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Biomedical subjects

P Barber

Publications and source records attributed to P Barber.

80 records · Page 5Linked to original sources
PubMed1975

Comparative ultrastructure of the nerves innervating the muscle of the body of the bladder.

The distribution and structure of the nerves supplying the muscle of the body of the bladder in mammals such as the mouse, guinea-pig, rabbit, cat and dog was compared with that previously demonstrated in the rat. The muscle of the arterioles located between the muscle bundles is innervated by a fine perivascular plexus and the nerves forming the muscular plexus can be divided into inter- and intra-fascicular nerves and the intrafascicular nerves are characterised by large numbers of terminals with the features of those of cholinergic axons. In addition to many small clear vesicles, the cholinergic terminals contained some small dense-cored vesicles, and it is suggested that, as in the rat, these contain a second transmitter which is released with acetylcholine at the terminals during impulse transmission. Adrenergic term-nals are more common in the muscular plexuses of the guinea-pig, dog and cat than in those of the other animals studied and there is evidence for the presence of two types of such terminal in the nerves. Of these, one contains a much smaller proportion of small vesicles with dense cores and many more large dense-dored vesicles than the second, and the possibility of a relationship between such terminals and those of short adrenergic neurones and neurones associated with non-adrenergic patterns of impulse transmission is discussed.

Animals↗
PubMed1975

Comparative ultrastructure of ureteric innervation.

The distribution and structure of the ureteric nerves in a small series of mammals was compared with that previously demonstrated in the rat. There was marked interspecies variation in the extent to which the nerves penetrated the wall of the ureter and in the degree of development of the deep submucous plexus. In animals with a highly developed deep submucous plexus, terminal arterioles frequently passed through the muscle coat before breaking up into capillaries. These vessels were surrounded by a fine periarteriolar plexus and were accompanied in their course through the muscle coat by one or more branches of the adventitial nerves. Intramuscular nerves not related to arterioles contained few axons with terminals classifiable as either adrenergic or cholinergic, and in animals in which the muscle cells were arranged in fascicles rather than in sheets, the nerves were typically interfascicular in position. As in the rat, only the periarteriolar plexuses contained large numbers of adrenergic axons. Cholinergic axons were generally few, but were not uncommon in the deep submucous plexus when this was well-developed. The majority of the terminals encountered in the intramural nerves contained variable and usually small numbers of both clear and large dense-cored vesicles. The relationship between these terminals and those defined in the submucous nerves of the rat ureter was discussed and it was suggested that the marked variations in the diameter of the axons in the terminal areas and in the number of vesicles in the terminals were related to the effects of the mechanical and other derangements which occur during processing.

Animals↗
PubMedDate not supplied

A morphometric analysis of osteoid collagen fibril diameter in osteogenesis imperfecta.

Osteogenesis imperfecta is a genetic disorder of connective tissue characterised by frequent bone fracture following minimal trauma. Mutations of type I procollagen genes have been widely reported as the cause of OI and such mutations have been shown to introduce kinks into the collagen molecule. A study was performed to examine type I collagen fibrils at the ultrastructural level in the transmission electron microscope (TEM). Type I collagen fibrils from the bone osteoid of OI patients and age- and site-matched normal control bone were photographed in the electron microscope. A histomorphometric analysis of the diameters of collagen fibrils photographed in the TEM indicated that type I collagen in OI bone was larger in diameter compared with normal bone. This increase in diameter of type I collagen fibrils may represent an alteration in the quaternary structure of the collagen fibril as a consequence of kinked, poorly packed collagen molecules. Such alteration in the collagen fibrils may affect the formation and stability of bone mineral associated with it.

Adolescent↗
PubMedDate not supplied

Further studies of blood infectivity in an experimental model of transmissible spongiform encephalopathy, with an explanation of why blood components do not transmit Creutzfeldt-Jakob disease in humans.

BACKGROUND: Solid evidence from experimentally infected animals and fragmentary evidence from naturally infected humans indicate that blood may contain low levels of the infectious agent of Creutzfeldt-Jakob disease (CJD), yet blood components have never been identified as a cause of CJD in humans. STUDY DESIGN AND METHODS: Blood components and plasma fractions were prepared from the pooled blood of mice that had earlier been infected with a mouse-adapted strain of human transmissible spongiform encephalopathy (TSE). Infectivity bioassays were conducted in healthy mice, and the brains of all assay animals dying during the course of the experiments were examined for the presence of proteinase-resistant protein. RESULTS: Infectivity in the blood during the preclinical phase of disease occurred in the buffy coat at infectious unit (IU) levels between 6 and 12 per mL and was either absent or present in only trace amounts in plasma and plasma fractions. Infectivity rose sharply at the onset of clinical signs to levels of approximately 100 IU per mL of buffy coat, 20 IU per mL of plasma, 2 IU per mL of cryoprecipitate, and less than 1 IU per mL of fractions IV and V. Plasma infectivity was not eliminated by either white cell-reduction filtration or high-speed centrifugation. Approximately seven times more plasma and five times more buffy coat were needed to transmit disease by the intravenous route than by the intracerebral route. CONCLUSION: Epidemiologic evidence of the absence in humans of disease transmission from plasma components can probably be explained by 1) the absence of significant plasma infectivity until the onset of symptomatic disease, and comparatively low levels of infectivity during the symptomatic stage of disease; 2) the reduction of infectivity during plasma processing; and 3) the need for at least five to seven times more infectious agent to transmit disease by the intravenous than intracerebral route. These and other factors probably also account for the absence of transmission after the administration of whole blood or blood components.

Animals↗