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AbstractWith the high-speed and high-frequency operation of CPU chips, as well as miniaturization and dense assembly of integrated circuits, the heat generated by the Raspberry Pi CPU is constantly increasing. To address the urgent need for efficient Raspberry Pi CPU heat dissipation and ensure normal operation within a safe temperature range, this study first established a model to simulate the CPU's thermal physics parameters during operation using CFD simulation software. An experimental platform was then set up to validate the CFD simulation results. Based on the validated CFD model, initial heat dissipation design was carried out. On this basis, the heat dissipation system was optimized by altering the heat sink’s length, width, fin height, thickness, spacing, and the thermal grease’s thermal conductivity between the heat sink and CPU chip. A surrogate model was established using the response surface methodology, and the NSGA-II genetic algorithm was employed for multi-objective optimization of the heat dissipation system’s cooling performance. Compared to the initial solution, the chip temperature was reduced by 6.19 °C, but the heat sink mass was increased by 0.65 g. By conducting multi-objective optimization design and making reasonable choices for the parameters, a suitable and an optimum design, in terms of both economics and efficiency, is obtained. These results demonstrate that this research can provide theoretical guidance and technical support for practical production. Furthermore, the methods and findings from this study can be applied to the design of heat dissipation systems for similar applications. [ABSTRACT FROM AUTHOR]

Objective To study the effects of Baishao (White Peony Root, Radix Paeoniae Alba) on liver yin deficiency pattern in mice with alcoholic liver injury and mechanism. Methods ICR mice were randomly divided into blank group, model group, Yiguan Jian ( Effective Integration Decoction, YGJ) group and Baishao group, with 10 mice in each group. Mice models of alcoholic liver injury with liver yin deficiency pattern were established by intragastric administration of Lieber-DeCarli alcohol diet plus thyroid hormone. Meanwhile, the blank group and the model group were given physiological saline by gavage, the YGJ group was given YGJ (9. 07 g/kg, 20 mL/kg) by gavage, and the Baishao group baishao exact (4. 3 g/kg, 20 mL/kg) by gavage. After 28 days, the state of mice in each group was observed, and their body weight, body temperature and heart rate were measured. Levels of transaminase activities, cytokine, enzyme activities related to ethanol and fat metabolism and antioxidant enzyme activities of the serum and liver tissue were detected. Frozen liver sections were examined with Oil Red 0 staining and liver biopsies with H&E staining. Results Compared with the blank group, the weight of the mice in the model group was significantly reduced, the body temperature increased, the heart rate increased, accompanied with symptoms like lusterless hair, tiredness, sleepiness and irritability. The levels of serum ALT, AST, TG, TC and cAMP and levels of liver MDA, CYP2E1, TNF-a, IL-1 (3 and IL-6 in the model group were significantly increased. The serum levels of cGMP and liver tissue levels of SOD, CAT, ADH, ALDH2, IL-10 and IL-1Ra were significantly reduced. In addition, lipid deposition ad hepatocyte necrosis occurred in the liver. Compared with the model group, serum levels of ALT, AST, TG, TC and cAMP in the Baishao group were significantly lowered (P <0. 05), and cGMP levels were significantly increased (P <0. 05). The liver levels of CYP2E1, TNF-a, IL-1 (3 and IL-6 were significantly decreased (P<0.05), and the levels of SOD, CAT, ADH, ALDH2, IL-10 and IL-1 Ra were significantly increased (P <0. 05). Also, the lipid content of the liver tissue was significantly decreased (P <0. 01), and hepatocyte necrosis was reduced. Conclusion Baishao has obvious curative effect on liver yin deficiency pattern caused by alcoholic liver injury. Its mechanism is related to the regulation of cAMP/cGMP levels and cytokine levels, the restoration of normal hepatocyte function and metabolism, enhanced activities of key enzymes and antioxidant enzymes of ethanol metabolism in liver tissue, inhibition of lipid peroxidation and reduction in lipid deposition. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects of Cyclocarya Paliurus aqueous extract (CPAE) on pancreatic (3 cell apoptosis in type 2 diabetic (T2D) rats. Methods T2D ract model was established by high-fat diet feeding for 8 weeks and single intraperitoneal injection of streptozotocin. From the ninth week, the rats in the model group (sodium chloride solution), metformin group (0.3 g/kg), low, medium and high dose CPAE groups (0.18, 0.36, 1.08 g/kg) were treated for 4 consecutive weeks. Glucose tolerance was measured at the last administration. After sacrifing the rats and removing the pancreas, the contents of superoxide dismutase (SOD), peroxidase (CAT), glutathione peroxidase (GSH-PX), malondialdehyde (MDA) and free fatty acid (FFA) were detected with colorimetric method. Tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were measured with radioimmunoassay. The levels of apoptosis factor (Fas) and its ligand (Fasl), activated cysteine protease (Caspase8) were detected by using ELISA. Western blot assay was used to detect total c-Jun N-terminal kinase 1 (T-JNK1), phosphorylated c-Jun N-terminal kinase 1 (P-JNK1), pancreatic duodenal homeobox 1 (PDX-1) protein expression; TUNEL staining was used to observe pancreatic cell's apoptosis. Results CPAE treated groups presented with increased contents of SOD, CAT, GSH-PX and increased expression of PDX-1 in the pancreas of the CPE groups; fasting blood glucose, area under the curve, MDA, FFA, TNFα, IL6, Fas, Fasl, Caspase8 content, T-JNK1, p-JNK1 expression, and pancreatic cell apoptosis rate were all reduced in the model group. Conclusion CPAE can improve the pancreas antioxidant, alleviate oxidative stress, and inhibit pancreatic β cell's apoptosis. The mechanism may be related to inhibiting the expression of T-JNK1 and P-JNK1 protein, increasing the expression of PDX-1 protein and decreasing the content of Fas, Fasl and Caspase8. [ABSTRACT FROM AUTHOR]