The effect of camphor on mitochondrial respiration

Summary Camphor at <8 moles/mg protein reduced the rate of oxygen consumption by rat liver mitochondria. The effect occurs only with NAD⁺-linked substrates. Succinate linked respiration was inhibited but this appears to be caused by some conversion of succinate to malate. At higher levels, camphor increases oxygen consumption with succinate substrate, by uncoupling at site II.Acknowledgment. D.F.G.-C. is grateful to the New Zealand Cancer Society (Wellington Branch), for financial support. We thank Mrs E. Dye for technical assistance and Dr W. Jordan for valuable discussions.     

氡及其子体对肺以外的组织器官是否有危险

吸入氡子体有致肺癌的危险是辐射防护界公认健康效应之一.文章总结了氡子体致肺癌的流行病调查结果.本文还给出了氡及其子体对其他组织器官所致剂量的计算结果,这些结果可用于评价氡及其子体对身体其他部分的可能危险.跟致肺癌的情况不一样,缺乏其他组织器官假设危害的流行病学调查结果.沉积到皮肤上的氡子体致皮癌的危险和溶于饮水中氡所致胃癌的危险没有过估,但其他危害好象不大.     

Identification of two related pentapeptides from the brain with potent opiate agonist activity.

Enkephalin, a natural ligand for opiate receptors is composed of the pentapepides H-Tyr-Gly-Gly-Phe-Met-OH and H-Tyr-Gly-Gly-Phe-Leu-OH. The evidence is based on the determination of the amino acid sequence of natural enkephalin by the dansyl-Edman procedure and by mass spectrometry followed by synthesis and comparison of the natural and synthetic peptides.     

Does Kant have a pre-Newtonian picture of force in the balance argument? An account of how the balance argument works

In this paper, I discuss whether the Metaphysical Foundations of Natural Science version of Kant’s argument that space-filling matter requires both attractive and repulsive forces betrays a pre-Newtonian picture of forces as Warren (2010) argues. More generally, I discuss Kant’s overall strategy for securing the possibility of space-filling matter and I describe what motivates Kant to think of the argument in the way, I believe, he does. Ultimately, I argue that Kant’s argument does not suggest a pre-Newtonian picture of forces. Along the way, I discuss the status of quantity of matter and the nature of forces in the Dynamics chapter of that work so as to better clarify what is at work in the balance argument.     

Causes of oxidative stress in Alzheimer disease

Oxidative stress is one of the earliest events of Alzheimer disease (AD), with implications as an important mediator in the onset, progression and pathogenesis of the disease. The generation of reactive oxygen species (ROS) and its consequent cellular damage/response contributes to much of the hallmark AD pathology seen in susceptible neurons. The sources of ROS-mediated damage appear to be multi-faceted in AD, with interactions between abnormal mitochondria, redox transition metals, and other factors. In this review, we provide an overview of these potential causes of oxidative stress in AD.     

A common variant of HMGA2 is associated with adult and childhood height in the general population

Human height is a classic, highly heritable quantitative trait. To begin to identify genetic variants influencing height, we examined genome-wide association data from 4,921 individuals. Common variants in the HMGA2 oncogene, exemplified by rs1042725, were associated with height (P = 4 x 10(-8)). HMGA2 is also a strong biological candidate for height, as rare, severe mutations in this gene alter body size in mice and humans, so we tested rs1042725 in additional samples. We confirmed the association in 19,064 adults from four further studies (P = 3 x 10(-11), overall P = 4 x 10(-16), including the genome-wide association data). We also observed the association in children (P = 1 x 10(-6), N = 6,827) and a tall/short case-control study (P = 4 x 10(-6), N = 3,207). We estimate that rs1042725 explains approximately 0.3% of population variation in height (approximately 0.4 cm increased adult height per C allele). There are few examples of common genetic variants reproducibly associated with human quantitativetraits; these results represent, to our knowledge, the first consistently replicated association with adult and childhood height.     

Prolyl 3-hydroxylase 1 deficiency causes a recessive metabolic bone disorder resembling lethal/severe osteogenesis imperfecta

A recessive form of severe osteogenesis imperfecta that is not caused by mutations in type I collagen has long been suspected. Mutations in human CRTAP (cartilage-associated protein) causing recessive bone disease have been reported. CRTAP forms a complex with cyclophilin B and prolyl 3-hydroxylase 1, which is encoded by LEPRE1 and hydroxylates one residue in type I collagen, alpha1(I)Pro986. We present the first five cases of a new recessive bone disorder resulting from null LEPRE1 alleles; its phenotype overlaps with lethal/severe osteogenesis imperfecta but has distinctive features. Furthermore, a mutant allele from West Africa, also found in African Americans, occurs in four of five cases. All proband LEPRE1 mutations led to premature termination codons and minimal mRNA and protein. Proband collagen had minimal 3-hydroxylation of alpha1(I)Pro986 but excess lysyl hydroxylation and glycosylation along the collagen helix. Proband collagen secretion was moderately delayed, but total collagen secretion was increased. Prolyl 3-hydroxylase 1 is therefore crucial for bone development and collagen helix formation.