PubMed Health⌕ Search

Biomedical subjects

K B Simons

Publications and source records attributed to K B Simons.

23 records · Page 2Linked to original sources
PubMed1983

Transient retinal striae.

Transient retinal folding was observed in a 28-year-old woman presenting with bilateral uveal inflammation. These retinal striae resolved within 5 weeks as the anterior uveal inflammation responded to topical cycloplegic and corticosteroid therapy. Ultrasonographic findings demonstrated choroidal thickening as a contributing factor in the production of these temporary retinal folds. We present this unusual case since transient retinal folding has been rarely documented, and as far as we are aware, has not been previously investigated by ultrasonography.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Pupillary response to atrial natriuretic factor in rabbits.

This study was designed to evaluate the pupillary and intraocular pressure (IOP) response to exogenously administered atrial natriuretic factor (ANF) in rabbits. Dose-response studies were conducted by administering intracameral (i.c.) ANF (0.1-5 micrograms). The effect of route of administration was evaluated by administering ANF (5 micrograms/kg) intravenous (i.v.) subcutaneous (s.c.) and intraperitoneal (i.p.). In a final study, normal rabbit serum or ANF antiserum were administered i.c. In all studies, pupillary diameter (PD) and IOP were evaluated. Intracameral administration of ANF (0.1-5 micrograms) produced a significant (P less than 0.01) dose-dependent unilateral miosis without affecting IOP. Peripheral (i.v., s.c., i.p.) administration ANF did not affect PD or IOP. Finally, ANF antiserum did not affect PD significantly. These data suggest that ocular, but not circulating ANF may contribute to regulate pupillary function. The mechanism of the miotic response to ANF probably involves interactions with other autonomic neurotransmitters because immunoneutralization of endogenous ocular ANF was without measurable effect.

Animals↗
PubMedDate not supplied

Antagonism of neurotensin induced miosis by thyrotropin-releasing hormone (TRH) in rabbits.

In previous studies we have shown that thyrotropin-releasing hormone (TRH) antagonizes many of the neural effects of neurotensin (NT). This study, evaluated the ability of TRH and two TRH analogs: 3 methyl-His-TRH and Phe2-TRH to affect NT-induced miosis in rabbits. In confirmation of previous findings, NT (30 micrograms) produced a significant miosis. The high (60 micrograms), but not the low (30 micrograms) dose of TRH significantly antagonized NT (30 micrograms)-induced miosis. Of interest was the observation that 3 methyl-His-TRH and Phe2-TRH were more effective than native TRH in blocking NT-induced miosis. The inhibitory effect of 3 methyl-His-TRH on the miotic response to NT exhibited long duration (approximately 60 min) when compared to native TRH and Phe2-TRH. TRH or the TRH congeners had no appreciable effects on pupillary diameter when administered alone. These findings indicate that TRH antagonizes the miotic response to NT, and suggest a hitherto undescribed peptide-peptide interaction involved in regulation of iris motility.

Animals↗
PubMedDate not supplied

Ligneous conjunctivitis: an autosomal recessive disorder.

Two siblings, a boy and a girl, developed a chronic, bilateral conjunctivitis with large recurrent pseudomembranes. The diagnosis of ligneous conjunctivitis was made by excisional biopsies in both. The family was referred for genetic counseling after the second child developed the disorder. On the basis of this family and previous reports, we believe that ligneous conjunctivitis is a genetic disorder inherited in an autosomal recessive pattern and that genetic counseling should be offered to the parents of affected children.

Child, Preschool↗