Biomedical subjects
Publications and source records attributed to R F Gilbert.
A case of adenocarcinoma involving a müllerian duct cyst is presented. The presentation, treatment, and pathological and radiological appearance are discussed. The embryology and history of this entity are reviewed.
Ten patients with metastatic carcinoid tumors in the liver showed elevated 5-hydroxytryptamine and substance P levels in plasma samples taken from hepatic or peripheral veins. Chromatographic characterization of the substance P-immunoreactivity showed that by gel permeation and high pressure liquid chromatography the substance P-immunoreactivity was indistinguishable from synthetic undecapeptide substance P. The results suggest that substance P, in addition to the 5-hydroxyinoles, may serve as a circulatory marker for some forms of carcinoid tumors.
1. The highest spinal cord levels of 5-hydroxytryptamine (5-HT) and thyrotrophin releasing hormone (TRH) were found in the ventral lumbar cord, in contrast to substance P which was found predominantly in the dorsal cord. 2. 5,6- and 5,7-dihydroxytryptamine, administered into the lateral ventricles reduced 5-HT in the dorsal and ventral spinal cord by up to 90%. 3. There was a parallel reduction in substance P and TRH in ventral spinal cord while methionine-enkephalin and somatostatin in ventral and dorsal cord increased. 4. Reserpine and tetrabenazine depleted 5-HT and partially depleted substance P and TRH in the ventral cord, but had no effect on either methionine-enkephalin or somatostatin. 5. The rates of loss and recovery, after reserpine and tetrabenazine, of 5-HT were different from those of the two peptides. 6. Endogenous 5-HT and TRH release from slices of lumbar cord was enhanced by high potassium. 7. p-Chloroamphetamine and fenfluramine increased 5-HT release but reduced or had no effect on TRH release. The effect of p-chloroamphetamine on TRH release was not dependent on either the presence of 5-HT or 5-HT receptor activity. 8. The results are discussed in terms of the possible co-existence, co-storage and release of 5-HT, substance P and TRH in descending bulbospinal neurones.
The coexistence of two neuronally-localised peptides, substance P and thyrotropin-releasing hormone (TRH), in descending serotoninergic nerve fibres to the spinal cord was investigated using immunocytochemical and biochemical methods. Substance P-like material in the spinal cord was shown to be identical to the undecapeptide substance P by the criteria of gel filtration, high performance liquid chromatography and behaviour in substance P specific radioimmunoassays. Immunocytochemical staining for 5-hydroxytryptamine, substance P, and TRH showed that all three substances had a similar distribution in nerve fibres and terminals in the ventral and lateral grey matter of the spinal cord. After treatment with the serotonin neurotoxin 5,7-dihydroxytryptamine, neuronal elements containing 5-hydroxytryptamine, substance P and TRH degenerated and disappeared from these parts of the spinal cord in parallel with one another. Biochemical measurements of 5-hydroxytryptamine, substance P and TRH in the spinal cord after treatment with 5,7-dihydroxytryptamine confirmed that these three substances were all depleted from the ventral horn and, in addition, showed that there was a small depletion of substance P from the dorsal horn. Two other neuropeptides, somatostatin and methionine-enkephalin were not depleted from the spinal cord by treatment with 5,7-dihydroxytryptamine nor was substance P in other parts of the brain. Substance P in the spinal cord was unaffected by 6-hydroxydopamine, a drug known to destroy catecholamine-containing neurones. These results are consistent with coexistence of substance P and TRH together with 5-hydroxytryptamine in the descending axons and terminals of bulbospinal neurones.
The ventral spinal cord content of several neuronally localised peptides was measured after treatment with a number of drugs which deplete spinal cord monoamines. Reserpine and tetrabenazine, but not p-chlorophenylalanine caused a partial depletion of ventral spinal cord substance P (SP) and thyrotropin-releasing hormone (TRH). Two other peptides, methionine-enkephalin and somatostatin were not depleted by any of the drugs. The rates of loss and recovery of SP and TRH after reserpine and tetrabenazine were different from that of 5-hydroxytryptamine (5-HT), though in the ventral spinal cord these two peptides probably coexist with 5-HT in the terminals of bulbospinal neurones. The results are discussed in relation to the possible costorage of SP and TRH with 5-HT in the same vesicles in nerve terminals in the ventral spinal cord.
The demonstration of depolarization-induced release of substance P, Met- and Leu-enkephalin, somatostatin, neurotensin, vasoactive intestinal polypeptide and cholecystokinin-like material from various regions of rat brain in vitro supports the hypothesis that these and other neuropeptides may act as neurotransmitters. In each case the stimulus-evoked release, but not the basal release, of peptide was dependent on the presence of calcium ions in the external medium. The stimulus-evoked release of substance P from nerve terminals in rat substantia nigra may be regulated by presynaptic gamma-aminobutyric acid (GABA) receptors. The possible existence of presynaptic opiate receptors on substance P-containing sensory nerve terminals may offer an explanation for the analgesic effects of opiates at spinal cord level, and for the existence of enkephalin neurons in substantia gelatinosa. Capsaicin releases substance P from spinal cord nerve terminals and may impair their function, while having no effect on substance P neurons in supraspinal regions. The possibility of cosecretion of peptide and amine products from the same cells is discussed.
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A case of cecal infarction proximal to an obstructing fecaloma is presented. The patient's medical records revealed a 19-year history of the abuse of prescribed narcotic, sedative, psychotropic, and anticholinergic drugs. Gangrene in this case was caused by compression of intramural vessels secondary to a sustained increased in intracolonic pressure. The greatest effect of this increased pressure was found in the cecum, where wall tension and colonic distention were greatest. This report indicates that the colonic effects of chronic drug abuse have the potential for becoming a true surgical emergency.
Accumulations of the neuropeptides substance P (SP), somatostatin (ST), and vasoactive intestinal polypeptide (VIP) proximal to a crush in the cervical vagus nerve of the rat have been measured using sensitive radioimmunoassays. Each of the peptides was rapidly transport towards the peripheral terminals of vagal afferent fibres, with average rates of flow ranging from 0.8 to 2.7 mm h-1. In the rabbit vagus nerve, SP was transported with an average rate of 4 mm h-1, which is more than double the rate for this peptide in the rat. Double crush experiments in rabbit vagus nerves indicated that the rapidly transported proportion of the total content of SP in the nerve free was about 34%. From this, the rate of transport of SP in the rapidly transported pool in the rabbit vagus nerve can be calculated to be 12 mm h-1 (280 mm day-1). Since such double crush experiments were not possible in the rat, it is not clear whether the different average rates of transport of SP in the rat and the rabbit reflect real differences in the rate of rapid transport in the two species. In common with rapid axonal transport of other neurotransmitters, the transport of SP and ST in the rat vagus nerve was blocked by colchicine, a drug that disrupts microtubules.
The development of VIP-containing neurones in the rat CNS and duodenum has been studied using a specific radioimmunoassay and immunohistochemistry. In the brain, VIP immunoreactivity appears entirely postnatally, while VIP in peripheral neurones in the duodenum was present before birth. The developmental changes observed in cerebral cortex appear to represent the maturation of a population of intrinsic cortical interneurones which contain VIP. These neurones develop entirely after birth. They are first seen in deep cortical layers, but later spread out into all cortical layers, particularly layers II--IV. Changes in the intensity of VIP cell body fluorescence can be correlated with changes in VIP content in the cortex measured by radioimmunoassay. Thus VIP forms a unique chemical marker for studying the maturation of a cortical neurone.
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1. The binding of [3H]-( +/- )-quinuclidinyl benzilate ([3H]-( +/- )-QNB) to muscarinic sites in rat brain slice and homogenate preparations was compared. 2. Evidence is presented in support of the view that only the (-)-enantiomer of QNB binds with high affinity to muscarinic sites. 3. The Kd value for [3H]-(-)-QNB binding in slices was eight times higher than that measured in homogenates. 4. Similarly, the potencies of various muscarinic ligands as inhibitors of [3H]-(-)-QNB binding were consistently lower in slices than in homogenates. 5. It is proposed that the results may reflect differences in the binding properties of muscarinic receptors in intact tissue slice and homogenate preparations.
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A surgically treated case of a mesenchymal hamartoma, a rare, benign liver tumor of infants and occasionally children, is reported. The clinical picture is characterized by marked, usually rapid abdominal enlargement. If untreated, the tumor may compromise other organ systems, resulting in death. The treatment is surgical removal. The tumor is characterized by proliferation of collagenous connective tissue, immature mesenchyme, and multiple cysts or pseudocysts of varying sizes. The origin of the tumor has not yet been definitely determined. Ultrasonography combined with radionuclide scanning was useful in establishing a working, preoperative diagnosis.
We show how statistical methods based on directed graphs may be useful in modeling traffic fatalities by comparing models specified using directed graphs to a model originally developed by Peltzman. The comparison uses Peltzman's original data, as well as up-dated data (and coefficients) through 1993. Out-of-sample forecasts of traffic fatalities from Peltzman's model are compared with those from a model constructed using directed graphs over data for the more recent period. The directed graphs model outperforms Peltzman's model in root mean squared forecast error.