Life Sciences

Data of Weight Blood pressure, Blood Glucose, and Dose-response curves in isolated aorta rings from pregnant and preeclamptic rats. to Phenylephrine

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Figure 1. Inhibition of Rac1 reduced radiation-induced intestinal injury of mice. Figure 2. Inhibition of Rac1 reduced the sensitivity of MODE-k cells to irradiation. Figure 3. Inhibition of Rac1 enhanced the sensitivity of CT-26 to irradiation. Figure 4. Inhibition of Rac1 reduced the ROS production of MODE-k after irradiation, while had little effect on CT-26. Figure 5. Inhibition of Rac1 could remit cycle arrest induced by irradiation in MODE-k while aggravate cycle arrest in CT-26.

ERS caused ER-phagy with a decrease in cell viability and an increase in cell death in H9c2 cardiomyoblasts.(A) Live/Dead staining of H9c2 cardiomyoblasts was performed using a LIVE/DEAD® Viability/Cytotoxicity Kit (bar=40 μm, n=3). TG- or TM-treated H9c2 cardiomyoblasts were incubated with calcein-AM (green) and EthD-1 (red) for 10 min, and the fluorescence was visualized using a confocal microscope. Green fluorescence indicates live cells, while red fluorescence indicates dead cells. (E) Ultrastructural lesions in the ER caused by TG or TM and the occurrence of ER-phagy were observed via transmission electron microscopy (bar=500 nm). (F) Representative confocal microscopy images corresponding to analysis of ER-phagy for TG- or TM-treated H9c2 cardiomyoblasts and showing colocalization of autophagosomes with ER-fragments (bar=15 μm; n=3). LC3B was labeled with Texas Red, while calreticulin was labeled with Alexa Fluor 488.

Aims: To investigate the effects of malignant fibrous histiocytoma amplified sequence 1 (MFHAS1) on cognitive dysfunction, the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and amyloid β peptide (Aβ) in the hippocampus, as well as dendritic pathology in the hippocampal CA1 region in sepsis-associated encephalopathy (SAE) rats. Main methods: The rats were randomly divided into four groups, 1) control group (subjected to sham surgery), 2) control plus Mfhas1 siRNA group (rats received intracerebroventricular injection of Mfhas1 siRNA after sham surgery), 3) CLP plus control siRNA group (rats received intracerebroventricular injection of control siRNA after cecal ligation and puncture (CLP)), 4) CLP plus Mfhas1 siRNA group (rats received intracerebroventricular injection of Mfhas1 siRNA after CLP). The learning and memory capabilities of the rats were examined by means of fear conditioning and Barnes maze test. The concentration of TNF-α and IL-1β was determined by enzyme-linked immunosorbent assay. The efficiency of siRNA transfection, MFHAS1 and Aβ expression were detected by Western blotting. Total branch lengths of the pyramidal dendrites of the CA1 basilar tree and spine density were determined by Golgi staining. Key findings: We observed that MFHAS1 knock-down by Mfhas1 siRNA intracerebroventricular injection could improve cognitive impairment, reduce the expression of TNF-α, IL-1β and Aβ in the hippocampus induced by CLP, and alleviate the dendritic spinal loss of the pyramidal neurons, as well as increase the dendritic branching of the CA1 basilar tree of septic rats. Significance: MFHAS1 knock-down can alleviate cognitive impairment, neuroinflammation and dendritic spinal loss in SAE rats. Key Words: MFHAS1, sepsis-associated encephalopathy, IL-1β, dendritic spine density

Effects of microwave radiation and CRT incubation on F-actin arrangement in HMECs. We evaluated the actin cytoskeleton and demonstrated that high-power microwave radiation inhibited actin polymerization, thus disrupting the F-actin arrangement.

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Raw data of Western blot