建筑室外风环境数值模拟的湍流模型比较

对日本建筑学会提供的室外无污染物扩散和有污染物扩散的建筑风洞实验模型,采用15种湍流模型分别求解其室外流场,通过模拟结果与风洞实验结果的对比分析,确定建筑室外风环境数值模拟所用的最优湍流模型.结果表明,Suga三次式高Re k-ε模型对风场和浓度场的求解具有很高的精度,是最优的模拟室外风环境的湍流模型,不足之处是该模型...     

Cnd2 has dual roles in mitotic condensation and interphase

Chromosome condensation requires condensin, which comprises five subunits. Two of these subunits--both being structural maintenance of chromosome (SMC) proteins-are coiled-coils with globular terminal domains that interact with ATP and DNA. The remaining three, non-SMC subunits also have essential, albeit undefined, roles in condensation. Here we report that Cnd2 (ref. 6), a non-SMC subunit of fission yeast similar to Drosophila Barren and the budding yeast protein Brn1 (refs 8, 9), is required for both interphase and mitotic condensation. In cnd2-1 mutants, ultraviolet-induced DNA damage is not repaired, and cells arrested by hydroxyurea do not recover. A definitive defect of interphase is abolishment of Cds1 (a checkpoint kinase) activation in the presence of hydroxyurea in both cnd2-1 mutant cells and in cells where other condensin subunits have been genetically disrupted. In the absence of hydroxyurea, a G2 checkpoint delay occurred in cnd2-1 mutants in a manner dependent on Cds1 and ATM-like Rad3, but not Chk1 (refs 10-13), before the mitotic condensation defect. Furthermore, cnd2-1 was synthetic-lethal with mutations of excision repair, RecQ helicase and DNA replication enzymes. These interphase and mitotic defects provide insight into the mechanistic role of non-SMC subunits that interact with the globular SMC domains in the heteropentameric holocomplex.     

Between two worlds: Yamanouchi Shigeo and eugenics in early twentieth-century Japan

This paper explores the eugenic through of Yamanouchi Shigeo (1876-1973), who was trained in plant cytology under the tutelage of botanist and eugenicist John Coulter (1851-1928) in the USA, and later become one of the early and important popularizers of eugenic ideas in Japan. His career demonstrates a direct link between Japanese and US eugenics. Despite his academic training and research at various internationally renowned institutions, numerous publications, and longevity, his life has received little scholarly attention. By the early twentieth century, most biologists in Japan, as in the USA, began accepting Mendelian evolutionary theory and rejecting the Lamarckian notion of inheritance of acquire characteristics. However, Yamanouchi Shigeo's eugenic view represents a paradox: he was a mendelian cytologist sympathetic to Lamarckism. Was his 'nurture'-oriented eugenic view unscientific? is that why he was largely ignored in the history of botany in Japan? This study attempts to answer these questions and to analyse the origins and distinct features of Yamanouchi's eugenic ideas by situating Yamanouchi's eugenic through historically and culturally. After examining his scientific papers, popular writings, and documents of various organizations to which he belonged, I argue that Yamanouchi's 'softer' (or less biologically deterministic) perspective may have reflected the Japanese desire to catch up with the dominant 'race' by using eugenics without accepting permanent inferior status.     

Calcineurin is required to release Xenopus egg extracts from meiotic M phase

Fertilization induces a transient increase in cytoplasmic Ca2+ concentration in animal eggs that releases them from cell cycle arrest in the second meiotic metaphase. In frog eggs, Ca2+ activates Ca2+/calmodulin-activated kinase, which inactivates cytostatic factor, allowing the anaphase-promoting factor to turn on and ubiquitinate cyclins and securin, which returns the cell cycle to interphase. Here we show that the calcium-activated protein phosphatase calcineurin is also important in this process. Calcineurin is transiently activated after adding Ca2+ to egg extracts, and inhibitors of calcineurin such as cyclosporin A (ref. 8) delay the destruction of cyclins, the global dephosphorylation of M-phase-specific phosphoproteins and the re-formation of a fully functional nuclear envelope. We found that a second wave of phosphatase activity directed at mitotic phosphoproteins appears after the spike of calcineurin activity. This activity disappeared the next time the extract entered M phase and reappeared at the end of mitosis. We surmise that inhibition of this second phosphatase activity is important in allowing cells to enter mitosis, and, conversely, that its activation is required for a timely return to interphase. Calcineurin is required to break the deep cell cycle arrest imposed by the Mos-MAP (mitogen-activated protein) kinase pathway, and we show that Fizzy/Cdc20, a key regulator of the anaphase-promoting factor, is an excellent substrate for this phosphatase.     

CD38 is critical for social behaviour by regulating oxytocin secretion

CD38, a transmembrane glycoprotein with ADP-ribosyl cyclase activity, catalyses the formation of Ca2+ signalling molecules, but its role in the neuroendocrine system is unknown. Here we show that adult CD38 knockout (CD38-/-) female and male mice show marked defects in maternal nurturing and social behaviour, respectively, with higher locomotor activity. Consistently, the plasma level of oxytocin (OT), but not vasopressin, was strongly decreased in CD38-/- mice. Replacement of OT by subcutaneous injection or lentiviral-vector-mediated delivery of human CD38 in the hypothalamus rescued social memory and maternal care in CD38-/- mice. Depolarization-induced OT secretion and Ca2+ elevation in oxytocinergic neurohypophysial axon terminals were disrupted in CD38-/- mice; this was mimicked by CD38 metabolite antagonists in CD38+/+ mice. These results reveal that CD38 has a key role in neuropeptide release, thereby critically regulating maternal and social behaviours, and may be an element in neurodevelopmental disorders.     

Mutations in WDR62, encoding a centrosome-associated protein, cause microcephaly with simplified gyri and abnormal cortical architecture

Genes associated with human microcephaly, a condition characterized by a small brain, include critical regulators of proliferation, cell fate and DNA repair. We describe a syndrome of congenital microcephaly and diverse defects in cerebral cortical architecture. Genome-wide linkage analysis in two families identified a 7.5-Mb locus on chromosome 19q13.12 containing 148 genes. Targeted high throughput sequence analysis of linked genes in each family yielded > 4,000 DNA variants and implicated a single gene, WDR62, as harboring potentially deleterious changes. We subsequently identified additional WDR62 mutations in four other families. Magnetic resonance imaging and postmortem brain analysis supports important roles for WDR62 in the proliferation and migration of neuronal precursors. WDR62 is a WD40 repeat-containing protein expressed in neuronal precursors as well as in postmitotic neurons in the developing brain and localizes to the spindle poles of dividing cells. The diverse phenotypes of WDR62 suggest it has central roles in many aspects of cerebral cortical development.     

Between Two Worlds: Yamanouchi Shigeo and Eugenics in Early Twentieth‐Century Japan

The 1935 conflict on the nature of relativistic degeneracy that pitted Subrahmanyan Chandrasekhar against Arthur Stanley Eddington is part of astronomical lore. In recountings of the events surrounding the dispute, the complaint is frequently aired that Chandrasekhar, who faced the pre-eminent astrophysicist of his time, did not enjoy the support of the astronomical community, which opted to side instead with Eddington. We reconsider these statements in the light of the published record and argue that the reception of Chandrasekhar's ideas was, if anything, rather favourable and that any perceived lack of support may have been due in great part to the inability to distinguish, on an observational basis, between the predictions of the competing theories. We further argue that the observational situation improved little over the subsequent thirty years, but that this did not prevent Chandrasekhar's version of relativistic degeneracy, and associated theory of electron-degenerate stars, from gaining a central position within the realm of stellar structure and evolution. We briefly compare this status to that enjoyed by general relativity before 1960.     

Mutations in SLC6A19, encoding B0AT1, cause Hartnup disorder

Hartnup disorder, an autosomal recessive defect named after an English family described in 1956 (ref. 1), results from impaired transport of neutral amino acids across epithelial cells in renal proximal tubules and intestinal mucosa. Symptoms include transient manifestations of pellagra (rashes), cerebellar ataxia and psychosis. Using homozygosity mapping in the original family in whom Hartnup disorder was discovered, we confirmed that the critical region for one causative gene was located on chromosome 5p15 (ref. 3). This region is homologous to the area of mouse chromosome 13 that encodes the sodium-dependent amino acid transporter B(0)AT1 (ref. 4). We isolated the human homolog of B(0)AT1, called SLC6A19, and determined its size and molecular organization. We then identified mutations in SLC6A19 in members of the original family in whom Hartnup disorder was discovered and of three Japanese families. The protein product of SLC6A19, the Hartnup transporter, is expressed primarily in intestine and renal proximal tubule and functions as a neutral amino acid transporter.