Polar ocean stratification in a cold climate

The low-latitude ocean is strongly stratified by the warmth of its surface water. As a result, the great volume of the deep ocean has easiest access to the atmosphere through the polar surface ocean. In the modern polar ocean during the winter, the vertical distribution of temperature promotes overturning, with colder water over warmer, while the salinity distribution typically promotes stratification, with fresher water over saltier. However, the sensitivity of seawater density to temperature is reduced as temperature approaches the freezing point, with potential consequences for global ocean circulation under cold climates. Here we present deep-sea records of biogenic opal accumulation and sedimentary nitrogen isotopic composition from the Subarctic North Pacific Ocean and the Southern Ocean. These records indicate that vertical stratification increased in both northern and southern high latitudes 2.7 million years ago, when Northern Hemisphere glaciation intensified in association with global cooling during the late Pliocene epoch. We propose that the cooling caused this increased stratification by weakening the role of temperature in polar ocean density structure so as to reduce its opposition to the stratifying effect of the vertical salinity distribution. The shift towards stratification in the polar ocean 2.7 million years ago may have increased the quantity of carbon dioxide trapped in the abyss, amplifying the global cooling.     

Dynamics of fat cell turnover in humans

Obesity is increasing in an epidemic manner in most countries and constitutes a public health problem by enhancing the risk for cardiovascular disease and metabolic disorders such as type 2 diabetes. Owing to the increase in obesity, life expectancy may start to decrease in developed countries for the first time in recent history. The factors determining fat mass in adult humans are not fully understood, but increased lipid storage in already developed fat cells (adipocytes) is thought to be most important. Here we show that adipocyte number is a major determinant for the fat mass in adults. However, the number of fat cells stays constant in adulthood in lean and obese individuals, even after marked weight loss, indicating that the number of adipocytes is set during childhood and adolescence. To establish the dynamics within the stable population of adipocytes in adults, we have measured adipocyte turnover by analysing the integration of 14C derived from nuclear bomb tests in genomic DNA. Approximately 10% of fat cells are renewed annually at all adult ages and levels of body mass index. Neither adipocyte death nor generation rate is altered in early onset obesity, suggesting a tight regulation of fat cell number in this condition during adulthood. The high turnover of adipocytes establishes a new therapeutic target for pharmacological intervention in obesity.     

The algal flora of the campus of Brigham Young University, Provo, Utah

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Biallelic mutations in PALB2 cause Fanconi anemia subtype FA-N and predispose to childhood cancer

PALB2 was recently identified as a nuclear binding partner of BRCA2. Biallelic BRCA2 mutations cause Fanconi anemia subtype FA-D1 and predispose to childhood malignancies. We identified pathogenic mutations in PALB2 (also known as FANCN) in seven families affected with Fanconi anemia and cancer in early childhood, demonstrating that biallelic PALB2 mutations cause a new subtype of Fanconi anemia, FA-N, and, similar to biallelic BRCA2 mutations, confer a high risk of childhood cancer.     

Birc2 (cIap1) regulates endothelial cell integrity and blood vessel homeostasis

Integrity of the blood vessel wall is essential for vascular homeostasis and organ function. A dynamic balance between endothelial cell survival and apoptosis contributes to this integrity during vascular development and pathological angiogenesis. The genetic and molecular mechanisms regulating these processes in vivo are still largely unknown. Here, we show that Birc2 (also known as cIap1) is essential for maintaining endothelial cell survival and blood vessel homeostasis during vascular development. Using a forward-genetic approach, we identified a zebrafish null mutant for birc2, which shows severe hemorrhage and vascular regression due to endothelial cell integrity defects and apoptosis. Using genetic and molecular approaches, we show that Birc2 positively regulates the formation of the TNF receptor complex I in endothelial cells, thereby promoting NF-kappaB activation and maintaining vessel integrity and stabilization. In the absence of Birc2, a caspase-8-dependent apoptotic program takes place that leads to vessel regression. Our findings identify Birc2 and TNF signaling components as critical regulators of vascular integrity and endothelial cell survival, thereby providing an additional target pathway for the control of angiogenesis and blood vessel homeostasis during embryogenesis, regeneration and tumorigenesis.     

Integrated knowledge-based modeling and its application for classification problems

Knowledge discovery from data directly can hardly avoid the fact that it is biased towards the collected experimental data, whereas, expert systems are always baffled with the manual knowledge acquisition bottleneck. So it is believable that integrating the knowledge embedded in data and those possessed by experts can lead to a superior modeling approach. Aiming at the classification problems, a novel integrated knowledge-based modeling methodology, oriented by experts and driven by data, is proposed. It starts from experts identifying modeling parameters, and then the input space is partitioned followed by fuzzification. Afterwards, single rules are generated and then aggregated to form a rule base, on which a fuzzy inference mechanism is proposed. The experts are allowed to make necessary changes on the rule base to improve the model accuracy. A real-world application, welding fault diagnosis, is presented to demonstrate the effectiveness of the methodology.     

Thromboxane synthase mutations in an increased bone density disorder (Ghosal syndrome)

Studying consanguineous families with Ghosal hematodiaphyseal dysplasia syndrome (GHDD), a disorder of increased bone density, we identified mutations in TBXAS1, which encodes thromboxane synthase (TXAS). TXAS, an enzyme of the arachidonic acid cascade, produces thromboxane A(2) (TXA(2)). Platelets from subjects with GHDD showed a specific deficit in arachidonic acid-produced aggregation. We also found that TXAS and TXA(2) modulated expression of TNFSF11 and TNFRSF11B (encoding RANKL and osteoprotegerin (OPG), respectively) in primary cultured osteoblasts.