ½æ¶åŒ–çš„å½±å“.

OBJECTIVES: To investigate the association between baseline hemoglobin level and early neurologic deterioration (END) after intravenous thrombolysis in patients with acute ischemic stroke (AIS). METHODS: Data of AIS patients who received intravenous thrombolytic therapy at multiple hospitals across the country between January 2017 and July 2020 were collected from the online database Acute Stroke Patients for Stroke Management Quality Evaluation (CASE-Ⅱ, NCT04487340). Binary logistic regression analysis was used to study the factors affecting the occurrence of END after intravenous thrombolytic therapy, and the correlation between baseline hemoglobin level and END was investigated by limiting cubic spline curve analysis. RESULTS: A total of 8162 patients were included. Patients with END had lower baseline hemoglobin levels (136 and 140 g/L, P<0.01) and higher rates of anemia (24.2% and 16.9%, P<0.01) compared with non-END patients. Binary logistic regression analysis showed that baseline hemoglobin level (OR=0.995, 95%CI: 0.991-0.999, P<0.05) and anemia (OR=1.238, 95%CI: 1.055-1.454, P<0.01) were independently correlated with the occurrence of END after intravenous thrombolysis in AIS patients. Restricted cubic spline regression showed that there was a U-shaped relationship between hemoglobin level and the risk of END after intravenous thrombolysis in AIS patients (P<0.01), although this relationship was only significant in male patients (P<0.05) and not in female patients (P>0.05). CONCLUSIONS: There is a correlation between baseline hemoglobin level and the risk of END in AIS patients after intravenous thrombolysis, especially in male patients, in whom both lower and higher hemoglobin level may increase the risk of END.

Metallothionein III Decreases the Proliferation of Astrocytes and Enhances Pathological Improvements in a Mouse Model of Alzheimer's Disease.

BACKGROUND: Alzheimer's disease (AD) affects the brain and causes difficulties with cognition and emotions. At present, there are no viable therapies to halt or slow down the advancement of AD. Metallothionein III (MT-III) exhibits antioxidant and anti-inflammatory characteristics, indicating possible therapeutic benefits. This study aimed to explore the influence of MT-III on AD pathological alterations and cognitive abilities. METHODS: In this research, we employed the universally accepted AD mouse models (3xTg-AD) as test subjects and administrated vehicle or MT-III. The mice were subjected to the Morris water maze test to assess their spatial learning and memory capabilities. Moreover, to evaluate the consequent effects on neuronal groups in the hippocampus, the Nissl staining and neuronal nuclear antigen (NeuN) immunohistochemistry were used to identify the cellular morphology changes and density. Immunohistochemistry was also used to detect ß-amyloid (Aß) and glial fibrillary acidic protein (GFAP) to measure Aß accumulation and astrocyte growth. Western blot was also used to measure Tau pathology-related PHD finger protein 1 (PHF-1), phosphorylated Tau (AT-8), and total Tau protein. RESULTS: The administration of MT-III notably enhanced spatial learning and memory function in 3xTg-AD mice, as evidenced by the Morris water maze test (p < 0.01). According to immunohistochemistry and the obtained findings, it was observed that brain tissues of mice treated with MT-III showed a notable increase of Nissl bodies and NeuN intensity (p < 0.01) while a remarkable decrease in Aß accumulation and GFAP (p < 0.01). Additionally, MT-III largely decreased levels of Tau phosphorylation-related PHF-1 and AT-8 (p < 0.01) and slightly reduced the level of Tau 5 (p < 0.05). CONCLUSION: In summary, our research indicates that MT-III has the capacity to ameliorate pathological alterations in AD mouse models and safeguard their cognitive and emotional abilities. By decreasing ß-amyloid accumulation and reducing the intensity of Tau pathology, MT-III protected hippocampal subfield neurons against pathological harm. Furthermore, MT-III reduced inflammation by inhibiting abnormal proliferation of astrocytes. Of utmost importance, MT-III greatly enhanced the cognitive abilities related to spatial learning and memory in mice, suggesting its promising therapeutic properties for AD.

How do the main components influence the VOCs emission characteristics and formation pathways during moso bamboo heat treatment?

Bamboo heat treatment will cause plenty of release of volatile organic compounds (VOCs) into the atmosphere which are important precursors for ozone (O3) formation. In this study, dewaxed bamboo was heat-treated at 180 °C for 2 h to investigate the emission characteristics and the formation pathways of VOCs during heat treatment by removing different main components. The results showed that aldehydes (22.61%-57.54%) and esters (14.64%-38.88%) are the primary VOCs released during heat treatment. These compounds mainly originate from the degradation of hemicellulose, lignin, cellulose, and the linkage bonds between them in bamboo. During the bamboo heat treatment, the degradation of CO, CH, and CO bonds in hemicellulose results in the release of 5-hydroxymethylfurfural, 3-furfural, and 1-(+)-ascorbic acid 2,6-dihexadecanoate. The breakage of benzene ring group and the CO and CH bonds of lignin leading to the emission of VOCs including m-Formylphenol, Vanillin, and Syringaldehyde. The degradation of aliphatic CH, CC, and CO bonds in the amorphous region of cellulose contributes to an enhanced release of alcohols, olefins, and alkanes. It is calculated that acids (28.92%-59.47%), esters (10.10%-22.03%) and aldehydes (17.88%-39.91%) released during heat treatment contributed more to Ozone Formation Potential (OFP).

circ-Gucy1a2 Protects Mice from Cerebral Ischemia-Reperfusion Injury by Attenuating Neuronal Apoptosis and Mitochondrial Membrane Potential Loss.

Cerebral ischemia-reperfusion (I/R) injury (CI/RI) is a severe problem in patients with cerebral ischemia. The current study explored the influences of circular (circ)-Gucy1a2 on neuronal apoptosis and mitochondrial membrane potential (MMP) in the brain tissue of CI/RI mice. Forty-eight mice were randomized into the sham group, transient middle cerebral artery occlusion (tMCAO) group, lentivirus negative control (LV-NC) group, and LV-Gucy1a2 group. Mice were first injected with lentivirus loaded with LV-Gucy1a2 or LV-NC via lateral ventricle, followed by the establishment of CI/RI models 2 weeks later. Twenty-four hours after CI/RI, the neurological impairment of mice was assessed using a 6-point scoring system. The cerebral infarct volume and brain histopathological changes were determined in CI/RI mice through histological staining. In vitro, pcDNA3.1-NC and pcDNA3.1-Gucy1a2 were transfected into mouse primary cortical neurons for 48 hours, followed by the establishment of oxygen-glucose deprivation/reoxygenation (OGD/R) models. The levels of circ-Gucy1a2 in mouse brain tissues and neurons were examined using RT-qPCR. Neuronal proliferation and apoptosis, MMP loss, and oxidative stress (OS)-related indexes in neurons were detected using CCK-8 assay, flow cytometry, JC-1 staining, and H2DFFDA staining. CI/RI mouse models and OGD/R cell models were successfully established. After CI/RI, neurons in mice were impaired and the cerebral infarction volume was increased. circ-Gucy1a2 was poorly expressed in CI/RI mouse brain tissues. Overexpression of circ-Gucy1a2 increased OGD/R-induced neuronal proliferation and mitigated apoptosis, MMP loss, and OS. Overall, circ-Gucy1a2 was down-regulated in brain tissues of CI/RI mice, and overexpression of circ-Gucy1a2 can protect mice from CI/RI.