A Comment on Nishimura, Nakajima, and Kiyota's "Does the natural selection mechanism still work in severe recessions? Examination of the Japanese economy in the 1990s"

Nishimura et al. (2005) analyze the entry/exit behavior of Japanese firms during the 1990s and find that relatively efficient firms exited while relatively inefficient firms survived during the banking-crisis period of 1996-97. They conclude that the natural selection mechanism (NSM) apparently malfunctions during severe recessions, but we offer a more plausible interpretation: NSM continued to function effectively even during this period, but aberrant banking practices caused a shift in the type of natural selection from directional to disruptive selection, with the most efficient as well as the least efficient firms being favored and firms of intermediate efficiency being selected against.

A Comment on Nishimura, Nakajima, and Kiyota's "Does the Natural Selection Mechanism Still Work in Severe Recessions? Examination of the Japanese Economy in the 1990s"

Nishimura, Nakajima, and Kiyota (2005) analyze the entry/exit behavior patterns of Japanese firms during the 1990s and find that relatively efficient (high total factor productivity (TFP)) firms exited while relatively inefficient (low TFP) firms survived during the banking-crisis period of 1996-97. They conclude from this finding that the natural selection mechanism (NSM) apparently malfunctions during severe recessions, but we offer a much more plausible interpretation: the NSM continued to function effectively even during this period, but aberrant banking practices (in particular, "forbearance lending" ("evergreening") and the "forcible withdrawal of loans" and/or the "reluctance to lend") caused a shift in the type of natural selection from "directional selection" to "disruptive selection," with the most efficient (highest TFP) firms as well as the least efficient (lowest TFP) firms being favored and firms of intermediate efficiency and TFP being selected against.

Do Banks Reduce Lending Preemptively in Response to Capital Losses?

We empirically examined whether declining bank loans in Japan in the late 1990s are the result of banks' downward adjustments of lending supply (a "credit crunch") in response to capital losses (a "capital crunch"). Estimating the new lending supply function as a non-linear function of the capital to asset ratio, we found that the (new lending supply) function is not only increasing in bank capital but also concave in bank capital, which supports the view that a "credit crunch" occurs since forward-looking banks have an incentive to avoid failing to meet regulatory requirements in the future.

Changes in Plasma Metabolites Concentrations in Obese Dogs Supplemented With Anti-oxidant Compound

The aim of this study is to discuss the effect of anti-oxidant supplement (Rv-PEM01-99, Kibun Foods, Inc., Tokyo, Japan) on changes in energy metabolism in obese dogs. 200 mg/kg/day of Rv-PEM01-99 (equivalent to 5 mg kg/day of quercetin derivative) were applied for 6 weeks to the Beagle dogs fed high fat diet (HFD) or control diet (CD). In the present study, body weight (BW) decreasing effect of Rv-PEM 01-99 in obese dogs was not clear. However, plasma alkaline phosphatase (ALP) activities at the end of experiment were significantly decreased compared to those at the start of experiment in obese dogs supplemented with Rv-PEM 01-99 (paired-t test, p < 0.05). In control dogs supplemented with Rv-PEM 01-99, Plasma malondialdehyde (MDA), and triglycerides (TG) levels and lactate dehydrogenase (LDH) activities were significantly decreased compared to those at the start of experiment (paired-t test, p < 0.05). From these findings, Rv-PEM 01-99 seems to be not harmful for dogs. Anti-lipid peroxide effect and liver function improvement are expected in the dogs supplemented with Rv-PEM 01-99

Humerus Varus in a Patient with Pseudohypoparathyroidism

A 7-yr-old girl presented with progressive shortening of the right upper arm and limitation of shoulder motion. Pseudohypoparathyroidism associated with Albright's hereditary osteodystrophy was diagnosed by biochemical, hormonal and radiographic studies. Her condition was complicated by severe humerus varus on the right side. Proximal humeral valgization osteotomy and concomitant humeral lengthening resulted in an improvement of the shoulder joint motion and activity in daily life

Abnormal Motion of the Interventricular Septum after Coronary Artery Bypass Graft Surgery: Comprehensive Evaluation with MR Imaging

OBJECTIVE: To define the mechanism associated with abnormal septal motion (ASM) after coronary artery bypass graft surgery (CABG) using comprehensive MR imaging techniques. MATERIALS AND METHODS: Eighteen patients (mean age, 58 +/- 12 years; 15 males) were studied with comprehensive MR imaging using rest/stress perfusion, rest cine, and delayed enhancement (DE)-MR techniques before and after CABG. Myocardial tagging was also performed following CABG. Septal wall motion was compared in the ASM and non-ASM groups. Preoperative and postoperative results with regard to septal wall motion in the ASM group were also compared. We then analyzed circumferential strain after CABG in both the septal and lateral walls in the ASM group. RESULTS: All patients had normal septal wall motion and perfusion without evidence of non-viable myocardium prior to surgery. Postoperatively, ASM at rest and/or stress state was documented in 10 patients (56%). However, all of these had normal rest/stress perfusion and DE findings at the septum. Septal wall motion after CABG in the ASM group was significantly lower than that in the non-ASM group (2.1+/-5.3 mm vs. 14.9+/-4.7 mm in the non-ASM group; p < 0.001). In the ASM group, the degree of septal wall motion showed a significant decrease after CABG (preoperative vs. postoperative = 15.8+/-4.5 mm vs. 2.1+/-5.3 mm; p = 0.007). In the ASM group after CABG, circumferential shortening of the septum was even larger than that of the lateral wall (-20.89+/-5.41 vs. -15.41+/-3.7, p < 0.05) CONCLUSION: Abnormal septal motion might not be caused by ischemic insult. We suggest that ASM might occur due to an increase in anterior cardiac mobility after incision of the pericardiumope

High-Resolution Diffusion Tensor MR Imaging for Evaluating Myocardial Anisotropy and Fiber Tracking at 3T: the Effect of the Number of Diffusion-Sensitizing Gradient Directions

Objective: We wanted to evaluate the effect of the number of diffusion-sensitizing gradient directions on the image quality for evaluating myocardial anisotropy and fiber tracking by using in vitro diffusion tensor MR imaging (DT-MRI). Materials and Methods: The DT-MR images, using a SENSE-based echo-planar imaging technique, were acquired from ten excised porcine hearts by using a 3T MR scanner. With a b-value of 800 S/mm(2), the diffusion tensor images were obtained for 6,15 and 32 diffusion-sensitizing gradient directions at the mid-ventricular level. The number of tracked fibers, the fractional anisotropy (FA), and the length of the tracked fibers were measured for the quantitative analysis. Two radiologists assessed the image quality of the fiber tractography for the qualitative analysis. Results: By increasing the number of diffusion-sensitizing gradient directions from 6 to 15, and then to 32, the FA and standard deviation were significantly reduced (p < 0.01), and the number of tracked fibers and the length of the tracked fibers were significantly increased (p < 0.01). The image quality of the fiber tractography was significantly increased with the increased number of diffusion-sensitizing gradient directions (p < 0.01). Conclusion: The image quality of in vitro DT-MRI is significantly improved as the number of diffusion-sensitizing gradient directions is increased.Jiang Y, 2007, AM J PHYSIOL-HEART C, V293, pH2377, DOI 10.1152/ajpheart.00337.2007Wu EX, 2007, MAGN RESON MED, V58, P687, DOI 10.1002/mrm.21350Wu EX, 2007, MAGN RESON IMAGING, V25, P1048, DOI 10.1016/j.mri.2006.12.008Wu MT, 2006, CIRCULATION, V114, P1036, DOI 10.1161/CIRCULATIONHAHA.105.545863Lee JW, 2006, INVEST RADIOL, V41, P553Okada T, 2006, RADIOLOGY, V238, P668, DOI 10.1148/radiol.2382042192CHANG YM, 2005, J KOREAN RADIOL SOC, V52, P87Tanenbaum LN, 2004, AM J NEURORADIOL, V25, P1626Nagae-Poetscher LM, 2004, AM J NEURORADIOL, V25, P1325Jones DK, 2004, MAGNET RESON MED, V51, P807, DOI 10.1002/mrm.20033Jaermann T, 2004, MAGNET RESON MED, V51, P230, DOI 10.1002/mrm.10707Naganawa S, 2004, EUR RADIOL, V14, P234, DOI 10.1007/s00330-003-2163-6Zhai GH, 2003, RADIOLOGY, V229, P673, DOI 10.1148/radiol.2293021462Cercignani M, 2003, AM J NEURORADIOL, V24, P1254Tseng WYI, 2003, J MAGN RESON IMAGING, V17, P31, DOI 10.1002/jmri.10223Jeong AK, 2001, KOREAN J RADIOL, V2, P21Holmes AA, 2000, MAGNET RESON MED, V44, P157Choi SI, 2000, RADIOLOGY, V215, P863Spotnitz HM, 2000, J THORAC CARDIOV SUR, V119, P1053Pruessmann KP, 1999, MAGNET RESON MED, V42, P952Tseng WI, 1999, MAGNET RESON MED, V42, P393Scollan DF, 1998, AM J PHYSIOL-HEART C, V275, pH2308Pierpaoli C, 1996, MAGNET RESON MED, V36, P893Taber LA, 1996, J BIOMECH, V29, P745REESE TG, 1995, MAGNET RESON MED, V34, P786EDELMAN RR, 1994, MAGNET RESON MED, V32, P423RADEMAKERS FE, 1994, CIRCULATION, V89, P1174STREETER DD, 1969, CIRC RES, V24, P339