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Biomedical subjects

C McCulloch

Publications and source records attributed to C McCulloch.

At least 19 recordsLinked to original sources
PubMed1989

Excitatory effect of morphine and opioid peptides in the rat isolated colon.

Morphine and the opioid peptides cause isolated segments of rat colon to contract and relax rhythmically. This study re-examines two hypotheses to explain this phenomenon: Release of 5-hydroxytryptamine (5-HT)/acetylcholine by morphine or inhibition of a tonically active non-adrenergic, non-cholinergic (NANC) inhibitory mechanism. Rhythmic contractions induced by morphine (5 x 10(-6) M) were naloxone sensitive (10(-6) M) but unaffected by methysergide (10(-6) M), atropine (10(-6) M) or pretreatment of rats with p-chlorophenylalanine (200 mg kg-1 i.p. for four days) which lowered the 5-HT level in the colon from 3.73 +/- 0.83 mg g-1 in controls to 0.41 +/- 0.06 mg g-1 (P less than 0.001). The pattern of rhythmic contractions produced by morphine was unlike those produced by 5-HT (5 x 10(-6) M), acetylcholine (5 x 10(-6) M) or potassium chloride (30 mM). Tetrodotoxin (10(-6) M), apamin (10(-8) M), clonidine (2 x 10(-8) M), phentolamine (10(-5) M) or oxprenolol (10(-5) M) caused rhythmic contractions which were unaffected by naloxone. Clonidine contractions were inhibited by yohimbine (10(-7) M) but not by prazosin (10(-6) M). Electrical field stimulation at the peak of a contraction induced by morphine, apamin or clonidine, produced an inhibitory response which was unaffected by atropine, phentolamine, propranolol and guanethidine (all 10(-5) M). It persisted in colon segments from the rats with reserpine or 6-hydroxydopamine. These results suggest that neither the 5-HT/acetylcholine hypothesis nor inhibition of the NANC mechanism adequately explains the excitatory effect of morphine in the rat colon.

Acetylcholine↗
PubMed1988

Pathological study in a female carrier of choroideremia.

We present the pathological findings in one eye of a 68-year-old woman with choroideremia. There was widespread malformation of the outer receptor segments. A second retinal finding was patches of atrophy, involving loss of the retinal outer cell layer. The pigment epithelium was intact, although there were areas showing depigmentation of the cells. The choriocapillaris was present. The findings suggest that the primary defect in choroideremia lies at the retina-pigment epithelium interface. Possible mechanisms are discussed.

Aged↗
PubMed1986

Effects of 30% intestinal resection on whole population cell kinetics of mouse intestinal epithelium.

The intestine remaining after resection undergoes a well known compensatory response. Crypts and villi grow in size, and the number of proliferating cells in a crypt increases. The crypt labeling index, however, is unchanged, which is thought to suggest that the growth fraction also remains unchanged and hence that the system is enlarged, but otherwise the new steady-state is similar to that of the controls. It is also generally accepted that no new crypts or villi are added to the adapting bowel. In this study we applied recently developed tools to study the response of the intestinal epithelium as a whole. Thus, the effects of 30% intestinal resection on whole population cell kinetics were determined by using flow cytometry, Coulter particle counting, and simple morphometric techniques. In addition to the classic response, we found an increase in the rate of crypt production, which was due mainly to a shorter crypt replication cycle. Thus, new crypts were produced at a faster rate in the resected animals than in the transected controls. This resulted in an expansion of the crypt cell population in the epithelium following resection. There was a corresponding expansion of the cycling cell population and thus an increase in the growth fraction of the resected epithelium. We conclude that for the crypt population, the classic story is correct with the exception that new crypts are added to the epithelium after resection. However, for the epithelium as a whole, the classic story is misleading as there appears to be an increase in the growth fraction of the epithelium after intestinal resection.

Animals↗
PubMed1986

Recurrent corneal erosion, microcystic epithelial dystrophy, map configurations and fingerprint lines in the cornea.

A 45-year-old lady presented with a recurrent corneal erosion. On closer examination, she was found to have epithelial microcysts and fingerprint dystrophy. Pathologic material from the affected cornea showed microcysts, protrusions of basement membrane and evidence of poor adhesion between the basement membrane and the epithelial cells, as well as between the epithelial cells themselves. The case demonstrated the clinical and pathologic features of recurrent corneal erosion, microcystic disease and fingerprint dystrophy of the cornea, together with the pathologic findings of map dystrophy. The authors suggest that these four diseases are various expressions of a clinicopathologic entity, epithelial basement membrane corneal dystrophy. A pathologic explanation for recurrent corneal erosion is apparent.

Cornea↗
PubMed1979

Hereditary lens dislocation with angle closure glaucoma.

Eight patients in one family showed dislocation of the lens and secondary angle-closure glaucoma coming on in the 50's. They all displayed the sequence of myopia, angle shallowing, followed by angle-closure glaucoma. This sequence should alert the clinician to the possibility of a hereditary disease. The cause of the disease is unknown. It is suggested that treatment should be an iridectomy in the early stages and a lens extraction if glaucoma develops.

Age Factors↗
PubMed1979

Epithelial downgrowth following cataract extraction.

This case of epithelial downgrowth following cataract extraction shows the typical sequence of a noneventful cataract extraction with satisfactory recovery but after a time, the appearance of conjunctival injection, iritis and attacks of elevated ocular pressure. A minimal membrane on the posterior surface of the cornea could be seen but the diagnosis rested on the sequence of events and was confirmed by the pathologic investigation. The apithelial cells grow freely on the iris, but extend onto the cornea and posteriorly apparently without hindrance. The epithelial cells form a basement membrane next to the iris, much as they do on the surface of the cornea next to Bowman's membrane. The source of the cells in this case was not identified; they presumably came from conjunctiva although no track through the sclera was found and the cells themselves did not show goblet cells.

Aged↗
PubMed1978

Whorl-like degeneration of corneal epithelium a clinico-pathologic study.

A case of epithelial corneal degeneration that was first seen as a pigmented plaque but changed to a whrol-like pattern and then partially regressed is described. The pathologic abnormality was an intra-cellular inclusion of lipid in the basal cells and of lipid and mucopolysaccharide in the wing and superficial cells. No duplication of basement membrane or thickening of Bowman's layer was present. It is suggested that despite different origins the pathologic entity in this case, in Fabry's disease and in chloroquine keratopathy is similar. The whorled pattern is due to a sliding of the corneal epithelial cells as they rise from the basal cells to the surface, much as a cyclonic flow forms about an atmospheric low in the southern hemisphere.

Aged↗
PubMed1978

A coronary teaching program in a community hospital.

In conclusion, the teaching program we developed appears to meet the needs originally established by the audit. Nurses are provided with a method of assessment, evaluation, and documentation. The program also provides a means of teaching continuity while following a structured time schedule that allows for recognition and satisfaction of individual patient needs. The patient teaching record provides the final tool as a reference and ongoing source of evaluation.

Coronary Disease↗
PubMed1977

Crystalline dystrophy of the cornea: a light and electron microscopic study.

We examined biopsy material from a case of stromal crystalline dystrophy of the cornea by light and electron microscopy. Frozen sections were positive for neutral fat and negative for cholesterol. Electron microscopy showed that the empty spaces at the site of the crystals did not have typical crystalline profiles. We concluded that in our case the crystals were composed of neutral fat.

Adult↗
PubMed1977

The presence of cell-mediated immunity in uveitis.

We have attempted to demonstrate cell mediated immunity in cases of uveitis. We tested blood samples of patients for leucocyte migration inhibition (LMI) and lymphocyte transformation (LT). The gel diffusion test was used to detect humoral antibody. Allogeneic uveal, retinal and corneal antigens were prepared for the tests from eye bank eyes. The LMI and LT tests gave positive results in 9 out of 16 cases. In these 9 cases 8 were positive to retinal antigen, three with corneal antigen and only one was positive against uveal antigen. Humoral antibodies were not detected. We suggest that cell mediated autoimmunity is present but the relationship of this to the uveitis itself is obscure.

Adolescent↗
PubMed1976

Optic disc observations in glaucoma.

In glaucomatous eyes, contrary to normal eyes, the blind spot size is not correlated with the disc or cup size, and the size of the optic disc, cup and optic rim also varies. The variation in area of the glaucomatous optic disc correlates with variation in area of the optic cup. The rim width and total rim area in glaucomatous eyes are decreased. In glaucoma the upper, lower and nasal rim widths are about the same, whereas the smallest rim width occurs temporally. Thus, clinically cupping in glaucoma eyes need not be vertically oval.

Glaucoma↗
PubMed1975

Gyrate atrophy of the choroid and retina with hyperornithinemia.

A case of gyrate atrophy of the choroid and retina and hyperornithinemia in a 28-year-old man was subjected to extensive clinical and biochemical investigation. The familial occurrence of the ocular disease and of abnormality of amino acids was unique to this patient, being absent in parents and siblings. He presented with progressive visual loss, and had cataracts and large areas of peripheral lacumar atrophy. Clinically there was no other abnormality. However, he was hyperuricemic and had an abnormal electroencephalogram. Despite otherwise normal biochemical indices of hepatic, renal, and muscle function, selective catheterization of an artery, the hepatic vein, the renal vein, and a deep forearm vein showed all of these circulatory beds to be producing ornithine according to arteriovenous difference measurements. Cerebrospinal fluid and urine contained increased amounts of ornithine. Though electromyography was normal a muscle biopsy specimen was abnormal. Clinical tests including arginine loading, glucose tolerance testing, and other measurements of blood variables provided inferences as to the metabolic locus of the abnormality. The syndrome is a systemic multiorgan disorder in which the choriod and retina would appear to be target organs and the hyperornithinemia to be of as yet undetermined cause and pathogenic significance.

Adult↗
PubMed1975

Anterior subcapsular cataract. An electron microscopic study.

Electron microscopic findings from a case of anterior subcapsular cataract are presented. It is suggested that the epithelial cells increase in activity, form fibrillae and multiple layers of basement membrane, and these make up the anterior plaque. The same activity, to a lesser degree, is present under the posterior capsule. This abnormal function of forming fibrillae and basement membrane along with increased ribosomal activity may be called pseudometaplasia.

Basement Membrane↗
PubMed1975

Gyrate atrophy of the choroid and retina: clinical, ophthalmologic, and biochemical considerations.

A case of gyrate atrophy of the choroid and retina associated with hyperornithinemia has been subjected to extensive clinical and biochemical investigation. The familial occurrence of the ocular disease and of abnormality of amino acid was unique to this 28-year-old male, being absent in parents and siblings. He presented with progressive visual loss, and was found to have cataracts and large areas of peripheral lacunar atrophy. Clinically there was no other abnormality. However, he was hyperuricemic and has an abnormal EEG. Despite otherwise normal biochemical indices of hepatic, renal, and muscle function; selective catheterization of an artery, the hepatic vein, the renal vein, and a deep forearm vein showed all of these circulatory beds to be producing ornithine according to arteriovenous difference measurements. Cerebrospinal fluid and urine contained increased amounts of ornithine. Though electromyography was normal, the muscle biopsy was abnormal. Clinical tests including arginine loading, glucose tolerance testing, and other measurements of blood variables provided inferences as to the metabolic locus of the abnormality. The syndrome is a systemic multiorgan disorder in which the choroid and retina would appear to be target organs and the hyperornithinemia to be of, as yet, undetermined cause and pathogenic significance.

Adult↗