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Biomedical subjects

K Milner

Publications and source records attributed to K Milner.

9 recordsLinked to original sources
PubMed1999

Antipsychotics from theory to practice: integrating clinical and basic data.

The recent introduction of the atypical antipsychotics into the treatment arena for psychoses and related disorders comes with justifiable excitement. These newer antipsychotics offer several clinical benefits over the conventional antipsychotics, which have been the mainstays of care thus far. The primary advantage of these atypical agents is their superior side effect profiles, particularly with regard to extrapyramidal side effects (EPS). The implications from a reduction in EPS touch on virtually every aspect of pathology in schizophrenic illness, including short- and long-term movement disorders, negative symptoms, noncompliance, cognitive dysfunction, and dysphoria. It should be emphasized that while atypical antipsychotics share many clinical attributes, there are also substantial differences among them. This review will examine the pharmacology, clinical efficacy, and side effect profiles of the atypical antipsychotics and attempt to relate the attributes observed in clinical practice and clinical trials to their basic pharmacologic profiles. There is a fair, but not perfect, correspondence between the pharmacologic profiles of the different atypical antipsychotics and their respective clinical attributes. After a comparative overview of their receptor-binding profiles, a brief pharmacokinetic summary will be provided. Finally, the clinical profiles of these agents will be summarized with regard to both their efficacy and adverse effects.

Animals↗
PubMed1992

The communicative Effectiveness Index: its use with South African stroke patients.

The functional communication of a group of 28 South African stroke patients was examined using the Communicative Effectiveness Index (CETI). It was translated into Afrikaans, Sotho and Zulu and administered to the significant others of 22 aphasic patients with left hemisphere damage and 6 patients with right hemisphere damage. Results were related to the results of standardized language testing and to case history factors such as cultural factors and time since onset. The CETI was readministered in the case of eight of the aphasic subjects after a mean period of six months in order to assess its sensitivity to recovery. Results showed that the CETI seems applicable across different language groups, that it is sensitive to change across time as well as sensitive to the communication disorders resulting from both right and left hemisphere damage. Further it appears to correlate well with overall level of severity. It does not appear to differentiate patients in terms of time since onset. Its potential use as a relatively culture free assessment tool in the South African context is discussed.

Adult↗
PubMed1986

A reexamination of the gain of the vestibuloocular reflex.

The properties of the vestibuloocular reflex (VOR) when the axis of rotation is behind the eyes and fixation of a near target is required were studied in the monkey. The magnitude of VOR gain in each eye was found to be above 1.0 and near the ideal value for stabilizing a retinal image. Evidence that this large VOR gain was not visually mediated was provided by the observations that no reduction in gain and no phase lag were observed at high frequencies of head rotation (2 Hz), large gain was observed in the dark, and large gain was observed within 10-20 ms of the start of head rotation. The magnitude of VOR gain was found to increase with increasing radius of head rotation and also to increase with decreasing target distance. When the distances from the two eyes to the target were different the instantaneous velocities and VOR gains of the eyes were also different. The dependence on radius of rotation indicates that the VOR is mediated by a combination of otolith and canal inputs. A general model for otolith-canal interaction is proposed in which VOR gain is based on a computation of target location relative to the head. This model simplifies to the classical VOR reflex when a cyclopean eye is subjected only to angular displacement.

Adaptation, Ocular↗
PubMed1984

Ultrastructure of trypan blue-induced ocular defects II. Cornea and mesenchyme.

Using scanning and transmission electron microscopy, the histological and cytological alterations induced in the developing eye by trypan blue were examined. Microphthalmic and anophthalmic eyes were analyzed from 16-day rat fetuses whose dams had received a teratogenic dose of trypan blue. Cell and tissue damage within cornea and mesenchyme were assessed. Corneas from the treated groups were undulating and uneven owing to abnormal lens placement and corneal cell injury. Extensive extracellular spacing, few cell-to-cell contacts, patchy glycocalyces, and abnormal surface morphology characterized the corneal cells of treated tissues. Mesenchyme of severely malformed eyes typically filled the eye field in regions normally occupied by retina and lens. As a tissue, mesenchyme lacked organization and those surface features normally present in component cells were altered. Mesenchymal cells were packed so closely that extracellular spaces were nearly obliterated. Microvilli, filopodia, and lamellipodia, cell processes observed in normal mesenchyme, were altered in both number and structure. The cytoplasm of mesenchymal cells was condensed and decreased in volume. These data suggested that 1) in this trypan blue ocular model, virtually all major tissue types were morphologically altered; 2) because healthy mesenchyme and cornea are required for normal development of lens, optic vesicle and ocular adnexa it follows that abnormal cornea and mesenchyme also will compromise these tissues; and 3) since necrotic reminants were not present, this trypan blue model probably causes developmental arrest. The most likely teratogenic pathway is presented with emphasis on the cell surface as a probable site of dye action.

Abnormalities, Drug-Induced↗
PubMed1983

Ultrastructure of trypan blue induced ocular defects: I. Retina and lens.

The histological and cytological basis of trypan blue-induced ocular defects were studied using scanning and transmission electron microscopy. Microphthalmic and anophthalmic eyes of 16-day rat fetuses were utilized from dams exposed to a teratogenic dose of trypan blue. Retinal and lenticular anlagen were specifically examined for architectural and cellular changes. Nearly all severely abnormal eyes showed no evidence of retina development: Of 41 such eyes, only two retinal rudiments were observed. Those eyes with mild microphthalmia always demonstrated retinae although architectural changes were present. In every abnormal eye, some degree of lenticular morphogenesis was always present. Lenses were small, displaced in the eye field, and arrested at the lens vesicle stage. Lens cells were markedly undifferentiated and thus lacked most of the cytological features normally present at this developmental stage. Neither retinal nor lenticular rudiments were necrotic despite major architectural and cytological disturbances. The data offer three conclusions: First, the absence of necrosis suggests that trypan blue causes developmental arrest in this eye model; second, absence of retinae is most likely due to primary failure of optic vesicle development; third, lack of lens differentiation is attributed to absence of the retina, the primary lens inducer.

Abnormalities, Drug-Induced↗
PubMed1970

Some structural and biological properties of Brucella endotoxin.

Hot phenol-water extraction of smooth Brucella abortus and B. melitensis cells yielded a toxic fraction which was recovered from the phenol phase (fraction 5). Chemically, fractions 5 from both Brucella species were lipid-carbohydrate-protein-2 keto-3-deoxyoctulosonic acid complexes which were stable to heat and resistant to Pronase digestion. Electron micrographs of the Brucella toxins were morphologically indistinguishable from those of enterobacterial endotoxins. Biologically, Brucella toxins were lethal for mice and immunogenic for rabbits. An intravenous injection of Brucella toxin induced severe leukopenia with subsequent leukocytosis in mice. Cross-tolerance experiments with mice demonstrated that pretreatment with B. abortus toxin lessened the hypoferremia produced by challenge with Escherichia coli endotoxin. Furthermore, fractions 5 from B. abortus and B. melitensis were able to form hybrids with E. coli and Salmonella enteritidis endotoxins and also with each other. Although Brucella toxins possess many structural and biological properties in common with endotoxins from the Enterobacteriaceae, some quantitative differences in their biological potencies were observed. Brucella toxins were relatively innocuous in tests for pyrogenicity in rabbits and lethality for chick embryos. In nonspecific protection tests, Brucella toxin had only 1/75 the potency of E. coli endotoxin in protecting mice against challenge with virulent S. typhi. However, on the basis of the data presented and on the work done previously, we concluded that the heat-stable toxins of B. abortus and B. melitensis were endotoxins.

Journal Article↗