Biomedical subjects
Publications and source records attributed to F Tang.
By solution-hybridization-RNase protection assay, the preproenkephalin (PPek) mRNA in the anterior pituitary (AL) of male rats was found to decrease by 42% after 3 weeks haloperidol treatment. It is concluded that dopamine may stimulate the AL enkephalinergic system at the level of gene expression.
Autoradiographic study was conducted to localize 2-[125I]iodomelatonin binding in the rat epididymis. In the peripubertal (6 weeks old), postpubertal (8 weeks old) and adult (3 months old) rats, intense specific 2-[125I]iodomelatonin labelling of the corpus epididymidis was observed. The intensity of 2-[125I]iodomelatonin binding in the distal epididymal segment was significantly decreased in orchidectomized rats but the effect could be reversed with testosterone replacement. The intensity of 2-[125I]iodomelatonin binding in the distal rat epididymal segment did not show any diurnal rhythmicity when mid-light period and mid-dark period levels were compared, and was unaffected by constant lighting. Our data suggest androgen-dependent expression of 2-[125I]iodomelatonin binding sites, independent of light-induced changes in circulating melatonin, in the rat corpus epididymidis. A novel role of melatonin and its receptor in the regulation of the functions of rat corpus epididymidis is strongly implicated.
A compound (L-655,708) has been identified which has at least 50-fold selectivity for the benzodiazepine site on GABAA receptors containing an alpha 5 subunit over those containing an alpha 1, alpha 2, alpha 3 or alpha 6 subunit in combination with beta 3 and gamma 2. The compound was radiolabelled with tritium and investigated as a novel radioligand which recognizes the benzodiazepine site of GABAA receptors which contain the alpha 5 subunit. [3H]L-655,708 labels one saturable and specific population of binding sites in rat hippocampus with a Kd of 2.4 +/- 0.7 nM and a Bmax of 256 +/- 42 fmol/mg protein. The pharmacology of the binding site labelled was consistent with that of receptors present in cells transfected with alpha 5, beta 2 and gamma 2 and with receptors immunoprecipitated from rat brain with an alpha 5-selective antiserum. It is concluded that [3H]L-655,708 is the first radioligand to date which is selective for any BZ2 subtype of the GABAA receptor and should provide a valuable tool for elucidating the structure and function of the alpha 5-containing GABAA receptor subtype.
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1. Haloperidol increased the Met-enk level in the striatum at all age groups. However, the Met-enk level was decreased in AL of young and middle-aged rats by the drug. 2. Haloperidol elevated the beta-end level in AL and CCK level in NIL in young rats only. 3. The SP content in NIL was decreased by haloperidol in all age groups. 4. With regard to the effect of aging, Met-enk level in AL of middle-aged rats was higher than that in young rats. The beta-end level in AL also increased in old rats. 5. Aging modified the haloperidol effect on beta-end level in AL and CCK level in NIL as the effect was only observed in young rats. 6. In addition, aging caused a blunted response of Met-enk level to haloperidol in the striatum but an increased response of SP content to haloperidol in the NIL.
Primary Sjögren's syndrome is an autoimmune disease whose etiology is unknown. Recent studies show that there is T cell abnormalities in addition to B cell hyperreactivity. In order to better understand the immunoregulatory abnormalities of primary Sjögren's syndrome, cellular immunology has become the main focus of recent studies. As such, the function of CD2 and CD3 pathways constitutes an integral part of these studies. The proliferation of PBMC, non-adhesive cells (mainly T cells) and adhesive cells (mainly B cells) has been investigated in patients with primary Sjögren's syndrome and normal controls; the results show that the proliferation of PMBC and non-adhesive cells in patients is much lower than that in normal controls (P < 0.05), whereas there is no difference in that of adhesive cells between these two groups (P > 0.05). It is also found that the non-adhesive cells' abnormality can not be adjusted by adding adhesive cells of normal controls. In addition, it seems that there is a relationship between the proliferation of PBMC via CD2 pathway in patients and the positivity of anti-SSA and anti-SSB antibodies. However, the underlying mechanism behind the pathogenesis of primary Sjögren's syndrome has yet to be fully understood. This study warrants further research into gaining a better concept of the CD2 pathway at molecular levels.
Enzymatic assays for acetylcholine esterase (AChE) and choline acetyltransferase (ChAT) were applied to dorsal and ventral cervical spinal cord regions taken from the Wobbler mouse, a model for inherited motoneuron disease. Early in the disease, ChAT (but not AChE) activity is significantly greater compared with the control littermate specimens. The high ChAT activity correlates with the high thyrotropin releasing hormone (also leucine-enkephalin) concentrations measured in the Wobbler ventral horn early in the disease. Late in the motoneuron disease, both AChE and ChAT activities are significantly lower than in the control littermate specimens. These data correlate with the high substance P, methionine and leucine enkephalin concentrations measured in the Wobbler ventral horn late in the motoneuron disease.
The effects of 1-week drug treatment on the brain contents of neuropeptides were investigated. The cholecystokinin (CCK) concentrations in the hypothalamus were significantly decreased by tryptophan treatment but not by imipramine and cyproheptadine, which changed the serotonergic function. Proglumide, the CCK antagonist, induced in the hypothalamic and hippocampal-striatal areas an increase in CCK concentration, which was not reversed in the presence of tryptophan. Dynorphin and substance P(SP) concentrations were also modified by proglumide treatment.
The immunosuppressive effect of chronic glucocorticoid treatment on 2[125I]iodomelatonin binding in the duck thymus was studied. Two-week-old ducks were injected intraperitoneally with either 1 mg of cortisol per day (experimental group) or an equivalent volume of vehicle (control group) in the middle of the light period for 7 days. 2[125I]Iodomelatonin binding assays were performed on thymic membranes. Cortisol injection reduced the body weight gain, size of the bursa of Fabricius and absolute weights of the primary lymphoid organs but had no effect on the spleen weights. The relative weights of the spleen were increased while those of the primary lymphoid organs were unchanged. The density of the thymus 2[125I]iodomelatonin binding sites was decreased while the affinity was not affected. The modulation of the thymic 2[125I]iodomelatonin binding sites by changes in the immune status of the duck suggests that these binding sites represent physiologically relevant melatonin receptors and that melatonin exerts its action on the lymphoid tissues directly. Our findings support the hypothesis that the thymus is the target site for the immunomodulatory interactions between the pineal melatonin and the adrenal steroids. A possible inhibitory influence of adrenal steroids on the immuno-enhancing effect of melatonin is also suggested.
To evaluate the effect of GG activity on tongue backwardness during sleep, we conducted experiments on 16 rabbits. The electric activities of the muscles involved in tongue motion were recorded in different phases (wakefulness, presnoring and snoring) with unipolar electrodes inserted into the muscles under direct vision. The observations demonstrated that GG played a more active role in the occurrence of tongue backwardness during sleep.
1. Fourteen days after hypothyroidism was induced either by propylthiouracil (PTU) treatment or by thyroidectomy, the serum thyrotropin (TSH) responses to morphine (5 or 20 mg/kg bw), ether stress (30 min) and cold exposure (60 min) were compared with those in normal rats. 2. The decrease in serum TSH levels after morphine and ether stress found in the normal rats were abolished or much reduced respectively. 3. The increase in serum TSH in response to cold exposure and the diurnal rhythm of serum TSH (lower level at night) were also absent in the hypothyroid rat. 4. The stimulating effects of low dose of thyrotropin releasing hormone (TRH) and the inhibitory effects of somatostatin and apomorphine were completely abolished, while the stimulating effects of a high dose of TRH were much reduced in the hypothyroid rat. 5. These results indicate that in the hypothyroid rat the effect of a lack of negative feedback action of thyroid hormone predominates, and that hypothalamic factors are probably unimportant in the regulation of TSH secretion.
Glucocorticoid excess inhibits somatic growth in man and laboratory animals. While the mechanism involved is likely to be multifactorial, indirect evidence suggesting the role of an enhanced endogenous somatostatin (SS) tone has been reported. However, there has been no direct evidence indicating an increased synthesis or secretion of hypothalamic SS. In this study, we investigated the effects of glucocorticoids on hypothalamic SS expression by measuring the peptide and mRNA content of SS in whole hypothalamic blocks of male Sprague-Dawley rats sacrificed 4 weeks after adrenalectomy or sham operation. Adrenalectomy decreased the SS content in the rat hypothalamus (p < 0.05), an effect which was reversed by dexamethasone treatment for 10 days. On the other hand, total hypothalamic SS mRNA levels were unaffected by adrenalectomy, but became significantly decreased following dexamethasone treatment (p < 0.05). Using in situ hybridization, this reduction in SS gene expression was shown to occur consistently in the periventricular nucleus and in the parvocellular subdivision of the paraventricular nucleus. The effects of adrenalectomy and dexamethasone on SS mRNA levels were further quantitated in hypothalamic fragments containing predominantly the periventricular and paraventricular nuclei. Somatostatin mRNA levels in these tissue fragments were marginally increased by adrenalectomy (p < 0.05), but showed a 50% reduction following dexamethasone treatment (p < 0.0001). In conclusion, our findings suggest that the inhibitory effect of glucocorticoids on somatic growth is probably not mediated via an effect on hypothalamic SS gene expression.
A series of trachoma inclusion color photograph is taken from the conjunctival smears of 48 trachoma cases. These smears were Giemsa-stained and stored in the slide-boxes for more than 30 years with no distinct changes in color. A description is given to the Pleomorphism of trachoma inclusion and its relation to the host cells. According to the gradual morphological changes of Chlamydia trachomatis multiplied in the infected cells, a 5-staged classification for trachoma inclusions is provided which may be benefit to understanding the pleomorphism of the trachoma inclusion and clinical laboratory diagnosis.
Anti-SSB antibodies were measured by ELISA in patients with various kinds of connective tissue diseases using SSB antigen purified from fresh rabbit thymus. The SSB antigen reacted with anti-SSB standard serum, and the positive rates in SS, SLE, RA, PBS and MCTD were 55.1%, 48.3%, 32.8%, 30.8% and 26.3%, respectively. The titers of anti-SSB antibodies were higher in SS and SLE patients than in other connective tissue disease patients. However, 10% of normal individuals were found to have anti-SSB antibodies with low titers. The anti-SSB antibodies detected were mainly of IgG isotype. Preliminary analysis of clinical data showed no relationship between anti-SSB and systemic involvement in SS.
The Wobbler mouse possesses an inherited motoneuron disease, which expresses itself primarily at cervical spinal levels and in cranial motor nuclei. Cell degeneration is sporatic and negligible in other motor regions of the brain (e.g., cerebellum, corpus striatum). However, enkephalin concentrations are consistently lower in the Wobbler cerebellum throughout the motoneuron disease, whereas substance P concentrations are significantly higher late in the disease compared with the normal phenotype littermates. The data imply that early changes in enkephalin (also shown for leucine enkephalin in the spinal cord and brainstem) may be important to the etiology of the Wobbler disorder. Like the late increase of substance P, this may reflect a yet-to-be described response to parent cell degeneration in the raphe nuclei. TRH remained unchanged in Wobbler cerebellum and corpus striatum, wherein the other peptides studied herein also maintained similar concentrations to the normal phenotype littermates.
Administration of ovine prolactin to castrated guinea pigs for 2 weeks induced hypertrophy of secretory cells in the lateral prostate when compared with the castrated controls. This was accompanied by an apparent increase in the number of profiles of granular endoplasmic reticulum and well developed Golgi complexes with dilated cisternae. An increase in the number of low-contrast electron-dense secretory granules was observed 4 weeks after prolactin treatment. In the seminal vesicle, dilatation and degranulation of granular endoplasmic reticulum and an apparent decrease in the number of secretory granules were observed 4 weeks after prolactin administration. Following castration and 2 weeks after prolactin treatment, thiamine pyrophosphatase (TPPase)-reaction product was mainly confined to 1-2 trans cisternae of the Golgi complexes in secretory cells of the lateral prostate and the seminal vesicle. In both glands, a reduction of TPPase activity was observed 2 weeks following prolactin administration, and the reaction product was totally absent after prolonged treatment for 4 weeks. The present study has provided morphological evidence that prolactin is capable of stimulating the secretory function of the lateral prostate while exerting some inhibitory effects on the seminal vesicle of the castrated guinea pig. In both glands, TPPase activity, and hence the process of glycosylation was inhibited after prolactin administration. The results from radioimmunoassay indicated that the action of prolactin on these glands could be a direct effect and not mediated through testosterone.
The present study was undertaken to quantify selected neuropeptides (thyrotropin releasing hormone, substance P, methionine and leucine enkephalin) in the cervical spinal cord and other regions of the central nervous system of Wobbler mice by radioimmunoassays during several stages of the motoneuron disease compared with age- and sex-matched normal phenotype littermates. In Wobbler spinal cord, thyrotropin releasing hormone is higher early in the disease, whereas in the brainstem it is higher at a later stage. Substance P in spinal cord is also higher late in the disease. Leucine enkephalin levels are greater at all stages in diseased spinal cord and brainstem, but methionine enkephalin increases only late in the disease. Highly significant increases of the peptides (except thyrotropin releasing hormone) appear in hypothalamus and midbrain only late in the motoneuron disease. Regression analyses show that thyrotropin releasing hormone in spinal cord and brainstem decreases normally with age in the control mice and at a faster rate related to the extent of motor impairment in Wobbler mice. Thyrotropin releasing hormone and methionine enkephalin in the Wobbler brainstem correlate (P less than 0.05) with the progress of the motoneuron disease. Methionine enkephalin increases faster in Wobbler brainstem and decreases faster in control spinal cord with age. The increase of leucine enkephalin in the Wobbler spinal cord correlates significantly with age and with the progress of the disease, but leucine enkephalin declines slightly with age in the controls. The changes of substance P in spinal cord and brainstem do not correlate significantly with the progress of the disease. In the hypothalamus, increasing values for substance P in control specimens and enkephalins in Wobbler specimens are significantly correlated with age. However, in the midbrain, higher methionine and leucine enkephalin levels are significantly associated with age only in the control mice. Alterations of neuropeptides in the Wobbler mouse spinal cord and brainstem may result from the degeneration of bulbospinal raphe neurons projecting to the ventral spinal cord, or from primary afferent or interneuronal nerve terminals. The data imply that the neuronal degeneration process in the Wobbler motoneuron disease is not limited to motoneurons. In the spinal cord, the data support our previous hypothesis that neuronal sprouting presynaptic to the motoneurons may account for increased neuropeptide concentrations. Alternatively, synthesis and/or degradation of these peptides may be altered. In addition, it is proposed that enkephalinergic neurons may develop abnormally in Wobbler mice. The early increase of leucine enkephalin in the Wobbler spinal cord possibly indicates its importance in the etiology of the motoneuron disease.
Nonpathogenic mutants of Xanthomonas campestris pv. campestris, generated from transposon mutagenesis, accumulated extracellular polygalacturonate lyase, alpha-amylase, and endoglucanase in the periplasm. The transposon Tn5 was introduced by a mobilizable, suicidal plasmid, pSUP2021 or pEYDG1. Genomic banks of wild-type X. campestris pv. campestris, constructed on the broad-host-range, mobilizable cosmid pLAFR1 or pLAFR3, were conjugated with one of the mutants, designated XC1708. Recombinant plasmids isolated by their ability to complement XC1708 can be classified into two categories. One, represented by pLASC3, can complement some mutants, whereas the other, represented by a single plasmid, pLAHH2, can complement all of the other mutants. Restriction mapping showed that the two recombinant plasmids shared an EcoRI fragment of 8.9 kb. Results from subcloning, deletion mapping, and mini-Mu insertional mutation of the 8.9-kb EcoRI fragment suggested that a 4.2-kb fragment was sufficient to complement the mutant XC1708. Sequence analysis of this 4.2-kb fragment revealed three consecutive open reading frames (ORFs), ORF1, ORF2, and ORF3. Hybridization experiments showed that Tn5 in the genome of XC1708 and other mutants complemented by pLASC3 was located in ORF3, which could code for a protein of 83.5 kDa. A signal peptidase II processing site was identified at the N terminus of the predicted amino acid sequence. Sequence homology of 51% was observed between the amino acid sequences predicted from ORF3 and the pulD gene of Klebsiella species.