Multiaxial Kitagawa analysis of A356-T6

Experimental Kitagawa analysis has been performed on A356-T6 containing natural and artificial defects. Results are obtained with a load ratio of R = -1 for three different loadings: tension, torsion and combined tension-torsion. The critical defect size determined is 400 \pm 100 \mum in A356-T6 under multiaxial loading. Below this value, the microstructure governs the endurance limit mainly through Secondary Dendrite Arm Spacing (SDAS). Four theoretical approaches are used to simulate the endurance limit characterized by a Kitagawa relationship are compared: Murakami relationships [Y Murakami, Metal Fatigue: Effects of Small Defects and Nonmetallic Inclusions, Elsevier, 2002.], defect-crack equivalency via Linear Elastic Fracture Mechanics (LEFM), the Critical Distance Method (CDM) proposed by Susmel and Taylor [L. Susmel, D. Taylor. Eng. Fract. Mech. 75 (2008) 15.] and the gradient approach proposed by Nadot [Y. Nadot, T. ~Billaudeau. Eng. Fract. Mech. 73 (2006) 1.]. It is shown that the CDM and gradient methods are accurate; however fatigue data for three loading conditions is necessary to allow accurate identification of an endurance limit.Comment: 27 pages, 11 figure

Dihydropteroate synthase gene mutations in Pneumocystis and sulfa resistance

Pneumocystis pneumonia (PCP) remains a major cause of illness and death in HIV-infected persons. Sulfa drugs, trimethoprim-sulfamethoxazole (TMP-SMX) and dapsone are mainstays of PCP treatment and prophylaxis. While prophylaxis has reduced the incidence of PCP, its use has raised concerns about development of resistant organisms. The inability to culture human Pneumocystis, Pneumocystis jirovecii, in a standardized culture system prevents routine susceptibility testing and detection of drug resistance. In other microorganisms, sulfa drug resistance has resulted from specific point mutations in the dihydropteroate synthase (DHPS) gene. Similar mutations have been observed in P. jirovecii. Studies have consistently demonstrated a significant association between the use of sulfa drugs for PCP prophylaxis and DHPS gene mutations. Whether these mutations confer resistance to TMP-SMX or dapsone plus trimethoprim for PCP treatment remains unclear. We review studies of DHPS mutations in P. jirovecii and summarize the evidence for resistance to sulfamethoxazole and dapsone

Pilomatrix carcinoma: a rare cutaneous adnexal tumor

Pilomatrix carcinoma is a rare tumor that is generally not diagnosed clinically. An 80-year-old man presented with a 5-month history of rapidly growing nodule of the submandibular area. Histological examination revealed a pilomatrix carcinoma, an aggressive malignancy with metastatic potential

Diffuse dermal angiomatosis of the breast: an emerging entity in the setting of cutaneous reactive angiomatoses

New and emerging types of cutaneous vascular (capillary) proliferations have been described or better categorized in the last few years. They include reactive angioendotheliomatosis, acroangiodermatitis (pseudo-Kaposi sarcoma), diffuse dermal angiomatosis, intravascular histiocytosis, glomeruloid angioendotheliomatosis, and angiopericytomatosis (angiomatosis with cryoproteins). Clinically, they are characterized by multiple, red violaceous, and purpuric patches and plaques, sometimes evolving toward necrosis and ulceration with a wide distribution but a propensity to involve the extremities. Histologically, they are characterized by different patterns of intravascular or extravascular lobular or diffuse hyperplasia of endothelial cells, pericytes, and sometimes histiocytes. Although these angioproliferations can histologically have a pseudoangiosarcomatous pattern, they are reactive in that they originate from the (sub)occlusion of vascular lumina by different localized or systemic disorders. The vascular proliferation stops after the inducing hypoxic stimulus has been withdrawn. Among them, diffuse dermal angiomatosis of the breast is a variant of diffuse dermal angiomatosis involving middle-aged women with macromastia, obesity, smoking, and vasculopathic disorders, considered a distinct disorder in the spectrum of cutaneous reactive angiomatoses. It presents with reticulated erythematous to purple patches with sometimes a tendency to ulcerate and bleeding, appearing on large, pendulous breasts. The pathogenesis is related to tissue hypoxemia resulting from subclinical torsion, compression, and increased venous hydrostatic pressure due to the macromastia, aggravated by the associated ischemic conditions such as hypertension and diabetes. There is no evidence-based therapy, but reduction mammoplasty is a viable treatment option. This should be evaluated in all patients who fail conservative therapy