Forest tree neighborhoods are structured more by negative conspecific density dependence than by interactions among closely related species

Interactions among neighbors influence the structure of communities of sessile organisms. Closely related species tend to share habitat and resource requirements and to interact with the same mutualists and natural enemies so that the strength of interspecific interactions tends to decrease with evolutionary divergence time. Nevertheless, the degree to which such phylogenetically related ecological interactions structure plant communities remains unclear. Using data from five large mapped forest plots combined with a DNA barcode mega‐phylogeny, we employed an individual‐based approach to assess the collective effects of focal tree size on neighborhood phylogenetic relatedness. Abundance‐weighted average divergence time for all neighbors (ADT_all) and for heterospecific neighbors only (ADT_hetero) were calculated for each individual of canopy tree species. Within local neighborhoods, we found phylogenetic composition changed with focal tree size. Specifically, significant increases in ADT_all with focal tree size were evident at all sites. In contrast, there was no significant change in ADT_hetero with tree size in four of the five sites for both sapling‐sized and all neighbors, even at the smallest neighbourhood scale (0–5 m), suggesting a limited role for phylogeny‐dependent interactions. However, there were inverse relationships between focal tree size and the proportion of heterospecific neighbors belonging to closely related species at some sites, providing evidence for negative phylogenetic density dependence. Overall, our results indicate that negative interaction with conspecifics had a much greater impact on neighborhood assemblages than interactions among closely related species and could contribute to community structure and diversity maintenance in different forest communities.     

Disruption of murine Hexa gene leads to enzymatic deficiency and to neuronal lysosomal storage,similar to that observed in Tay-Sachs disease

Tay-Sachs disease is an autosomal recessive lysosomal storage disease caused by -hexosaminidase A deficiency and leads to death in early childhood. The disease results from mutations in the HEXA gene, which codes for the chain of -hexosaminidase. The catastrophic neurodegenerative progression of the disease is thought to be a consequence of massive neuronal accumulation of G_M2 ganglioside and related glycolipids in the brain and nervous system of the patients. Fuller understanding of the pathogenesis and the development of therapeutic procedures have both suffered from the lack of an animal model. We have used gene targeting in embryonic stem (ES) cells to disrupt the mouse Hexa gene. Mice homozygous for the disrupted allele mimic several biochemical and histological features of human Tay-Sachs disease. Hexa-/-mice displayed a total deficiency of -hexosaminidase A activity, and membranous cytoplasmic inclusions typical of G_M2 gangliosidoses were found in the cytoplasm of their neurons. However, while the number of storage neurons increased with age, it remained low compared with that found in human, and no apparent motor or behavioral disorders could be observed. This suggests that the presence of -hexosaminidase A is not an absolute requirement of ganglioside degradation in mice. These mice should help us to understand several aspects of the disease as well as the physiological functions of hexosaminidase in mice. They should also provide a valuable animal model in which to test new forms of therapy, and in particular gene delivery into the central nervous system.     

Adverse effects of tempol on hidrosaline balance in rats with acute sodium overload

We studied the effects of tempol, an oxygen radical scavenger, on hydrosaline balance in rats with acute sodium overload. Male rats with free access to water were injected with isotonic (control group) or hypertonic saline solution (0.80 mol/l NaCl) either alone (Na group) or with tempol (Na-T group). Hydrosaline balance was determined during a 90 min experimental period. Protein expressions of aquaporin 1 (AQP1), aquaporin 2 (AQP2), angiotensin II (Ang II) and endothelial nitric oxide synthase (eNOS) were measured in renal tissue. Water intake, creatinine clearance, diuresis and natriuresis increased in the Na group. Under conditions of sodium overload, tempol increased plasma sodium and protein levels and increased diuresis, natriuresis and sodium excretion. Tempol also decreased water intake without affecting creatinine clearance. AQP1 and eNOS were increased and Ang II decreased in the renal cortex of the Na group, whereas AQP2 was increased in the renal medulla. Nonglycosylated AQP1 and eNOS were increased further in the renal cortex of the Na-T group, whereas AQP2 was decreased in the renal medulla and was localized mainly in the cell membrane. Moreover, p47-phox immunostaining was increased in the hypothalamus of Na group, and this increase was prevented by tempol. Our findings suggest that tempol causes hypernatremia after acute sodium overload by inhibiting the thirst mechanism and facilitating diuresis, despite increasing renal eNOS expression and natriuresis.     

Timing of valve replacement in chronic aortic regurgitation. A pathophysiological approach

Timing of valve replacement (AVR) in chronic aortic regurgitation remains a difficult problem in clinical practice. When the disease takes a favorable natural course, this may be attributed to excellent compensatory mechanisms - especially an increase in left ventricular end-diastolic volume (LVEDV) in relation to regurgitant volume (RV) - whereas a rapid clinical and hemodynamic deterioration may usually be ascribed to a vicious circle consisting in a marked increase in afterload leading to an increase in LVEDV and so on. 54 patients with aortic regurgitation underwent pre- and postoperative as well as long-term follow-up radionuclide ventriculographic (RNV) studies in order to determine LVEDV and RV and to measure left ventricular ejection fraction (LVEF). These measures were expected to provide information on 'physiologic' LVEDV elevation in relation to RV. Our results indicate that if LVEDV exceeds 300-400 ml there may be an increase in afterload for LV. Factors counteracting this increased afterload (LV hypertrophy, increased diastolic stretching) will eventually preserve LVEF and keep LVEDV/RV within the normal range, but are accompanied by an elevation of LV filling pressure leading to dyspnea on exertion. With an LVEDV exceeding 400-500 ml these factors generally cannot prevent the initiation of the above mentioned vicious circle. Hence, in these severely symptomatic cases LVEDV/RV exceeds the normal range and LVEF becomes markedly depressed. An unfavorable postoperative result must be expected in these patients, while the postoperative result will be good in cases with an LVEDV/RV within the normal range. Hence, we conclude that AVR should ideally be performed in those patients with an EDV exceeding 300 ml, who still have an LVEDV/RV within the normal range, but who show clinical symptoms and/or an only moderately depressed LVEF, indicating that the limits of the compensatory mechanism are reached. The indications for AVR in other conditions characterized by the clinical status, the level of the LVEDV and LVEDV/RV are discussed.     

A gene that encodes a protein consisting solely of zinc finger domains is preferentially expressed in transformed mouse cells.

We describe the cloning and characterization of the mouse MOK-2 gene, a new member of the Krüppel family of zinc finger proteins. Sequencing of both cDNA and genomic clones showed that the predicted MOK-2 protein consists of seven zinc finger domains with only five additional amino acids. The finger domains of MOK-2 are highly homologous to one another but not to those of other zinc finger proteins. MOK-2 is preferentially expressed in transformed cell lines, brain tissue, and testis tissue. Its possible role in cellular transformation is discussed.     

Effect of tunicamycin and cycloheximide on the secretion of acid hydrolases from I-cell cultured fibroblasts.

I-cell cultures fibroblasts secrete excessive amounts of N-acetyl-beta-D-hexosaminidase and alpha-L-fucosidase into the culture media as compared with normal fibroblasts. Addition of tunicamycin or cyd [14C]leucine (40--50%) into trichloroacetic acid-precipitable material decreased the secretion of these I-cell hydrolases to normal values within 24 h, but had no effect on the secretion of acid hydrolases from normal fibroblasts. These results indicate that I-cell cultured fibroblasts secrete at least two types of acid hydrolases: one is tunicamycin- and cycloheximide-sensitive and constitutes the greater proportion of the secreted hydrolases, and a smaller proportion is insensitive to tunicamycin and cycloheximide, similar t9 the acid hydrolases secreted by normal cultured fibroblasts.     

Ergebnisse von Untersuchungen an kurzbehaarten und kleinsamigen Mutanten vonLupinus Luteus

Ohne ZusammenfassungMit I Textabbildung