温度和pH值对羊毛织物尺寸稳定性的影响

通过一系列实验分析了温度和pH值对羊毛纤维的膨胀和羊毛织物尺寸变化的影响．在pH2．1的溶液中，羊毛织物的尺寸随温度的升高而下降，变化的幅度取决于织物组织和织物的定型率．在羊毛等电点pH4．8时，纤维的膨胀达到最小值，而织物的尺寸则随着溶液酸性的增加而减小．     

脉冲激光照射下生物质材料的传热特性

采用快速瞬态温度检测系统测定高能脉冲激光作用下生物质材料的温度动态变化,研究生物质材料瞬态传热特性以及激光脉冲宽度、功率密度、材料厚度与初始含湿量对温度变化规律的影响.根据实验现象,尝试提出脉冲激光作用下生物质材料传热的数学模型,数值模拟分析表明,计算与实验结果基本吻合,能较好地反应脉冲激光作用下生物质材料的传热特性,为进一步深入研究和理论分析积累了有价值的实验资料,提供了可供参考的经验.     

Palaeolake and palaeoenvironment between 42 and 18 kaBP in tengger desert, NW China

Comprehensive field investigations and laboratory analyses show that palaeolakes, including fresh- mesohaline water Megalake Tengger and other semi-con- nected, isolated water bodies, during late Pleistocene covered an area of more than 20000 km², which is more than half of the Tengger Desert in NW China. Stratigraphic correlation and chronological evidence indicate that before ca. 42000 aBP the area was more arid. The palaeolakes started to develop around 40000 uncal. ¹⁴C aBP but until 37000 ¹⁴C aBP their scope was limited. High water levels established from 35000 ¹⁴C aBP lasted until 22000 ¹⁴CaBP. Lake levels regressed between 22000 and 20000 ¹⁴C aBP but transgressed from 20000 to 18600 ¹⁴C aBP. Subsequently, water level declined further and the Megalake Tengger finally desiccated at around 18000 ¹⁴C aBP. Megalake Tengger possessed a fresh-mesohaline water property, implying that the regional precipitation increased significantly. During the period of Megalake Tengger, the climate was warmer-humid than present. The annual rainfall was 250 to 350 mm more than that of today and the temperature was 1.5 to 3.0℃ higher.     

Superoxide activates mitochondrial uncoupling proteins.

Uncoupling protein 1 (UCP1) diverts energy from ATP synthesis to thermogenesis in the mitochondria of brown adipose tissue by catalysing a regulated leak of protons across the inner membrane. The functions of its homologues, UCP2 and UCP3, in other tissues are debated. UCP2 and UCP3 are present at much lower abundance than UCP1, and the uncoupling with which they are associated is not significantly thermogenic. Mild uncoupling would, however, decrease the mitochondrial production of reactive oxygen species, which are important mediators of oxidative damage. Here we show that superoxide increases mitochondrial proton conductance through effects on UCP1, UCP2 and UCP3. Superoxide-induced uncoupling requires fatty acids and is inhibited by purine nucleotides. It correlates with the tissue expression of UCPs, appears in mitochondria from yeast expressing UCP1, and is absent in skeletal muscle mitochondria from UCP3 knockout mice. Our findings indicate that the interaction of superoxide with UCPs may be a mechanism for decreasing the concentrations of reactive oxygen species inside mitochondria.     

Mutations in a human homologue of Drosophila crumbs cause retinitis pigmentosa (RP12).

Retinitis pigmentosa (RP) comprises a clinically and genetically heterogeneous group of diseases that afflicts approximately 1.5 million people worldwide. Affected individuals suffer from a progressive degeneration of the photoreceptors, eventually resulting in severe visual impairment. To isolate candidate genes for chorioretinal diseases, we cloned cDNAs specifically or preferentially expressed in the human retina and the retinal pigment epithelium (RPE) through a novel suppression subtractive hybridization (SSH) method. One of these cDNAs (RET3C11) mapped to chromosome 1q31-q32.1, a region harbouring a gene involved in a severe form of autosomal recessive RP characterized by a typical preservation of the para-arteriolar RPE (RP12; ref. 3). The full-length cDNA encodes an extracellular protein with 19 EGF-like domains, 3 laminin A G-like domains and a C-type lectin domain. This protein is homologous to the Drosophila melanogaster protein crumbs (CRB), and denoted CRB1 (crumbs homologue 1). In ten unrelated RP patients with preserved para-arteriolar RPE, we identified a homozygous AluY insertion disrupting the ORF, five homozygous missense mutations and four compound heterozygous mutations in CRB1. The similarity to CRB suggests a role for CRB1 in cell-cell interaction and possibly in the maintenance of cell polarity in the retina. The distinct RPE abnormalities observed in RP12 patients suggest that CRB1 mutations trigger a novel mechanism of photoreceptor degeneration.     

Susceptibility to testicular germ-cell tumours in a 129.MOLF-Chr 19 chromosome substitution strain.

The identification of genes that control susceptibility to testicular germ-cell tumours (TGCTs), the most common cancer affecting young men, has been difficult. In laboratory mice, TGCTs arise from primordial germ cells in only the 129 inbred strains, and susceptibility is under multigenic control. The spontaneously arising mutation Ter (ref. 5) on mouse chromosome 18 (Refs 6,7) increases TGCT frequency on a 129/Sv background. We originally used Ter in genetic crosses to identify loci that control tumorigenesis. A genome scan of tumour-bearing progeny from backcrosses between the 129/Sv-Ter/+ and MOLF/Ei strains provided modest evidence that MOLF-derived alleles on chromosome 19 enhance development of bilateral TGCTs (ref. 9). To obtain independent evidence for linkage to the MOLF chromosome, we made an autosomal chromosome substitution strain (CSS; or 'consomic strain') in which chromosome 19 of 129/Sv+/+ was replaced by its MOLF-derived homologue. The unusually high frequency of TGCTs in this CSS (even in the absence of the Ter mutation) provides evidence confirming the genome survey results, identifies linkage for a naturally occurring strain variant allele that confers susceptibility to TGCTs and illustrates the power of CSSs in complex trait analysis.     

Regulation of sodium and body fluid homeostasis during development: Implications for the pathogenesis of hypertension

The spontaneously hypertensive rat (SHR) is an important animal model of human essential hypertension. During the first month of life, increased retention of sodium is present in the SHR which appears to be mediated by the renin-angiotensin system. The present review will discuss the role that increased activity of the renin-angiotensin system plays in sodium/body fluid regulation during early development. It is hypothesized that disordered regulation of sodium/body fluid homeostasis during this stage leads to pathological cardiovascular regulation in adulthood. Through an understanding of the relationship between sodium/body fluid balance in the young and cardiovascular function in the adult insights may be gained into both the pathological state of hypertension and the critical role played by early development in shaping homeostatic mechanisms in adulthood.