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Biomedical subjects

A Legrand

Publications and source records attributed to A Legrand.

At least 109 records · Page 6Linked to original sources
PubMed1995

Involvement of cyclic AMP in the effects of phosphodiesterase IV inhibitors on arachidonate release from mononuclear cells.

The effects of selective phosphodiesterase inhibitors, cyclic AMP (cAMP) elevating agents and stable analogues of cyclic nucleotides, on the release of arachidonate induced by N-formyl-Met-Leu-Phe (fMLP) were investigated on human peripheral blood mononuclear cells. The selective phosphodiesterase IV inhibitors, rolipram and Ro 20-1724, and the non-selective phosphodiesterase inhibitor, theophylline, elicited a concentration-dependent inhibition of arachidonate release (EC50 = 1.3 x 10(-6) M, 3.2 x 10(-6) M and 3.7 x 10(-4) M respectively). The selective phosphodiesterase III inhibitor, milrinone (10(-5) M), only caused a slight effect while the phosphodiesterase V inhibitor, zaprinast (10(-5) M), the beta 2-adrenoceptor agonists, salbutamol and fenoterol (10(-5) M), failed to inhibit arachidonate release. Forskolin (10(-5) M) and N6,2'-O- dibutyryladenosine 3':5'-cyclic monophosphate (db-cAMP), 10(-3) M) elicited a moderate inhibition. Forskolin increased the effects of rolipram and Ro 20-1724 (EC50 = 4.5 10(-7) M and 4 x 10(-7) M respectively). Incubation of the cells with rolipram (10(-8) to 10(-5) M), Ro 20-1724 (10(-8) to 10(-5) M, forskolin (10(-5) M) or salbutamol (10(-5) M) alone, induced a moderate increase or no increase at all in intracellular cAMP. However, in the presence of forskolin, rolipram (10(-8) to 10(-6) M) and Ro 20-1724 (10(-8) to 10(-6) M) induced significant and concentration-dependent increase in intracellular levels of cAMP. These results suggest that the potent inhibition of arachidonate release from mononuclear cells by selective phosphodiesterase IV inhibitors may be due to increases in discrete pools of intracellular cAMP.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1995

Cloning of the cDNA encoding rabbit galectin-3.

The complete coding sequence of the rabbit galectin-3-encoding cDNA (LGALS3) has been cloned in a single step by using RT-PCR and specific human LGALS3 cDNA primers. The putative protein contains three domains with different degrees of homology to other known LGALS3. The homology is high in the C-terminal moiety corresponding to the carbohydrate-binding domain and is relatively low in the N-terminal moiety.

Amino Acid Sequence↗
PubMed1995

Oxysterol (7 beta-hydroxycholesteryl-3-oleate) promotes serotonergic reinnervation in the lesioned rat spinal cord by reducing glial reaction.

In the present study, following previous experience with electrolytic lesion of the rat brain, and subsequent reduction of reactive gliosis with 7 beta-hydroxycholesterol derivatives (Bochelen et al.: Neuroscience 51:827-834, 1992), we have performed a hemisection of the spinal cord in adult rats and investigated the influence of 7 beta-hydroxycholesteryl-3-oleate (oxysterol) on the intensity of the astrocytic reaction and the axonal regeneration. We have shown here that local administration of liposomes containing this oxysterol reduced the intensity of the astroglial reaction on the sectioned side, as seen with immunocytochemical detection of glial fibrillary acidic protein (GFAP) and by in situ hybridization with a specific RNA probe. Moreover, radioautographic evaluation of astrocyte proliferation with tritiated thymidine evidenced a reduction of the astrocyte labelling index. In addition, double immunocytochemical detection of GFAP and polysialylated neural cell adhesion molecule (E-NCAM) revealed a decrease of the expression of this molecule in reactive astrocytes of the treated animals. Finally, immunocytochemical detection of serotonin (5HT) was determined in the raphespinal projections, which constitute a major descending system. In treated animals, serotonergic axons originating from the intact side reinnervated the dorsal horn of the sectioned side, below the hemisection. These results demonstrate that 7 beta-hydroxycholesteryl-3-oleate can reduce the astrocytic reaction following spinal cord injury, promoting the serotonergic reinnervation of a denervated territory.

Animals↗
PubMed1995

The second intron of the human galectin-3 gene has a strong promoter activity down-regulated by p53.

Galectin-3 is a galactose-specific lectin which has been shown to be involved in several biological functions such as cell growth regulation, cell aggregation and cell differentiation. The partial cloning of the human genomic sequences reveals the presence of a 651 bp intron, 18 bp downstream of the translation initiation site. This intron contains several regulatory elements found in many eukaryotic genes. This sequence, when inserted upstream of a promoter-free luciferase gene, induces the expression of luciferase, demonstrating the promoter activity of the intron upon transfection in human or murine cells. This promoter activity is down-modulated by wild-type p53 but not by a mutated form of p53.

Antigens, Differentiation↗
PubMed1995

ERGIC-53, a membrane protein of the endoplasmic reticulum-Golgi intermediate compartment, is identical to MR60, an intracellular mannose-specific lectin of myelomonocytic cells.

A mannose-specific membrane lectin (MR60) isolated from human myelomonocytic HL60 cells by affinity chromatography is expressed in intracellular organelles of immature monocytes (Pimpaneau, V., Midoux, P., Monsigny, M., and Roche, A. C. (1991) Carbohydr. Res. 213, 95-108). It is not present at the cell surface and is immunochemically and structurally distinct from the M(r) 175,000 mannose receptor of mature macrophages. MR60 cDNA was isolated and characterized; on the basis of its sequence, MR60 is not related to any known mammalian lectins. Surprisingly, MR60 was found to be identical to ERGIC-53 (Schindler, R., Itin, C., Zerial, M., Lottspeich, F., and Hauri, H.P. (1993) Eur. J. Cell Biol. 61, 1-9), a type I integral membrane protein, defined as a marker of the intermediate compartment that recycles between the Golgi apparatus and endoplasmic reticulum; MR60/ERGIC-53 shares with VIP-36 significant homologies with leguminous plant lectins (Fiedler, K., and Simmons, K. (1994) Cell 77, 625-626). We extend these findings in evidencing a structural homology between MR60/ERGIC-53 and mammalian galectins (soluble beta galactose binding proteins). MR60/ERGIC-53 is the first lectin characterized as an endoplasmic reticulum-Golgi protein. Accordingly, this intracellular mannose binding protein could be involved in the traffic of glycoproteins between endoplasmic reticulum and the Golgi apparatus.

Amino Acid Sequence↗
PubMed1995

Response of the inspiratory intercostal [correction of intercoastal] muscles to increased inertial loads.

To test the hypothesis that the external intercostals and levator costae constitute an inspiratory reserve system, we have examined the response of these muscles to increased inertial loads. Weights were t hus attached sequentially to the ribs in ten lightly anesthetized, spontaneously breathing dogs. As weights were attached, the ribs were progressively displaced caudally at end-expiration, so that the external intercostal muscles were lengthened. In addition, the cranial motion of the ribs during inspiration was gradually reduced, the inspiratory shortening of external intercostal disappeared, and the external intercostal and levator costae inspiratory EMG activities increased. The parasternal intercostal inspiratory activity, however, remained unchanged. Studies also showed that: (1) the increases in external intercostal activity appeared with the first loaded breath and disappeared as soon as the load was removed; (2) these increases were related to the suppression of the inspiratory muscle shortening, rather than to the increase in precontraction muscle length or to vagal inputs; and (3) denervation of the external intercostal caused inspiratory muscle lengthening but had little effect on the inspiratory motion of the ribs. These observations thus indicate that increased inertial loads on the ribs trigger reflexes, possibly spindle reflexes, which cause selective increases in external intercostal and levator costae inspiratory EMG activities. In that sense, the present findings are consistent with the idea that these two muscles constitute an inspiratory reserve system. However, it appears that the major effect of these increased activities is simply to prevent the muscles from lengthening during inspiration.

Animals↗
PubMed1995

Inhomogeneous activation of the parasternal intercostals during breathing.

Recent computations of the mechanical advantage of the canine intercostal muscles have suggested that the inspiratory advantage of the parasternal intercostals is not uniform. In the present studies, we have initially tested this hypothesis. Using a caliper and markers implanted in the costal cartilages, we have thus measured, in four supine paralyzed dogs, the length of the medial, middle, and lateral parasternal fibers at functional residual capacity and after a 1-liter mechanical inflation. With inflation, the medial fibers always shortened more than did the middle fibers (-9.8 +/- 0.8 vs. -6.0 +/- 0.8%; P < 0.001), whereas the lateral fibers remained virtually constant in length (-0.2 +/- 0.8%). This gradient of mechanical advantage agreed well with the gradient of orientation of the muscle fibers. Therefore, we have also recorded the electromyograms of the medial, middle, and lateral parasternal bundles during spontaneous breathing in nine anesthetized animals (20 interspaces); each activity was expressed as a percentage of the activity recorded during tetanic, supramaximal stimulation of the internal intercostal nerve (maximal activity). The medial bundle was invariably more active than was the middle bundle during resting breathing (57.3 +/- 3.3 vs. 25.5 +/- 3.4% of maximum; P < 0.001), and in 10 interspaces, medial activity consistently preceded middle activity at the onset of inspiration. These differences persisted during hypercapnia, during inspiratory resistive loading, as well as after phrenicotomy. Activity was never recorded from the lateral bundle.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1995

Rapid diagnosis of long chain and medium chain fatty acid oxidation disorders using lymphocytes.

A method based on the release of tritiated water from [9,10(n)-3H] palmitic and myristic acids previously described for fibroblasts, was adapted for lymphocytes for the rapid diagnosis of fatty acid oxidation disorders. Optimal concentrations for both substrates and linearity of the assay were established. Normal values were established in control subjects of different age groups (58 children and 117 adults) and 16 patients with known fatty acid oxidation disorders were tested. Tritiated water production from patients' lymphocytes was expressed as a ratio between residual oxidations of palmitate and myristate and the results show that this method allows good differentiation between long chain and medium chain fatty acid oxidation defects.

Acyl-CoA Dehydrogenase↗
PubMed1995

Residual bodies activate Sertoli cell interleukin-1 alpha (IL-1 alpha) release, which triggers IL-6 production by an autocrine mechanism, through the lipoxygenase pathway.

Interleukin-1 (IL-1) and IL-6 are produced by Sertoli cells. As IL-1 stimulates IL-6 production in some tissues, the cascade of events that results in IL-6 secretion by Sertoli cells was studied. The addition of IL-1 alpha to Sertoli cells resulted in a time-dependent increase in IL-6 secretion. Incubation of Sertoli cells with two known stimulators of IL-1 production, lipopolysaccharide (LPS) and residual bodies, resulted in a significant increase in IL-1 release into the medium several hours before IL-6 release. That IL-1 is essential for IL-6 production from Sertoli cells was established by blocking the actions of LPS and residual bodies with an anti-IL-1 alpha antibody. An increase in the release of IL-1 before IL-6 was also observed in medium obtained from staged segments of intact seminiferous tubules; IL-1 reached a maximum level at stage VIII, when mature spermatozoa are released and residual bodies are formed and phagocytosed. The secretion of IL-6 was low during this stage and then increased progressively from stage IX onward, consistent with IL-1 stimulation of IL-6. The pathway of IL-1 alpha-induced release of IL-6 was studied in the presence of agents that influence arachidonic acid release and metabolism. IL-1 alpha was found to stimulate arachidonic acid release by Sertoli cells. Furthermore, a phospholipase A2 inhibitor, aristolochic acid, significantly decreased IL-1-, LPS-, and pyrularia pubera thionin-induced IL-6 secretion from Sertoli cells. Indomethacin, a specific inhibitor of the cyclooxygenase pathway, had no significant effect on basal, but enhanced IL-1- and LPS-stimulated IL-6 production. The involvement of arachidonic acid metabolites produced in the lipoxygenase pathway on the release of IL-6 was investigated indirectly, using nordihydroguaiaretic acid. This inhibitor reduced basal and IL-1 alpha- and LPS-stimulated IL-6 production. Ethacrynic acid, an inhibitor of peptido-leukotriene synthesis, also reduced basal IL-6 levels and blocked IL-1 alpha- as well as LPS-induced IL-6 secretion. It is concluded that IL-1 produced by Sertoli cells in response to LPS or residual bodies induces IL-6 through the lipoxygenase pathway.

Animals↗
PubMed1995

The serotonin-4 receptor agonist cisapride and angiotensin-II exert additive effects on aldosterone secretion in normal man.

In animals and man, serotonin (5-HT) exerts a direct stimulatory action on adrenocortical cells through activation of 5-HT4 receptors. In rats, 5-HT also potentiates the stimulatory effect of angiotensin-II (Ang II) on aldosterone secretion. The aim of the present study was to investigate the effect of concomitant administration of the 5-HT4 receptor agonist, cisapride, and Ang II on aldosterone secretion in normal human subjects. Eight healthy male volunteers pretreated with dexamethasone received, at 1-week intervals in random order and simple blind fashion, the following treatments: 1) a single oral dose of 10 mg cisapride, 2) a single oral dose of placebo, 3) a perfusion of graded doses of Ang II (from 1-4 ng/kg.min), 4) a perfusion of placebo, and 5) a single oral dose of 10 mg cisapride associated with a perfusion of Ang II. The oral doses of cisapride and placebo were also administered after a 3-day period of a low sodium diet (10 mmol/day). Plasma aldosterone levels increased significantly within 90 min after the administration of cisapride without any change in renin levels. The comparison between the net increase in aldosterone production induced by cisapride, Ang II, and cisapride plus Ang II showed that the stimulatory effects of cisapride and Ang II on aldosterone secretion were only additive. Similarly, the increase in plasma aldosterone levels induced by a sodium-restricted diet was just additive with the cisapride-evoked stimulation of aldosterone secretion. These results provide further evidence that the action of 5-HT on glomerulosa cells is mediated through activation of 5-HT4 receptors. The data also indicate that in humans, 5-HT does not potentiate the stimulatory effect of Ang II on aldosterone secretion.

Adult↗
PubMed1995

A sensitive time-resolved immunofluorometric assay for the measurement of apolipoprotein B in cerebrospinal fluid. Application to multiple sclerosis and other neurological diseases.

Although low density lipoprotein receptors have been described on oligodendrocytes, apolipoprotein B was thought to be absent or present in only very small amounts in cerebrospinal fluid (CSF). Several immunoassays have been used for the measurement of apolipoprotein B in serum. However, the majority of methods cannot be used to measure small amounts of apolipoprotein B in CSF. In this study, we describe a highly sensitive time resolved immunofluorometric assay (TR-IFMA) using europium as label (detection limit: 0.3 microgram/l). The reliability of the TR-IFMA for the measurement of apolipoprotein B was first studied in serum. Serum and CSF apolipoprotein B concentrations were then determined in subjects free of neurological disorders and in patients with multiple sclerosis. Local intrathecal apolipoprotein B synthesis was calculated. Although the high sensitivity of the TR-IFMA allowed low amounts of apolipoprotein B in CSF to be detected (0.11 +/- 0.06; 0.12 +/- 0.06 mg/l in controls and multiple sclerosis patients, respectively), no apolipoprotein B could be detected in CSF by electroimmunodiffusion. As suggested by the blood/CSF apolipoprotein B ratio (about 6000), no apolipoprotein B synthesis was observed by both using apolipoprotein B index and formula. This indicates its probable serum origin. Moreover, there was no difference between controls and multiple sclerosis patients in CSF, serum, blood/CSF, index, and local intrathecal apoliprotein B synthesis. Finally, these results suggest that the role of apolipoprotein B in lipid transport in the central nervous system may be questionable.

Adult↗
PubMed1994

A negative regulatory element of the macrophage-specific human mannose receptor gene represses its expression in nonmyeloid cells.

We have cloned the putative promoter of the human mannose receptor gene using the ligation-mediated polymerase chain reaction. This modified polymerase chain reaction method depends upon the ligation of restricted genomic DNA fragments to a sequence of DNA containing a generic primer site. Approximately 400 bp of genomic DNA sequence immediately upstream from the 5' end of the lectin gene was amplified with this strategy. Primer-extended reverse transcription identified several 5' ends of the mannose receptor mRNA corresponding to differential use of initiation transcription sites. DNA sequence analysis of the 5' flanking sequence of the mannose receptor gene indicated the presence of a TATA box and various putative binding sites for several transcription activators. The insertion of the sequence into a plasmid containing a promoterless luciferase reporter gene reveals a promoter activity with a high cell type specificity, efficient expression upon transfection into macrophage type cells, and lack of efficiency upon transfection into nonmyeloid cells. A series of deletion mutants reveals that this cell-type-specific promoter activity is mediated by a negative regulatory element located at the 5' end of the isolated promoter.

Base Sequence↗
PubMed1994

An EBV-based vector allowing a high level of LTRHIV-directed expression in human cells.

We have developed a vector that allows high and transactivable expression of inserted genes. The vector contains a transcription unit in which the LTR from HIV flanks a multicloning site. The plasmid is based on the EBV p205 plasmid, which allows stable replication in human cells. The ability of the vector to express an exogenous DNA in human cells has been tested using the firefly luciferase gene.

DNA, Complementary↗
PubMed1994

Discrepancies between lipoprotein(a) concentrations in icteric sera measured by immunonephelometry and electroimmunodiffusion.

We compared the lipoprotein(a) [Lp(a)] levels in 32 icteric sera determined both by an electroimmunodiffusion assay (EIA), using the Hydragel Lp(a) kit (Sebia, France) and by two immunonephelometric assays, one on a Behring Nephelometer Analyzer (BNA), using antiserum from immunofrance, and the other on a Beckman analyzer (Array), using antiserum from Dako (Denmark). With the EIA assay, the Lp(a) level was 0.09 +/- 0.09 (mean +/- SD in g/L), with the BNA assay, 1.01 +/- 1.51 and with the Array assay, 0.05 +/- 0.05. Sample blanks values (0.76 +/- 1.28 g/L) demonstrated that the high Lp(a) levels obtained in the BNA assay are caused by nonspecific precipitation. Analysis of the precipitate indicated the presence of Lipoprotein X, an abnormal lipoprotein that appears in the serum of patients with obstructive jaundice or with lecithin-cholesterol acyltransferase deficiency. The precipitant seems to be polyethyleneglycol (PEG) that was added to the reaction medium in both the BNA and the Array assays to stabilize the Lp(a)-anti Lp(a) immune complex. In the Array assay, interference by this nonspecific precipitation is eliminated by preliminary centrifugation of the diluted sample. However, coprecipitation of Lp(a) could occur during this step. Consequently, the results of Lp(a) measurement in serum from patients with hepatobiliary diseases should be interpreted with caution when immunonephelometric assays are used with a medium containing PEG.

Humans↗
PubMed1994

Study of 5-HT release with a chronically implanted microdialysis probe in the ventral horn of the spinal cord of unrestrained rats during exercise on a treadmill.

The ventral horn of the spinal cord is profusely innervated by serotonin (5-hydroxytryptamine, 5-HT) which presumably modulates locomotor activity through motoneurons. However, direct evidence of correlation between 5-HT release and activation of motoneurons is still lacking. In order to appreciate the functional characteristics of this innervation, we have used microdialysis to monitor the release of 5-HT in the spinal cord of rats spontaneously running on a treadmill. For this purpose, we developed an original surgical procedure adapted for the chronic implantation of a microdialysis probe in the lumbar spinal cord. The probe was kept in place for 40 days, and microdialysis experiments were carried out at days 8, 16, 20 and 32. 5-HT was detected with HPLC coupled to electrochemistry. This technique demonstrated that release of 5-HT is not increased during exercise. However, a significant decrease was measured during postexercise rest. 5-HT could still be detected 32 days after probe implantation. Detailed histological and immunocytochemical analysis based on glial fibrillary acidic protein and 5-HT immunocytochemistry showed minimal gliosis and the presence of serotonergic varicose fibers, respectively, at the probe contact. It thus appears that microdialysis can be performed through a probe implanted chronically in the spinal cord of unrestrained rat during an endurance running exercise.

Animals↗
PubMed1994

Pharmacokinetic and pharmacodynamic properties of a long-acting formulation of the new somatostatin analogue, lanreotide, in normal healthy volunteers.

1. The aims of the study were to assess the pharmacokinetic parameters and the hormonal effects of the slow-release formulation of the somatostatin analogue (SR-L) in normal male volunteers. 2. Eight healthy males were studied. For the determination of basal values blood was sampled before the injection of vehicle and then every other hour for 8 h in order to measure plasma GH, prolactin (PRL), TSH, free thyroxin (fT4), insulin and glucagon levels. Plasma insulin-like growth factor 1 (IGF-1) levels were measured on a single sample. On day 1 of the study, 30 mg SR-L was administered intramuscularly. Blood was drawn just before injection and then every other hour for a period of 8 h. Thereafter, blood was sampled three times a week for 3 weeks in order to measure lanreotide, IGF-1, TSH, fT4 and PRL concentrations. Plasma GH was determined on days 6 and 11 of the study. 3. Plasma lanreotide concentrations rose to 38.3 +/- 4.1 ng ml-1 2 h following injection. The levels then progressively decreased, remaining above 1.5 ng ml-1 until day 11 and reaching 0.92 +/- 0.28 ng ml-1 2 weeks after injection. The apparent plasma half-life and mean residence time were 4.52 +/- 0.50 and 5.48 +/- 0.51 days respectively. 4. By comparison with the control day, plasma insulin concentrations only decreased 2 h following injection, whereas plasma glucagon did not change at any time. 5. Plasma TSH concentrations were significantly (P < 0.01) reduced from 2 h to day 4 following SR-L injection.2+ '

Abdominal Pain↗
PubMed1994

Effects of a slow-release formulation of the new somatostatin analogue lanreotide in TSH-secreting pituitary adenomas.

OBJECTIVE: Somatostatin analogues have been proposed for the treatment of thyrotrophinomas. However, this treatment requires several s.c. injections a day to be effective. The present study had the following aims: (i) appraisal of the efficacy of a single dose of two somatostatin analogues (lanreotide and octreotide) to acutely inhibit TSH secretion of TSH-secreting pituitary adenomas; (ii) assessment of the efficacy of a single injection of a slow release formulation of lanreotide (SR-L) in reducing TSH and thyroid hormone secretions in the same cases; and (iii) evaluation of the effects of SR-L used for 3-6 months on hormone secretion and tumour size. PATIENTS: Four patients with hyperthyroidism linked to a TSH-secreting pituitary adenoma found on pituitary magnetic resonance imaging (MRI) and subsequently proved by immunohistochemistry were studied. METHODS: In the first step of the study the patients received in a random order, vehicle, 150 micrograms octreotide and 500 micrograms lanreotide as a single s.c. injection. Measurements of plasma TSH, free T4 (fT4), free T3 (fT3) and free alpha subunit (fAS) levels were carried out before injection and then every other hour for 8 hours. In the second part of the study, after a basal blood sample (0800 h), each patient received 30 mg lanreotide as an i.m. injection of SR-L. Blood was sampled 2 hours later and then three times a week for 3 weeks in order to measure plasma TSH, fT4, fT3 and lanreotide levels using radioimmunoassays. The patients then received one SR-L injection twice or in one case three times a month for 3-6 months. Plasma TSH, fT4 and fT3 levels were measured monthly and a pituitary MRI was performed at the end of the treatment with SR-L. RESULTS: 500 micrograms lanreotide acutely reduced plasma TSH and fAS levels to the same extent as 150 micrograms octreotide. Two hours after a single i.m. injection of SR-L plasma lanreotide levels reached 7.8 +/- 0.6 micrograms/l and then progressively decreased, being 1.8 +/- 0.2 microgram/l on day 2 and 1.1 +/- 0.3 microgram/l on day 14 after the injection. Plasma TSH level decreased from basal value (mean +/- SEM 4.4 +/- 1.2 mlU/l) within 2 hours (2.5 +/- 0.8 mlU/l) and further declined to 0.8 +/- 0.2 ml/Ul on day 2 following the injection. Depending on the patient, plasma TSH levels were reduced for a period of 6-15 days. Plasma fT4, fT3 levels were normalized on day 2 and remained in the normal range for a period of time of 9-20 days. During long-term treatment, abdominal cramps and diarrhoea appeared, leading to interruption of the treatment in one patient. The treatment was well tolerated in the other three patients. Plasma TSH and thyroid hormone levels progressively decreased during the treatment. No change in adenoma volume was observed after 3-6 months of therapy. CONCLUSIONS: This study shows that (i) lanreotide is able to inhibit acutely TSH secretion in thyrotrophinomas and that a single s.c. injection of 500 micrograms lanreotide is as effective as 150 micrograms octreotide; (ii) SR-L appears to be able to reduce plasma TSH and to normalize fT4 and fT3 levels for 9-20 days in patients with thyrotrophinomas; (iii) this effect is maintained throughout the treatment using two or three SR-L injections monthly for months. These results suggest that SR-L could be used as a treatment of thyrotrophinomas and avoids the drawbacks of the modes of administration of other somatostatin analogues used in such cases.

Adenoma↗