A New Bot Fly Species (Diptera: Oestridae) From Central Texas

The bot fly Cephenemyia albina (Diptera: Oestridae) is described from a relict pine forest in east-central Texas. This species presumably lives as a parasitic larva in the throat of white-tailed deer as do its two close relatives previously reported from both Texas and the Great Lakes region (C. phobifera (Clark) and C. jellisoni Townsend). Only the adult male is currently known

Male spatial distribution in the mating system of the northern field cricket, Gryllus veletis.

http://deepblue.lib.umich.edu/bitstream/2027.42/53658/1/2093.pdfDescription of 2093.pdf : Access restricted to on-site users at the U-M Biological Station

Notes on the natural history of Geocaulon lividum.

http://deepblue.lib.umich.edu/bitstream/2027.42/53596/1/2031.pdfDescription of 2031.pdf : Access restricted to on-site users at the U-M Biological Station

Notes on the population and territory size of winter wrens (Troglodytes troglodytes) in a section of Reese's swamp.

http://deepblue.lib.umich.edu/bitstream/2027.42/53595/1/2030.pdfDescription of 2030.pdf : Access restricted to on-site users at the U-M Biological Station

Transforming growth factor-? and atherosclerosis: Interwoven atherogenic and atheroprotective aspects

Age-related progression of cardiovascular disease is by far the largest health problem in the US and involves vascular damage, progressive vascular fibrosis and the accumulation of lipid-rich atherosclerotic lesions. Advanced lesions can restrict flow to key organs and can trigger occlusive thrombosis resulting in a stroke or myocardial infarction. Transforming growth factor-beta (TGF-β) is a major orchestrator of the fibroproliferative response to tissue damage. In the early stages of repair, TGF-β is released from platelets and activated from matrix reservoirs; it then stimulates the chemotaxis of repair cells, modulates immunity and inflammation and induces matrix production. At later stages, it negatively regulates fibrosis through its strong antiproliferative and apoptotic effects on fibrotic cells. In advanced lesions, TGF-β might be important in arterial calcification, commonly referred to as “hardening of the arteries”. Because TGF-β can signal through multiple pathways, namely the SMADs, a MAPK pathway and the Rho/ROCK pathways, selective defects in TGF-β signaling can disrupt otherwise coordinated pathways of tissue regeneration. TGF-β is known to control cell proliferation, cell migration, matrix synthesis, wound contraction, calcification and the immune response, all being major components of the atherosclerotic process. However, many of the effects of TGF-β are essential to normal tissue repair and thus, TGF-β is often thought to be “atheroprotective”. The present review attempts to parse systematically the known effects of TGF-β on both the major risk factors for atherosclerosis and to isolate the role of TGF-β in the many component pathways involved in atherogenesis