Biomedical subjects
Publications and source records attributed to C Shaw.
Detection of small, dense, rectangular opacities that follow the course of pulmonary vessels on chest radiographs should raise the suspicion of a prior therapeutic occlusion of the blood supply of a mass or of an arteriovenous fistula elsewhere with embolization of the occlusive material to the lungs. This article demonstrates the radiographic findings of such an occurrence in an asymptomatic woman.
Tachykinin immunoreactivity has been quantified and characterized in extracts of bovine retinae by combining radioimmunoassay, gel permeation chromatography, and reverse-phase HPLC. Using an antiserum specific for the C-terminal hexapeptide amide of substance P, levels of 3.43 +/- 0.33 ng g-1 and 12.45 +/- 0.76 ng g-1 (mean +/- SD, n = 5) were measured in extracts prepared by acidified ethanol and boiling 0.5 M acetic acid, respectively. Levels of neurokinin A immunoreactivity, assayed using an antiserum cross-reacting with neurokinin A (100%), neurokinin B (50%), neuropeptide K (85%), and substance P (less than 0.1%) were 12.46 +/- 0.47 ng g-1 and 7.20 +/- 0.37 ng g-1 in the same extracts. Gel permeation chromatography identified a single substance P immunoreactant eluting with substance P standard, whereas two neurokinin A immunoreactants were resolved eluting with neuropeptide K and neurokinin A standards. Reverse-phase HPLC analysis resolved immunoreactivity eluting with substance P, neurokinin A, neuropeptide K, and neurokinin B and their respective methionine sulphoxides. The amount of immunoreactive material co-eluting with the respective sulphoxides was higher in acidified ethanol extracts, and substance P was most susceptible to oxidative modification. Subsequent incubation of synthetic substance P with dispersed bovine retinal cells resulted in rapid conversion to three metabolites identified and isolated by reverse-phase HPLC. Each had an amino acid composition identical to that of substance P, and the major product had the same retention time as substance P sulphoxide.(ABSTRACT TRUNCATED AT 250 WORDS)
Metastatic spread of nonpulmonary malignancies to the lung is a common clinical problem. However, the evaluation and treatment of metastatic lung disease may be confusing. This article considers both pulmonary and pleural metastases. The basic biology of the metastatic process is discussed, together with the pathologic, clinical, radiologic, diagnostic, and therapeutic features of pulmonary metastases. Metastatic disease to the pleura is reviewed in detail, including etiology and incidence, pathogenesis, clinical manifestations, diagnosis, prognosis, and treatment.
Tritiated phorbol-12,13-dibutyrate [( 3H]PDBu), a phorbol ester, was utilized to autoradiographically localize protein kinase C (PKC) in the cat visual cortex. Thin, slide-mounted sections of adult cat brain were used to characterize binding of [3H]PDBu. This was found to be saturable, reversible, and more readily displaced by phorbol ester than by synthetic diacylglycerols. Binding sites displayed a tissue concentration of 20 pmol/mg protein, and a dissociation constant of 8.0 nM. [3H]PDBu was slow to associate with its receptor, requiring 9.5 h to reach equilibrium. Autoradiograph revealed that PKC is heterogeneously distributed in the cat brain, and displays a laminar-specific pattern in the visual cortex. This laminar distribution undergoes marked changes during the first two months of postnatal life. In the visual cortex of neonatal kittens, [3H]PDBu binding is confined to layers I and V. Layer III acquires high levels of binding by postnatal day 15, layer II by 28 days, and layer VI becomes labelled by 40 days of age. Adult animals exhibit high levels of binding in all laminae except layer IV. Age-dependent changes in PKC's laminar distribution do not seem to be correlated with specific anatomical, neurochemical, or behavioural events during development. PKC appears to be associated with cell bodies or processes intrinsic to the visual cortex, and is probably not located on the terminals of cortical afferents.
Using radioimmunoassay, reverse phase high pressure liquid chromatography (rp HPLC) and immunohistochemistry, we have identified gastrin releasing peptide-immunoreactivity (GRP-IR) in the rat retina. The concentration of GRP-IR in retinal extracts was 7.4 +/- 0.6 ng/g wet wt. (mean +/- S.E.M. n = 15). There was no significant difference between the levels of immunoreactivity in 12-h light and 12-h dark adapted retinae. rp HPLC analysis of retinal extracts demonstrated that two main immunoreactive components were present which corresponded in retention time to GRP10 (neuromedin C) and GRP14 (GRP14-27). A small amount of material also co-eluted with GRP27. Using immunohistochemistry, the immunoreactivity has been localised in the inner retinal layers. Immunoreactive somata were present in the proximal inner nuclear layer and in the ganglion cell layer. Fibre staining was present in laminae 2 and 4 of the inner plexiform layer. Somatal staining was increased by pretreatment of retinae with vincristine while the laminar staining was markedly reduced. These results demonstrate the existence of GRP-like peptides in the rat retina which has not previously been reported.
We have examined the number, characteristics and distribution of GABAA receptor in the visual cortex of normal cats and in cats monocularly deprived by unilateral eyelid suture from early in postnatal life. Receptor densities were about 100% higher in the deprived animals than in their normal counterparts. No changes in receptor affinity were noted. The GABAA receptor increase appeared to affect all laminae in the visual cortex. The results suggest that an increase in GABAA receptors may underlie or result from the physiological consequences of early monocular deprivation.
In vitro autoradiographic techniques using [3H]nicotine were used to characterise nicotine binding sites in developing kitten visual cortex. These binding sites in adult animals have a Bmax of 3.91 fmol/mg protein and a Kd of 4.40 nM. Displacement experiments indicate that [3H]nicotine binds to a nicotinic receptor site that is similar to central nicotinic sites described by investigators in other mammals. The number of binding sites increases during postnatal development, peaking near 60 days of age and levelling-off thereafter. There is no evidence for large changes in affinity during postnatal development for this binding site. [3H]Nicotine binding sites are densely concentrated in layer IV in the visual cortex of adult animals, with sharply reduced binding outside of cortical areas 17 and 18. This laminar pattern does not change during postnatal development, but an increase in the number of binding sites in layer IV as well as in layers I and VI occurs during early postnatal life. These binding sites disappear when extrinsic cortical inputs are severed. However, they survive when neurons in the visual cortex are selectively destroyed with a cell-specific neurotoxin. Unilateral destruction of the lateral geniculate nucleus eliminates [3H]nicotine binding sites in the visual cortex ipsilateral to the lesion, suggesting that they are located presynaptically on the terminals of lateral geniculate nucleus afferent fibres. The laminar pattern of binding of [3H]nicotine during early development of the visual cortex is complimentary to that for muscarinic acetylcholine receptors. These latter receptors redistribute during postnatal development becoming less prominent in layer IV at the same time as the [3H]nicotine binding sites are increasing in number in this layer. For a short period of time at the height of the critical period for cortical plasticity, both populations of binding sites are located in layer IV.
The nature of xenopsin immunoreactivity in mammalian antral G-cells has been reassessed. Xenopsin immunostaining was most intense in human antral G-cells, present in those of the dog and pig and not detected in guinea pig or rat tissues. Rigorous specificity controls for ionic binding of immunoglobulins to antral G-cell granules indicated that this mechanism was not responsible for xenopsin immunostaining. Preincubation of the xenopsin antiserum with xenopsin, human gastrin 1-13 and gastrin 2-17 completely abolished immunostaining at similar molar concentrations. Gastrin 34 was ineffective at much higher concentrations. These results infer that xenopsin-immunoreactivity in antral G-cells resides in the N-terminal region of gastrin 17. Examination of the primary structures of xenopsin and the N-terminal regions of some mammalian gastrins reveals a hitherto unrecognized homology.
We have examined the influence of the sodium channel toxins veratrine and veratridine on mu-opioid ([3H]-DAGO), muscarinic ([3H] NMS) and beta-adrenergic ([3H] CGP) receptors in rat brain slices. These drugs reduce opioid and muscarinic binding while leaving beta-receptors unaffected. Veratrine is inhibitory at 0 degree or at 30 degrees C whereas veratridine is without effect at 0 degree C. These data suggest that some factor contained in the mixture of drugs (veratrine) can block opioid and muscarinic receptors independently of depolarization. Veratridine does not affect muscarinic receptors at ice temperature. Similar observations were made in thin sections of cat brain at 0 degree C. The concentrations of the toxins which cause 50% inhibition of binding are well within the range (5 x 10(-5) M-10(-4) M) routinely used for depolarization experiments. We suggest that caution be used in the interpretation of results obtained from veratrum alkaloid-induced depolarizations. It would not be surprising if the binding of other ligands to their receptors was also affected.
The characteristics and distribution of muscarinic acetylcholine (mACh) receptor binding in primary somatosensory (SI) cortex and the caudate nucleus of raccoons were studied using [3H]-QNB, a muscarinic antagonist. The binding characteristics were similar to reported values in rat and cat. Autoradiographs produced from tissue sections labeled with [3H]-QNB showed the distribution of mACh receptors in the forebrain of the raccoon. [3H]-QNB binding was highest in cerebral cortex, neostriatum and hippocampus. Within SI cortex, binding was high in layers I-III and VI and relatively low in layers IV and V. Autoradiographs obtained from animals that had undergone peripheral deafferentation of part of the forepaw revealed no changes in [3H]-QNB binding in the affected cortical region during the time that physiological reorganization is known to occur.
Mutants of Vibrio cholerae defective in intestinal colonization have been constructed. Characterization of these mutants has led to the identification of a gene cluster involved in the assembly of a pilus colonization factor called TCP. The tcp operon has been cloned and strains of V. cholerae have been constructed that overproduce this pilus and the B subunit of cholera toxin. Together these studies may contribute to the eventual construction of efficient live and killed, oral cholera vaccines.
Recent studies have shown that several receptor populations in cat visual cortex undergo alterations in their laminar distributions during postnatal development (Shaw et al., 1984a,b; 1986b). These redistributions occur during the first few months of postnatal life, coincident with the physiologically defined critical period for cortical plasticity. In the present communication, we demonstrate that receptor redistributions can be prevented from occurring, or progressing once started, by surgically isolating the visual cortex at appropriate postnatal ages. These data suggest that the maturation of the chemical circuitry of the visual cortex is dependent on factors of extrinsic origin.
Polymerised pyridoxylated haemoglobin solution (PPSFH) is a modified haemoglobin solution which has a normal oxygen carrying capacity, long half-life, and reasonable oxygen affinity, and is a leading candidate for use as an oxygen carrying blood substitute. Previous work has given indications that vasoactive factors may be present. A bioassay sensitive to vasoconstrictors was constructed. PPSFH prepared by chloroform extraction produced a mean pressure rise of 24.3 mm Hg. PPSFH prepared by a crystallisation method showed a mean rise of 2 mm Hg (p = 0.0004). Unmodified stroma-free haemoglobin (SFH) prepared from platelet- and white cell-free red blood cells showed a mean rise of 32.5 mm Hg. These data indicate that both PPSFH and SFH contain a vasoconstrictor factor which is of low molecular weight, is hydrophilic, and is derived from red blood cells.
Celiac disease is characterized by reversible, gluten-induced, architectural abnormalities of the intestinal mucosa. Villus atrophy is compensated for by an increase in the number of proliferating cells and an increase in crypt cell production rate, resulting in increased crypt length and girth. Several authors, employing various methods of quantitation, have reported enteric endocrine cell hyperplasia in celiac disease. The present study has re-evaluated enteric endocrine cell status in this disorder by employing methods of quantitation which more accurately take account of alterations of crypt morphology than those previously used. Numbers of endocrine cells expressed as cells per unit of crypt length are not increased in the celiac biopsies when contrasted with those from controls. Indeed, numbers of cells immunoreactive for gastrin, GIP, motilin and somatostatin were reduced in the celiac mucosa. Endocrine cell hyperplasia in the celiac small bowel is not as marked as was previously thought, and may lag behind that of the enterocyte population.
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[3H]Flunitrazepam (FNZ) binding sites were characterized in homogenates of cat visual cortex during normal postnatal development and following dark rearing from birth. In parallel experiments, the distribution and density of [3H]FNZ binding sites were examined by in vitro autoradiographic or 'scrape' methods. In homogenates, Bmax measurements showed low early values, rising to a peak in receptor density at about 60 days postnatal, followed by a decline in adulthood. At all ages, gamma-aminobutyric acid (GABA) altered the Kd, but not the Bmax of [3H]FNZ binding sites. Kd values showed a general increase with age, parallelled by an increased sensitivity to GABA. Receptor autoradiography revealed that the highest density of [3H]FNZ binding sites was in layer IV of cats of all ages. Deafferentation of extrinsic inputs to the visual cortex by surgical undercutting did not alter this pattern of laminar distribution, indicating that the receptors were associated with intrinsic cortical elements rather than subcortical inputs. Dark rearing had no effect on [3H]FNZ laminar distribution in the visual cortex. The Bmax was higher at 30 days postnatal, but did not differ significantly thereafter. Modulation by GABA was concomitantly higher at 30 days, but lower than normal in dark-reared animals at ages greater than 30 days postnatal. The results are discussed in relation to the normal and abnormal development of GABA receptors in the cat visual cortex.
Using the methods of in vitro receptor autoradiography, we have characterized a population of receptors for nicotine in cat visual cortex that is concentrated primarily in layer IV of areas 17 and 18. Surgically undercutting the visual cortex essentially abolished [3H]nicotine binding in the isolated zone. However, neuron-specific, quinolinic acid lesions of a region of visual cortex had little effect on binding, establishing a presynaptic locus on cortical inputs for these sites. Lesions of the lateral geniculate nucleus abolished binding in the corresponding cortical areas, thus localizing the [3H]nicotine binding sites to lateral geniculate nucleus terminals in the cortex.
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