SERUM LIPIDS IN NORMAL AND ABNORMAL SUBJECTS—Observations on Controlled Experiments

The relationship of diet to serum lipids and to atherosclerosis is a controversial subject. The data presented indicate that diets containing very large amounts of vegetable fat are consistently associated with a sharp fall in serum cholesterol and phospholipid, whereas administration of equal amounts of fat of animal origin is associated with a rise of the serum lipids to levels noted on an average mixed diet.In critical evaluation of elderly hospitalized diabetic patients with advanced atherosclerosis it was observed that there was close mathematical correlation between serum content of cholesterol, “lipoproteins,” and phospholipids. There was no obvious correlation between the degree or kind of atherosclerosis and any one of the lipid entities followed. Coronary occlusion occurred in a patient with one of the lowest levels of cholesterol and of lipoprotein.     

Mutations Causing Constitutive Invertase Synthesis in Yeast: Genetic Interactions with snf Mutations

We have selected 210 mutants able to grow on sucrose in the presence of 2-deoxyglucose. We identified recessive mutations in three major complementation groups that cause constitutive (glucose-insensitive) secreted invertase synthesis. Two groups comprise alleles of the previously identified HXK2 and REG1 genes, and the third group was designated cid1 (constitutive invertase derepression). The effect of cid1 on SUC2 expression is mediated by the SUC2 upstream regulatory region, as judged by the constitutive expression of a SUC2-LEU2-lacZ fusion in which the LEU2 promoter is under control of SUC2 upstream sequences. A cid1 mutation also causes glucose-insensitive expression of maltase. The previously isolated constitutive mutation ssn6 is epistatic to cid1, reg1 and hxk2 for very high level constitutive invertase expression. Mutations in SNF genes that prevent derepression of invertase are epistatic to cid1, reg1 and hxk2; we have previously shown that ssn6 has different epistasis relationships with snf mutations. The constitutive mutation tup1 was found to resemble ssn6 in its genetic interactions with snf mutations. These findings suggest that CID1, REG1 and HXK2 are functionally distinct from SSN6 and TUP1.     

Suppressors of snf2 Mutations Restore Invertase Derepression and Cause Temperature-Sensitive Lethality in Yeast

Mutations in the SNF2 gene of Saccharomyces cerevisiae prevent derepression of the SUC2 (invertase) gene, and other glucose-repressible genes, in response to glucose deprivation. We have isolated 25 partial phenotypic revertants of a snf2 mutant that are able to derepress secreted invertase. These revertants all carried suppressor mutations at a single locus, designated SSN20 (suppressor of snf2). Alleles with dominant, partially dominant and recessive suppressor phenotypes were recovered, but all were only partial suppressors of snf2, reversing the defect in invertase synthesis but not other defects. All alleles also caused recessive, temperature-sensitive lethality and a recessive defect in galactose utilization, regardless of the SNF2 genotype. No significant effect on SUC2 expression was detected in a wild-type (SNF2) genetic background. The ssn20 mutations also suppressed the defects in invertase derepression caused by snf5 and snf6 mutations, and selection for invertase-producing revertants of snf5 mutants yielded only additional ssn20 alleles. These findings suggest that the roles of the SNF2, SNF5 and SNF6 genes in regulation of SUC2 are functionally related and that SSN20 plays a role in expression of a variety of yeast genes.     

On the usage and measurement of landscape connectivity

This paper examines the usage and measurement of "landscape connectivity" in 33 recent studies. Connectivity is defined as the degree to which a landscape facilitates or impedes movement of organisms among resource patches. However, connectivity is actually used in a variety of ways in the literature. This has led to confusion and lack of clarity related to (1) function vs structure, (2) patch isolation vs landscape connectivity and, (3) corridors vs connectivity. We suggest the term connectivity should be reserved for its original purpose. We highlight nine studies; these include modeling studies that actually measured connectivity in accordance with the definition, and empirical studies that measured key components of connectivity. We found that measurements of connectivity provide results that can be interpreted as recommending habitat fragmentation to enhance landscape connectivity. We discuss reasons for this misleading conclusion, and suggest a new way of quantifying connectivity, which avoids this problem. We also recommend a method for reducing sampling intensity in landscape-scale empirical studies of connectivity.     

Genetic mode of action of cocarcinogens and tumor promoters in yeast and mice

Summary In experiments with yeast, cocarcinogens were found to be comutagenic and antirecombinogenic, tumor promoters to be corecombinogenic and antimutagenic. Substances that were cocarcinogens as well as tumor promoters had an intermediary effect. These results were confirmed in the mammalian spot test: By in vivo treatment of mice with the cocarcinogen catechol and the tumor promoter limonene carcinogen-induced recombination due to mitotic crossing over and gene mutations was reduced and enhanced, respectively.Our results support the hypothesis that mutagenesis is the mechanism by which chemicals induce malignancy, and that cocarcinogens modify the process by enhancement of mutagenicity whereas tumor promoters effect carcinogenesis by increase of the spontaneous frequency of recombination. In addition, induced mitotic recombination in mammals in vivo has been demonstrated for the first time.Dedicated to Prof. Dr. H. Remmer (Tübingen) on the occasion of his 65th birthday     

Mental Ill Health,Recovery and the Family Assemblage

The recovery approach is now among the most influential paradigms shaping mental health policy and practice across the English-speaking world. While recovery is normally presented as a deeply personal process, critics have challenged the individualism underpinning this view. A growing literature on “family recovery” explores the ways in which people, especially parents with mental ill health, can find it impossible to separate their own recovery experiences from the processes of family life. While sympathetic to this literature, we argue that it remains limited by its anthropocentricity, and therefore struggles to account for the varied human and nonhuman entities and forces involved in the creation and maintenance of family life. The current analysis is based on an ethnographic study conducted in Australia, which focused on families in which the father experiences mental ill health. We employ the emerging concept of the “family assemblage” to explore how the material, social, discursive and affective components of family life enabled and impeded these fathers’ recovery trajectories. Viewing families as heterogeneous assemblages allows for novel insights into some of the most basic aspects of recovery, challenging existing conceptions of the roles and significance of emotion, identity and agency in the family recovery process.