Coats' disease and persistent hyperplastic primary vitreous. Role of MR imaging and CT

Coats' disease is an idiopathic disorder in which telangiectatic and aneurysmal retinal vessels leak a lipoproteinaceous exudate, with consequent bullous retinal detachment. It is a diagnostic challenge, and CT and MR imaging provide valuable information to differentiate it from other pathologies, particularly from retinoblastoma. Typical, advanced Coats' disease shows on CT a denser substance posterior to the vitreous, which on MR is hyperintense on all pulse sequences. Contrast administration on both CT and MR might give slight linear enhancement at the boundary between vitreous and exudation. Persistent hyperplastic primary vitreous (PHPV) is a unilateral disorder in a microphthalmic eye, seen in full-term infants. PHPV rarely is bilateral in patients with Norrie's disease, Warburg syndrome, or patients with retinal dysplasia. Persistent fetal vasculature leads to fibrosis, resulting in elongation of the ciliary processes, retinal detachment, and spontaneous cataracts. The CT appearance in the disorder is quite variable; however, MR imaging may be superior in demonstrating the enhancing retrolental mass and the elongated ciliary processes.     

The recognition of sentences in noise by normal-hearing listeners using simulations of cochlear-implant signal processors with 6-20 channels

Sentences were processed through simulations of cochlear-implant signal processors with 6, 8, 12, 16, and 20 channels and were presented to normal-hearing listeners at +2 db S/N and at -2 db S/N. The signal-processing operations included bandpass filtering, rectification, and smoothing of the signal in each band, estimation of the rms energy of the signal in each band (computed every 4 ms), and generation of sinusoids with frequencies equal to the center frequencies of the bands and amplitudes equal to the rms levels in each band. The sinusoids were summed and presented to listeners for identification. At issue was the number of channels necessary to reach maximum performance on tests of sentence understanding. At +2 dB S/N, the performance maximum was reached with 12 channels of stimulation. At -2 dB S/N, the performance maximum was reached with 20 channels of stimulation. These results, in combination with the outcome that in quiet, asymptotic performance is reached with five channels of stimulation, demonstrate that more channels are needed in noise than in quiet to reach a high level of sentence understanding and that, as the S/N becomes poorer, more channels are needed to achieve a given level of performance.     

Disruption of IRS-2 causes type 2 diabetes in mice

Human type 2 diabetes is characterized by defects in both insulin action and insulin secretion. It has been difficult to identify a single molecular abnormality underlying these features. Insulin-receptor substrates (IRS proteins) may be involved in type 2 diabetes: they mediate pleiotropic signals initiated by receptors for insulin and other cytokines. Disruption of IRS-1 in mice retards growth, but diabetes does not develop because insulin secretion increases to compensate for the mild resistance to insulin. Here we show that disruption of IRS-2 impairs both peripheral insulin signalling and pancreatic beta-cell function. IRS-2-deficient mice show progressive deterioration of glucose homeostasis because of insulin resistance in the liver and skeletal muscle and a lack of beta-cell compensation for this insulin resistance. Our results indicate that dysfunction of IRS-2 may contribute to the pathophysiology of human type 2 diabetes.     

Selenium, calcium channel blockers, and cancer risk--the Yin and Yang of apoptosis?

It is increasingly clear that apoptosis plays a crucial role in the promotional phase of cancer development. Initiated pre-neoplastic clones in rat liver experience a high rate of apoptosis, and this rate has an important impact on the survival and growth of these clones. Suppression of apoptosis appears to be a universal property of cancer promoters, suggesting conversely that agents which inhibit cancer induction during the promotional phase increase the rate of apoptosis in initiated cells. Modulation of apoptosis is a likely explanation for recent striking evidence that use of calcium channel blockers substantially increases, whereas supplemental selenium substantially decreases, human cancer incidence. Non-genotoxic measures which are likely to upregulate apoptosis in pre-neoplastic/neoplastic cells--and thus may be useful in prevention and/or therapy--include selenium, retinoids/carotenoids, green tea polyphenols, caloric restriction, downregulation of IGF-I activity, high-dose tamoxifen and other protein kinase C antagonists, withdrawal or blockade of trophic hormones, isoflavones, limonene, vitamin D and cholecalciferol analogs, dietary fiber/sodium butyrate, hyperthermia, benzaldehyde derivatives, and creatine.