The expression of Visinin-like 1 during mouse embryonic development

Visinin like 1 (Vsnl1) encodes a calcium binding protein which is well conserved between species. It was originally found in the brain and its biological functions in central nervous system have been addressed in several studies. Low expression levels have also been found in some peripheral organs, but very little information is available regarding its physiological roles in non-neuronal tissues. Except for the kidney, the expression pattern of Vsnl1 mRNA and protein has not yet been addressed during embryogenesis. By in situ hybridization and immunolabeling we have extensively analyzed the expression pattern of Vsnl1 during murine development. Vsnl1 specifies the cardiac primordia and its expression becomes restricted to the atrial myocardium after heart looping. However, in the adult heart, Vsnl1 is expressed by all four cardiac chambers. It also serves as a specific marker for the cardiomyocyte-derived structures in the systemic and pulmonary circulation. Vsnl1 is dynamically expressed also by many other organs during development e.g. taste buds, cochlea, thyroid, tooth, salivary and adrenal gland. The stage specific expression pattern of Vsnl1 makes it a potentially useful marker particularly in studies of cardiac and vascular morphogenesis.     

Recent avian H5N1 viruses exhibit increased propensity for acquiring human receptor specificity

Adaptation of avian influenza viruses for replication and transmission in the human host is believed to require mutations in the hemagglutinin glycoprotein (HA) which enable binding to human α2-6 sialosides and concomitant reduction in affinity for avian α2-3 linked sialosides. Here, we show by glycan microarray analyses that the two mutations responsible for such specificity changes in 1957 H2N2 and 1968 H3N2 pandemic viruses, when inserted into recombinant HAs or intact viruses of some recent avian H5N1 isolates (clade 2.2), impart such attributes. This propensity to adapt to human receptors is primarily dependent on arginine at position 193 within the receptor-binding site, as well as loss of a vicinal glycosylation site. Widespread occurrence of these susceptible H5N1 clade 2.2 influenza strains has already occurred in Europe, the Middle East, and Africa. Thus, these avian strains should be considered high-risk, because of their significantly lower threshold for acquiring human receptor specificity and, therefore, warrant increased surveillance and further study.     

Ligation-based molecular tools for lab-on-a-chip devices

Molecular diagnostics can offer early detection of disease, improved diagnostic accuracy, and qualified follow-up. Moreover, the use of microfluidic devices can in principle render these analyses quickly and user-friendly, placing them within the reach of the general practitioner and maybe even in households. However, the progress launching such devices has been limited so far. We propose that an important limiting factor has been the difficulty of establishing molecular assays suitable for microfabricated formats. The assays should be capable of monitoring a wide range of molecules, including genomic DNA, RNA and proteins with secondary modifications and interaction partners, and they must exhibit excellent sensitivity and specificity. We discuss these problems and describe a series of molecular tools that may present new opportunities for lab-on-a-chip devices at the point-of-care.     

Hormone-sensitive lipase is necessary for normal mobilization of lipids during submaximal exercise

For the working muscle there are a number of fuels available for oxidative metabolism, including glycogen, glucose, and nonesterified fatty acids. Nonesterified fatty acids originate from lipolysis in white adipose tissue, hydrolysis of VLDL triglycerides, or hydrolysis of intramyocellular triglyceride stores. A key enzyme in the mobilization of fatty acids from intracellular lipid stores is hormone-sensitive lipase (HSL). The aim of the present study was to investigate the metabolic response of HSL-null mice challenged with exercise or fasting and to examine whether other lipases are able to fully compensate for the lack of HSL. The results showed that HSL-null mice have reduced capacity to perform aerobic exercise. The liver glycogen stores were more rapidly depleted in HSL-null mice during treadmill exercise, and HSL-null mice had reduced plasma concentrations of both glycerol and nonesterified fatty acids after exercise and fasting, respectively. The data support the hypothesis that in the absence of HSL, mice are not able to respond to an exercise challenge with increased mobilization of the lipid stores. Consequently, the impact of the lipid-sparing effect on liver glycogen is reduced in the HSL-null mice, resulting in faster depletion of this energy source, contributing to the decreased endurance during submaximal exercise.     

Measurement of net ecosystem exchange,productivity and respiration in three spruce forests in Sweden shows unexpectedly large soil carbon losses

Measurement of net ecosystem exchange was made using the eddy covariance method above three forests along a north-south climatic gradient in Sweden: Flakaliden in the north, Knottåsen in central and Asa in south Sweden. Data were obtained for 2 years at Flakaliden and Knottåsen and for one year at Asa. The net fluxes (N_ep) were separated into their main components, total ecosystem respiration (R_t) and gross primary productivity (P_g). The maximum half-hourly net uptake during the heart of the growing season was highest in the southernmost site with ?0.787 mg CO₂ m^?2 s^?1 followed by Knottåsen with ?0.631 mg CO₂ m^?2 s^?1 and Flakaliden with ?0.429 mg CO₂ m^?2 s^?1. The maximum respiration rates during the summer were highest in Knottåsen with 0.245 mg CO₂ m^?2 s^?1 while it was similar at the two other sites with 0.183 mg CO₂ m^?2 s^?1. The annual N_ep ranged between uptake of ?304 g C m^?2 year^?1 (Asa) and emission of 84 g C m^?2 year^?1 (Knottåsen). The annual R_t and P_g ranged between 793 to 1253 g C m^?2 year^?1 and ?875 to ?1317 g C m^?2 year^?1, respectively. Biomass increment measurements in the footprint area of the towers in combination with the measured net ecosystem productivity were used to estimate the changes in soil carbon and it was found that the soils were losing on average 96–125 g C m^?2 year^?1. The most plausible explanation for these losses was that the studied years were much warmer than normal causing larger respiratory losses. The comparison of net primary productivity and P_g showed that ca 60% of P_g was utilized for autotrophic respiration.