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Biomedical subjects

C Carani

Publications and source records attributed to C Carani.

At least 19 recordsLinked to original sources
PubMed2003

Riedel's thyroiditis and fibrous variant of Hashimoto's thyroiditis: a clinicopathological and immunohistochemical study.

The aim of this study was to analyze and compare clinico pathological aspects of Riedel's thyroiditis (RT) and the fibrous variant of Hashimoto's thyroiditis (HTFV), and to show their immunohistochemical features. We reviewed 6 cases of HTFV and 4 cases of RT. Compared to RT, HTFV patients had hypothyroidism, no pressure symptoms, and frequently diagnostic fine-needle aspiration biopsy (FNAB) cytology. At histology, invasion of surrounding tissues and presence of occlusive phlebitis distinguished RT from HTFV. At immunohistochemistry, RT--compared to HTVF--was characterized by: 1) a more abundant fibrous reaction, and granulocytic, monocytic and eosinophil infiltration; 2) few plasma-cells, CD8+ T- and B-lymphocytes. The results of our study add further evidence regarding the separation of RT and HTFV in their peculiar clinical, laboratory, cyto-histological and immunohistochemical aspects.

Adult↗
PubMed2003

Sex steroids and sexual desire mechanism.

Sexual behavior is mainly controlled by cognitive functions in men, though hormones, particularly sex steroids, may modulate some aspects of male sexuality. This review focuses on the role of both estrogens and androgens on male sexual desire, starting from both animal and human studies. Estrogens could play a role in human male sexual activity, similarly to what happens in animals, but even though physiological levels of estrogens could be probably required for a completely normal male sexual behavior, testosterone remains the major determinant of human male sexual behavior.

Androgens↗
PubMed2002

Short-term suppression of GH and IGF-I levels improves gonadal function and sperm parameters in men with acromegaly.

Experimental data support a role for GH and IGF-I in the reproductive process in humans, but the effect of chronic GH excess on gonadal and reproductive function in men has been never investigated. To understand the effects of short-term GH and IGF-I suppression on the gonadal axis and seminal fluid characteristics in men with acromegaly, we evaluated 35 patients (age 27-59 yr) with active disease and 35 age-matched healthy controls. Gonadal hormones and seminal fluid analysis were evaluated before and 6 months after surgery or lanreotide (LAN) (60 mg/month). At study entry, FSH, testosterone (T), and dihydrotestosterone (DHT) (P < 0.0001) levels, seminal volume, sperm count, total motility and forward progression, normal morphology, and vitality were significantly lower in patients with acromegaly than in controls. After 6 months, 22 patients achieved disease control after surgery (n = 11) or LAN (n = 11), whereas 13 had uncontrolled disease. Serum T and DHT levels and sperm number significantly increased in all groups. FSH and LH levels and total motility increased only in patients achieving disease control. Posttreatment IGF-I levels significantly correlated with total motility (r = -0.45; P = 0.006). In conclusion, short-term GH and IGF-I suppression after surgery or LAN significantly increased T and DHT levels and improved sperm number and motility in acromegalic men.

Acromegaly↗
PubMed2001

Congenital estrogen deficiency: in search of the estrogen role in human male reproduction.

Recently, a remarkable progress has been made in our understanding about the role of sex steroids in male physiology. In this paper, we consider the clinical aspects of congenital estrogen deficiency - notably, estrogen resistance and aromatase deficiency - in men and we discuss both well-established and supposed estrogen roles in the human male reproductive function. These topics include the role of estrogens in the control of gonadotropin secretion, in male fertility determination and psychosexual behavior. Briefly, estrogens play a pivotal role in the control of serum gonadotropin concentrations in the human male. Furthermore, a possible role of estrogens on both human male fertility and sexuality has also been suggested by recent studies, even though the available data are far from being conclusive. Conversely, for what concern fertility and sexual behavior, a well-established effect of estrogens has been provided by recent studies on male rodents, which show impaired sexual behavior and fertility as a consequence of estrogen defect.

Animals↗
PubMed2001

Role of estrogen on bone in the human male: insights from the natural models of congenital estrogen deficiency.

The reports of congenital estrogen deficiency - notably, estrogen resistance and aromatase deficiency - have completely changed our knowledge on the role of estrogen on bone in males. Particularly, the bone changes at puberty, which were classically considered androgen-dependent, are now considered to be induced at least in part by estrogen action. Clinical cases of congenital estrogen deficiency have clearly demonstrated that the role of estrogens in epiphyseal closure, skeletal proportions and bone mineralization is crucial not only in women but also in men. In addition progress have been made in the treatment of such a rare disease even though further studies are needed to a definitive understanding of this issue.

Aromatase↗
PubMed2000

Tumor progression is accompanied by significant changes in the levels of expression of polyamine metabolism regulatory genes and clusterin (sulfated glycoprotein 2) in human prostate cancer specimens.

Using Northern blotting, the expression levels of the genes for polyamine metabolism regulatory proteins and clusterin have been measured in a series of 23 human prostate cancers (CaPs) dissected from radical prostatectomy specimens. Patient matched, nontumor tissue was dissected from benign areas of the gland. The results indicate that transcripts encoding ornithine decarboxylase (ODC), ODC antizyme, adenosylmethionine decarboxylase, and spermidine/spermine N1-acetyltransferase (SSAT) were significantly higher, whereas clusterin (sulfated glycoprotein 2) mRNA was significantly lower in tumors compared with the benign tissue. All mRNA levels were compared with those of histone H3 and growth arrest-specific gene 1, markers of cell proliferation and cell quiescence, respectively, and glyceraldehyde 3-phosphate dehydrogenase, a housekeeping gene. In poorly differentiated and locally invasive CaPs and in tumors with unfavorable prognosis or total prostate-specific antigen (PSA) levels > 10.0 ng/ml at diagnosis, an overall increase in the levels of H3 mRNA and a decrease in growth arrest-specific gene 1 mRNA was detected, indicative of higher proliferation activity, whereas the differences in expression levels for the polyamine metabolism and clusterin genes were higher. ODC and SSAT changes were positively correlated in normal tissue but not in high-grade cancer, whereas ODC antizyme and SSAT changes were positively correlated in more malignant CaPs but not in normal tissue. Tumor classification based on the changes in expression levels of all of the genes studied could be correlated to differentiation grade and local invasiveness classification systems in 72.2 and 83.3% of the cases, respectively. In a 1-year follow-up period, three patients whose CaPs ranked as less aggressive according to clinical staging, but classified as advanced cancers with the proposed molecular classification, showed increases in total PSA levels, indicative of tumor relapse. Thus, molecular classification, based on gene expression, may enhance the available prognostic tools for prostate tumors.

Acetyltransferases↗
PubMed2000

Insights into the role of estrogen in the male genital tract: a report on an estrogen and male reproduction workshop, Isola Capo Rizzuto, Italy, 23-24 September 1999.

The first International Workshop on estrogen and male reproduction was held in Isola Capo Rizzuto, Italy and was organized by the University of Calabria (COSENZA), the University of Naples and the University of Modena and Reggio Emilia. The workshop, which was attended by general scientists, endocrinologists and andrologists, addressed the impressive recent progress in this area of male reproduction. Owing to space limitations, this report focuses on only a few of the recent advances related to the role of estrogen in the male genital tract.

Animals↗
PubMed2000

Estrogen replacement therapy in a man with congenital aromatase deficiency: effects of different doses of transdermal estradiol on bone mineral density and hormonal parameters.

The effects of different doses of transdermal estradiol (TE) on bone mineral density (BMD) in a man with aromatase deficiency were evaluated. The study protocol was divided in the following four phases: phase 1, before estradiol treatment; phase 2, 50 microg TE twice weekly for 6 months; phase 3, 25 microg TE twice weekly for 9 months; and phase 4, 12.5 microg TE twice weekly for 9 months. X-rays of hands, legs, and pelvis were performed, and BMD of the lumbar spine, hormonal parameters (LH, FSH, testosterone, and estradiol), and markers of bone turnover were determined during each phase. BMD in phase 1 was 0.933 g/cm2 and increased to 1.051 and 1.173 g/cm2 after 4 and 7 months of TE, respectively. In phase 3, BMD reached the maximum value (1.275 g/cm2). In phase 4, BMD decreased to 1.180 g/cm2 and was 1.029 g/cm2 at the end of the study protocol. A bilateral necrosis of femoral heads was also detected by x-ray films. In phase 1 serum testosterone was in the normal range, whereas serum estradiol was undetectable. During the 24-month period of treatment with TE (phases 2-4), estradiol was directly related to the amount of TE, whereas LH was inversely related to estradiol serum levels. Estradiol and gonadotropins reached optimal values only in phase 3, when FSH also was near normal; serum testosterone concentrations were normal in phases 3 and 4. This study confirms the role of estrogens in achieving and maintaining bone mineral content in the human male, providing further clinical tools useful in the management of bone loss in aromatase deficiency in the male. We suggest that the adequate substitutive dose of TE for maintaining both bone mass and normal estradiol serum levels in adult men with aromatase deficiency may be 25 microg twice weekly (0.47 microg/kg weekly).

Administration, Cutaneous↗
PubMed1999

Role of oestrogen in male sexual behaviour: insights from the natural model of aromatase deficiency.

OBJECTIVE: In order to evaluate the role of oestrogens on human male sexual behaviour, the gender-identity, psychosexual orientation and sexual activity of a man with a congenital lack of oestradiol resulting from an inactivating mutation of the aromatase P450 gene was investigated. The psychosexual and sexual behavioural evaluations were performed before and during testosterone treatment and before oestradiol treatment, during three phases of different dosages of oestradiol treatment. DESIGN: The study was performed before (phase A) and during (phase B) testosterone enanthate treatment (250 mg i.m. every 10 days, for 6 months), during testosterone withdrawal (phase C), and during each of the following transdermal oestradiol treatments: 50 microg twice a week for 6 months (phase D); 25 microg twice a week for 9 months (phase E), and 12.5 microg twice a week for 9 months (phase F). MEASUREMENTS: Sexual behaviour was investigated by a sexological interview and by a 2-month self-reported daily diary performed during each phase of the protocol study. Furthermore, during each oestradiol treatment (phase C, D, E and F), a study of depression, anxiety trait and sexual behaviour was performed by the Beck Depression Inventory (BDI), the Spielberger Trait Anxiety Inventory (STAI) and the Golombok-Rust Inventory of Sexual Satisfaction (GRISS), respectively. Sexual orientation and gender-identity were evaluated by the BEM Sex Role Inventory (BSRI). Serum testosterone and oestradiol were measured during each phase of the study. RESULTS: Before oestradiol treatment (phase C), serum oestradiol was undetectable, while it rose to 356.1, 88.1 and 55.1 pmol/l during phases D, E and F, respectively. Before any oestradiol treatment, during phase D, phase E and phase F serum testosterone was 18.13, 0.72, 14.3 and 18.51 nmol/l, respectively. The patient's gender-identity as assessed by BSRI and by the sexological interview was clearly male. The psychosexual orientation evaluated by BSRI, by the sexological interview and by the analysis of the self-filled diary was heterosexual. Relevant modification of the patient's sexual behaviour occurred only during oestrogen treatment. This was more evident during both phase E and phase F, and concerned the behavioural parameters with an increase of libido, frequency of sexual intercourse, masturbation and erotic fantasies. A reduction of BDI and STAI scores was detected during the oestrogen phases. CONCLUSIONS: The study of the sexual behaviour in this man with aromatase deficiency suggests that oestrogens in humans do not affect gender-identity and sexual orientation but could have a role in male sexual activity.

Adult↗
PubMed1999

GH/IGF-I axis in azoospermia in primary and secondary hypogonadism: a study before and during replacement therapy.

The growth hormone/insulin-like growth factor-I (GH/IGF-I) axis was studied in 15 azoospermic patients and in 10 control men. Eight patients were affected by hypergonadotrophic hypogonadism and 7 by hypogonadotrophic hypogonadism. All were studied before and during replacement therapy with testosterone and gonadotrophin, respectively, using the alpha 2 adrenergic agonist, clonidine (clonidine test). The data demonstrate no differences in basal levels for IGF-I and for the GH response to clonidine in azoospermic patients, affected by primary and secondary hypogonadism, before and during replacement therapy when compared with control fertile men. In contrast to some studies which describe a reduced GH response in azoospermia and oligozoospermia, we conclude that basal serum levels of IGF-I and the GH response to clonidine are not impaired in azoospermic patients affected by primary hypogonadism before and after the restoration of normal androgenization, and in azoospermic patients affected by secondary hypogonadism, both before and after restoration of spermatogenesis.

Adolescent↗
PubMed1999

The effect of chronic treatment with GH on gonadal function in men with isolated GH deficiency.

Eleven adult males, previously submitted to neurosurgery because of a pituitary lesion (three with craniopharyngioma, three with clinically non-functioning adenoma and five with macroprolactinoma) were treated with recombinant GH for 12 months after the diagnosis of GH deficiency was made. Circulating FSH, LH, prolactin, testosterone, 17 beta-estradiol (E2), dehyroepiandrosterone (DHEA-S), androstenedione. 17-OH-progesterone (17OHP), IFG-I, and steroid hormone-binding protein (SHBG) levels were assayed before and after CG test at study entry and 6 and 12 months after GH treatment. A significant increase in plasma IGF-I levels was obtained after 6 and 12 months of GH treatment. In addition, CG-stimulated, but not baseline, testosterone levels showed a significant increase after 6 and 12 months of GH treatment when compared with study entry (9.6 +/- 0.5 and 9.9 +/- 0.5 vs 7.9 +/- 0.5 ng/ml; P < 0.05). Baseline, but not CG-stimulated, serum 17OHP levels were significantly increased only after 12 months of GH treatment (1.7 +/- 0.1 vs 1.4 +/- 0.1 ng/ml; P < 0.05). No significant difference was found as far as both basal and CG-stimulated E2, androstenedione, DHEA-S and SHBG were concerned. With regards to the semen analysis, only seminal plasma volume was significantly increased after 12 months of GH treatment (2.9 +/- 0.3 vs 1.7 +/- 0.3 ml; P < 0.05). No significant change in sperm count, motility and abnormal forms was observed. These data show that GH treatment displays a clear-cut effect upon Leydig cell function and increases the production of seminal plasma volume in fertile adult males with isolated GH deficiency.

17-alpha-Hydroxyprogesterone↗
PubMed1998

Mitochondrial membrane potential and DNA stainability in human sperm cells: a flow cytometry analysis with implications for male infertility.

Sperm cells from control donors of proven fertility and men from barren couples were studied by conventional procedures, i.e., light microscopy as well as flow cytometry. Light microscopy analysis of semen included the measurement of spermatozoa concentration, morphology, and motility. All the men from barren couples were asthenozoospermic at the conventional analysis of semen samples. Flow cytometry was applied to study two important parameters of sperm cells: mitochondrial membrane potential (MMP) assessed by the cationic dye JC-1 and DNA stainability with propidium iodide (PI). JC-1 staining was more reliable than the classical procedure used for this purpose, i.e., rhodamine 123 (Rh123) staining, and allowed us to show a positive correlation between MMP and spermatozoa motility. Regarding DNA analysis, a higher relative percentage of immature spermatozoa, showing a high accessibility of DNA to the intercalating PI fluorochrome, was found in men from barren couples compared to donors of proven fertility. The relative percentage of immature spermatozoa was significantly higher in semen from oligoasthenozoospermic subjects. Moreover, a positive correlation was found between immature spermatozoa, as evaluated by PI staining, and cells with depolarized mitochondria, as evaluated by JC-1 staining, suggesting that spermatozoa defective for nuclear maturity could be functionally defective cells. No correlation between immature spermatozoa determined by FCM and immature spermatozoa determined by light microscopy was found, suggesting that these two techniques assess sperm cell maturity at different levels.

Adult↗
PubMed1997

Screening for deletions of the Y chromosome involving the DAZ (Deleted in AZoospermia) gene in azoospermia and severe oligozoospermia.

OBJECTIVE: To evaluate the occurrence and prevalence of microdeletions of the Y chromosome involving the DAZ (Deleted in AZoospermia) gene in patients with azoospermia or severe oligozoospermia. DESIGN: Controlled clinical study. SETTING: University infertility clinic. PATIENT(S): Infertile men (n = 168) with nonobstructive, idiopathic azoospermia or severe oligozoospermia and normal LH. The control group consisted of proven fathers (n = 86). INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Semen analysis; polymerase chain reaction amplification of the loci sY84, sY143, sY254, and sY255; serum FSH, LH, and T; testicular volume. RESULT(S): Deletions involving the sY254 and sY255 DAZ loci were found in three azoospermic patients and two men with sperm concentration < 1 x 10(6)/mL. Serum FSH was elevated in four patients and was normal in one. All five patients had decreased testicular volumes compared with controls. No deletions involving the sY84 and sY143 loci were found. The four loci were amplified normally in the control group. CONCLUSION(S): The estimated frequency of deletions involving the DAZ locus is 3% in azoospermic-severely oligozoospermic men consulting an infertility clinic. Polymerase chain reaction amplification of the DAZ locus is useful for the diagnosis of microdeletions of the Y chromosome. Deletions involving more proximal regions of the Y chromosome seem to be rare.

Adult↗
PubMed1997

cynDAZLA: a cynomolgus monkey homologue of the human autosomal DAZ gene.

A gene on the human Y chromosome, specifically deleted in azoospermic patients (DAZ: deleted in azoospermia), and a DAZ homologue (DAZH) on human chromosome 3, have been recently described. In the present work we report the isolation and characterization of the corresponding DAZH gene of the cynomolgus monkey (Macaca fascicularis), which we have named cynDAZLA (cynomolgus DAZ-like autosomal). Reverse transcription-polymerase chain reaction was used to amplify the monkey DAZ homologue, and sequence analysis revealed an open reading frame of 888 bp encoding 295 amino acids. Northern blot hybridization of different tissues to a probe derived from the cynDAZLA cDNA detected a transcript of 3.5 kb that, in the male, was expressed only in the testis. Comparison of the cynDAZLA sequence to autosomal DAZ homologues from human, mouse and Drosophila showed two RNA-recognition motifs (RRM) and the presence of only one DAZ consensus repeat compared with the seven repeats found in the human DAZ gene on the Y chromosome. The homology of the cynDAZLA cDNA compared with the human DAZH and mouse dazla cDNAs is 97.97 and 87.46% respectively. The identification of the monkey cynDAZLA enables further studies regarding the putative functions of DAZH, such as onset of expression and hormonal dependence of this gene.

Amino Acid Sequence↗
PubMed1996

The effects of clonidine on blood pressure, catecholamine and growth hormone release in hypogonadal men is preserved and not influenced by testosterone replacement therapy.

It has been demonstrated that castration impairs the hypotensive effect of clonidine in rat as well as its GH-releasing activity while testosterone replacement restores to normal the effects of alpha-2 adrenoceptor activation. Thus, these data point to main role of the gonadal steroid testosterone in modulating the effects of alpha-2 adrenergic activation on blood pressure, catecholamine and GH release in animal. Aim of the present study was to verify the activity of clonidine on blood pressure, catecholamine and GH release in human male hypogonadism before and after testosterone replacement. To this goal, 14 hypogonadal men (HP, age 33.8 +/- 2.9 yr; BMI < 25 kg/m2; 8 with hypergonadotropic and 6 with hypogonadotropic hypogonadism) received clonidine administration (CLON, 300 micrograms po at 0 min) before and after 3 months of testosterone replacement (testosterone propionate depot, 250 mg i.m. every 21 days). Ten normal adult volunteers (NS, age 31.5 +/- 1.9 yr; BMI < 25 kg/m2) were studied as control group. In all subjects, before and after clonidine administration, systolic and diastolic blood pressure (SBP and DBP), pulse rate (PR), norepinephrine (NE), epinephrine (E) and GH levels were recorded. In HP basal testosterone levels were lower than those in NS (1.25 +/- 0.3 vs 7.34 +/- 1.5 ng/ml, p < 0.05) and were restored to normal by hormonal replacement (6.91 +/- 1.3 ng/mL) in HP, both SBP and DBP as well as PR were normal in basal conditions and were not modified by testosterone replacement. Both before and during testosterone CLON lowered SBP, DBP and PR in HP to the same extent observed in NS. In HP, basal NE levels were lower than those in NS (0.85 +/- 0.15 vs 1.28 +/- 0.19 nmol/l, p < 0.05) and were restored to normal during testosterone replacement (1.25 +/- 0.13 nmol/l). On the other hand, basal E levels in HP were similar to those in NS (179 +/- 42 vs 197 +/- 38 pmol/l) and were not modified by testosterone therapy (167 +/- 28 pmol/l). In HP, both before and during testosterone replacement, CLON reduced NE (0.44 +/- 0.10 and 0.58 +/- 0.07 nmol/l) levels to the same levels recorded in NS (0.68 +/- 0.08 nmol/l). Basal GH and IGF-I levels in HP (1.15 +/- 0.5 and 234 +/- 42 micrograms/l, respectively) were similar to those in NS (1.18 +/- 0.4 and 221 +/- 38 micrograms/l, respectively) and were not modified by testosterone (1.35 +/- 0.6 and 256 +/- 32 micrograms/l, respectively). CLON administration induced a clear GH response in HP (F = 37; p < 0.001) which overlapped with that recorded in NS and was not modified by testosterone (F = 1.7; P = NS). Our present findings demonstrate that, differently from in animal, in man testosterone has no role in modulating the effects of alpha-2 adrenergic activation by clonidine on blood pressure, catecholamine and GH release. On the other hand, our data suggest the existence in male hypogonadism of a reduced basal noradrenergic activity which is restored by testosterone replacement.

Adult↗