Publications by authors named "Monfette G"

The advancement of new ceramic materials for dental crowns has prompted the need for improved methods of bonding orthodontic brackets to these surfaces. Currently, lithium-disilicate is the primary material being used for anterior crowns, while zirconia is the primary material being used in the posterior. The purpose of this study was to compare the shear bond strength of HEMA (Assure® Universal Bonding Resin) and bis-GMA (Assure® PLUS All Surface Bonding Resin) orthodontic bonding resins on enamel, lithium-disilicate, and zirconia materials.

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We followed total prostate and prostatic tumor volumes in patients who received combination endocrine therapy with the antiandrogen flutamide and the LHRH agonist [D-Trp6,des-Gly-NH2(10)]LHRH ethylamide. Twenty-three men with proved prostatic adenocarcinoma (Stages B1 to D2) were subjected to a transrectal ultrasound (TRUS) study before and after a three-month period of combination antihormonal therapy. A total prostatic volume reduction ranging from 17 percent to 70 percent (median 47%, p less than 0.

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The histopathology of 23 radical prostatectomies from patients with prostatic adenocarcinoma pretreated for 3-6 months with combination therapy including a luteinizing hormone-releasing hormone agonist and the antiandrogen drug flutamide was reviewed and compared with the pretreatment biopsies or transurethral resection material. After combination therapy, benign prostatic glands showed marked atrophy with prominent basal-cell layers, basal-cell hyperplasia, and epithelial-cell vacuolization. Immature squamous-cell metaplasia was present in seven cases.

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Three hundred and sixty-three patients with clinical stage D2 prostate cancer who had not received previous endocrine therapy or chemotherapy were treated with the combination therapy using the pure antiandrogen Flutamide and the LHRH agonist [D-Trp6,des-Gly-NH2(10)]LHRH ethylamide (or orchiectomy) for an average of 771 days (24-2607 days). Only 31 of the 308 evaluable patients (10.1%) did not show an objective positive response at the start of the combination therapy compared with an average of 18% in five recent studies using monotherapy.

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In order to achieve a more complete blockade of androgens of both testicular and adrenal origins, 223 patients with advanced prostate cancer (stage D2 with bone metastases) received the combination therapy with the antiandrogen Flutamide and the LH-RH agonist [D-Trp6,des-Gly-HN10(2)] LH-RH ethylamide as first treatment. As assessed by the objective criteria of the US NPCP, a positive response was obtained in 94% of patients, thus leaving only 6% of patients with no response at the start of treatment while, following standard therapy, 20-40% of patients do not respond to treatment. The duration of response was increased while longer survival (an advantage of approximately 14 months compared to standard therapy, 38.

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The concentrations of dehydroepiandrosterone (DHEA), its sulfate (DHEAS), androstenedione (A-dione), testosterone (T) and dihydrotestosterone (DHT) have been measured before and after castration in men and two animal models, namely the rat and the guinea pig. In adult men, the pre-castration levels of plasma DHEAS and DHEA were measured at 1839 +/- 320 and 2.4 +/- 0.

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One hundred and eighty-six previously untreated patients with clinical stage D2 prostate cancer have been followed according to the criteria of objective response of the National Prostatic Cancer Project (NPCP). All patients received combination therapy with the antiandrogen Flutamide and the LHRH agonist (D-Trp6, des-Gly-NH2(10)]LHRH ethylamide (or surgical castration, 10 patients) as first treatment. Forty-nine patients (26.

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Two hundred and nine patients with biopsy-proven stage D2 prostatic carcinoma showing disease progression after orchiectomy or treatment with DES (stilboestrol) or an LHRH agonist alone received combination therapy with the pure antiandrogen flutamide. In patients treated with DES, the oestrogen was replaced by the LHRH agonist [D-Trp6]LHRH ethylamide. The objective response to therapy was assessed according to the criteria of the US NPCP.

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One hundred and ninety-nine patients with clinical stage D2 prostate cancer who had not received previous endocrine therapy or chemotherapy were treated with the combination therapy using the pure antiandrogen Flutamide and the LHRH agonist [D-Trp6]LHRH ethylamide for an average of 26 months (3-59 months). The objective response to the treatment was assessed according to the criteria of the U.S.

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One hundred fifty-four patients with clinical stage D2 prostate cancer with no previous endocrine therapy or chemotherapy received the combination therapy with the pure antiandrogen Flutamide and the LHRH agonist [D-Trp]LHRH ethylamide for an average of 22 months (3 to 49). The objective response to the treatment was assessed according to the criteria of the US NPCP. There was a 6.

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Patients (154) with clinical stage D2 prostate cancer with no previous endocrine therapy or chemotherapy received the combination therapy with the pure antiandrogen Flutamide and the LHRH agonist [D-Trp6]LHRH ethylamide for an average of 22 months (3-49 months). The objective response to the treatment was assessed according to the criteria of the US NPCP. There was a 6.

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In order to achieve a more complete blockade of androgens of both testicular and adrenal origin at the start of treatment, we have administered the pure antiandrogen Flutamide in association with orchiectomy (13 patients) or the LHRH agonist [D-Trp6]LHRH ethylamide (118 patients) to previously untreated patients with clinical stage D2 prostate cancer. The mean duration of treatment was 491 days (102-1208 days). The response was assessed according to the criteria of the U.

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It is now well established that chronic treatment with GnRH agonists offers an advantageous alternative to orchiectomy and estrogens for the treatment of prostate cancer. Castration levels of androgens can thus be easily achieved without side effects other than those related to castration levels of serum androgens. However, man is unique among species in having a high secretion rate of precursor adrenal steroids which are converted into active androgens in the normal prostate and prostatic cancer.

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Since the first observation reported by Huggins et al. in 1941, hormonal treatment of advanced prostatic cancer has been directed primarily at neutralizing testicular androgens by orchiectomy or estrogen therapy. These two approaches yielded a 60 to 80% positive response rate in the many studies carried out over the last forty years.

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Eighty-seven previously untreated patients with clinical stage D2 (bone metastases) prostate cancer have received the combination therapy with a pure antiandrogen and an LHRH agonist (or orchiectomy) as first treatment in a multicentre study for up to 34 months (average = 16.2 months). A positive objective response assessed according to the criteria of the US NPCP has been observed in all cases.

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Although castration levels of serum androgens are consistently achieved after 2-3 weeks of treatment with luteinizing hormone-releasing hormone (LHRH) agonists, the administration of these peptides alone in adult men is always accompanied by a transient increase in plasma testosterone and dihydrotestosterone levels, which lasts for 5-15 days at the beginning of treatment and is accompanied by disease flare-up in some cases, thus seriously limiting the acceptability of this otherwise efficient and well-tolerated treatment. The present data show that the simultaneous administration of a pure antiandrogen neutralizes the influence of the transient increase in serum androgens on prostate cancer, as indicated by the 60% decrease in serum prostatic acid phosphatase observed within 5 days of combined treatment with an LHRH agonist and a pure antiandrogen. The addition of a pure antiandrogen thus makes fully acceptable the use of LHRH agonists as an advantageous substitute for surgical castration and estrogens in the treatment of prostate cancer.

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At doses which have no or minimal inhibitory effect when administered alone, the LHRH agonist [D-Ser(TBU)6,des-Gly-NH10(2)] LHRH ethylamide (HOE-766) and the antiandrogen RU-23908 administered simultaneously cause a marked inhibition of ventral prostate and seminal vesicle weight after 5 months of treatment. The effect of the LHRH agonist is due to a blockage of the testicular steroidogenic pathway. The same LHRH agonist administered to adult men with cancer of the prostate causes a marked inhibition of serum testosterone and dihydrotestosterone to castration levels within 1-2 weeks.

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To completely eliminate androgens of both testicular and adrenal origin, 37 previously untreated patients with advanced (stages C or D) prostatic cancer received the combination therapy using an LHRH agonist (HOE-766) and a pure antiandrogen (RU-23908). The response criteria developed by the National Prostatic Cancer Project were used. A positive response (assessed by bone scan and/or serum prostatic acid phosphatase measured by radioimmunoassay was observed in 29 of the 30 cases who could be evaluated by these objective criteria (97%).

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