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PubMed1976

Delayed pituitary hormone response to LRF and TRF in patients with anorexia nervosa and with secondary amenorrhea associated with simple weight loss.

The qualitative and quantitative responses of LRF-induced LH and FSH release and TRF-induced TSH and Prolactin (PRL) release were evaluated in 21 patients with anorexia nervosa, 19 patients with secondary amenorrhea associated with simple weight loss (SWL) who did not fulfill the psychologic criteria for anorexia nervosa, and 7 normal women in the early follicular phase of the menstrual cycle. Basal plasma LH and FSH were significantly lower in the anorexia nervosa group compared to the SWL group and normals (P less than 0.05). The LRF-induced integrated LH responses, however, were the same in the 3 groups and the integrated FSH responses were greater in the underweight groups when compared to normal. The time of the peak LH response (mean+/-SE) was signifantly delayed (P less than 0.01) in both the anorexia nervosa (49 +/- 6.1 min) and SWL (28 +/- 2.5 min) groups when compared to normal (17 +/- 2.3 min). The time of the FSH response was significantly delayed (P less than 0.05) in anorexia nervosa (95 +/- 9.6 min) when compared to normals (35 +/0 7.9 min) and SWL patients (62 +/- 11.7 min). Normal basal TSH and PRL and normal peak TSH and PRL responses to TRF were found in anorexia nervosa. The time of the TSH and PRL peak (56+/-8.9 and 36+/-3.6 min,, respectively) in anorexia nervosa was significantly later than normal (26 +/- 1.7 and 36 +/- 3.6 min respectively) (P less than 0.01). It is concluded that despite normal quantitative response to releasing hormones, there are abnormally delayed responses in both anorexia nervosa and SWL patients. The SWL responses were intermediate between those of the anorexia nervosa group and normals. The constellation of normal quantitative but abnormal kinetic LRF and TRF responses supports the hypothesis that the endocrine changes seen in anorexia nervosa are consistent with hypothalamic dysfunction.

Adolescent↗
PubMed1977

Plasma ACTH and cortisol responses to TRF, vasopressin or hypoglycemia in cushing's disease and nelson's syndrome.

The response of plasma ACTH and/or cortisol concentrations to thyrotropin-releasing-factor (TRF), vasopressin, and insulin administration was determined in 5 patients with Nelson's syndrome and 12 patients with untreated Cushing's disease. TRF administration was associated with a mean increment of 267 pg/ml in plasma ACTH concentrations in patients with Nelson's syndrome, and of 42 pg/ml in patients with Cushing's disease. The increment in plasma cortisol concentrations in the latter group was 12 mug%. No ACTH or cortisol response was observed in normal subjects. Patients with Cushing's disease or Nelson's syndrome exhibited significantly greater increments in plasma ACTH concentrations in response to vasopressin administration (P less than .05, P less than .02 respectively) than did normal subjects; the increment in cortisol concentration was also greater, (P less than .05), in patients with Cushing's disease than in normal subjects. No significant difference was present between patients with Cushing's disease and Nelson's syndrome with regard to the magnitude of the ACTH response to vasopressin administration. In contrast, the increment in plasma cortisol and plasma ACTH concentrations following insulin induced hypoglycemia was significantly less in patients with Cushing's disease than seen in normal subjects, (P less than .001, P less than .05 respectively); while this stimulus was associated with a significantly greater increment in plasma ACTH concentrations in patients with Nelson's syndrome as compared to that seen in normal subjects, (P less than .01) and in patients with Cushing's disease (P less than .01). These findings indicate that pituitary function in patients with Nelson's syndrome is not autonomous and suggest the possibility that altered central nervous regulatory mechanism might play a role in the etiology of the pituitary tumors which are frequently associated with this syndrome. The TRF induced rise in plasm cortisol and ACTH concentrations in patients with Cushing's disease and Nelson's syndrome suggests the possibility of altered hypothalamic or pituitary receptors in such patients.

Adolescent↗
PubMed1983

Culture conditions for selective and enhanced release of various murine lymphokines (CSF, IL-2, MCF, MIF and TRF).

The production of the lymphokines colony stimulating factor (CSF), interleukin-2 (IL-2), macrophage cytotoxicity factor (MCF), macrophage migration inhibitory factor (MIF) and T cell replacing factor (TRF) was optimized from mouse spleen cell cultures stimulated with concanavalin A (Con A). The cultivation was performed in bioreactors which allow regulation of dissolved oxygen concentration. The oxygen supply influenced the yields of individual lymphokines in different ways. High oxygen concentration was beneficial for high release of IL-2 and MCF, whereas MIF and TRF were better produced at low oxygen concentrations. CSF release did not depend on oxygen supply. Upon stimulation with Con A, lymphokine activities in the culture supernatant reached an optimum or plateau after 24 h Lymphocytes continued with lymphokine release, when they were restimulated for further 24 h. in fresh medium and mitogen. CSF could be induced for at least 4 times. MCF was released during the first 3 inductions, whereas IL-2 and TRF were only produced during the first and second induction. These findings led to specific culture conditions for selective and enhanced production of individual lymphokines.

Animals↗
PubMed1983

LRF and TRF test during long-term danazol treatment: increase of the LH and FSH responses but decrease of the prolactin and TSH responses.

Seven patients suffering from severe endometriosis were treated with danazol 200 mg X 3 daily for 6 months. Clinical symptoms were alleviated and menses disappeared in response to the treatment. After cessation of the treatment the menstrual bleedings returned in 1-3 months. Blood samples for determination of gonadotrophins, prolactin (Prl), oestradiol (E2), progesterone, thyroid hormones and thyrotrophin in radioimmunoassays were taken and a combined TRF and LRF test carried out in the follicular phase before treatment, at the 6th month of treatment and after reappearance of the first menses. There were no statistically significant changes in the basal levels of serum FSH, LH or TSH during the danazol treatment. Neither was there any change in episodic secretions of FSH, LH or Prl, as determined by the mean coefficients of variation of the hormone levels in seven consecutive samples taken at 20 min intervals. On the other hand, serum E2, Prl and thyroid hormone levels were significantly decreased in the 6th month of treatment. In the TRF-LRF test the responses of serum FSH and LH were significantly higher and those of serum Prl and TSH significantly lower during danazol treatment than before. Prl responses remained lowered after the treatment. It appears that low serum oestrogen levels, induced by the danazol treatment, sensitize the pituitary gonadotrophs to exogenous LRF, but make the sensitivity of thyrotrophs and lactotrophs lower to exogenous TRF. These results thus indicate that danazol does not make the pituitary gonadotrophs insensitive to LRF, but danazol may rather inhibit the secretion of hypothalamic LRF.

Adult↗
PubMed1980

Polyclonal activation of murine B lymphocytes by Fe fragments. II. Replacement of T cells by a soluble helper T cell-replacing factor (TRF).

Fc fragments of human gamma-globulin stimulate T cell-dependent polyclonal antibody responses in murine splenic B cells. The T cell signal can be delivered by a soluble T cell-replacing factor, derived by concanavalin A stimulation of spleen cells. TRF interacts directly with responding B cells and appears to provide the second, differentiative, trigger that initiates the polyclonal response. TRF is maximally active even if added at 24 hr after Fc and does not alter the response kinetics. Although macrophages are requird for the polyclonal activation of B cells in intact spleen cell cultures, they are not necessary for the delivery of the TRF signal to B cells.

Animals↗
PubMedDate not supplied

[Response of thyrotropin (TSH) to the stimulation with hypothalamic releasing factor (TRF) in hypothyroid children].

The normal human serum thyrotropin (TSH) measured by radioimmunoassay in 36 children was 3.3 +/- 1.13 muUI/ml. No differences dependent on age or sex were found. Stimulation by intravenous injection of 100 mug of TRF has been carried out in 7 euthyroid children and in 14 with hypothyroidism. TSH was determined prior to, and during TRF stimulation. Among other thyroid tests included in this study were: serum T3 uptake, total thyroxine, serum protein-bound iodine, 131INa uptake and thyroid scanning. In the euthyroid children, TSH at zero time was 4.4 muUI/ml.; a significant increase was reached at 30-40 minutes. In 13 children with a light primary hypothyroidism, TSH was little increased in correlation with other parameters assessed. In two children with true primary hypothyroidism, TSH at zero time was X 465 muUI/ml., showing an increase at 30 minutes of X 550 muUL/ml. which was in agreement with the absence of thyroid tissue, showed by the scanning image and with the low concentration of thyroid hormones. The synthetic thyrotropin-releasing factor (TRF) should be a useful agent for clinical assessment of pituitary reserve. TSH, T3, T4 and T4I serum concentration measurement in pediatric age, makes possible to evaluate the physiopathology of the pituitary - thyroid axis.

Adolescent↗
PubMed1998

Transcription: TRF walks the walk but can it talk the talk?

The TBP-related factor TRF binds to a TATA box promoter sequence and mediates basal transcription in vitro. A central question is: does TRF function in vivo to transduce the effects of activators in a tissue-specific fashion?

Amino Acid Sequence↗
PubMed2002

A comparison of ALPHAScreen, TR-FRET, and TRF as assay methods for FXR nuclear receptors.

New developments in detection technologies are providing a variety of biomolecular screening strategies from which to choose. Consequently, we performed a detailed analysis of both separation-based and non-separation-based formats for screening nuclear receptor ligands. In this study, time-resolved fluorescence resonance energy transfer (TR-FRET), ALPHAScreen, and time-resolved fluorescence (TRF) assays were optimized and compared with respect to sensitivity, reproducibility, and miniaturization capability. The results showed that the ALPHAScreen system had the best sensitivity and dynamic range. The TRF assay was more time consuming because of the number of wash steps necessary. The TR-FRET assay had less interwell variation, most likely because of ratiometric measurement. Both the ALPHAScreen and the TR-FRET assays were miniaturized to 8-microl volumes. Of the photomultiplier tube-based readers, the ALPHAScreen reader (ALPHAQuest) presented the advantage of faster reading times through simultaneous reading with four photomultiplier tubes.

Animals↗
PubMed1987

Specific antibody responses by high- and low-density human peripheral blood B cells: T-helper cells and T-cell replacing factor (TRF) act on different B-cell subpopulations.

Antibody production to influenza A strain virus X31 (H3N2) was measured in cultures of peripheral blood mononuclear cells (PBMC) stimulated with either antigen (X31) or pokeweed mitogen (PWM). With some donors, X31 antibody was produced in response to antigenic stimulation, but not as part of the polyclonal response to PWM, suggesting that antigen and PWM may be acting on different B-cell subpopulations. To test this hypothesis, T-cell depleted PBMC (E-) cells were fractionated on discontinuous Percoll gradients and assayed for antibody production in response to antigen or PWM. Fraction I (FrI = SG less than 1.070) cultured in the presence of T cells responded well to PWM, but not at all to X31. FrII (1.070 less than SG less than 1.075) and FrIII (SG greater than 1.075) cultured in the presence of T cells both responded well to X31, but only the medium-density B cells (FrII) were able to make specific antibody when T cells were replaced with T-cell replacing factor (TRF). Specific X31 antibody responses by medium- and high-density B cells (FrII and FrIII) were suppressed equally by the addition of allogeneic T-suppressor (Ts) cells. When allo-activated Ts cells were inactivated by irradiation, allogeneic T-helper (Th) cells were able to collaborate with both FrII and FrIII B cells in specific antibody responses to X31. Since TRF was not able to substitute for T cells in specific antibody responses by FrIII B cells, this result shows that allogeneic T-cell help was not mediated by non-specific 'allogeneic effect' factors and apparently requires cognate T cell-B cell interactions.

Adjuvants, Immunologic↗
PubMedDate not supplied

Regulation of antibody synthesis to sheep red cells in cultures of nu/nu spleen cells by T-cell replacing factor (TRF) and immunoglobulin-binding factor (IBF).

Fc receptor positive alloantigen-activated T cells release an immunoglobulin binding factor (IBF) which suppresses in vitro antibody synthesis. The present work was undertaken to approach the mechanisms by which IBF suppresses the response, and we obtained the following results. First, IBF does not inhibit DNA synthesis in lipopolysaccharide stimulated spleen cells while suppressing the polyclonal plaque response, indicating that IBF does not interfere with B-cell proliferation. Second, antibody synthesis by spleen cells from Nude (nu/nu) mice, stimulated with sheep red blood cells triggered by concanavalin A induced T-cell replacing factor (TRF) was suppressed by IBF, indicating that the factor does not need mature T cells to express its activity. Kinetics experiments showed that IBF does not destroy TRF but rather acts sequentially with the helper factor on the late phase of the differentiation of B cells to antibody producing cells.

Animals↗
PubMed1982

Human helper T cell factor(s) (ThF). II. Induction of IgG production in B lymphoblastoid cell lines and identification of T cell-replacing factor- (TRF) like factor(s).

IgG-PFC was induced in Epstein-Barr virus-transformed B lymphoblastoid cell lines (LCL) by the addition of allogeneic T cells. T cells involved in the induction of IgG-PFC were shown to belong to the Leu 3a+/2a- T cell subset. Furthermore, partially purified soluble factors obtained from the culture supernatant of PPD-stimulated pleural T cells or PWM-stimulated tonsillar mononuclear cells was shown to induce IgG-PFC in LCL across the major histocompatibility complex barrier. The induction of IgG-PFC was observed only in surface IgG-positive LCL cell populations and was not accompanied by the increase in the number of LCL cells. The factors with such a TRF-like activity were found in two fractions corresponding to the m.w. range of 18,000 to 25,000 (22K fraction) and 28,000 to 38,000 (36K fraction) by gel filtration. Isoelectric focusing of these fractions revealed that TRF-like activity of both 22K and 36K fractions distributed in the pI range of 5.0 to 6.0, and both fractions were found to be devoid of TCGF activity. These results appear to indicate that the factors act on the B cells in terminal stages to trigger final differentiation to Ig-producing cells.

Animals↗
PubMed1999

The human homologue of Drosophila TRF-proximal protein is associated with an RNA polymerase II-SRB complex.

Mammalian RNA polymerase II holoenzymes are large complexes that have been reported to contain, in addition to RNA polymerase II, homologues of several yeast SRBs, various general transcription factors, and other polypeptides. On the basis of its copurification with an SRB-containing RNA polymerase II complex by conventional chromatography procedures, we have identified a human homologue of Drosophila TRF-proximal protein, designated hTRFP, and isolated its cognate cDNA. Antibody specific for SRB7 can immunoprecipitate hTRFP and RNA polymerase II and, reciprocally, antibody specific for hTRFP can immunoprecipitate RNA polymerase II and SRB7. These data indicate that hTRFP is an integral component of an RNA polymerase II-SRB complex. Whereas the precise function of hTRFP remains to be determined, the hTRFP-containing RNA polymerase II-SRB complex supports basal level transcription and, relative to RNA polymerase II alone, enhances transcriptional activation by Gal4-VP16 in the presence of cofactor PC4. Thus, hTRFP may regulate transcription of class II genes through association with the RNA polymerase II-SRB complex.

Amino Acid Sequence↗
PubMed1978

Cyproheptadine treatment of Nelson's syndrome: restoration of plasma ACTH circadian periodicity and reversal of response to TRF.

Administration of cyproheptadine for four months to a patient with Nelson's Syndrome was associated with evidence of skin lightening, decreased plasma ACTH concentrations, return of a normal circadian periodicity of plasma ACTH concentrations, and lack of responsiveness of plasma ACTH concentrations to TRF administration, in contrast to the response seen in the untreated state.

Adrenocorticotropic Hormone↗
PubMed1976

Myxedematous madness without myxedema. Selective defect of TSH release on TRF loading in a young woman with a history of severe depressive illness cured with thryoid hormone replacement therapy.

A young woman, whose psychiatric history covered 16 years, has been treated several times as in-patient for psychotic depression, which were finally cured with thyroid replacement therapy. Recent reports of the connection between depression and disturbances in the hypothalamic-pituitary-thyroid axis are discussed. The authors question the suggestion that selective pituitary insufficiency and a defect in TSH release on TRF loading are rare phenomena.

Adolescent↗
PubMedDate not supplied

Time-resolved fluorometry (TRF)-based immunoassay concept for rapid and quantitative determination of biochemical myocardial infarction markers from whole blood, serum and plasma.

We report the development of a time-resolved fluorometry-based immunoassay concept for the rapid measurement of three cardiac markers from whole blood, serum or plasma. Using a universal all-in-one (AIO) dry reagent concept, all the analyte specific reagents are built into a single microtire well, to which an identical assay protocol is applied. Addition of 5-20 microL sample (whole blood, serum or plasma) together with a universal buffer initiates the reaction, which is brought close to equilibrium in 15 min. After the wash step the Eu chelate-derived signal is measured directly from the dried surface. Application of this concept to the three cardiac markers illustrates its ability to provide rapid, highly sensitive and fully quantitative results over a large dynamic range with good reproducibility. Such a performance, especially when using whole blood specimens, is largely a consequence of the inherently fluorescent and stable Eu-chelate employed in the system. Correlation to commercial assays was excellent for all three analytes, as was between-sample matrix correlation using the AIO assays. The presented assay concept enabling a simple automation is particularly suited for point-of-care applications, where the performance characteristics are fully comparable to state-of-the-art central laboratory immunoassays.

Biomarkers↗