Influence of Nearby Plants and Artificial Structures on the Surface Air Temperature Statistics : An in-situ Measurement at Central Tokyo (Otemachi) throughout Years

In order to clarify the influence of obstacles on temperature measurement, two years\u27 continuous observation was made in the meteorological enclosure of the Japan Meteorological Agency in central Tokyo (Otemachi), by installing an extra thermometer at a spot that was surrounded by trees and was 20 m distant from the thermometer for operational observation. In the early afternoon of the warm season, the temperature at the spot surrounded by trees was found to be higher than the operational temperature. The temperature difference at 15JST was about 0.5 degrees Celsius on theaverage, and was correlated with daily solar radiation with a correlation coefficient of over 0.7 from March to September. On the other hand, difference of nighttime temperature was generally small, so that the monthly mean difference of daily mean temperatures was less than 0.1 degree Celsius for all the months of the year

Three‐dimensional myocardial scarring along myofibers after coronary ischemia–reperfusion revealed by computerized images of histological assays

Abstract Adverse left ventricular (LV) remodeling after acute myocardial infarction is characterized by LV dilatation and development of a fibrotic scar, and is a critical factor for the prognosis of subsequent development of heart failure. Although myofiber organization is recognized as being important for preserving physiological cardiac function and structure, the anatomical features of injured myofibers during LV remodeling have not been fully defined. In a mouse model of ischemia–reperfusion (I/R) injury induced by left anterior descending coronary artery ligation, our previous histological assays demonstrated that broad fibrotic scarring extended from the initial infarct zone to the remote zone, and was clearly demarcated along midcircumferential myofibers. Additionally, no fibrosis was observed in longitudinal myofibers in the subendocardium and subepicardium. However, a histological analysis of tissue sections does not adequately indicate myofiber injury distribution throughout the entire heart. To address this, we investigated patterns of scar formation along myofibers using three‐dimensional (3D) images obtained from multiple tissue sections from mouse hearts subjected to I/R injury. The fibrotic scar area observed in the 3D images was consistent with the distribution of the midcircumferential myofibers. At the apex, the scar formation tracked along the myofibers in an incomplete C‐shaped ring that converged to a triangular shape toward the end. Our findings suggest that myocyte injury after transient coronary ligation extends along myofibers, rather than following the path of coronary arteries penetrating the myocardium. The injury pattern observed along myofibers after I/R injury could be used to predict prognoses for patients with myocardial infarction

Systemic PPARγ deletion impairs circadian rhythms of behavior and metabolism.

Compelling evidence from both human and animal studies suggests a physiological link between the circadian rhythm and metabolism but the underlying mechanism is still incompletely understood. We examined the role of PPARγ, a key regulator of energy metabolism, in the control of physiological and behavioral rhythms by analyzing two strains of whole-body PPARγ null mouse models. Systemic inactivation of PPARγ was generated constitutively by using Mox2-Cre mice (MoxCre/flox) or inducibly by using the tamoxifen system (EsrCre/flox/TM). Circadian variations in oxygen consumption, CO(2) production, food and water intake, locomotor activity, and cardiovascular parameters were all remarkably suppressed in MoxCre/flox mice. A similar phenotype was observed in EsrCre/flox/TM mice, accompanied by impaired rhythmicity of the canonical clock genes in adipose tissues and liver but not skeletal muscles or the kidney. PPARγ inactivation in isolated preadipocytes following exposure to tamoxifen led to a similar blockade of the rhythmicity of the clock gene expression. Together, these results support an essential role of PPARγ in the coordinated control of circadian clocks and metabolic pathways