Stress plays a role in the association between cognitive constructs and measures of eating disorders in male subjects.

OBJECTIVE: Several theorists have hypothesized that stressful situations may trigger abnormal eating and even eating disorders in predisposed people. The purpose of this study was to assess whether a stressful situation would reveal an association between perfectionism and low self-esteem, and measures of eating disorder symptoms in male high school students. METHOD: A sample of 61 male high school students completed the Eating Disorder Inventory, the Multidimensional Perfectionism Scale, and the Self Liking and Competence Scale three times: on an average school day, on the day of an exam and on the day the subjects received the results of that exam. Linear regression analysis was carried out to verify whether the dimensions of perfectionism were associated with the measures of eating disorders. RESULTS: Interoceptive awareness was associated with 'Bulimia' only during the stressful situation and with 'Drive for thinness' both in stress and non stress situations. Other results were contradictory and difficult to interpret. DISCUSSION: The results suggest that in nonclinical male individuals stress might bring out a previously absent association between some psychological predisposing factors for eating disorders and an actual desire or plan for ED related thoughts and behaviours. Such a finding suggests that stress may stimulate behaviours related to eating disorders in a predisposed personality. A central role may be played by interoceptive awareness in male subjects.

Comparative analysis of the Borrelia garinii genome.

Three members of the genus Borrelia (B.burgdorferi, B.garinii, B.afzelii) cause tick-borne borreliosis. Depending on the Borrelia species involved, the borreliosis differs in its clinical symptoms. Comparative genomics opens up a way to elucidate the underlying differences in Borrelia species. We analysed a low redundancy whole-genome shotgun (WGS) assembly of a B.garinii strain isolated from a patient with neuroborreliosis in comparison to the B.burgdorferi genome. This analysis reveals that most of the chromosome is conserved (92.7% identity on DNA as well as on amino acid level) in the two species, and no chromosomal rearrangement or larger insertions/deletions could be observed. Furthermore, two collinear plasmids (lp54 and cp26) seem to belong to the basic genome inventory of Borrelia species. These three collinear parts of the Borrelia genome encode 861 genes, which are orthologous in the two species examined. The majority of the genetic information of the other plasmids of B.burgdorferii is also present in B.garinii although orthology is not easy to define due to a high redundancy of the plasmid fraction. Yet, we did not find counterparts of the B.burgdorferi plasmids lp36 and lp38 or their respective gene repertoire in the B.garinii genome. Thus, phenotypic differences between the two species could be attributable to the presence or absence of these two plasmids as well as to the potentially positively selected genes.

Connexin genes in the mouse and human genome.

Gap junctions serve for direct intercellular communication by docking of two hemichannels in adjacent cells thereby forming conduits between the cytoplasmic compartments of adjacent cells. Connexin genes code for subunit proteins of gap junction channels and are members of large gene families in mammals. So far, 17 connexin (Cx) genes have been described and characterized in the murine genome. For most of them, orthologues in the human genome have been found (see White and Paul 1999; Manthey et al. 1999; Teubner et al. 2001; Söhl et al. 2001). We have recently performed searches for connexin genes in murine and human gene libraries available at EMBL/Heidelberg, NCBI and the Celera company that have increased the number of identified connexins to 19 in mouse and 20 in humans. For one mouse connexin gene and two human connexin genes we did not find orthologues in the other genome. Here we present a short overview on distinct connexin genes which we found in the mouse and human genome and which may include all members of this gene family, if no further connexin gene will be discovered in the remaining non-sequenced parts (about 1-5%) of the genomes.

Lack of phenobarbital-mediated promotion of hepatocarcinogenesis in connexin32-null mice.

Connexin32 (Cx32) is the major gap junction forming protein in liver. We have recently shown that hepatocarcinogenesis is strongly enhanced in mice deficient in Cx32, demonstrating that lack of functional Cx32 accelerates liver tumorigenesis. Many tumor-promoting agents, including phenobarbital, block gap junctional intercellular communication in vitro, and it has been suggested that this effect is relevant for clonal expansion of neoplastic cells in vivo. We have now tested this hypothesis by analyzing the potency of phenobarbital as a liver tumor promoter in male Cx32-wild-type (Cx32(Y/+)) and Cx32-null (Cx32(Y/-)) mice. Preneoplastic and neoplastic liver lesions were induced in 6-week-old male mice by a single injection of 90 microg/g body weight of N-nitrosodiethylamine, and groups of mice were subsequently kept on phenobarbital-containing (0.05%) or control diet for 39 weeks. Frozen liver sections were prepared, and (pre)neoplastic lesions were identified by their deficiency in glucose-6-phosphatase staining. In addition, the number and size of macroscopically visible tumors were monitored. Phenobarbital led to a approximately 5-fold increase in the volume fraction occupied by glucose-6-phosphatase-deficient liver lesions in Cx32(Y/+) mice, whereas there was no such increase in Cx32(Y/-) mice. Even more pronounced differences were observed with respect to tumor response. Whereas phenobarbital clearly promoted the occurrence of numerous large hepatomas in Cx32(Y/+) mice, no such effect was seen in Cx32(Y/-) mice. These results demonstrate, for the first time, that functional Cx32 protein is required for tumor promotion by phenobarbital.

The "Kergin pneumonectomy".

Out of a series of 211 stage III (A and B) lung cancers radically resected with routine lymphadenectomy from 1971 to 1987, a total of 11 were squamous cell carcinomas invading the right main bronchus and lateral portion of the trachea. These patients were managed using a particular technique that we have always arbitrarily called, "Kergin pneumonectomy," after the Toronto surgeon who described it in 1952. These patients, today, are staged III B. There was no operative mortality and only 2 minor complications. Two patients survived 3 years and 1 is alive and free of disease 7 years from surgery. This technique should be considered before embarking on more perilous surgery such as "sleeve pneumonectomy," a procedure which still carries high mortality and morbidity rates and requires special equipment and intensive postoperative care.