Impaired Development of Somatotropes, Lactotropes and Thyrotropes in Growth-Retarded (grt) Mice

Congenitally primary hypothyroid growth-retarded (grt) mice exhibit a characteristic growth pause followed by delayed onset of pubertal growth. We characterized the developmental pattern of somatotropes, lactotropes and thyrotropes in the anterior pituitary, as well as plasma levels of their secretory hormones, in grt mice. Compared with normal mice, the weight of grt pituitary gland was similar at 8 weeks of age but significantly heavier after 12 weeks of age. Compared with normal mice, there were significantly fewer somatotropes in the grt pituitary until 8 weeks of age, but the number gradually increased up to 48 weeks. The number of lactotropes in grt mice was consistently lower than that in normal mice from 2 through 48 weeks, whereas the number of thyrotropes in the grt pituitary was consistently higher than in the normal pituitary. Thyrotropes in the grt pituitary exhibited hypertrophy and hyperplasia with less intensive thyroid-stimulating hormone (TSH) immunoreactivity than normal thyrotropes. In normal mice, the sum of the relative proportions of these cells plateaued at 8 weeks, where it remained up to 48 weeks of age. In grt mice, these proportions almost reached normal levels at 12 weeks of age but gradually declined after 24 weeks. Plasma growth hormone concentrations did not differ between grt and normal mice until 24 weeks of age. Compared with normal mice, grt mice exhibited significantly lower plasma prolactin and thyroxine levels but higher TSH levels. These findings indicate that development of somatotropes, lactotropes and thyrotropes in grt mice is impaired, being followed by altered hormone secretion

Electrically Triggered All-or-None Ca2+-Liberation during Action Potential in the Giant Alga Chara

Electrically triggered action potentials in the giant alga Chara corallina are associated with a transient rise in the concentration of free Ca2+ in the cytoplasm (Ca2+cyt). The present measurements of Ca2+cyt during membrane excitation show that stimulating pulses of low magnitude (subthreshold pulse) had no perceivable effect on Ca2+cyt. When the strength of a pulse exceeded a narrow threshold (suprathreshold pulse) it evoked the full extent of the Ca2+cyt elevation. This suggests an all-or-none mechanism for Ca2+ mobilization. A transient calcium rise could also be induced by one subthreshold pulse if it was after another subthreshold pulse of the same kind after a suitable interval, i.e., not closer than a few 100 ms and not longer than a few seconds. This dependency of Ca2+ mobilization on single and double pulses can be simulated by a model in which a second messenger is produced in a voltage-dependent manner. This second messenger liberates Ca2+ from internal stores in an all-or-none manner once a critical concentration (threshold) of the second messenger is exceeded in the cytoplasm. The positive effect of a single suprathreshold pulse and two optimally spaced subthreshold pulses on Ca2+ mobilization can be explained on the basis of relative velocity for second messenger production and decomposition as well as the availability of the precursor for the second messenger production. Assuming that inositol-1,4,5,-trisphosphate (IP3) is the second messenger in question, the present data provide the major rate constants for IP3 metabolism

A Wireless Method for Stimulating Characeae Internofal Cells

　車軸藻節間細胞を電気刺激するための，ピエゾ素子を用いる方法を開発した．この方法は電線の接続を要しない非接触のものであるので，遠心顕微鏡観察のもとで細胞を電気刺激することができた．またこの刺激方法は，オジギソウ，アメーバ，ラッパムシにも適用できた

Evolution of the Corticotropin-releasing Hormone Signaling System and Its Role in Stress-induced Phenotypic Plasticity

Developing animals respond in variation in their habitats by altering their rules of development and/or their morphologies (i.e., they exhibit phenotypic plasticity). In vertebrates, one mechanism by which plasticity is expressed is through activation of the neuroendocrine system, which transduces environmental information into a physiological response. Recent findings of ours with amphibians and of others with mammals show that the primary vertebrate stress neuropeptide, corticotropin-releasing hormone (CRH), is essential for adaptive developmental responses to environmental stress. For instance, CRH-dependent mechanisms cause accelerated metamorphosis in response to pond-drying in some amphibian species, and intrauterine fetal stress syndromes in humans precipitate preterm birth. CRH may be a phylogenetically ancient developmental signaling molecule that allows developing organisms to escape deleterious changes in their larval/fetal habitat. The response to CRH is mediated by at least two different receptor subtypes and may also be modulated by a secreted binding protein.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73287/1/j.1749-6632.1999.tb07877.x.pd

Kalamazoo River Watershed Land Conservation Plan

The Kalamazoo River Watershed Land Conservation Plan was developed to select for conservation targets among ownership parcels in the Kalamazoo River Watershed (MI). The watershed, while historically degraded, features large areas of preserved Midwestern habitats. To facilitate for the permanent protection of these lands, this plan was developed using an ArcGIS-based analysis that scored ownership parcels based on the following conservation criteria: land cover, presence of wetlands, proximity to hydrology, proximity to existing conserved lands, presence of cold lands, and presence of threatened and endangered species habitat. These criteria were developed using a literature review of existing conservation plans and Kalamazoo River Watershed stakeholder input. The results from this analysis were used to identify conservation priorities, including: the top 100 scoring parcels in the basin, a database of the top 20% scoring parcels and their contact information, and priority subwatersheds for conservation.Master of ScienceNatural Resources and EnvironmentUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/106543/1/KRWLCP_Final_2014.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/106543/2/KRWLCP_Owner_Database.xls