[Movement Control of Striatum Neural Pathway].

Striatum is the central structure controlling movement. It plays a pivotal role in the regulation of voluntary movement, unconscious movement, muscle tone, posture adjustment and fine movement. Dysfunction of striatum causes a variety of movement disorders ranging from the hypokinetic disorders with increased muscle tone, such as Parkinson's disease, to the hyperkinetic disorders with decreased muscle tone, such as Huntington's disease. It is generally recognized that striatum receives the neural movement signals from the motor cortex, and then processes and modifies these signals and subsequently transfers the signals back to the motor cortex via thalamus for execution of the movement through pyramidal system. The movement control function of striatum depends on a complex neural circuit system. In this review, the studies on the movement control function of striatum as well as the striatal neural circuit system are summarized with an emphasis on the progress made during recent years for better understanding the mechanism underlying the movement control function as well as the disease association of striatum.

[Protein Kinase A and Lipid Metabolism].

Protein kinase A(PKA),as a pivotal factor in the cellular signal transduction,plays an es-sential role in the regulation of lipid metabolism.PKA activates the key lipases including hormone sensi-tive lipase (HSL)and adipose triglyceride lipase (ATGL)to promote the fat mobilization.PKA signaling up-regulates the mitochondrial thermogenesis by enhancing the expression of uncoupling protein-1 (UCP-1),which critically contributes to the body heat production.PKA is closely involved in the regulation of lipogenesis in the liver.Notably,the dysregulation of PKA signaling is associated with the pathogenic mechanisms underlying the obesity,cardiovascular diseases and diabetes mellitus.The pharmacological studies show that PKA is linked to the pharmacological effects of the major lipid regulating agents.In this review,the studies on roles of PKA in the regulation of lipid metabolism are summarized with an emphasis on progress made during the last five years for providing insights into the mechanism by which PKA regu-lates the lipid metabolism as well as the novel therapeutic strategy for lipid-metabolic diseases.

Hemodynamic changes in hepatic sinusoids of hepatic steatosis mice.

BACKGROUND: Fatty liver (FL) is now a worldwide disease. For decades, researchers have been kept trying to elucidate the mechanism of FL at the molecular level, but rarely involve the study of morphology and medical physics. Traditionally, it was believed that hemodynamic changes occur only when fibrosis occurs, but it has been proved that these changes already show in steatosis stage, which may help to reveal the pathogenesis and its progress. Because the pseudolobules are not formed during the steatosis stage, this phenomenon may be caused by the compression of the liver microcirculation and changes in the hemodynamics. AIM: To understand the pathogenesis of hepatic steatosis and to study the hemodynamic changes associated with hepatic steatosis. METHODS: Eight-week-old male C57BL/6 mice were divided into three groups randomly (control group, 2-wk group, and 4-wk group), with 16 mice per group. A hepatic steatosis model was established by subcutaneous injection of carbon tetrachloride in mice. After establishing the model, liver tissue from mice was stained with hematoxylin and eosin (HE), and oil red O stains. Blood was collected from the angular vein, and hemorheological parameters were estimated. A two-photon fluorescence microscope was used to examine the flow properties of red blood cells in the hepatic sinusoids. RESULTS: Oil red O staining indicated lipid accumulation in the liver after CCl4 treatment. HE staining indicated narrowing of the hepatic sinusoidal vessels. No significant difference was observed between the 2-wk and 4-wk groups of mice on morphological examination. Hemorheological tests included whole blood viscosity (mPas, γ = 10 s-1/γ = 100 s-1) (8.83 ± 2.22/4.69 ± 1.16, 7.73 ± 2.46/4.22 ± 1.32, and 8.06 ± 2.88/4.22 ± 1.50), red blood cell volume (%) (51.00 ± 4.00, 42.00 ± 5.00, and 40.00 ± 3.00), the content of plasma fibrinase (g/L) (3.80 ± 0.50, 2.90 ± 0.80, and 2.30 ± 0.70), erythrocyte deformation index (%) (44.49 ± 5.81, 48.00 ± 15.29, and 44.36 ± 15.01), erythrocyte electrophoresis rate (mm/s per V/m) (0.55 ± 0.11, 0.50 ± 0.11, and 0.60 ± 0.20), revealing pathological changes in plasma components and red blood cells of hepatic steatosis. Assessment of blood flow velocity in the hepatic sinusoids with a laser Doppler flowmeter (mL/min per 100 g) (94.43 ± 14.64, 80.00 ± 12.12, and 67.26 ± 5.92) and two-photon laser scanning microscope (µm/s) (325.68 ± 112.66, 213.53 ± 65.33, and 173.26 ± 44.02) revealed that as the modeling time increased, the blood flow velocity in the hepatic sinusoids decreased gradually, and the diameter of the hepatic sinusoids became smaller (µm) (10.28 ± 1.40, 6.84 ± 0.93, and 5.82 ± 0.79). CONCLUSION: The inner diameter of the hepatic sinusoids decreases along with the decrease in the blood flow velocity within the sinusoids and the changes in the systemic hemorheology.