Biomedical subjects

W M Hart

Publications and source records attributed to W M Hart.

At least 55 records · Page 3Linked to original sources

PubMed1979

The metabolism of dihomo-gamma-linolenic acid in man.

Orally administered dihomo-gamma-linolenic acid (DHLA) is well absorbed in man; it appears in blood after ca. 4 hr first as triglyceride ester and later as phospholipid. After sustained-dosing, DHLA penetrated membrane pools and all phospholipid components but, depending on the dosage, reached a metabolic equilibrium in 4-16 days. Intact platelets do not accumulate arachidonate following DHLA administration, and species differences occur in the capacity of animals to metabolize DHLA to arachidonic acid (AA). The rat appears to be unusual in having a very active hepatic delta5-desaturase enzyme system. Potentially antithrombotic changes in platelet function which followed the administration of DHLA to man were accompanied by a significant increase in the capacity of platelets to synthesize PGE1. Concomitant increases in PGE2 synthesis do not apparently result from an increased production of AA and suggest that DHLA, or a DHLA metabolite, interferes with the metabolism of AA. Effects on thromboxane and prostacyclin synthesis are being studied.

8,11,14-Eicosatrienoic Acid↗

PubMed1979

Optic disk edema in sarcoidosis.

A 24-year-old woman had bilateral optic disk edema. A granulomatous uveitis and macular edema subsequently ensued. Histologic examination of a biopsy specimen taken from an area of marked hilar adenopathy revealed noncaseating epithelioid cell tubercles. No other associated systemic findings were noted, and after a course of topical and systemic corticosteroid therapy, the ocular manifestations disappeared.

Adult↗

PubMed1978

Quantitative visual field and optic disc correlates early in glaucoma.

A retrospective study was made of persons with ocular hypertension and normal initial visual fields. Seventy eyes were followed, and glaucomatous visual field defects developed in 25 of these eyes. In eyes with ocular hypertensio, the area enclosed by the central visual field isopter (I2e) was significantly smaller than that previously reported for an age-corrected group of eyes with normal intraocular pressure. In the absence of glaucomatous visual field defects, isopter areas were not releated to cup-disc ratios. Coincident with visual field loss, reductions in both peripheral (I4e) and central (I2e) isopter areas correlated linearly with increases in the cup-disc ratio. Prior to visual field loss, the I4e isopter area wassignificantly smaller among those eyes destined to lose visual field.

Adult↗

PubMed1978

Cytomegalovirus in juvenile iridocyclitis.

We cultured cytomegalovirus from lens material aspirated from the eye of a 4-year-old boy who had a severe bilateral iridocyclitis and secondary cataracts. There were neither systemic manifestations of congenital disease nor chorioretinitis.

Child, Preschool↗

PubMed1977

Visual field changes in ocular hypertension. A computer-based analysis.

A minicomputer system has been developed to digitize and store visual field data. In 110 cortiocosteroid-nonresponding subjects aged 10 to 75, the area of the i4e and i2e isopters and of the blind spot changed linearly as a function of age. Within this population the same visual field parameters were randomly distributed with respect to intraocular pressure. In 32 cortiocosteroid responders (increase in intraocular pressure to over 31 mm Hg after topical administration of corticosteroids) with normal visual fields, the central visual field area (i2e isopter) was reduced as a nonlinear function of IOP. Increases in IOP in excess of 8 mm Hg were required to produce significant mean reductions in central visual field area.

Adolescent↗

PubMed1977

Management of dysthyroid optic neuropathy.

The diagnosis of dysthyoid ophthalmopathy is based on clinical observation of characteristic ophthalmic abnormalities. Proper diagnosis and initiation of treatment should not be delayed because a patient is found to be euthyroid. Although visual problems in dysthyroid ophthalmopathy are uncommon this disorder can result in permanent severe visual loss if optic neuropathy is not detected early and managed properly. Oral corticosteroid therapy and surgical decompression both seem to have a place in the treatment of dysthyroid ophthalmopathy with optic neuropathy.

Adrenal Cortex Hormones↗

PubMed1974