Bold colouration pattern in southern bottlenose whales, a preliminary assessment of external variation. Scientific Committee document SC/57/SM12, International Whaling Commission, May-June 2005, Ulsan, Korea

Insights in the variation in pigmentation patterns and other external features in Hyperoodon planifrons are few, in particular, variability contributed by each of individual, ontogenetic, sexual, and geographic factors. A preliminary assessment is based on two close-up sightings of juveniles during IWC-SOWER Cruises and stranded specimens from South Africa, Australia and New Zealand. Bold, cream-white facial fields separated by a distinct dark blowhole stripe are diagnostic of all juvenile/neonates examined and may persist in subadults. Dark eyepatches may be pronounced or almost absent, a light nuchal band behind the blowhole may be prominent or muted, and the dorsal aspect of flippers may be light or dark. A light flank patch on the tailstock is consistent in juveniles. With maturation the head pattern gradually blurs, apparently because facial fields and the nuchal band gain pigmentation. The slate-grey or dark brownish-grey spinal field in juveniles is appreciably darker than in most adults, in which it varies widely, ranging from brownish-grey (most common), bluish-black to yellowish. Diatoms have been blamed as cause for the brown hue, however the evidence is unclear. Large, almost-white animals have been reported but no such specimens were available for study. Much of the external variation seen may be individual and ontogenetic, however sexual dimorphism and geographic variation remain unassessed due to small samples. A comprehensive morphological study is indicated. The bold features in juvenile H. planifrons are diagnostically distinct from juvenile Tasmacetus shepherdi and Indopacetus pacificus. Non-priority status and long dive durations have allowed scant time for data collection on H. planifrons during Antarctic surveys. This study shows that maximizing opportunistic encounters through allowance for some flexibility in schedules, valuable data can be obtained. A rule-of-thumb is recommended for avoiding ziphiid species identification at distances exceeding 0.8 nmiles

Endogenous transforming growth factor β1 suppresses inflammation and promotes survival in adult CNS

Transforming growth factor β1 (TGFβ1) is a pleiotropic cytokine with potent neurotrophic and immunosuppressive properties that is upregulated after injury, but also expressed in the normal nervous system. In the current study, we examined the regulation of TGFβ1 and the effects of TGFβ1 deletion on cellular response in the uninjured adult brain and in the injured and regenerating facial motor nucleus. To avoid lethal autoimmune inflammation within 3 weeks after birth in TGFβ1-deficient mice, this study was performed on a T- and B-cell-deficient RAG2-/- background. Compared with wild-type siblings, homozygous deletion of TGFβ1 resulted in an extensive inflammatory response in otherwise uninjured brain parenchyma. Astrocytes increased in GFAP and CD44 immunoreactivity; microglia showed proliferative activity, expression of phagocytosis-associated markers [αXβ2, B7.2, and MHC1 (major histocompatibility complex type 1)], and reduced branching. Ultrastructural analysis revealed focal blockade of axonal transport, perinodal damming of axonal organelles, focal demyelination, and myelin debris in granule-rich, phagocytic microglia. After facial axotomy, absence of TGFβ1 led to a fourfold increase in neuronal cell death (52 vs 13%), decreased central axonal sprouting, and significant delay in functional recovery. It also interfered with the microglial response, resulting in a diminished expression of early activation markers [ICAM1 (intercellular adhesion molecule 1), α6β1, and αMβ2] and reduced proliferation. In line with axonal and glial findings in the otherwise uninjured CNS, absence of endogenous TGFβ1 also caused an ∼10% reduction in the number of normal motoneurons, pointing to an ongoing and potent trophic role of this anti-inflammatory cytokine in the normal as well as in the injured brain. Copyright © 2007 Society for Neuroscience

2004-2005 International Whaling Commission-Southern Ocean Whale and Ecosystem Research (IWC-SOWER) Cruise, Area III

We conducted the 27th annual IWC-SOWER (formerly IDCR) Cruise in Area III (000°-070°E) aboard the Japanese Research Vessels Shonan Maru and Shonan Maru No.2. The 65-day cruise departed Cape Town, South Africa on 4 January 2005 and returned to Fremantle, Australia on 9 March 2005. After transiting to the study area, we carried out a minke whale survey and several research experiments from 12 January to 25 February. A systematic minke whale survey was conducted in Area IIIW (000°-035°E) from 12 January until 8 February. The survey design was intentionally similar to that used during the IWC/IDCR second circumpolar series of cruises (CPII) to provide information towards addressing the effect of changing cruise track design on Antarctic minke whale abundance estimates. 000°-020°E was surveyed in two contiguous strata (Northern and Southern), from 64°30'S to the ice edge. Poor weather limited the coverage 020°E-035°E to the Southern Stratum only. A total of 1788.2 nmiles was surveyed (000°-035°E) including 935.5 nmiles in closing mode and 930.3 nmiles in independent observer mode, and a total of 466 minke whales were sighted. Minke whale visual dive time experiments were conducted during the minke whale survey. 35 trials were completed, recording surfacing cues for a total of 45.81 hours. From 10-22 February the ships conducted collaborative studies with the Japanese icebreaker, Shirase to investigate the relationship between minke whale abundance and the sea ice. During this study the SOWER vessels surveyed for minke whales in the near-ice area from 035°-050°E. 575.3 nmiles were covered and a total of 22 minke whales were detected. The Shirase surveyed in the pack ice zone 040°-050°E from 12-15 February. Two methods-testing experiments were carried out during the cruise: Adaptive Line Transect Sampling and ‘BT Mode.’ Adaptive Line Transect Sampling was tested during survey in Area IIIW. BT Mode trials were conducted 22-25 February in the area between 050° and 065°E. A direct electronic data acquisition program was evaluated during the cruise on both ships. Sightings for the entire cruise included: minke whales (237 groups/515 animals); blue whales (13 groups/46 individuals) of which 6 groups (28 individuals) were identified as true blue whales and 3 groups (3 individuals) were identified as pygmy blue whales; fin whales (14/132); humpback whales (251/646); sperm whales (35/49); killer whales (23/217); southern bottlenose whales (32/60); Gray’s beaked whales (1/7); Layard’s beaked whales (2/3); pilot whales (4/265); hourglass dolphins (4/17); striped dolphins (3/435) and common bottlenose dolphins (1/20). Opportunistic research during the cruise included blue whale research on 8 groups/29 animals resulting in 5 biopsies and images of 23 individuals for photo-identification studies. Biopsy samples and photo-ID images were also obtained opportunistically from other species. Biopsies were collected from 6 humpback whales and 1 southern right whale. Photo-ID images were collected from 45 humpback whales, 1 southern right whale and 8 groups of killer whales. Estimated Angle and Distance Training Exercise and Experiment were each completed on both vessels

Obesity-induced insulin resistance in human skeletal muscle is characterised by defective activation of p42/p44 MAP kinase

Insulin resistance (IR), an impaired cellular, tissue and whole body response to insulin, is a major pathophysiological defect of type 2 diabetes mellitus. Although IR is closely associated with obesity, the identity of the molecular defect(s) underlying obesity-induced IR in skeletal muscle remains controversial; reduced post-receptor signalling of the insulin receptor substrate 1 (IRS1) adaptor protein and downstream effectors such as protein kinase B (PKB) have previously been implicated. We examined expression and/or activation of a number of components of the insulin-signalling cascade in skeletal muscle of 22 healthy young men (with body mass index (BMI) range, 20–37 kg/m2). Whole body insulin sensitivity (M value) and body composition was determined by the hyperinsulinaemic (40 mU. min−1.m−2.), euglycaemic clamp and by dual energy X-ray absorptiometry (DEXA) respectively. Skeletal muscle (vastus lateralis) biopsies were taken before and after one hour of hyperinsulinaemia and the muscle insulin signalling proteins examined by western blot and immunoprecipitation assay. There was a strong inverse relationship between M-value and BMI. The most striking abnormality was significantly reduced insulin-induced activation of p42/44 MAP kinase, measured by specific assay, in the volunteers with poor insulin sensitivity. However, there was no relationship between individuals' BMI or M-value and protein expression/phosphorylation of IRS1, PKB, or p42/44 MAP kinase protein, under basal or hyperinsulinaemic conditions. In the few individuals with poor insulin sensitivity but preserved p42/44 MAP kinase activation, other signalling defects were evident. These findings implicate defective p42/44 MAP kinase signalling as a potential contributor to obesity-related IR in a non-diabetic population, although clearly multiple signalling defects underlie obesity associated IR

Glucose tolerance is associated with differential expression of microRNAs in skeletal muscle: results from studies of twins with and without type 2 diabetes.

AIMS/HYPOTHESIS: We aimed to identify microRNAs (miRNAs) associated with type 2 diabetes and risk of developing the disease in skeletal muscle biopsies from phenotypically well-characterised twins. METHODS: We measured muscle miRNA levels in monozygotic (MZ) twins discordant for type 2 diabetes using arrays. Further investigations of selected miRNAs included target prediction, pathway analysis, silencing in cells and association analyses in a separate cohort of 164 non-diabetic MZ and dizygotic twins. The effects of elevated glucose and insulin levels on miRNA expression were examined, and the effect of low birthweight (LBW) was studied in rats. RESULTS: We identified 20 miRNAs that were downregulated in MZ twins with diabetes compared with their non-diabetic co-twins. Differences for members of the miR-15 family (miR-15b and miR-16) were the most statistically significant, and these miRNAs were predicted to influence insulin signalling. Indeed, miR-15b and miR-16 levels were associated with levels of key insulin signalling proteins, miR-15b was associated with the insulin receptor in non-diabetic twins and knockdown of miR-15b/miR-16 in myocytes changed the levels of insulin signalling proteins. LBW in twins and undernutrition during pregnancy in rats were, in contrast to overt type 2 diabetes, associated with increased expression of miR-15b and/or miR-16. Elevated glucose and insulin suppressed miR-16 expression in vitro. CONCLUSIONS: Type 2 diabetes is associated with non-genetic downregulation of several miRNAs in skeletal muscle including miR-15b and miR-16, potentially targeting insulin signalling. The paradoxical findings in twins with overt diabetes and twins at increased risk of the disease underscore the complexity of the regulation of muscle insulin signalling in glucose homeostasis.JB-J was supported by a grant from the Danish PhD School for Molecular Metabolism. The study was supported by grants from the Danish Medical Research Council, the Danish Strategic Research Council. The Novo Nordisk Foundation, the Danish Ministry of Science, Technology and Innovation. DSF-T was supported by the Biotechnology and Biological Sciences Research Council project grant BB/F-15364/1. SEO is a British Heart Foundation Senior Fellow (FS/09/029/27902).This is the final version of the article. It was first published by Springer at http://link.springer.com/article/10.1007%2Fs00125-014-3434-

Pre- and early-postnatal nutrition modify gene and protein expressions of muscle energy metabolism markers and phospholipid fatty acid composition in a muscle type specific manner in sheep.

We previously reported that undernutrition in late fetal life reduced whole-body insulin sensitivity in adult sheep, irrespective of dietary exposure in early postnatal life. Skeletal muscle may play an important role in control of insulin action. We therefore studied a range of putative key muscle determinants of insulin signalling in two types of skeletal muscles (longissimus dorsi (LD) and biceps femoris (BF)) and in the cardiac muscle (ventriculus sinister cordis (VSC)) of sheep from the same experiment. Twin-bearing ewes were fed either 100% (NORM) or 50% (LOW) of their energy and protein requirements during the last trimester of gestation. From day-3 postpartum to 6-months of age (around puberty), twin offspring received a high-carbohydrate-high-fat (HCHF) or a moderate-conventional (CONV) diet, whereafter all males were slaughtered. Females were subsequently raised on a moderate diet and slaughtered at 2-years of age (young adults). The only long-term consequences of fetal undernutrition observed in adult offspring were lower expressions of the insulin responsive glucose transporter 4 (GLUT4) protein and peroxisome proliferator-activated receptor gamma, coactivator 1α (PGC1α) mRNA in BF, but increased PGC1α expression in VSC. Interestingly, the HCHF diet in early postnatal life was associated with somewhat paradoxically increased expressions in LD of a range of genes (but not proteins) related to glucose uptake, insulin signalling and fatty acid oxidation. Except for fatty acid oxidation genes, these changes persisted into adulthood. No persistent expression changes were observed in BF and VSC. The HCHF diet increased phospholipid ratios of n-6/n-3 polyunsaturated fatty acids in all muscles, even in adults fed identical diets for 1½ years. In conclusion, early postnatal, but not late gestation, nutrition had long-term consequences for a number of determinants of insulin action and metabolism in LD. Tissues other than muscle may account for reduced whole body insulin sensitivity in adult LOW sheep

IntAct—open source resource for molecular interaction data

IntAct is an open source database and software suite for modeling, storing and analyzing molecular interaction data. The data available in the database originates entirely from published literature and is manually annotated by expert biologists to a high level of detail, including experimental methods, conditions and interacting domains. The database features over 126 000 binary interactions extracted from over 2100 scientific publications and makes extensive use of controlled vocabularies. The web site provides tools allowing users to search, visualize and download data from the repository. IntAct supports and encourages local installations as well as direct data submission and curation collaborations. IntAct source code and data are freely available from

Endogenous TGF-beta 1 suppresses inflammation and promotes survival in adult CNJS

Transforming growth factor β1 (TGFβ1) is a pleiotropic cytokine with potent neurotrophic and immunosuppressive properties that is upregulated after injury, but also expressed in the normal nervous system. In the current study, we examined the regulation of TGFβ1 and the effects of TGFβ1 deletion on cellular response in the uninjured adult brain and in the injured and regenerating facial motor nucleus. To avoid lethal autoimmune inflammation within 3 weeks after birth in TGFβ1-deficient mice, this study was performed on a T- and B-cell-deficient RAG2−/− background. Compared with wild-type siblings, homozygous deletion of TGFβ1 resulted in an extensive inflammatory response in otherwise uninjured brain parenchyma. Astrocytes increased in GFAP and CD44 immunoreactivity; microglia showed proliferative activity, expression of phagocytosis-associated markers [αXβ2, B7.2, and MHC1 (major histocompatibility complex type 1)], and reduced branching. Ultrastructural analysis revealed focal blockade of axonal transport, perinodal damming of axonal organelles, focal demyelination, and myelin debris in granule-rich, phagocytic microglia. After facial axotomy, absence of TGFβ1 led to a fourfold increase in neuronal cell death (52 vs 13%), decreased central axonal sprouting, and significant delay in functional recovery. It also interfered with the microglial response, resulting in a diminished expression of early activation markers [ICAM1 (intercellular adhesion molecule 1), α6β1, and αMβ2] and reduced proliferation. In line with axonal and glial findings in the otherwise uninjured CNS, absence of endogenous TGFβ1 also caused an ∼10% reduction in the number of normal motoneurons, pointing to an ongoing and potent trophic role of this anti-inflammatory cytokine in the normal as well as in the injured brain

CHEK2 1100delC in patients with metachronous cancers of the breast and the colorectum

BACKGROUND: Development of multiple primary tumors is a hallmark of hereditary cancer. At least 1/10 of breast cancers and colorectal cancers occur because of heredity and recently the cell cycle kinase 2, CHEK2 1100delC allele has been identified at a particularly high frequency in families with hereditary breast and colorectal cancer. METHODS: We utilized the Southern Sweden population-based cancer registry to identify women with double primary breast and colorectal cancer and sequenced tumor material in order to assess the contribution of the CHEK2 1100delC to the development of such metachronous tumors. RESULTS: Among the 75 patients successfully analyzed, 2 (2.5%) carried the CHEK2 1100delC allele. which was not significantly different (p = 0.26) from the 1% (3/300) carriers identified in the control group. CONCLUSION: In summary, our data suggest that the CHEK2 1100delC is not a major cause of double primary breast and colorectal cancer in Sweden, which suggests that this patient group should not routinely be screened for the CHEK2 1100delC variant