Tropical forests are thermally buffered despite intensive selective logging

Tropical rainforests are subject to extensive degradation by commercial selective logging. Despite pervasive changes to forest structure, selectively logged forests represent vital refugia for global biodiversity. The ability of these forests to buffer temperature‐sensitive species from climate warming will be an important determinant of their future conservation value, although this topic remains largely unexplored. Thermal buffering potential is broadly determined by: (i) the difference between the “macroclimate” (climate at a local scale, m to ha) and the “microclimate” (climate at a fine‐scale, mm to m, that is distinct from the macroclimate); (ii) thermal stability of microclimates (e.g. variation in daily temperatures); and (iii) the availability of microclimates to organisms. We compared these metrics in undisturbed primary forest and intensively logged forest on Borneo, using thermal images to capture cool microclimates on the surface of the forest floor, and information from dataloggers placed inside deadwood, tree holes and leaf litter. Although major differences in forest structure remained 9–12 years after repeated selective logging, we found that logging activity had very little effect on thermal buffering, in terms of macroclimate and microclimate temperatures, and the overall availability of microclimates. For 1°C warming in the macroclimate, temperature inside deadwood, tree holes and leaf litter warmed slightly more in primary forest than in logged forest, but the effect amounted to <0.1°C difference between forest types. We therefore conclude that selectively logged forests are similar to primary forests in their potential for thermal buffering, and subsequent ability to retain temperature‐sensitive species under climate change. Selectively logged forests can play a crucial role in the long‐term maintenance of global biodiversity.     

Restriction fragment length polymorphism analysis and direct sequencing for determination of HBV genotypes in a Turkish population

The aim of this study was to analyze the restriction fragment length polymorphism and direct sequencing results in genotyping of hepatitis B virus from a Turkish population in a clinical virology laboratory. Serum samples of 54 chronic hepatitis B patients attending the Ege University Hospital were studied. Sequences of partial S gene PCR products were analysed and RFLP was performed. Fifty-three isolates could be identified by direct sequencing as genotype D. One sample needed to be cloned and determined as genotype D. Forty-two isolates were genotyped as D with RFLP according to published determinative patterns. Twelve isolates had undefined patterns. Eight of them suggested a mixture of isolates with different patterns and cloning of these samples confirmed the presence of heterogeneous isolates. Four isolates with undefined pattern were determined as genotype D by direct sequencing. All the studied isolates were genotype D. The results of this studied population suggest that RFLP is suitable for HBV genotyping in a routine clinical virology laboratory setting. However sequence analysis and even cloning may be needed to clarify indeterminate results.     

Craniosynostosis and maternal smoking

BACKGROUND: Several previous studies suggested increased risk of craniosynostosis among infants born to women who smoked. METHODS: This study used data from the National Birth Defects Prevention Study, a multi‐state, population‐based case‐control study of infants delivered from 1997–2003. Nonmalformed, liveborn controls were selected randomly from birth certificates or birth hospitals. Data from maternal telephone interviews were available for 531 cases and 5008 controls. RESULTS: Smoking during the first month of pregnancy was not associated with craniosynostosis. Smoking later in pregnancy was associated with increased risk, but only among mothers who smoked at least one pack/day. For example, during the second trimester, the odds ratio for smoking <5 cigarettes/day was 1.0 (95% confidence interval [CI] 0.6, 1.8), but the odds ratio (OR) for smoking 15 or more cigarettes/day was 1.6 (95% CI 0.9, 2.8), after adjustment for maternal age, education, race‐ethnicity, sub‐fertility, parity, folic acid supplement intake, body mass index, and study center. Among women who did not smoke, adjusted odds ratios suggested that secondhand smoke exposure at home, but not at work/school, was associated with modestly increased risk; the OR for home exposure was 1.3 (95% CI 0.9, 1.9). Results followed a similar pattern for some, but not all, specific suture types, but numbers for some groupings were small. CONCLUSIONS: The results suggest moderately increased risk of craniosynostosis among mothers who were the heaviest smokers and who continued to smoke after the first trimester. Results are somewhat equivocal, given that most confidence intervals included one. Birth Defects Research (Part A), 2008. © 2007 Wiley‐Liss, Inc.     

Nutrient intakes in women and congenital diaphragmatic hernia in their offspring

BACKGROUND: Congenital diaphragmatic hernia (CDH) is a severe birth defect where there is an opening in the diaphragm through which a portion of the abdominal contents protrudes into the thoracic cavity. The etiologies of CDH remain unknown, although experimental animal data suggest dietary factors might play a role. This study examined whether maternal nutrient intakes were associated with delivering infants with CDH. METHODS: We analyzed infants with isolated CDH who were born from 1997 to 2003 and recruited into the National Birth Defects Prevention Study (NBDPS), a multisite, population‐based case‐control study. Exposure data were obtained from telephone interviews, which were completed within 24 months after delivery, and were available for 377 case mothers and 5,008 control mothers. A food frequency questionnaire was used to derive nutrient intakes during the year before pregnancy. RESULTS: A crude OR of 0.6 (95% CI: 0.3–1.0) was observed for higher intake of choline. Elevated ORs (1.4 to 1.7) were found for lower intakes of choline, cysteine, methionine, and protein. Among women who took vitamin supplements, higher intakes of B vitamins (i.e., folate, vitamin B1, B2, B6, and B12), minerals (i.e., calcium, iron, magnesium, and zinc), and vitamin E were inversely associated with CDH (ORs from 0.7–0.3). Moreover, among women who did not take vitamin supplements, lower intakes of calcium, retinol, selenium, vitamin B12, and vitamin E had positive associations with CDH (ORs from 1.4 to 2.1). CONCLUSIONS: Our observations contribute to a limited body of evidence suggesting a woman's periconceptional diet might be associated with CDH in her offspring. Birth Defects Research (Part A), 2008. © 2007 Wiley‐Liss, Inc.     

The recent evolution of a pseudogene: diversity and divergence of a mitochondria-localized small heat shock protein in Arabidopsis thaliana

In this study we examined the evolution of the genes for three organelle-localized small heat shock proteins in Arabidopsis thaliana: the chloroplast-localized (CP) protein HSP21 and two mitochondria-localized (MT) proteins, HSP23.5 and HSP23.6. We found that the CP protein and one of the MT proteins, HSP23.6, are evolving under purifying selection to maintain function. In contrast, the gene for HSP23.5, the other MT protein, is highly variable within A. thaliana, and in some accessions or ecotypes this gene may be a pseudogene. HSP23.5 and HSP23.6 are related via a segmental duplication event, and the presence of orthologs of each gene in other species within the Brassicaceae indicates that the duplication generating HSP23.5 and HSP23.6 may have occurred as much as 20 million years ago. This is considerably longer than the 4 million year half-life of gene duplicates (functional genes as well as pseudogenes) reported by some studies. Our results are consistent with the prediction that after gene duplication one gene duplicate can be maintained for some time under relaxed selection while it accumulates random mutations. By capturing a pseudogene in the making our study provides important information on how pseudogenes are formed.     

A mutation in the ProteosomalRegulatory Particle AAA-ATPase-3 in Arabidopsis impairs the light-specific hypocotyl elongation response elicited by a glutamate receptor agonist, BMAA

BMAA is a cycad-derived glutamate receptor agonist that causes a two- to three-fold increase in hypocotyl elongation on Arabidopsis seedlings grown in the light. To probe the role of plant glutamate receptors and their downstream mediators, we utilized a previously described genetic screen to identify a novel, BMAA insensitive morphology (bim) mutant, bim409. The normal BMAA-induced hypocotyl elongation response observed on wild-type seedlings grown in the light is impaired in the bim409 mutant. This BMAA-induced phenotype is light-specific, as the bim409 mutant exhibits normal hypocotyl elongation in etiolated (dark grown) plants (+ or − BMAA). The mutation in bim409 was identified to be in a gene encoding the Proteosomal Regulatory Particle AAA-ATPase-3 (RPT3). Possible roles of the proteosome in Glu-mediated signaling in plants is discussed. Electronic supplementary material  The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Non-hypoxic activation of the negative regulatory feedback loop of prolyl-hydroxylase oxygen sensors

Hypoxia inducible factors (HIF) coordinate cellular responses towards hypoxia. HIFs are mainly regulated by a group of prolyl-hydroxylases (PHDs) that in the presence of oxygen, target the HIFα subunit for degradation. Herein, we studied the role of nitric oxide (NO) in regulating PHD activities under normoxic conditions. In the present study we show that different NO-donors initially inhibited endogenous PHD2 activity which led to accumulation of HIF-1α subsequently to enhance HIF-1 dependent increased PHD2 promoter activity. Consequently PHD2 abundance and activity were strongly induced which caused downregulation of HIF-1α. Interestingly, upregulation of endogenous PHD2 activity by NO was not found in cells that lack an intact pVHL dependent degradation pathway. Recovery of PHD activity required intact cells and was not observed in cell extracts or recombinant PHD2. In conclusion induction of endogenous PHD2 activity by NO is dependent on a feedback loop initiated despite normoxic conditions.     

Functional basis for complement evasion by staphylococcal superantigen‐like 7

The human pathogen Staphylococcus aureus has a plethora of virulence factors that promote its colonization and survival in the host. Among such immune modulators are staphylococcal superantigen‐like (SSL) proteins, comprising a family of 14 small, secreted molecules that seem to interfere with the host innate immune system. SSL7 has been described to bind immunoglobulin A (IgA) and complement C5, thereby inhibiting IgA‐FcαRI binding and serum killing of Escherichia coli. As C5a generation, in contrast to C5b‐9‐mediated lysis, is crucial for immune defence against staphylococci, we investigated the impact of SSL7 on staphylococcal‐induced C5a‐mediated effects. Here, we show that SSL7 inhibits C5a generation induced by staphylococcal opsonization, slightly enhanced by its IgA‐binding capacity. Moreover, we demonstrate a strong protective activity of SSL7 against staphylococcal clearance in human whole blood. SSL7 strongly inhibited the C5a‐induced phagocytosis of S. aureus and oxidative burst in an in vitro whole‐blood inflammation model. Furthermore, we found that SSL7 affects all three pathways of complement activation and inhibits the cleavage of C5 by interference of its binding to C5 convertases. Finally, SSL7 effects were also demonstrated in vivo. In a murine model of immune complex peritonitis, SSL7 abrogated the C5a‐driven influx of neutrophils in mouse peritoneum.     

C. elegans MCM-4 is a general DNA replication and checkpoint component with an epidermis-specific requirement for growth and viability

DNA replication and its connection to M phase restraint are studied extensively at the level of single cells but rarely in the context of a developing animal. C. elegans lin-6 mutants lack DNA synthesis in postembryonic somatic cell lineages, while entry into mitosis continues. These mutants grow slowly and either die during larval development or develop into sterile adults. We found that lin-6 corresponds to mcm-4 and encodes an evolutionarily conserved component of the MCM2-7 pre-RC and replicative helicase complex. The MCM-4 protein is expressed in all dividing cells during embryonic and postembryonic development and associates with chromatin in late anaphase. Induction of cell cycle entry and differentiation continues in developing mcm-4 larvae, even in cells that went through abortive division. In contrast to somatic cells in mcm-4 mutants, the gonad continues DNA replication and cell division until late larval development. Expression of MCM-4 in the epidermis (also known as hypodermis) is sufficient to rescue the growth retardation and lethality of mcm-4 mutants. While the somatic gonad and germline show substantial ability to cope with lack of zygotic mcm-4 function, mcm-4 is specifically required in the epidermis for growth and survival of the whole organism. Thus, C. elegans mcm-4 has conserved functions in DNA replication and replication checkpoint control but also shows unexpected tissue-specific requirements.     

Raloxifene attenuates Gas6 and apoptosis in experimental aortic valve disease in renal failure

Renal failure is associated with aortic valve calcification. Using our rat model of uremia-induced reversible aortic valve calcification, we assessed the role of apoptosis and survival pathways in that disease. We also explored the effects of raloxifene, an estrogen receptor modulator, on valvular calcification. Gene array analysis was performed in aortic valves obtained from three groups of rats (n = 7 rats/group): calcified valves obtained from rats fed with uremic diet, valves after calcification resolution following diet cessation, and control. In addition, four groups of rats (n = 10 rats/group) were used to evaluate the effect of raloxifene in aortic valve calcification: three groups as mentioned above and a fourth group fed with the uremic diet that also received daily raloxifene. Evaluation included imaging, histology, and antigen expression analysis. Gene array results showed that the majority of the altered expressed genes were in diet group valves. Most apoptosis-related genes were changed in a proapoptotic direction in calcified valves. Apoptosis and decreases in several survival pathways were confirmed in calcified valves. Resolution of aortic valve calcification was accompanied by decreased apoptosis and upregulation of survival pathways. Imaging and histology demonstrated that raloxifene significantly decreased aortic valve calcification. In conclusion, downregulation of several survival pathways and apoptosis are involved in the pathogenesis of aortic valve calcification. The beneficial effect of raloxifene in valve calcification is related to apoptosis modulation. This novel observation is important for developing remedies for aortic valve calcification in patients with renal failure.