超低速压铸慢压射速度下ADC12铝合金的显微组织和性能

采用光学显微镜、扫描电镜、X线衍射和能谱等显微分析技术,结合力学性能检测,研究超低速压铸条件下慢压射速度对ADC12铝合金铸件显微组织及力学性能的影响,以优化超低速压铸工艺及其参数。通过对相同高速起速位置、不同低速速度及不同起速位置、相同低速速度2种超低速工艺得到的铸件比较发现:在超低速压铸工艺下,慢压射速度对铸件密度的影响不明显;当起速位置相同时,随着低速速度的增大,铸件的α(Al)枝晶越来越粗大,其性能降低;在相同低速速度、不同高速起速位置时,起速位置有最佳值,当铸件性能在高速起速位置为260mm时,α(Al)枝晶较细小,其性能也较好。     

In vitro secretion of ecdysteroids by Y-organs of the crayfish,Procambarus clarkii

It was demonstrated that excised Y-organs of the crayfish,Procambarus clarkii, synthesize in vitro 3-dehydroecdysone (3-DHE) as the major product, together with small amounts of ecdysone. Both were identified by immunological and spectroscopic methods. The increase of ecdysteroidogenesis in the Y-organs was accompanied by an increase of the major free ecdysteroid, 20-hydroxyecdysone, in the hemolymph. This suggests a physiological role of 3-DHE, the details of which are still to be elucidated.     

The gene mutated in ataxia-ocular apraxia 1 encodes the new HIT/Zn-finger protein aprataxin

The newly recognized ataxia-ocular apraxia 1 (AOA1; MIM 208920) is the most frequent cause of autosomal recessive ataxia in Japan and is second only to Friedreich ataxia in Portugal. It shares several neurological features with ataxia-telangiectasia, including early onset ataxia, oculomotor apraxia and cerebellar atrophy, but does not share its extraneurological features (immune deficiency, chromosomal instability and hypersensitivity to X-rays). AOA1 is also characterized by axonal motor neuropathy and the later decrease of serum albumin levels and elevation of total cholesterol. We have identified the gene causing AOA1 and the major Portuguese and Japanese mutations. This gene encodes a new, ubiquitously expressed protein that we named aprataxin. This protein is composed of three domains that share distant homology with the amino-terminal domain of polynucleotide kinase 3'- phosphatase (PNKP), with histidine-triad (HIT) proteins and with DNA-binding C2H2 zinc-finger proteins, respectively. PNKP is involved in DNA single-strand break repair (SSBR) following exposure to ionizing radiation and reactive oxygen species. Fragile-HIT proteins (FHIT) cleave diadenosine tetraphosphate, which is potentially produced during activation of the SSBR complex. The results suggest that aprataxin is a nuclear protein with a role in DNA repair reminiscent of the function of the protein defective in ataxia-telangiectasia, but that would cause a phenotype restricted to neurological signs when mutant.     

A gene encoding a putative GTPase regulator is mutated in familial amyotrophic lateral sclerosis 2

Amyotrophic lateral sclerosis 2 (ALS2) is an autosomal recessive form of juvenile ALS and has been mapped to human chromosome 2q33. Here we report the identification of two independent deletion mutations linked to ALS2 in the coding exons of the new gene ALS2. These deletion mutations result in frameshifts that generate premature stop codons. ALS2 is expressed in various tissues and cells, including neurons throughout the brain and spinal cord, and encodes a protein containing multiple domains that have homology to RanGEF as well as RhoGEF. Deletion mutations are predicted to cause a loss of protein function, providing strong evidence that ALS2 is the causative gene underlying this form of ALS.     

Expression cloning and cDNA sequencing of the Na+/glucose co-transporter

Organic substrates (sugars, amino acids, carboxylic acids and neutrotransmitters) are actively transported into eukaryotic cells by Na+ co-transport. Some of the transport proteins have been identified--for example, intestinal brush border Na+/glucose and Na+/proline transporters and the brain Na+/CI-/GABA transporter--and progress has been made in locating their active sites and probing their conformational states. The archetypical Na+-driven transporter is the intestinal brush border Na+/glucose co-transporter (see ref. 8), and a defect in the co-transporter is the origin of the congenital glucose-galactose malabsorption syndrome. Here we describe cloning of this co-transporter by a method new to membrane proteins. We have sequenced the cloned DNA and have found no homology between the Na+/glucose co-transporter and either the mammalian facilitated glucose carrier or the bacterial sugar transport proteins. This suggests that the mammalian Na+-driven transporter has no evolutionary relationship to the other sugar transporters.     

Development of the Q2 induced contractions in the ductus arteriosus of the guinea-pig

Zusammenfassung Die Wirkung von Sauerstoff und Norepinephrin auf die Kontraktionen des isolierten Ductus arteriosus des Meerschweinchens nimmt mit zunehmendem Alter des Feten bis zur Geburt zu und verschwindet kurze Zeit hernach wieder.

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Supported by grants from USPHS No. HL-05157 and No. HL-5696, American Heart Association No. 69880 and No. 69127 and the Los Angeles County Heart Association No. 437 IG.     

Chlorpromazine causes vesicle population changes in the monoaminergic synapse of the rat caudate nucleus

Summary The population of monoaminergic synaptic vesicles in the rat caudate nucleus remained unchanged or slightly decreased 3 h after chlorpromazine (CP) administration, and clearly increased after 24 h. The diameter of synaptic vesicles became smaller when the vesicles increased. These findings suggest that CP causes presynaptic blocking in part of its actions and leads to a condition in which neural transmission is inactive. In the control animals, population of the vesicles tended to fluctuate following the circadian rhythm.     

Design of an Interpolated Controller for Stabilization of a Plant with Variable Operating Condition

1.INTRODUCTIONDynamicsofalmostallthere4lplantschangeaccordingtotheiroperatingconditions.Todescribethechangeofdynamics,therehavebeenconsideredvariousinterpolationsofanum-berofrepresentativemodelsdefinedatrepresentativeoperatingpoints.OneofthemisalinearinterpolationoftheproperstablecChprimefactorizationsofthetransferfunctionsoftworepresentativemodels[1,2].Forsuchinterpolatedplants,thestabilizationproblemhasbeenstudiedusing"fixed"controller.Ifwecanadaptcontrollerstothechangeofplantdynamics,…     

对14.9MeV中子核反应产生的反冲核能谱的测量

测量了由１４ ．９ Ｍｅ Ｖ 中子入射金属产生的反冲核的能谱．用活化技术测量溅射产额随靶与收集器之间距离的变化,用统一的原子阻止本领公式来计算溅射粒子在空气中的能量损失．溅射粒子的能量分布可由不同距离的溅射产额和能量损失导出．用这种方法第一次测量了 Ｍｇ 、 Ａｌ 、 Ｃｒ 、 Ｆｅ 、 Ｃｏ 、 Ｎｂ 和３１６ 型不锈钢等７ 种样品的８ 种核反应所产生的反冲核的能谱