Biomedical subjects

A Pappalardo

Publications and source records attributed to A Pappalardo.

At least 37 records · Page 2Linked to original sources

PubMed2000

Comparison of intravenously administered dofetilide versus amiodarone in the acute termination of atrial fibrillation and flutter. A multicentre, randomized, double-blind, placebo-controlled study.

AIMS: This study compared the efficacy and safety of intravenous dofetilide with amiodarone and placebo in converting atrial fibrillation or flutter to sinus rhythm. METHODS AND RESULTS: One hundred and fifty patients with atrial fibrillation or flutter (duration range 2 h-6 months) were given 15-min intravenous infusions of 8 microg. kg(-1)of dofetilide (n=48), 5 mg. kg(-1)of amiodarone (n=50), or placebo (n=52) and monitored continuously for 3 h. Sinus rhythm was restored in 35%, 4%, and 4% of patients, respectively (P<0.001, dofetilide vs placebo;P=ns, amiodarone versus placebo). Dofetilide was more effective in atrial flutter than in atrial fibrillation (cardioversion rates 75% and 22%, respectively;P=0.004). The mean time to conversion with dofetilide was 55+/-15 min. Dofetilide prolonged the QTc interval (+16% at 20 min). Amiodarone substantially decreased the ventricular rate in non-converters (-18 beats. min(-1)at 30 min). Two patients given dofetilide (4%) had non-sustained ventricular tachycardias, and four (8%) had torsade de pointes, in one case requiring electrical cardioversion. CONCLUSION: Intravenous dofetilide is significantly more effective than amiodarone or placebo in restoring sinus rhythm in patients with atrial fibrillation or flutter. However, when infused intravenously at this dose and rate, dofetilide causes a significant incidence of torsade de pointes.

Acute Disease↗

PubMed2000

Basic fibroblast growth factor inhibits apoptosis of spontaneously immortalized granulosa cells by regulating intracellular free calcium levels through a protein kinase Cdelta-dependent pathway.

Previous studies have shown that basic fibroblast growth factor (bFGF) inhibits primary granulosa cells from undergoing apoptosis. The present studies were designed to determine whether spontaneously immortalized granulosa cells (SIGCs) undergo apoptosis when deprived of growth factors and whether bFGF prevents apoptosis. In the absence of serum, the SIGCs lost cell contact and underwent apoptosis as indicated by the presence of annexin V binding, DNA ladders, and nuclear fragmentation. Basic FGF maintained cell contact and reduced the percentage of apoptotic cells. This antiapoptotic action was not observed ifbFGF was added 30 min after serum withdrawal. Further, intracellular free calcium ([Ca2+]i) levels gradually increased 3- to 4-fold within 10 min of serum withdrawal. This increase was inhibited by bFGF. The intracellular calcium chelator, BAPTA, completely prevented the SIGCs from undergoing apoptosis in the absence of serum. These observations suggest that bFGF's ability to regulate [Ca2+]i is an essential component of its antiapoptotic action. The phorbol ester TPA, an activator of protein kinase C (PKC), blocked apoptosis due to serum deprivation. Conversely, bisindolylmaleimide II, an inhibitor of PKC, completely attenuated, whereas bisindolylmaleimide V, an inactive bisindolylmaleimide analog, did not influence bFGF's antiapoptotic action. Also, treatment with the PKC inhibitor, chelerythrine chloride, interfered with bFGF's ability to maintain calcium homeostasis. Western blot analysis revealed that SIGCs expressed PKCdelta, tau, lambda, and zeta. Of these PKC isoforms, only PKCdelta has been shown to be activated by TPA. In apoptotic SIGCs, PKCdelta levels were depleted. When PKCdelta levels were reduced by pretreatment with 500 nM TPA, neither bFGF nor 10 nM TPA suppressed apoptosis. Collectively, these observations suggest that bFGF maintains [Ca2+]i and thereby SIGC viability through a PKCdelta-dependent pathway.

Animals↗

PubMed2000

Effect of disrupting cell contact on the nuclear accumulation of beta-catenin and subsequent apoptosis of rat ovarian surface epithelial cells in vitro.

The present studies were designed to determine how disrupting cell contact induces rat ovarian surface epithelial cells (i.e., ROSE-179 cells) to undergo apoptosis. In the first series of studies, the effect of depleting serum and calcium on the levels of the adhesion proteins N-cadherin and beta-catenin was examined. These studies revealed that the depletion of serum and calcium results in the degradation of N-cadherin but not beta-catenin. However, the localization of beta-catenin changed from principally the plasma membrane to the nucleus. The nuclear localization of beta-catenin was demonstrated by Western blot and confocal microscopy. A second series of studies demonstrated that cells that lost contact in response to the depletion of serum and calcium showed enhanced beta-catenin-dependent transcription. Finally, forced expression of a stable form of beta-catenin resulted in an increase in beta-catenin within the cytoplasm of transfected ROSE-179 cells. When these beta-catenin transfected ROSE-179 cells were deprived of serum and calcium, beta-catenin accumulated within the nucleus and accelerated the rate at which these cells became apoptotic. These data indicate that in viable cells, beta-catenin is part of the adhesion complex that maintains cell contact. If calcium-dependent cell contacts are broken, beta-catenin accumulates within the nucleus, where it promotes transcription and ultimately the apoptotic death of ROSE-179 cells.

Animals↗

PubMed1999

Progesterone maintains large rat granulosa cell viability indirectly by stimulating small granulosa cells to synthesize basic fibroblast growth factor.

Ovarian follicles are composed of small and large granulosa cells (GCs). Since progesterone (P4) inhibits large GCs from undergoing apoptosis, studies were designed to determine whether both sizes of GCs bind P4. These studies revealed that fluorescein isothiocyanate-BSA-P4 bound only to the surface membranes of small GCs. This binding was steroid-specific and inhibited by an antibody directed against the ligand-binding domain of the nuclear P4 receptor (PR). In addition, a cell-impermeable derivative of P4, BSA-conjugated P4, was as effective as P4 in preventing apoptosis. Quantitative in situ hybridization studies showed that P4 increased the relative amount of basic fibroblast growth factor (bFGF) mRNA expressed per cell as well as the percentage of small GCs that expressed bFGF. To determine whether the anti-apoptotic action of P4 was mediated by bFGF, GCs were cultured in control medium supplemented with either P4, a neutralizing antibody to bFGF, or both P4 and the bFGF antibody. The results from this study demonstrated that P4 suppressed apoptosis and that this effect was attenuated in presence of the bFGF antibody. Basic FGF also prevented GC apoptosis, and its action was not influenced by either the PR antagonist (RU-486), an inhibitor of P4 synthesis (aminoglutethimide), or a PR antibody. Finally, FGF receptors were detected on both small and large GCs. Collectively, these data support the hypothesis that P4 acts through a putative membrane receptor on small GCs to stimulate the synthesis of bFGF. Basic FGF then activates its receptors within large GCs, and this initiates a signal transduction pathway that maintains large GC viability.

Aminoglutethimide↗

PubMed1998

Progesterone mediates its anti-mitogenic and anti-apoptotic actions in rat granulosa cells through a progesterone-binding protein with gamma aminobutyric acidA receptor-like features.

Progesterone (P4) inhibits small granulosa cell (GC) mitosis and large GC apoptosis. These actions are steroid specific and dose dependent and are inhibited by the progesterone receptor (PR) antagonist, RU-486. However, these cells do not express the nuclear PR but rather an ill-defined P4-binding protein (P4BP). This binding protein could function as a receptor and mediate P4's actions in GCs. Therefore, a series of studies was designed to characterize this P4BP. First, an antibody directed against the ligand-binding site of the nuclear PR was used in a Western blot analysis. This analysis revealed the presence of a 60-kDa P4BP within ovarian and GC lysates as well as within an ovarian membrane preparation. This protein was not observed in lysates of cells derived from the ovarian surface epithelium. In addition, this P4BP was immunoprecipitated by an antibody to the alpha1 chain of the gamma aminobutyric acidA (GABA(A)) receptor, suggesting that the P4BP could be the ovarian GABA(A) receptor. Since activation of the rat ovarian GABA(A) receptor increases intracellular cAMP levels, GCs were cultured with control medium supplemented with either 8-bromo-cAMP (8-br-cAMP), P4, or muscimol (a GABA agonist). Increases in cAMP were detected by monitoring the cAMP-dependent phosphorylation of cAMP response element-binding protein (CREB). Phosphorylated CREB was not observed in control or P4-treated cultures, but it was detected in the majority of both small and large GCs exposed to either 8-br-cAMP or muscimol. Since activation of the GABA(A) receptor with muscimol increases phosphorylated CREB but P4 does not, this study indicates that P4 does not activate the ovarian GABA(A) receptor. However, both bicuculline, a GABA(A) receptor antagonist, and the antibody to PR inhibited P4's ability to prevent both insulin-dependent mitosis and apoptosis. Collectively, these studies suggest that P4 mediates its anti-mitotic and anti-apoptotic effects through this 60-kDa P4BP, which has GABA(A) receptor-like properties and is localized within the surface membrane of GCs.

Animals↗

PubMed1998

[Magnetic resonance imaging of seronegative sacroiliitis].

INTRODUCTION: The inflammatory involvement of the sacroiliac joint is frequent during seronegative spondylarthritis. The clinical diagnosis of sacroiliitis may be very difficult, especially in the early stage, because joint motion cannot be assessed directly and the clinical picture is very similar to that of lumbar pain. Conventional radiography is negative as long as the structural change in the joint is limited to the synovial membrane and the cartilage (early stage). Computed Tomography (CT) also has many drawbacks, and thus the changes can be shown only when chondritis and enthesitis have already damaged the bone. The disease onset is usually preceded by a long latency; early diagnosis is needed for a proper and timely treatment, which can be made only with a highly sensitive and specific technique. We investigated the diagnostic accuracy of MRI in the early detection of sacroiliitis during seronegative spondylarthritis. MATERIAL AND METHODS: Forty patients with suspected sacroiliitis and negative radiographic findings were submitted to MRI; thirty-seven of them were HLA B27 positive. MRI was performed with a .5 T superconducting unit; T1-weighted SE, T2-weighted FSE, T2* GE, and STIR images were acquired on the oblique coronal plane parallel to the anterior sacrum. Ten asymptomatic volunteers were also examined as a control group. RESULTS: An irregular sacral border and marrow changes at the insertion of the sacroiliac ligaments were seen in 3/10 asymptomatic volunteers. MRI was negative in 7/40 patients, while the synovial compartment was replaced by some tissue with low signal intensity of T1 and high signal on T2 in the other 33 patients; this finding was referred to synovial pannus. Persisting low-signal foci were seen in the synovial compartment in 16/33 patients, which were referred to spared cartilage. High-signal regions were depicted at the bone periphery in 9/33 patients, which areas were consistent with bone erosion; the subchondral bone was markedly hypointense in 5 of these patients, indicating sclerosis. Finally, diffuse high signal intensity was found in the bone marrow in 3/33 patients and referred to infectious sacroiliitis. CONCLUSIONS: MRI appears the method of choice for the early detection of seronegative sacroiliitis because it can show the early changes in cartilage and subchondral bone, filling the gap between the onset of symptoms and radiographic evidence. Moreover, MRI uses no ionizing radiations and makes therefore a precious tool for the diagnosis and follow-up of young patients, hopefully decreasing the use of CT which however provides better detailing of bone and bone degeneration.

Arthritis↗

PubMed1997

Basic fibroblast growth factor and N-cadherin maintain rat granulosa cell and ovarian surface epithelial cell viability by stimulating the tyrosine phosphorylation of the fibroblast growth factor receptors.

Both granulosa cells (GCs) and ovarian surface epithelial cells undergo apoptosis in vivo. Although basic fibroblast growth factor (bFGF) and N-cadherin-mediated cell contact inhibit GC apoptosis, little is known about the factors that influence rat ovarian surface epithelial (ROSE) cell apoptosis. The present studies were designed to determine whether bFGF and N-cadherin maintain the viability of both GC and ROSE cells by stimulating separate signaling pathways. For the GC studies, large GCs were collected from immature rat ovaries after Percoll gradient centrifugation and placed in serum-free culture for 24 h. These studies confirmed that about 10% of the aggregated GCs and more than 50% of single GCs were apoptotic after culture. bFGF reduced the percentage of apoptotic single GCs, but did not influence aggregated GCs. A neutralizing antibody to bFGF blocked bFGF's antiapoptotic action, but did not alter the percentage of apoptotic aggregated GCs. The antibody to N-cadherin not only increased the percentage of aggregated apoptotic GCs, but also blocked bFGF's ability to maintain the viability of single GCs. The effect of the FGF receptor antibody was similar to that of the N-cadherin antibody. Like GCs, ROSE cells also undergo apoptosis in serum-free medium. Exposure to either the N-cadherin or FGF receptor antibody, even in the presence of serum, increased the percentage of apoptotic aggregated ROSE cells. As tyrosine kinase activity is involved in maintaining cell viability, the pattern of tyrosine-phosphorylated proteins was examined after culture in control (ascites) or N-cadherin antibody-supplemented medium. Exposure to the N-cadherin antibody altered the pattern of tyrosine-phosphorylated proteins, decreasing the tyrosine phosphorylation of proteins in the 130- to 180-kDa range and increasing the tyrosine phosphorylation of one or more proteins of about 50 kDa. The identity of the 50-kDa protein is unknown. However, immunoprecipitation studies demonstrated that the N-cadherin antibody reduced the amount of tyrosine-phosphorylated FGF receptor in both GCs and ROSE cells by 50%. This decrease corresponds to an increase in apoptosis among aggregated cells. Taken together, these data suggest that homophilic N-cadherin binding and bFGF-FGF receptor binding activate signal transduction pathways that converge at the level of the FGF receptor and subsequently promote the viability of both GC and ROSE cells.

Animals↗

PubMed1997

[Renal angiomyolipoma].

Renal angiomyolipoma is a benign tumor that can be observed in two distinct types: the solitary type and the tuberous sclerosis associated type. It is now diagnosed, even if asymptomatic, with increasing frequency by means of ultrasonography and computerized tomography owing to its particular features. The possibility of preoperative diagnosis and the biological characteristics of this benign lesion should induce a more conservative management.

Angiomyolipoma↗

PubMed1996

Steroidogenic factor-1 as a positive regulator of rat granulosa cell differentiation and a negative regulator of mitosis.

Ovarian follicles contain small nonaromatase-expressing and large aromatase-expressing granulosa cells (GCs). The present studies were designed to determine whether small GCs can differentiate into large GCs and/or express aromatase. Additional studies were conducted to assess the role of steroidogenic factor-1 (SF-1), an orphan nuclear receptor, in regulating GC differentiation and proliferation. For these studies, small GCs were isolated from immature rats by Percoll gradient centrifugation and cultured for up to 48 h with FSH and/or 8-bromo-cAMP (8-br-cAMP). FSH/8-br-cAMP induced a 2-fold increase in SF-1 messenger RNA levels within 4 h. This increase was maintained throughout the culture period. By 24 h culture, FSH/8-br-cAMP increased the percentage of large GCs. It was not until 48 h of culture with FSH and 8-br-cAMP that aromatase expression increased. This increase was detected by both Western blot and quantitative immunocytochemistry. 8-br-cAMP alone did not promote GC differentiation. Small GCs were then cultured with FSH/8-br-cAMP in the presence or absence of an antisense oligonucleotide complementary to the putative SF-1 ligand-binding site (SF-1 AS). As a control, small GCs were cultured with FSH/8-br-cAMP and an 18-mer nonsense oligonucleotide (SF-1 NS). The SF-1 AS, but not the SF-1 NS, prevented FSH/8-br-cAMP from increasing 1) SF-1 messenger RNA levels, 2) transcription of a SF-1(x2) promoter/luciferase construct, 3) GC size, and 4) aromatase expression. In a third series of experiments, small GCs were cultured for 24 h in 1) control media supplemented with 2) a mitogen, phorbol ester [12-O-tetraphorbol acetate (TPA)], 3) FSH/8-br-cAMP, or 4) both. TPA increased the number of GCs by 51 +/- 9%. FSH/8-br-cAMP completely blocked TPA-induced mitosis. When small GCs were cultured with FSH/cAMP, TPA, and SF-1 AS, the number of GCs increased by 50 +/- 7%. This increase was not observed with SF-1 NS. Taken together, these data demonstrate that SF-1 is expressed in both small and large GCs, and enhanced SF-1 expression is part of the molecular mechanism associated with GC differentiation. Interestingly, SF-1 not only regulates differentiation, but also inhibits TPA-induced GC mitosis.

Animals↗

PubMed1996

N-cadherin-mediated cell contact inhibits granulosa cell apoptosis in a progesterone-independent manner.

Previous studies have shown that both progesterone and cell contact inhibit granulosa cell (GC) apoptosis in vitro. Since the progesterone concentration associated with aggregated GCs may be higher than that of single GCs, experiments were conducted to differentiate progesterone's action from that of cell contact. For these studies, GCs were isolated from immature rats. Large GCs were collected after Percoll gradient centrifugation and placed in serum-free culture for 24 h. These studies confirmed that the rate of apoptosis was 2-3 times higher for single GCs than for aggregated GCs. This relationship was observed in the presence of aminoglutethimide, where progesterone concentrations were 3 ng/ml or less. A dose-response studied revealed that a minimum of 100 ng/ml progesterone were required to suppress apoptosis of single GCs. In addition, a single cell contact was shown to be sufficient to suppress apoptosis, with a small nonsteroidogenic GC being as effective as a large steroidogenic GC. Taken together, these data support the concept that cell contact blocks apoptosis in a progesterone-independent manner. GC contact is due to the presence of gap and adhesion-type junctions. To assess which, if either, of these junctions is involved in mediating the antiapoptotic action of cell contact, cocultures were set-up between GCs and R2C cells. Contact with R2C cells inhibits GC apoptosis, but does not result in the formation of functional gap junctions. This demonstrates that gap junctions are not essential to maintain GC viability. Adhesion-type junctions result from a homophilic binding of N-cadherin, which is expressed by both GCs and R2C cells. When this binding is inhibited by treatment with either an antibody to N-cadherin or a synthetic N-cadherin peptide, cell aggregation is attenuated. For those cells that form cell contacts in the presence of these N-cadherin-binding inhibitors, the percentage of apoptotic cells is increased compared to that in controls. These observations suggest that homophilic binding of N-cadherin molecules on the surface membranes of adjacent GCs initiates a signal transduction cascade that ultimately inhibits apoptosis.

Animals↗

PubMed1996

[Exfoliative conjunctival cytology in Sjögren's syndrome].

The study has been performed in order to give a contribution to the knowledge of the conjunctival cytology in Sjögren's syndrome. Exfoliated cells were obtained by a tampon from the inferior conjunctival sac of 11 patients affected by primary or secondary Sjögren's syndrome; the material was placed onto a microscope slide and it was stained with May-Grumwald-Giemsa, after the ferning test had been performed. Tear production had been previously assessed in all patients by Schirmer's I test and basic secretion test that showed an evident tear fluid hyposecretion. Cytoanalysis of tear fluid showed, in all patients, a marked lymphocytosis, presence of epithelial cells (sometimes cell-adhesion) and a number of "snake-cells", with a nucleus-cytoplasm ratio in favour of cytoplasm. Some of those cells have a thicker cytoplasmic membrane and/or a spindle-shaped peripheral nucleus, characteristic finding of keratoconjunctivitis sicca. In all cases we found mucus and fibrin (sometimes with included cells), organic debris and big crystals, some of which aggregated.

Aged↗

PubMed1995

Cellular and molecular mechanisms that mediate insulin-dependent rat granulosa cell mitosis.

Rat ovarian follicles are composed of small and large granulosa cells (GC). The present studies demonstrate that small GCs undergo insulin- or phorbol ester-dependent mitosis in vitro. In order to examine the cellular and molecular events that account for insulin's mitogenic action, small GCs were cultured with either insulin, phorbol ester (TPA), or both insulin and TPA. Insulin and TPA increased GC numbers by 21 +/- 3% and 20 +/- 2% over control values, respectively (p < 0.05). Simultaneous addition of insulin and TPA increased GC numbers by 20 +/- 3% (p < 0.05). In a second experiment, small GCs were exposed to control medium, insulin, staurosporine (a protein kinase C [PKC] inhibitor), or both insulin and staurosporine. These studies revealed that insulin induced a 21 +/- 5% increase in GC numbers and that staurosporine blocked insulin's mitogenic action. These observations suggest that insulin mediates its mitogenic action through a PKC-dependent mechanism. Since the proto-oncogenes, c-fos and c-jun, are expressed during GC mitosis, studies were undertaken to determine whether or not the expression of these two proto-oncogenes products was enhanced by insulin. The expression of c-fos and c-jun proteins was assessed by immunocytochemistry. These studies showed that after 5 h, insulin increased the percentage of cells that stained for c-fos and c-jun by 15 +/- 2% and 19 +/- 4, respectively (p < 0.05). The expression of these proto-oncogenes was blocked by staurosporine. Both progesterone and 8-br-cAMP, which block insulin-dependent GC mitosis, also inhibited the expression of c-fos and c-jun.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1995

Proliferative and steroidogenic capabilities of rat granulosa cells of different sizes.

Equine chorionic gonadotrophin stimulates both rat granulosa cell mitoses and oestradiol secretion. However, the mitotic potential of oestradiol-secreting granulosa cells is not known. In the first study, granulosa cells of different sizes were isolated and their ability to secrete oestradiol and proliferate in vitro was determined. Granulosa cells were harvested from equine chorionic gonadotrophin-primed immature rats, separated on a 15-45% Percoll gradient, and collected in 12 fractions. An enriched population of small granulosa cells (44 +/- 1 micron2) was collected in fractions 3 and 4 and an enriched population of large granulosa cells (97 +/- 2 microns2) in fractions 6-8. When granulosa cells from each fraction were cultured for 24 h in the presence of testosterone, the large cells secreted 50% more oestradiol than did the small cells (P < 0.05). Aromatase was shown, by immunocytochemistry, to be expressed mainly by granulosa cells larger than 73 microns2, with the relative amount of aromatase expressed per cell increasing with increasing cell size. However, not all large granulosa cells expressed aromatase. To test proliferative capacity, cells from each fraction were cultured with testosterone and the mitogen, insulin. This study showed that only small cells were able to undergo insulin-induced mitosis. In a second study, follicles of different sizes were isolated from immature and equine chorionic gonadotrophin-primed immature rats and the granulosa cell size distribution determined for each follicle size. This study confirmed that equine chorionic gonadotrophin altered the size distribution from principally small mitotically competent cells to large oestradiol-secreting cells.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1995

[Reflexions on the Tietze syndrome. Clinical contribution].

The authors report 4 cases of Tietze's syndrome. In 3 of them the syndrome onset during a rheumatic disease (psoriatic arthritis, sternoclavicular hyperostosis). It is thus necessary to distinguish between the idiopathic of unknown ethiology and the secondary form due to, a well defined disease, in 3 cases observed.

Adult↗

PubMed1994

Epidermal growth factor inhibits large granulosa cell apoptosis by stimulating progesterone synthesis and regulating the distribution of intracellular free calcium.

The initial study was designed to determine whether all granulosa cells (GCs) undergo apoptosis in vitro. GCs were isolated from immature rat ovaries and separated on a 15-45% Percoll gradient. Twelve fractions were collected, and GCs were pooled according to size: small GCs (approximately 50 mu 2; fractions 2-5) and large GCs (> or = 75 mu 2; fractions 6-8). GCs were cultured in serum-free medium for 24 h. After 24 h of culture, fragmented DNA, detected by in situ end labeling of the 3'OH ends of DNA fragments, was observed within 70-80% of large GCs. Similarly, in situ DNA staining demonstrated that at least 50% of large GCs possessed apoptotic nuclei. These degenerative changes in DNA were observed within < or = 5% of small GCs. These studies demonstrate that in serum-free medium, most large GCs die via an apoptotic mechanism within 24 h. Subsequent studies focused on the mechanism by which epidermal growth factor (EGF) inhibits large GC apoptosis. EGF reduced the percentage of large GCs with apoptotic nuclei from 47 +/- 1% for controls to 18 +/- 2% (p < 0.05). EGF also increased progesterone (P4) secretion from large GCs (6.3 +/- 0.7 for controls vs. 18.7 +/- 1.0 ng/ml for EGF treatment; p < 0.05). The effect of EGF on apoptosis was mimicked by P4 and attenuated by the P4 antagonist, RU 486, and aminoglutethimide (AG), an inhibitor of P4 synthesis. The effect of AG was overridden by P4. Therefore, EGF reduces large GC apoptosis by stimulating P4 synthesis, with P4 mediating its action through its receptor.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoglutethimide↗

PubMed1994

[Evaluation of the use of calcitonin in rheumatoid arthritis by bone densitometry and the study of of phospho-calcium metabolism].

Forty-eight patients were subdivided into three groups according to the stage of their rheumatoid arthritis and to whether or not they received glucocorticoids; they were compared to healthy volunteers of similar sex, age, and body weight. Before calcitonin treatment, bone mineral content (BMC) of RA patients was significantly lowered, especially in patients with 3rd and 4th Steinbroker degree and in those taking glucocorticoids. Synthetic eel calcitonin was administered in three 60-day cycles separated by 40-day intervals with daily dosage 40 U.M.R.C. (1 vial). This treatment did not result in a increase of BMC compared to baseline. A further decrease of BMC observed at the end of treatment was not statistically significant. No appreciable variation was found in parameters of phospho-calcic metabolism.

Arthritis, Rheumatoid↗

PubMed1993

Control of rat granulosa cell mitosis by phorbol ester-, cyclic AMP-, and estradiol-17 beta-dependent pathways.

The present studies examined the effect of 8-bromo-cAMP (8-Br-cAMP), phorbol ester (TPA), and estradiol-17 beta (E2) on the capacity of rat granulosa cells (GC) to undergo mitosis. In the first series of experiments, GC were either maintained within immature rat ovaries in perifusion culture or isolated and placed in tissue culture. GC were cultured for 24 h with 1) control medium, 2) 8-Br-cAMP, 3) TPA, or 4) 8-Br-cAMP plus TPA in the presence of 3H-thymidine (3H-T). In perifusion culture, 8-Br-cAMP stimulated both 3H-T incorporation (p < 0.05) and E2 secretion (p < 0.05) while TPA increased 3H-T (p < 0.05) without altering E2 secretion (p > 0.05). Simultaneous exposure to 8-Br-cAMP and TPA enhanced 3H-T incorporation and suppressed E2 as compared to 8-Br-cAMP treatment alone (p < 0.05). In tissue culture, 8-Br-cAMP did not increase 3H-T incorporation or cell number. TPA increased both 3H-T incorporation (p < 0.05) and cell number (p < 0.05), while 8-Br-cAMP suppressed both of these TPA-induced responses. In the presence of testosterone, 1) TPA's mitogenic action was also observed, 2) basal E2 secretion ranged between 30 and 35 pg/ml, 3) neither 8-Br-cAMP nor TPA stimulated E2 secretion over basal levels, and 4) Rp-cAMP, a cAMP antagonist, blocked TPA-induced cell proliferation. E2 at 250 pg/ml also blocked TPA's mitogenic action. In a second series of experiments, GC were collected from eCG-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1992

[Telethermography in the diagnosis of lumbo-sciatica syndromes].

Thermal maps of the lumbo-sacral and gluteal regions and of the lower limbs were obtained with telethermography in 30 subjects suffering from painful lumbo-sciatic syndromes in order to assess whether there were differences of thermal index between painful and opposite side, and to evaluate the telethermographic patterns of the irritative and deficitary forms. Among 25 patients with lumbo-sciatalgia in the irritative or early stage, 16 showed hypothermia of the affected side; in three of the five patients in the deficitary stage, hyperthermia of the affected side was observed while two did not show changes of the thermal gradient. The authors stress the importance of telethermography and suggest that this method, which is not costly, non-invasive and easily reproducible, should be used to complete diagnosis of and to monitor lumbo-sciatalgic syndromes.

Adult↗