Causes and consequences of past and projected Scandinavian summer temperatures, 500-2100 AD

Tree rings dominate millennium-long temperature reconstructions and many records originate from Scandinavia, an area for which the relative roles of external forcing and internal variation on climatic changes are, however, not yet fully understood. Here we compile 1,179 series of maximum latewood density measurements from 25 conifer sites in northern Scandinavia, establish a suite of 36 subset chronologies, and analyse their climate signal. A new reconstruction for the 1483–2006 period correlates at 0.80 with June–August temperatures back to 1860. Summer cooling during the early 17th century and peak warming in the 1930s translate into a decadal amplitude of 2.9°C, which agrees with existing Scandinavian tree-ring proxies. Climate model simulations reveal similar amounts of mid to low frequency variability, suggesting that internal ocean-atmosphere feedbacks likely influenced Scandinavian temperatures more than external forcing. Projected 21st century warming under the SRES A2 scenario would, however, exceed the reconstructed temperature envelope of the past 1,500 years.

Physiological Consequences Of White-Nose Syndrome

White-nose syndrome (WNS) is a disease that has caused the mass mortality of hibernating bat species. Since its first discovery in the winter of 2006-2007, an estimated five million bats or more have been killed. Although infection with Pseudogymnoascus destructans (Pd, the causative agent of WNS) does not always result in death, bats that survive Pd infection may experience fitness consequences. To understand the physiological consequences of WNS, I measured reproductive rates of free-ranging hibernating bat species of the Northeastern United States. In addition, captive little brown myotis (Myotis lucifugus) bats that were infected by Pd but survived (¿WNS survivors¿) and uninfected bats were studied in order to understand the potential consequences (e.g., lower reproductive rates, decreased ability to heal wounds, degradation of wing tissue, and altered metabolic rates) of surviving WNS. No differences in reproductive rates were found between WNS-survivors and uninfected bats in either the field or in captivity. In addition, wound healing was not affected by Pd infection. However, wing tissue degradation was worse for little brown myotis 19 days post-hibernation, and mass specific metabolic rate (MSMR) was significantly higher for those infected with Pd 22 days post-hibernation. While it is clear that these consequences are a direct result of Pd infection, further research investigating the long-term consequences for both mothers and pups is necessary.

The Unintended Consequences of Requiring a Licence to Help

Comments that current proposals for licensure, accreditation, and 3rd-party reimbursement may have several unintended consequences. Until now discussion has focused on the effects of the proposed regulations on the development of psychology as a profession. Recent proposals, however, may have unexpected adverse consequences on 3 other areas as well: the education of professionals within psychology, the delivery of psychological and other helping services, and the self-definition of the consumer of psychological services. Any changes in licensure, accreditation, and reimbursement require compromises of concerns for the profession, for the consumer, and for psychologists' livelihood.

Human leukocyte antigens (HLA) associated drug hypersensitivity: consequences of drug binding to HLA

Recent publications have shown that certain human leukocyte antigen (HLA) alleles are strongly associated with hypersensitivity to particular drugs. As HLA molecules are a critical element in T-cell stimulation, it is no surprise that particular HLA alleles have a direct functional role in the pathogenesis of drug hypersensitivity. In this context, a direct interaction of the relevant drug with HLA molecules as described by the p-i concept appears to be more relevant than presentation of hapten-modified peptides. In some HLA-associated drug hypersensitivity reactions, the presence of a risk allele is a necessary but incomplete factor for disease development. In carbamazepine and HLA-B*15:02, certain T-cell receptor (TCR) repertoires are required for immune activation. This additional requirement may be one of the 'missing links' in explaining why most individuals carrying this allele can tolerate the drug. In contrast, abacavir generates polyclonal T-cell response by interacting specifically with HLA-B*57:01 molecules. T cell stimulation may be due to presentation of abacavir or of altered peptides. While the presence of HLA-B*58:01 allele substantially increases the risk of allopurinol hypersensitivity, it is not an absolute requirement, suggesting that other factors also play an important role. In summary, drug hypersensitivity is the end result of a drug interaction with certain HLA molecules and TCRs, the sum of which determines whether the ensuing immune response is going to be harmful or not.

Consequences of depleted SERCA2-gated calcium stores in the skin

Sarco(endo)plasmic reticulum Ca2+-ATPase isoform 2 (SERCA2) pumps belong to the family of Ca2+-ATPases responsible for the maintenance of calcium in the endoplasmic reticulum. In epidermal keratinocytes, SERCA2-controlled calcium stores are involved in cell cycle exit and onset of terminal differentiation. Hence, their dysfunction was thought to provoke impaired keratinocyte cohesion and hampered terminal differentiation. Here, we assessed cultured keratinocytes and skin biopsies from a canine family with an inherited skin blistering disorder. Cells from lesional and phenotypically normal areas of one of these dogs revealed affected calcium homeostasis due to depleted SERCA2-gated stores. In phenotypically normal patient cells, this defect compromised upregulation of p21(WAF1) and delayed the exit from the cell cycle. Despite this abnormality it failed to impede the terminal differentiation process in the long term but instead coincided with enhanced apoptosis and appearance of chronic wounds, suggestive of secondary mutations. Collectively, these findings provide the first survey on phenotypic consequences of depleted SERCA-gated stores for epidermal homeostasis that explain how depleted SERCA2 calcium stores provoke focal lesions rather than generalized dermatoses, a phenotype highly reminiscent of the human genodermatosis Darier disease.