Severe herpetic keratitis. I: Prevalence of visual impairment in a clinic population.

We report a prevalence study of the best visual acuity in the affected eye of 100 selected patients with herpetic keratitis seen during a two-year period. Sixty-two patients retained an acuity of 6/9 or better without requiring penetrating keratoplasty (PK). The prevalence of reduced visual acuity severe enough to warrant PK was 33%. Patients requiring PK for whom full clinical records were available suffered a mean of 6.8 episodes of keratitis. In this group of patients the vision of 18 fell from 6/6 to 6/60 over a mean period of 8.5 years. Once visual acuity was permanently reduced to 6/12, 78% of patients proceeded to lose vision to 6/60. Unilateral visual impairment occurs in at least a third of patients with severe herpetic keratitis. Once vision falls permanently to 6/12, the long-term prognosis for vision appears to be poor.     

A review of professional liability cases affecting the practice of optometry

In establishing the liability of optometrists for negligence the courts have applied the same standard of care that is imposed upon other health care professionals, holding that optometrists must employ the minimum degree of skill, care and learning that is ordinarily exhibited by members of the profession who are in good standing. The leading cases establishing this standard have involved glaucoma, retinal detachment, and intraocular tumors. Optometrists have also been held liable under product liability law for injuries caused by ophthalmic lenses, which illustrates the trend toward strict liability. Other cases have involved the doctrine of informed consent.     

Successful bridge to transplantation in a patient with Becker muscular dystrophy-associated cardiomyopathy.

A 28-year-old male patient diagnosed with Becker muscular dystrophy (BMD)-associated cardiomyopathy was successfully bridged to transplantation with the Cardiowest total artificial heart. Dramatic improvement of muscular functional status occurred following transplantation.     

Mutational analysis of HOXD13 and HOXA13 genes in the triphalangeal thumb-brachyectrodactyly syndrome.

The triphalangeal thumb-brachyectrodactyly syndrome is a very rare autosomal dominant disorder of unknown etiology characterized by an unusual pattern of limb malformations: triphalangeal thumbs and brachyectrodactyly in the hands, and ectrodactyly in the feet. In a previous report, we described the clinical and radiographical features of three related subjects with the disease and suggest that due to the unusual combination of limb defects and to its phenotypic similarity with the limb malformative pattern induced by disrupting the Hoxd13 gene in mouse, the triphalangeal thumb-brachyectrodactyly syndrome might be caused by mutations in a HOX gene. After sequencing the entire coding region of HOXD13 and the highly conserved homeodomain encoding region of HOXA13, we do not detect any deleterious mutation in any of the patients excluding that alterations at these sequences are responsible for the disease. Mutations in regulatory regions of these genes or in other genes involved in limb development might be responsible for the disease.     

Effects of galanin on insulin and glucagon secretion in the rat

Galanin-like immunoreactivity has been visualized in nerve fibers in the islets of Langerhans, suggesting an involvement of galanin in the neural regulation of islet function. In this study, we investigated the effects of galanin on basal and stimulated insulin and glucagon secretion by infusing the peptide at three different dose rates in rats. We also studied the direct effect of galanin on insulin secretion from freshly isolated rat islets. At 320 pmol/kg/min, but not at 20 or 80 pmol/kg/min, galanin lowered basal plasma insulin levels. In contrast, basal plasma glucagon levels were lowered by galanin already at 20 and 80 pmol/kg/min. Furthermore, galanin inhibited both glucose- and arginine-induced insulin release at all three dose levels, whereas arginine-induced glucagon release was not affected by galanin. Glucose-stimulated insulin secretion from isolated rat islets was dose-dependently suppressed by galanin (10^-6-10^-8M). Therefore, it is concluded that galanin in rats inhibits insulin secretion, both in vivo and in vitro, and that at lower dose levels, the peptide also inhibits basal glucagon release.