On the Contribution of Turbulent Boundary Layers to the Noise inside a Fuselage

The following report deals i preliminary fashion with the transmission through a fuselage of random noise generated on the fuselage skin by a turbulent boundary layer. The concept of attenuation is abandoned and instead the problem is formulated as a sequence of two linear couplings: the turbulent boundary layer fluctuations excite the fuselage skin in lateral vibrations and the skin vibrations induce sound inside the fuselage. The techniques used are those required to determine the response of linear systems to random forcing functions of several variables. A certain degree of idealization has been resorted to. Thus the boundary layer is assumed locally homogeneous, the fuselage skin is assumed flat, unlined and free from axial loads and the "cabin" air is bounded only by the vibrating plate so that only outgoing waves are considered. Some of the details of the statistical description have been simplified in order to reveal the basic features of the problem. The results, strictly applicable only to the limiting case of thin boundary layers, show that the sound pressure intensity is proportional to the square of the free stream density, the square of cabin air density and inversely proportional to the first power of the damping constant and to the second power of the plate density. The dependence on free stream velocity and boundary layer thickness cannot be given in general without a detailed knowledge of the characteristics of the pressure fluctuations in the boundary layer (in particular the frequency spectrum). For a flat spectrum the noise intensity depends on the fifth power of the velocity and the first power of the boundary layer thickness. This suggests that boundary layer removal is probably not an economical means of decreasing cabin noise. In general, the analysis presented here only reduces the determination of cabin noise intensity to the measurement of the effect of any one of four variables (free stream velocity, boundary layer thiclkness, plate thickness or the characteristic velocity of propagation in the plate). The plate generates noise by vibrating in resonance over a wide range of frequencies and increasing the damping constant is consequently an effective method of decreasing noise generation. One of the main features of the results is that the relevent quantities upon which noise intensity depends are non-dimensional numbers in which boundary layer and plate properties enter as ratios. This is taken as an indication that in testing models of structures for boundary layer noise it is not sufficient to duplicate in the model the structural characteristics of the fuselage. One must match properly the characteristics of the exciting pressure fluctuations to that of the structure

The determinants of intrafirm trade: Evidence from French firms

How well does the theory of the firm explain the choice between intrafirm and arms' length trade? This paper uses firm-level import data from France to look into this question. We find support for three key predictions of property-rights theories of the multinational firm. Intrafirm imports are more likely: (i) in capital- and skill-intensive firms; (ii) in highly productive firms; (iii) from countries with well-functioning judicial institutions. We further bridge previous aggregate findings with our investigation by decomposing intrafirm imports into an extensive and intensive margin. Doing so we uncover interesting patterns in the data that require further theoretical investigation.intrafirm trade; outsourcing; firm heterogeneity; incomplete contracts; internationalization strategies; quality of institutions, extensive margin, intensive margin.

The Splenic Injury Outcomes Trial: An American Association For the Surgery of Trauma Multi-Institutional Study

BACKGROUND: Delayed splenic hemorrhage after nonoperative management (NOM) of blunt splenic injury (BSI) is a feared complication, particularly in the outpatient setting. Significant resources, including angiography (ANGIO), are used in an effort to prevent delayed splenectomy (DS). No prospective, long-term data exist to determine the actual risk of splenectomy. The purposes of this trial were to ascertain the 180-day risk of splenectomy after 24 hours of NOM of BSI and to determine factors related to splenectomy. METHODS: Eleven Level I trauma centers participated in this prospective observational study. Adult patients achieving 24 hours of NOM of their BSI were eligible. Patients were followed up for 180 days. Demographic, physiologic, radiographic, injury-related information, and spleen-related interventions were recorded. Bivariate and multivariable analyses were used to determine factors associated with DS. RESULTS: A total of 383 patients were enrolled. Twelve patients (3.1%) underwent in-hospital splenectomy between 24 hours and 9 days after injury. Of 366 discharged with a spleen, 1 (0.27%) required readmission for DS on postinjury Day 12. No Grade I injuries experienced DS. The splenectomy rate after 24 hours of NOM was 1.5 per 1,000 patient-days. Only extravasation from the spleen at time of admission (ADMIT-BLUSH) was associated with splenectomy (odds ratio, 3.6; 95% confidence interval, 1.4–12.4). Of patients with ADMIT-BLUSH (n = 49), 17 (34.7%) did not have ANGIO with embolization (EMBO), and 2 of those (11.8%) underwent splenectomy; 32 (65.3%) underwent ANGIO with EMBO, and 2 of those (6.3%, p = 0.6020 compared with no ANGIO with EMBO) required splenectomy. CONCLUSION: Splenectomy after 24 hours of NOM is rare. After the initial 24 hours, no additional interventions are warranted for patients with Grade I injuries. For Grades II to V, close observation as an inpatient or outpatient is indicated for 10 days to 14 days. ADMIT-BLUSH is a strong predictor of DS and should lead to close observation or earlier surgical intervention. LEVEL OF EVIDENCE: Prognostic/epidemiological study, level III; therapeutic study, level IV

Refined localization of human connexin32 gene locus, GJB1, to Xq13.1

Connexins are the peptide subunits of gap junctions that interconnect cells to allow the direct, intercellular transfer of small molecules. Recently, the human connexin32 gene (locus designation GJB1) has been regionally mapped by three other laboratories to Xp11-q13, Xcen-q22, and Xp11-q22. The smallest region of overlap from these studies is Xcen-q13. By using a series of somatic cell hybrid mapping panels and a rat connexin32 cDNA probe, we have localized the human GJB1 locus to a much smaller region in proximal Xq13.1, in interval 8, as described by Lafreniere et al. (8).Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/30018/1/0000386.pd