The validity of obesity based on self-reported weight and height: Implications for population studies

Objective: To validate self‐reported information on weight and height in an adult population and to find a useful algorithm to assess the prevalence of obesity based on self‐reported information. Research Methods and Procedures: This was a cross‐sectional survey consisting of 1703 participants (860 men and 843 women, 30 to 75 years old) conducted in the community of Vara, Sweden, from 2001 to 2003. Self‐reported weight, height, and corresponding BMI were compared with measured data. Obesity was defined as measured BMI ≥ 30 kg/m². Information on education, self‐rated health, smoking habits, and physical activity during leisure time was collected by a self‐administered questionnaire. Results: Mean differences between measured and self‐reported weight were 1.6 kg (95% confidence interval, 1.4; 1.8) in men and 1.8 kg (1.6; 2.0) in women (measured higher), whereas corresponding differences in height were ?0.3 cm (?0.5; ?0.2) in men and ?0.4 cm (?0.5; ?0.2) in women (measured lower). Age and body size were important factors for misreporting height, weight, and BMI in both men and women. Obesity (measured) was found in 156 men (19%) and 184 women (25%) and with self‐reported data in 114 men (14%) and 153 women (20%). For self‐reported data, the sensitivity of obesity was 70% in men and 82% in women, and when adjusted for corrected self‐reported data and age, it increased to 81% and 90%, whereas the specificity decreased from 99% in both sexes to 97% in men and 98% in women. Discussion: The prevalence of obesity based on self‐reported BMI can be estimated more accurately when using an algorithm adjusted for variables that are predictive for misreporting.     

Exposure of neural crest cells to elevated glucose leads to congenital heart defects, an effect that can be prevented by N-acetylcysteine

BACKGROUND: Diabetes mellitus during pregnancy increases the risk for congenital heart disease in the offspring. The majority of the cardiovascular malformations occur in the outflow tract and pharyngeal arch arteries, where neural crest cells are essential for normal development. We studied the effects of specific exposure of neural crest cells to elevated glucose on heart development. Antioxidants reduce the damaging effect of glucose on neural crest cells in vitro; therefore, we investigated the effect of supplementing N-acetylcysteine in vivo. METHODS: Cardiac neural crest of HH 8-12 chicken embryos was directly exposed by a single injection in the neural tube with 30 mM D-glucose (or 30 mM L-glucose as a control). To examine the effect of a reduction in oxidative stress, we added 2 mM N-acetylcysteine to the injected D-glucose. RESULTS: Exposure of neural crest cells to elevated D-glucose-induced congenital heart malformations in 82% of the embryos. In the embryos injected with L-glucose, only 9% developed a heart malformation. As expected, all malformations were located in the outflow tract and pharyngeal arch arteries. The frequency of heart malformations decreased from 82% to 27% when 2 mM N-acetylcysteine was added to the injected D-glucose. CONCLUSIONS: These data are the first to confirm that the vulnerability of neural crest cells to elevated glucose induces congenital heart malformations. The fact that N-acetylcysteine limits the teratogenicity of glucose implies that its damaging effect is mediated by an increase of oxidative stress in the neural crest cells.     

Tomographic molecular imaging and 3D quantification within adult mouse organs

A convenient technology to quantify three-dimensional (3D) morphological features would have widespread applications in biomedical research. Based on combined improvements in sample preparation, tomographic imaging and computational processing, we present a procedure for high-resolution 3D quantification of structures within intact adult mouse organs. Using the nonobese diabetic (NOD) mouse model, we demonstrate a correlation between total islet beta-cell volume and the onset of type-1 diabetes.     

Water availability shapes edaphic and lithic cyanobacterial communities in the Atacama Desert

In the Atacama Desert, cyanobacteria grow on various substrates such as soils (edaphic) and quartz or granitoid stones (lithic). Both edaphic and lithic cyanobacterial communities have been described but no comparison between both communities of the same locality has yet been undertaken. In the present study, we compared both cyanobacterial communities along a precipitation gradient ranging from the arid National Park Pan de Azúcar (PA), which resembles a large fog oasis in the Atacama Desert extending to the semiarid Santa Gracia Natural Reserve (SG) further south, as well as along a precipitation gradient within PA. Various microscopic techniques, as well as culturing and partial 16S rRNA sequencing, were applied to identify 21 cyanobacterial species; the diversity was found to decline as precipitation levels decreased. Additionally, under increasing xeric stress, lithic community species composition showed higher divergence from the surrounding edaphic community, resulting in indigenous hypolithic and chasmoendolithic cyanobacterial communities. We conclude that rain and fog water, respectively, cause contrasting trends regarding cyanobacterial species richness in the edaphic and lithic microhabitats.     

ZMAT3 hypomethylation contributes to early senescence of preadipocytes from healthy first‐degree relatives of type 2 diabetics

Senescence of adipose precursor cells (APC) impairs adipogenesis, contributes to the age‐related subcutaneous adipose tissue (SAT) dysfunction, and increases risk of type 2 diabetes (T2D). First‐degree relatives of T2D individuals (FDR) feature restricted adipogenesis, reflecting the detrimental effects of APC senescence earlier in life and rendering FDR more vulnerable to T2D. Epigenetics may contribute to these abnormalities but the underlying mechanisms remain unclear. In previous methylome comparison in APC from FDR and individuals with no diabetes familiarity (CTRL), ZMAT3 emerged as one of the top‐ranked senescence‐related genes featuring hypomethylation in FDR and associated with T2D risk. Here, we investigated whether and how DNA methylation changes at ZMAT3 promote early APC senescence. APC from FDR individuals revealed increases in multiple senescence markers compared to CTRL. Senescence in these cells was accompanied by ZMAT3 hypomethylation, which caused ZMAT3 upregulation. Demethylation at this gene in CTRL APC led to increased ZMAT3 expression and premature senescence, which were reverted by ZMAT3 siRNA. Furthermore, ZMAT3 overexpression in APC determined senescence and activation of the p53/p21 pathway, as observed in FDR APC. Adipogenesis was also inhibited in ZMAT3‐overexpressing APC. In FDR APC, rescue of ZMAT3 methylation through senolytic exposure simultaneously downregulated ZMAT3 expression and improved adipogenesis. Interestingly, in human SAT, aging and T2D were associated with significantly increased expression of both ZMAT3 and the P53 senescence marker. Thus, DNA hypomethylation causes ZMAT3 upregulation in FDR APC accompanied by acquisition of the senescence phenotype and impaired adipogenesis, which may contribute to FDR predisposition for T2D.     

Distribution, abundance, behavior and metabolism of Periphylla periphylla, a mesopelagic coronate medusa in a Norwegian fjord

The distribution, behavior and metabolism of the mesopelagic jellyfish, Periphylla periphylla (Péron & Lesueur), were investigated in Lurefjorden, Norway. Field studies, conducted in 1998–1999 with plankton nets and a remotely operated vehicle, indicated that 80-90% of the dense (up to 2.5 m^–3) population migrated 200–400 m vertically each day throughout the year. In situ observations with red light revealed that swimming rates and feeding activity varied with age and time of day. Detection of turbulence and contact with surfaces caused this medusa to conceal one or all of its tentacles in the stomach or to shed nematocyst-laden tissue from the tentacles. Stomachs of medusae collected with nets were often full of prey entangled with the sloughed tissue. Stomachs of medusae captured individually with ROV samplers were empty or contained only a few prey in their stomachs (typically, 1–4 copepods Calanus spp. or chaetognaths Eukrohnia hamata Möbius per medusa). Low rates (0.4–5.6 l O₂ mg C^–1 h^–1) of oxygen consumption of P. periphylla suggested that this species was sustained by relatively few (1–34) prey d^–1.     

Immunohistochemical Detection of Induced Expression of Wild-type p53 Tumor Supressor Protein in the Livers of Rats Treated with Diethylnitrosamine

Paraffin sections of formalin-perfused rat livers were stained immunohistochemically for p53. In livers from untreated rats, no p53 expression was observed. p53 expression was induced in a response to treatment with diethylnitrosamine 24h prior to sacrifice. Staining for p53 was localized in the nucleus of perivenous hepatocytes. In serial sections p53-immunopositive areas were found to co-localize with increased expression of TUNEL-positive cells. Without formalin perfusion, the staining for p53 was uneven and often barely detectable. Perfusion with saline prior to formalin resulted in a rapid decrease in the detectability of p53, indicating rapid degradation of this protein under these conditions. We conclude that rapid fixation by formalin perfusion increases the detectability of p53 by immunohistochemical staining. This provides a convenient procedure for studying the response of wild-type p53 in rodent liver. This procedure is also suitable for in situ investigations on the degradation of p53 protein stabilized by DNA damage.     

Genomic rearrangements at the <Emphasis Type="Italic">IGHMBP2</Emphasis> gene locus in two patients with SMARD1

Autosomal recessive spinal muscular atrophy with respiratory distress type 1 (SMARD1) is caused by mutations in the immunoglobulin -binding protein 2 (IGHMBP2) gene. Patients affected by the infantile form of SMARD1 present with early onset respiratory distress. So far, patients with neither juvenile onset nor with larger deletions/rearrangements in IGHMBP2 have been reported. In this study, we investigated one patient with infantile (4 months) and another with juvenile (4.3 years) onset of respiratory distress. Direct sequencing of all exons and flanking intron sequences in both patients revealed a mutation on only one allele. In both patients, we identified genomic rearrangements of the other allele of IGHMBP2 by means of Southern blotting. Putative breakpoints were confirmed by polymerase chain reaction on genomic and cDNA. The patient with juvenile onset had an Alu/Alu mediated rearrangement, which resulted in the loss of ~18.5 kb genomic DNA. At the mRNA level, this caused an in-frame deletion of exons 3–7. The patient with infantile onset had a complex rearrangement with two deletions and an inversion between intron 10 and 14. This rearrangement led to a frameshift at the mRNA level. Our results show that SMARD1 can be caused by genomic rearrangements at the IGHMBP2 gene locus. This may be missed by mere sequence analysis. Additionally, we demonstrate that juvenile onset SMARD1 may also be caused by mutations of IGHMBP2. The complex nature of the genomic rearrangement in the patient with infantile SMARD1 is discussed and a deletion mechanism is proposed.     

Epidermal UV-screening in vascular plants from Svalbard (Norwegian Arctic)

Stratospheric ozone depletion is most pronounced at high latitudes, and the concurring increased UV-B radiation might adversely affect plants from polar areas. However, vascular plants may protect themselves against UV-B radiation by UV-absorbing compounds located in the epidermis. In this 3-year study, epidermal UV-B (_max 314 nm) and UV-A (_max 366 nm) screening was assessed using a fluorescence method in 12 vascular species growing in their natural environment at Svalbard. The potential for acclimation to increased radiation was studied with artificially increased UV-B, simulating 11% ozone depletion. Open-top chambers simulated an increase in temperature of 2–3°C in addition to the UV-B manipulation. Adaxial epidermal UV-B transmittance varied between 1.6 and 11.4%. Artificially increased UV-B radiation and temperature did not consistently influence the epidermal UV-B transmittance in any of the measured species, suggesting that they may not have the potential to increase their epidermal screening, or that the screening is already high enough at the applied UV-B level. We propose that environmental factors other than UV-B radiation may influence epidermal UV-B screening.