Ordering behaviors and age-hardening in experimental AuCu-Zn pseudobinary alloys for dental applications

Age-hardening mechanisms and related ordering behaviors of the experimental (AuCu)_1−xZn_x alloys with x0.2 were investigated for dental applications. The addition of Zn to equiatomic AuCu greatly increased the age-hardening rate and delayed overaging. It was suggested that the quenched-in excess vacancies were greatly related to the age-hardening rate in the AuCu–Zn pseudobinary alloys. In these alloys, the hardness became maximum during the very initial stage of ordering, and with the development of ordered phase, the hardness began to decrease. Transmission electron microscopy revealed that the age-hardening of AuCu–Zn pseudobinary alloys is caused by lattice distortion that occurred during the very early stage of atomic ordering. The addition of Zn to AuCu effectively increased the density of antiphase boundaries per unit volume of the AuCu II superstructure. This is suggested to be the main cause for the retardation of the overaging in the alloys containing Zn of 5 at% or more. This pronounced effect of Zn addition to AuCu alloy on its age-hardening characteristics may be advantageous for obtaining stable mechanical properties of dental casting gold alloys.     

Two cases of limited cutaneous nodular amyloidosis with primary Sj?gren's syndrome]

We described two female patients with primary Sj?gren's syndrome associated with localized cutaneous nodular amyloidosis (LCNA), in which amyloid protein was derived from immunoglobulin light chain. Case 1; a 70-year-old female had complained with polyarthralgia, low-grade fever and parotid gland swelling. She was diagnosed as primary Sj?gren's syndrome. Three years later she noticed brown color small tumor on the thigh and yellow to brown nodules on the bilateral calves of legs. Skin biopsy from the left thigh revealed amyloid L protein deposition, which was positive for anti-lambda light chain staining, in almost entire dermis. Infiltration of lymphocytes and plasma cells around the amyloid deposit were prominent. Case 2; a 51-year-old female had noticed increasing eruption on the hip. Skin biopsy revealed amyloid L protein deposition in the dermis, which was negative for anti-lambda nor kappa light chain staining. When she was refereed to our hospital, she complained of xerostomia and xerophthalmia. She was diagnosed as primary Sj?gren's syndrome. In both cases, histological examination of a minor salivary gland biopsy revealed infiltration of lymphocytes and plasma cells but not amyloid deposit. Serum M protein and urine Bence-Jones protein were not detected. These cases represent localized amyloidosis without systemic involvement. It is widely recognized that Sj?gren's syndrome is frequently accompanied by B cell lymphoproliferative disorders. In LCNA, infiltration of plasma cells around the amyloid deposits was frequently prominent. The relation between these two disorders is discussed.     

Suppression of allergic inflammation by the prostaglandin E receptor subtype EP3

Prostaglandins, including PGD(2) and PGE(2), are produced during allergic reactions. Although PGD(2) is an important mediator of allergic responses, aspirin-like drugs that inhibit prostaglandin synthesis are generally ineffective in allergic disorders, suggesting that another prostaglandin-mediated pathway prevents the development of allergic reactions. Here we show that such a pathway may be mediated by PGE(2) acting at the prostaglandin E receptor EP3. Mice lacking EP3 developed allergic inflammation that was much more pronounced than that in wild-type mice or mice deficient in other prostaglandin E receptor subtypes. Conversely, an EP3-selective agonist suppressed the inflammation. This suppression was effective when the agonist was administered 3 h after antigen challenge and was associated with inhibition of allergy-related gene expression. Thus, the PGE(2)-EP3 pathway is an important negative modulator of allergic reactions.     

Comparative anatomical study of the kidney position in amniotes using the origin of the renal artery as a landmark

The anatomical relationship between the kidney position and its arterial supply was investigated in 21 mammals, 1 bird, and 3 reptiles (n = 1 for each species) and in 43 human cadavers. The following observations were made. (1) Although the right kidney was located caudal to the left kidney in 29 out of 43 human cadavers (67.4%), the origin of the right renal artery from the aorta was located cranial to the origin of the left renal artery in 36 human cadavers (83.7%). Therefore, the relative positions of the kidneys do not correspond with the relative origins of the renal arteries in humans. (2) Among the mammals that were examined, the position of the kidney and the branching level of the renal artery on the right side were usually cranial to those on the left side. (3) In the bird and most reptiles that were examined, kidneys were typically located in the pelvic region and were supplied by segmental arterial branches. These results suggest that the right kidney and its arterial supply are generally located cranial to the left kidney in phylogeny of mammals. While the presence of a human accessory renal artery in 9 out of 86 sides (10.5%) and a cranial origin of the left renal artery relative to the right renal artery in 7 out of 43 cadavers (16.3%), shows some variation in the arterial supply to the kidneys, the origin of the renal arteries can generally be used as phylogenetic landmarks indicating the relative positions of the kidneys. Hence, from an ontological perspective, the human right kidney may be initially situated cranial to the left kidney during the early stages of development. Thereafter, the human right kidney may shift downwards secondary.     

Idiopathic hypertrophic cranial pachymeningitis with perifocal brain edema--case report

A 51-year-old female presented with an extremely rare case of idiopathic hypertrophic cranial pachymeningitis manifesting as markedly thickened frontotemporal meninges with expanding perifocal edema. Magnetic resonance imaging with gadolinium revealed enhancement of the thickened dura mater protruding into the brain parenchyma accompanied by focal edema causing a mass effect. Histological examination of a biopsy specimen revealed thickened dura with infiltrating lymphocytes. Serological and immunological tests were normal. No inflammatory response or evidence of malignant tumors was observed. The patient was treated with predonisolone, resulting in marked improvement of the mass effect. High-dose steroid therapy appears to be effective for intracranial pachymeningitis associated with expanding perifocal brain edema.