Controllable Negative Thermal Expansion by Mechanical Pulverizing in Hexagonal Mn0.965Co1.035Ge Compounds.

Negative thermal expansion (NTE) material as a compensator is very important for accurately controlling the thermal expansion of materials. Along with the magnitude of the coefficient of thermal expansion, the operating temperature window of the NTE materials is also a major concern. However, only a few of the NTE materials possess both a large operating temperature range and a large thermal expansion coefficient. To explore this type of new NTE material, the Mn0.965Co1.035Ge fine powders were prepared by mechanical ball milling (BM). These fine powders show a largely extended NTE operation temperature window simultaneously possessing a giant thermal expansion coefficient. For samples treated with different BM times, such as the BM-0.5h, BM-4h, and BM-12 h samples, the operating temperature window (Δ T) and linear thermal expansion coefficient (αL) are 167 K (222-389 K) and ∼ -63 ppm/K, 221 K (140-360 K) and ∼ -41.3 ppm/K, and 208 K (234-442 K) and ∼ -40 ppm/K, respectively, which are larger than most well-known NTE materials. More strikingly, all BM samples have a large constant linear NTE coefficient with an ultrawide temperature window covering room temperature. For these three samples, these values are ∼ -52 ppm/K (140 K), ∼ -58.3 ppm/K (110 K), and ∼ -65 ppm/K (80 K), respectively. The origin of the excellent NTE properties is discussed based on the thermomagnetic measurements and X-ray absorption spectroscopic results.

[Early-stage changes of caliber and blood flow of cat pial microvessels following craniocerebral missile wound].

OBJECTIVE: To investigate the early-stage changes of cerebral microcirculation after craniocerebral missile wound (CMW) in cats. METHODS: Twelve mongrel cats of either sex were used for measuring the caliber (D), velocity (V) and blood flow (Q) of the pial microvessels and observing the vital signs 10 min before CMW and from 5 min to 5 h after CMW. The pathological changes of the brain tissue were also examined. RESULTS: After CMW, the D, V and Q of the pial arteriole decreased within the initial 5 to 20 min, followed by elevation of Da and Qa at 90 min. No significant changes were noted in the Dv of the pial venule but its Vv and Qv remained at low levels. CONCLUSION: After CMW, the Q of microvessels may increase progressively in the areas of concussion, contusion and laceration injuries to induce reperfusion injury following ischemia and hypoxia of the brain tissue resulting from microcirculation disorder caused by the wound.

[Three-dimensional architecture and ultrastructure of the cerebral microvasculature of missile brain wound in cats].

OBJECTIVE: To explore the changes of cerebral microvasculature in cats with missile brain wound. METHODS: The microvascular corrosion casts of the brain were examined by scanning electron microscopy, and the ultra-thin slices of the brain were inspected by transmission electron microscopy. RESULTS: The brain microvasculature showed evidently abnormal morphological changes, with both vasospasm and vasodilation as well as concurrent bleeding and ischemia. Strong pathological contraction of vascular sphincter, rupture of some microvessels, and increased microvilli and vacuoles in the endothelial cells were observed. Loosening of the intercellular tight junction and basal membrane rupture occurred along with perivascular swelling and neural cell damages. CONCLUSION: Morphological or functional changes occur in the cerebral microvasculature leading to secondary brain injury after missile brain wound in cats.

[Effect of L-arginine on the changes of cerebral microcirculation following craniocerebral missile wound at early stage in cats].

OBJECTIVE: To study the alterations of cerebral microcirculation and the effect of L-Arginine after craniocerebral missile wound (CMW) at early stage in cats. METHODS: The CMW animal model in cat was constructed by Carey method. Altogether 12 mongrel cats with either sex were divided into the CMW group and the L-Arginine treatment group. The caliber (D), velocity (V) and blood flow (Q) of pial microvessels and pathological examination of brain tissue at 10 min before CMW and from 5 min to 5 h after CMW were evaluated in each group. RESULTS: 1. In CMW group, although the Da, Va and Qa of pial arteriole decreased from 5 to 20 minutes, Da and Qa elevated at 90 minutes after CMW. There were no significant changes in the Dv of pial venule, but the levels of Vv and Qv were lower at 5 min and 20 min after CMW. Qv increased from 45 min to 3 h after CMW. The pial venules were in congestion situation. 2. In the L-Arginine treatment group, the pial aterioles persistently dilated after CMW. The blood flow of pial aterioles increased at 20 min after CMW and the higher level lasted 5 h. Similarly, the dilation of pial venules was observed, and the blood flow increased at 20 min after the injury, followed by venules constriction temporarily. 3. Petechial hemorrhage, microthrombosis and nerve cell swelling were found in the cortex on the opposite side of the trauma area. The pathological changes were less severe in the L-Arginine treatment group than those in the CMW group. CONCLUSION: At the early stage after CMW, there are obstructions to cerebral microcirculation, which induce brain ischemia, hypoxia and secondary failure of cerebral function. The mechanism by which L-Arginine alleviates the impaired cerebral microcirculation may lie in the vascular activation of L-Arginine-NO system.