Postoperative refractive error of secondary intraocular lens implantation after simultaneous vitrectomy and lensectomy.

To determine postoperative refractive errors of secondary intraocular lens (IOL) implantation, this study was performed in 42 eyes of 42 patients following secondary IOL implantation fixed in the sulcus after simultaneous vitrectomy and phacoemulsification and aspiration. Controls were 138 eyes of 124 patients with cataract who underwent phacoemulsification and aspiration and IOL implantation. The spread between expected and actual refraction (actual - expected) was -0.81 +/- 0.86 diopters (average +/- standard deviation) in the study group and 0.01 +/- 0.91 diopters in the control group (statistically significant, P < .001, Student's t test). The actual refractive errors in the study subjects were shifted toward myopia compared with the controls.     

Dermal fillers. The next generation.

In today's busy and demanding world, we no longer have the luxury of taking weeks to recover from a surgical procedure and are more frequently seeking quicker alternatives. The use of dermal fillers meets this need but in no way replaces a surgical intervention. Previously, bovine collagen was the only approved dermal filler. However, today there are several options available including a human collagen, a variety of hyaluronic acids, and a permanent injectable product. Each of the products has different uses, indications, and adverse reactions. The experienced injector now has a wider selection of products from which to choose to ensure that the patient receives what is best suited for his or her particular situation. These new products are becoming increasingly popular, due to acceptability and affordability, but are not without potential complications and adverse reactions. This article discusses the use of Cosmoderm/Cosmoplast, Hylaform, Restylane/Perlane, and Artecoll dermal fillers.     

Aneurysms of the anterior communicating artery and subclavian artery in association with congenital absence of unilateral internal carotid artery]

We encountered a rare case of unilateral internal carotid arterial defect complicated with anterior communicating aneurysm and subclavian artery aneurysm. The patient was a 56-year-old man in whom cerebral angiography and 3D-CTA revealed defects in the right internal carotid artery and the right carotid canal, and an unruptured aneurysm in the anterior communicating artery. In addition, the patient was also found to have an unruptured aneurysm in the right subclavian artery. As both the aneurysms were considered to have a high risk of rupture and such subclavian aneurysms were likely to cause an embolism, radical surgery was performed for each aneurysm. The postoperative course was uneventful, and the patient was discharged without ambulatory limitations. Although the defect in the internal carotid artery is a relatively rare vascular deformity, the incidence of cerebral aneurysm is about 30% in such cases due to the marked hemodynamic stress involved. On the other hand, there have been only two previous case reports of internal carotid arterial defect complicated with a subclavian aneurysm. Moreover, there have been no previous reports of internal carotid arterial defect complicated with both an intracranial aneurysm and a subclavian aneurysm, as observed in the present case. Thus, this case was very rare and is reported here.     

Three human osteosarcoma cell lines exhibiting different phenotypic expressions.

to elucidate the differences in histological features and biological behavior of osteosarcomas, three human osteoblastic-type osteosarcomas were studied in vitro and in nude mice. The secretory processing and extracellular fiber formation of type I collagen proved to be the most important factor in bone formation in the osteosarcomas. Alkaline phosphatase also seemed to be important. However, we were unable to find any particular protooncogene abnormalities which could have been implicated in the occurrence or biological behavior of these osteosarcomas.     

Molecular biological study of the rhodopsin gene in Japanese patients with autosomal dominant retinitis pigmentosa]

The author analyzed codon 347 of the rhodopsin gene using PCR (polymerase chain reaction) amplification and restriction enzymes in 19 unrelated Japanese families including 28 patients with autosomal dominant retinitis pigmentosa (ADRP). An allele of codon 347 mutation was found in a family (father and daughter). Sequence analysis shows that the mutation is from CCG to CTG. This mutation appears to be the cause of one form of ADRP, since it was also found in Japanese cases of ADRP which have a different racial background from families reported by Dryja et al.     

Cerebellopontine angle ganglioneuroblastoma

Summary The CT, MR and histological features of a rare ganglioneuroblastoma of the cerebellopontine angle and cavernous sinus are reported.     

Lectin-mediated enhancement of dengue virus infection in a mouse macrophage cell line Mk1

Summary Treatment of a mouse macrophage cell line Mk1 with pokeweed mitogen (PWM) either before or during but not after virus inoculation resulted in an enhancement of dengue virus (DV) infection. The infection enhancement was primarily due to an increase in the number of DV-infected cells but not to increased virus production in a cell. These results suggested that PWM treatment mediated increased DV binding and/or penetration to Mk1 cells, thereby resulting in the infection enhancement.N-acetylglucosamine (GlucNAc) did not suppress PWM-mediated enhancement of DV infection when added to Mk1 cells after PWM treatment was done, although GlucNAc clearly suppressed the effect of PWM when added simultaneously with PWM. The results implied the possibility that the PWM-mediated increase in viral binding/penetration was not due to a cross-linking by PWM between DV and a cell-surface receptor, but due to another mechanism, presumably exposure of a masked DV receptor(s). The DV receptor, unidentified as yet, involved in the PWM-mediated infection enhancement appeared to have no relation with IgG Fc receptors that are known to be involved in antibody-mediated enhancement of DV infection.     

Camostat mesilate attenuates pancreatic fibrosis via inhibition of monocytes and pancreatic stellate cells activity

Camostat mesilate (CM), an oral protease inhibitor, has been used clinically for the treatment of chronic pancreatitis in Japan. However, the mechanism by which it operates has not been fully understood. Our aim was to evaluate the therapeutic efficacy of CM in the experimental pancreatic fibrosis model induced by dibutyltin dichloride (DBTC), and we also determined the effect of CM on isolated monocytes and panceatic stellate cells (PSCs). In vivo, chronic pancreatitis was induced in male Lewis rats by single administration of 7 mg/kg DBTC and a special diet containing 1 mg/g CM was fed to the DBTC+CM-treated group from day 7, while the DBTC-treated group rats were fed a standard diet. At days 0, 7, 14 and 28, the severity of pancreatitis and fibrosis was examined histologically and enzymologically in both groups. In vitro, monocytes were isolated from the spleen of a Lewis rat, and activated with lipopolysaccharide stimulation. Thereafter, the effect of CM on monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) production from monocytes was examined. Subsequently, cultured rat PSCs were exposed to CM and tested to see whether their proliferation, MCP-1 production and procollagen alpha1 messenger RNA expression was influenced by CM. In vivo, the oral administration of CM inhibited inflammation, cytokines expression and fibrosis in the pancreas. The in vitro study revealed that CM inhibited both MCP-1 and TNF-alpha production from monocytes, and proliferation and MCP-1 production from PSCs. However, procollagen alpha1 expression in PSCs was not influenced by CM. These results suggest that CM attenuated DBTC-induced rat pancreatic fibrosis via inhibition of monocytes and PSCs activity.     

Loss of suppressor T cell function and circulating immune complexes in chronic active liver diseases

Suppressor T cell function is decreased in patients with chronic active liver diseases (CALD). To account for the alterations, we examined the effect of sera of patients with various liver diseases on concanavalin A (Con A) induced suppressor T cell activity of normal individuals. The suppressor T cell activity was inhibited by heat-inactivated serum pretreatment in 13 of 27 cases of patients with CALD and in five of 11 cases of patients with acute viral hepatitis, whereas only two sera of 18 patients with other liver diseases affected suppressor cell activity. Using a 125I-C1q-binding test, a significant correlation (P less than 0.01) was detected between the degree of inhibition in the development of suppressor T cells and the level of circulating immune complexes in the sera of CALD patients. The blocking effect of patients' sera disappeared when the immune complexes were removed with polyethylene glycol. These data suggest that circulating immune complexes modulate cellular immunity in patients with CALD by influencing the suppressor T cell function.