8 results on '"Ciampani, T."'
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2. Italian Study Group on Idiopathic Central Hypogonadism (ICH). Germline prokineticin receptor 2 (PROKR2) variants associated with central hypogonadism cause differental modulation of distinct intracellular pathways
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Libri, D. V., Kleinau, G., Vezzoli, V., Busnelli, M., Guizzardi, F., Sinisi, A. A., Pincelli, A. I., Mancini, A., Russo, G., Eccoz, P. Beck P., Loche, S., Crivellaro, C., Maghnie, M., Krausz, C., Persani, L., Bonomi, M., Aimaretti, G., Altobelli, M., Arnaldi, G., Baldi, M., Bartalena, Luigi, Beccaria, L., Bellastella, G., Bellizzi, M., Bona, G., Borretta, G., Buzi, F., Cannavò, S., Cappa, M., Cariboni, A., Ciampani, T., Cicognani, A., Cisternino, M., Corbetta, S., Corciulo, N., Corona, G., Cozzi, R., D’Elia, A. V., Degli Uberti, E., De Marchi, M., Forti, G., di Iorgi, N., Isidori, A., Fabbri, A., Ferlin, A., Foresta, C., Franceschi, R., Garolla, A., Gaudino, R., Giagulli, V., Grosso, E., Jannini, E., Lanfranco, F., Larizza, L., Lenzi, A., Lombardo, F., Limone, P., Maggi, M., Maggi, R., Maggio, M. C., Mandrile, G., Marino, M., Mencarelli, M. A., Migone, N., Neri, G., Perroni, L., Pignatti, E., Pilotta, A., Pizzocaro, A., Pontecorvi, A., Pozzobon, G., Prodam, F., Radetti, G., Razzore, P., Salerno, M. C., Salvatoni, Alessandro, Salvini, F., Secco, A., Segni, M., Simoni, M., Vigneri, R., and Weber, G.
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- 2014
3. New understandings of the genetic basis of isolated idiopathic central hypogonadism
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Bonomi, M, Libri, Dv, Guizzardi, F, Guarducci, E, Maiolo, E, Pignatti, E, Asci, R, Persani, L, Idiopathic Central Hypogonadism Study Group of the Italian Societies of Endocrinology, Pediatric, Endocrinology, Diabetes Aimaretti, G, Altobelli, M, Arnaldi, G, Baldi, M, Bartalena, L, Beccaria, L, Beck Peccoz, P, Bellastella, G, Borretta, G, Buzi, F, Cannavo', Salvatore, Cappa, M, Cariboni, A, Ciampani, T, Cicognani, A, Cisternino, M, Corbetta, S, Corciulo, N, Cozzi, R, D'Elia, Av, Uberti, Ed, De Marchi, M, Forti, G, di Iorgi, N, Fabbri, A, Ferlin, A, Gaudino, R, Grosso, E, Krausz, C, Lanfranco, F, Larizza, D, Limone, P, Maggi, M, Maggi, R, Maghnie, M, Mancini, A, Mandrile, G, Marino, M, Mencarelli, Ma, Migone, N, Neri, G, Perroni, L, Pilotta, A, Pincelli, Ai, Pizzocaro, A, Pontecorvi, A, Radetti, G, Razzore, P, Russo, G, Salvini, F, Secco, A, Segni, M, Simoni, M, Sinisi, A, Vigneri, R, and Weber, G.
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Male ,Infertility ,central hypogonadism ,congenital hypogonadism ,GnRH ,hypogonadotropic hypogonadism ,hypothalamus–pituitary–gonadal axis ,Kallmann syndrome ,male infertility ,Hypothalamo-Hypophyseal System ,medicine.medical_specialty ,Urology ,Context (language use) ,Review ,Disease ,Bioinformatics ,Male infertility ,Mice ,Hypogonadotropic hypogonadism ,Internal medicine ,medicine ,Animals ,Humans ,Animals, Humans, Hypogonadism ,complications/genetics/physiopathology, Hypothalamo-Hypophyseal System ,physiopathology, Infertility ,genetics, Italy, Kallmann Syndrome ,complications/genetics, Male, Mice, Mice ,Knockout, Models ,Animal ,cardiovascular diseases ,Infertility, Male ,Mice, Knockout ,business.industry ,Hypogonadism ,General Medicine ,medicine.disease ,Penetrance ,nervous system diseases ,Endocrinology ,Italy ,Models, Animal ,central hypogonadism, congenital hypogonadism, GnRH, hypogonadotropic hypogonadism, hypothalamus–pituitary–gonadal axis, Kallmann syndrome, male infertility ,business ,gnrh ,hypothalamus-pituitary-gonadal axis ,kallmann syndrome ,Rare disease - Abstract
Idiopathic hypogonadotropic hypogonadism is a rare disease that is characterized by delayed/absent puberty and/or infertility due to an insufficient stimulation of an otherwise normal pituitary–gonadal axis by gonadotrophin-releasing hormone (GnRH) action. Because reduced or normal luteinizing hormone (LH)/follicle-stimulating hormone (FSH) levels may be observed in the affected patients, the term idiopathic central hypogonadism (ICH) appears to be more appropriate. This disease should be distinguished from central hypogonadism that is combined with other pituitary deficiencies. Isolated ICH has a complex pathogenesis and is fivefold more prevalent in males. ICH frequently appears in a sporadic form, but several familial cases have also been reported. This finding, in conjunction with the description of numerous pathogenetic gene variants and the generation of several knockout models, supports the existence of a strong genetic component. ICH may be associated with several morphogenetic abnormalities, which include osmic defects that, with ICH, constitute the cardinal manifestations of Kallmann syndrome (KS). KS accounts for approximately 40% of the total ICH cases and has been generally considered to be a distinct subgroup. However, the description of several pedigrees, which include relatives who are affected either with isolated osmic defects, KS, or normo-osmic ICH (nICH), justifies the emerging idea that ICH is a complex genetic disease that is characterized by variable expressivity and penetrance. In this context, either multiple gene variants or environmental factors and epigenetic modifications may contribute to the variable disease manifestations. We review the genetic mechanisms that are presently known to be involved in ICH pathogenesis and provide a clinical overview of the 227 cases that have been collected by the collaborating centres of the Italian ICH Network.
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- 2012
4. Characteristics of a nationwide cohort of patients presenting with isolated hypogonadotropic hypogonadism (IHH)
- Author
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Marco Bonomi, Valeria Vezzoli, Csilla Krausz, Fabiana Guizzardi, Silvia Vezzani, Manuela Simoni, Ivan Bassi, Paolo Duminuco, Natascia Di Iorgi, Claudia Giavoli, Alessandro Pizzocaro, Gianni Russo, Mirella Moro, Letizia Fatti, Alberto Ferlin, Laura Mazzanti, Maria Chiara Zatelli, Salvo Cannavò, Andrea M Isidori, Angela Ida Pincelli, Flavia Prodam, Antonio Mancini, Paolo Limone, Maria Laura Tanda, Rossella Gaudino, Mariacarolina Salerno, Pregnolato Francesca, Mohamad Maghnie, Mario Maggi, Luca Persani, G Aimaretti, M Altobelli, M R Ambrosio, M Andrioli, G Angeletti, F Arecco, G Arnaldi, M Arosio, A Balsamo, M Baldassarri, L Bartalena, N Bazzoni, L Beccaria, P Beck-Peccoz, G Bellastella, M Bellizzi, F Benedicenti, S Bernasconi, C Bizzarri, G Bona, S Bonadonna, G Borretta, M Boschetti, A Brunani, V Brunelli, F Buzi, C Cacciatore, B Cangiano, M Cappa, R Casalone, A Cassio, P Cavarzere, V Cherubini, T Ciampani, D Cicognani, A Cignarelli, M Cisternino, P Colombo, S Corbetta, N Corciulo, G Corona, R Cozzi, C Crivellaro, I Dalle Mule, L Danesi, A V D’Elia, E degli Uberti, S De Leo, E Della Valle, M De Marchi, N Di Iorgi, A Di Mambro, A Fabbri, C Foresta, G Forti, A R Franceschi, A Garolla, M Ghezzi, C Giacomozzi, M Giusti, E Grosso, G Guabello, M P Guarneri, G Grugni, A M Isidori, F Lanfranco, A Lania, R Lanzi, L Larizza, A Lenzi, S Loche, P Loli, V Lombardi, M C Maggio, G Mandrile, C Manieri, G Mantovani, S Marelli, M Marzullo, M A Mencarelli, N Migone, G Motta, G Neri, G Padova, G Parenti, B Pasquino, A Pia, E Piantanida, E Pignatti, A Pilotta, B Pivetta, M Pollazzon, A Pontecorvi, P Porcelli, G B Pozzan, G Pozzobon, G Radetti, P Razzore, L Rocchetti, R Roncoroni, G Rossi, E Sala, A Salvatoni, F Salvini, A Secco, M Segni, R Selice, P Sgaramella, F Sileo, A A Sinisi, F Sirchia, A Spada, A Tresoldi, R Vigneri, G Weber, S Zucchini, Bonomi, Marco, Vezzoli, Valeria, Krausz, Csilla, Guizzardi, Fabiana, Vezzani, Silvia, Simoni, Manuela, Bassi, Ivan, Duminuco, Paolo, Di Iorgi, Natascia, Giavoli, Claudia, Pizzocaro, Alessandro, Russo, Gianni, Moro, Mirella, Fatti, Letizia, Ferlin, Alberto, Mazzanti, Laura, Zatelli Maria, Chiara, Cannavò, Salvo, Isidori Andrea, M., Pincelli Angela, Ida, Prodam, Flavia, Mancini, Antonio, Limone, Paolo, Tanda Maria, Laura, Gaudino, Rossella, Salerno, Mariacarolina, Francesca, Pregnolato, Maghnie, Mohamad, Maggi, Mario, Persani, Luca, Italian Network on Central, Hypogonadism., Zatelli, Maria Chiara, Cannavã², Salvo, Isidori, Andrea M., Pincelli, Angela Ida, Tanda, Maria Laura, Aimaretti, G., Altobell, M., Ambrosio, M. R., Andrioli, M., Angelett, G., Arecco, F., Arnald, G., Arosio, M., Balsamo, A., Baldassarr, M., Bartalena, L., Bazzon, N., Beccari, L., Beck-Peccoz, P., Bellastella, G., Bellizz, M., Benedicent, F., Bernasconi, S., Bizzarri, C., Bona, G., Bonadonna, S., Borrett, G., Boschetti, M., Brunani, A., Brunelli, V., Buz, F., Cacciatore, C., Cangiano, B., Cappa, M., Casalone, R., Cassio, A., Cavarzere, P., Cherubini, V., Ciampani, T., Cicognan, D., Cignarell, A., Cisternin, M., Colombo, P., Corbetta, S., Corciul, N., Corona, G., Cozzi, R., Crivellaro, C., Dalle Mule, I., Danesi, L., Eli, A. V. D., Degli Uberti, E., De Leo, S., Della Valle, E., De Marchi, M., Di Iorgi, N., Di Mambr, A., Fabbri, A., Foresta, C., Forti, G., Franceschi, A. R., Garolla, A., Ghezzi, M., Giacomozzi, C., Giusti, M., Grosso, E., Guabello, G., Guarneri, M. P., Grugni, G., Isidori, A. M., Lanfranco, F., Lania, A., Lanzi, R., Larizza, L., Lenzi, A., Loche, S., Loli, P., Lombardi, V., Maggi, M. C., Mandrile, G., Manieri, C., Mantovani, G., Marelli, S., Marzullo, M., Mencarelli, M. A., Migone, N., Motta, G., Neri, G., Padov, G., Parenti, G., Pasquino, B., Pia, A., Piantanida, E., Pignatti, E., Pilotta, A., Pivett, B., Pollazzon, M., Pontecorvi, A., Porcelli, P., Pozza, G. B., Pozzobon, G., Radetti, G., Razzore, P., Rocchett, L., Roncoron, R., Rossi, G., Sala, E., Salvatoni, A., Salvini, F., Secc, A., Segni, M., Selice, R., Sgaramella, P., Sileo, F., Sinisi, A. A., Sirchia, F., Spada, A., Tresoldi, A., Vigneri, R., Weber, G., Zucchini, S., Marco Bonomi, Valeria Vezzoli, Csilla Krausz, Fabiana Guizzardi, Silvia Vezzani, Manuela Simoni, Ivan Bassi, Paolo Duminuco, Natascia Di Iorgi, Claudia Giavoli, Alessandro Pizzocaro, Gianni Russo, Mirella Moro, Letizia Fatti, Alberto Ferlin, Laura Mazzanti, Maria Chiara Zatelli, Salvo Cannavò, Andrea M Isidori, Angela Ida Pincelli, Flavia Prodam, Antonio Mancini, Paolo Limone, Maria Laura Tanda, Rossella Gaudino, Mariacarolina Salerno, Pregnolato Francesca, Mohamad Maghnie, Mario Maggi, Luca Persani, Italian Network on Central Hypogonadism […, A. Cassio, …, S. Zucchini, ], Isidori, Andrea M, Weber, Giovanna, and Italian Network on Central, Hypogonadism
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0301 basic medicine ,Male ,Pediatrics ,Synkinesis ,Kallmann syndrome ,diagnosis ,genotype ,Endocrinology, Diabetes and Metabolism ,Gonadal Steroid Hormone ,Cohort Studies ,Olfaction Disorders ,0302 clinical medicine ,Endocrinology ,Olfaction Disorder ,Young adult ,Age of Onset ,Gonadal Steroid Hormones ,Gonadotropin ,Pituitary Hormone ,Isolated hypogonadotropic hypogonadism ,General Medicine ,isolated hypogonadotropic hypogonadism, pubertal delay ,genetic-basis ,gonadotropin-deficiency ,Diabetes and Metabolism ,Phenotype ,Italy ,Cohort ,Female ,complex ,Cohort study ,Human ,Adult ,medicine.medical_specialty ,Adolescent ,Gonadotropins ,Humans ,Hypogonadism ,Obesity ,Overweight ,Pituitary Hormones ,Young Adult ,030209 endocrinology & metabolism ,NO ,03 medical and health sciences ,Hypogonadotropic hypogonadism ,Adolescent, Adult, Age of Onset, Cohort Studies, Female, Gonadal Steroid Hormones, Gonadotropins, Humans, Hypogonadis, Italy, Male, Obesity, Olfaction Disorders, Overweight, Phenotype, Pituitary Hormones, Synkinesis, Young Adult, Endocrinology, Diabetes and Metabolism, Endocrinology ,Internal medicine ,medicine ,Isolated hypogonadotropic hypogonadism, Kallmann syndrome, Observational cohort study ,gnrh deficiency ,disease ,business.industry ,Settore MED/13 - ENDOCRINOLOGIA ,isolated Hypogonadotropic hypogonadism, kallmann syndrome ,medicine.disease ,body regions ,030104 developmental biology ,Sex steroid ,linked kallmann-syndrome ,heterogeneity ,phenotype ,Observational cohort study ,Synkinesi ,Age of onset ,Cohort Studie ,business - Abstract
Objective Isolated hypogonadotropic hypogonadism (IHH) is a rare disorder with pubertal delay, normal (normoosmic-IHH, nIHH) or defective sense of smell (Kallmann syndrome, KS). Other reproductive and non-reproductive anomalies might be present although information on their frequency are scanty, particularly according to the age of presentation. Design Observational cohort study carried out between January 2008 and June 2016 within a national network of academic or general hospitals. Methods We performed a detailed phenotyping of 503 IHH patients with: (1) manifestations of hypogonadism with low sex steroid hormone and low/normal gonadotropins; (2) absence of expansive hypothalamic/pituitary lesions or multiple pituitary hormone defects. Cohort was divided on IHH onset (PPO, pre-pubertal onset or AO, adult onset) and olfactory function: PPO-nIHH (n = 275), KS (n = 184), AO-nIHH (n = 36) and AO-doIHH (AO-IHH with defective olfaction, n = 8). Results 90% of patients were classified as PPO and 10% as AO. Typical midline and olfactory defects, bimanual synkinesis and familiarity for pubertal delay were also found among the AO-IHH. Mean age at diagnosis was significantly earlier and more frequently associated with congenital hypogonadism stigmata in patients with Kallmann’s syndrome (KS). Synkinesis, renal and male genital tract anomalies were enriched in KS. Overweight/obesity are significantly associated with AO-IHH rather than PPO-IHH. Conclusions Patients with KS are more prone to develop a severe and complex phenotype than nIHH. The presence of typical extra-gonadal defects and familiarity for PPO-IHH among the AO-IHH patients indicates a common predisposition with variable clinical expression. Overall, these findings improve the understanding of IHH and may have a positive impact on the management of patients and their families.
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- 2018
5. Derivation and validation of the clinical prediction model for COVID-19.
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Foieni F, Sala G, Mognarelli JG, Suigo G, Zampini D, Pistoia M, Ciola M, Ciampani T, Ultori C, and Ghiringhelli P
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- Adult, Aged, Aged, 80 and over, COVID-19, Coronavirus Infections physiopathology, Female, Humans, Male, Middle Aged, Pandemics, Pneumonia, Viral physiopathology, Reproducibility of Results, Risk Assessment methods, Risk Assessment statistics & numerical data, Severity of Illness Index, Clinical Decision Rules, Coronavirus Infections diagnosis, Pneumonia, Viral diagnosis, Risk Assessment standards
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The epidemic phase of Coronavirus disease 2019 (COVID-19) made the Worldwide health system struggle against a severe interstitial pneumonia requiring high-intensity care settings for respiratory failure. A rationalisation of resources and a specific treatment path were necessary. The study suggests a predictive model drawing on clinical data gathered by 119 consecutive patients with laboratory-confirmed COVID-19 admitted in Busto Arsizio hospital. We derived a score that identifies the risk of clinical evolution and in-hospital mortality clustering patients into four groups. The study outcomes have been compared across the derivation and validation samples. The prediction rule is based on eight simple patient characteristics that were independently associated with study outcomes. It is able to stratify COVID-19 patients into four severity classes, with in-hospital mortality rates of 0% in group 1, 6-12.5% in group 2, 7-20% in group 3 and 60-86% in group 4 across the derivation and validation sample. The prediction model derived in this study identifies COVID-19 patients with low risk of in-hospital mortality and ICU admission. The prediction model that the study presents identifies COVID-19 patients with low risk of in-hospital mortality and admission to ICU. Moreover, it establishes an intermediate portion of patients that should be treated accurately in order to avoid an unfavourable clinical evolution. A further validation of the model is important before its implementation as a decision-making tool to guide the initial management of patients.
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- 2020
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6. Growth hormone-releasing hormone in testicular interstitial and germ cells: potential paracrine modulation of follicle-stimulating hormone action on Sertoli cell function.
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Fabbri A, Ciocca DR, Ciampani T, Wang J, and Dufau ML
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- Aging physiology, Animals, Antibodies, Cells, Cultured, Drug Interactions, Growth Hormone-Releasing Hormone analysis, Immunohistochemistry, Male, Rats, Rats, Sprague-Dawley, Sertoli Cells cytology, Sertoli Cells drug effects, Spermatids drug effects, Spermatids physiology, Testis cytology, Testis growth & development, Cyclic AMP metabolism, Follicle Stimulating Hormone pharmacology, Growth Hormone-Releasing Hormone pharmacology, Growth Hormone-Releasing Hormone physiology, Sertoli Cells physiology, Sexual Maturation, Testis physiology
- Abstract
GH-releasing hormone (GHRH) is present in the interstitial and germ cells of the rat testis. In previous studies we found that GHRH is secreted from rat adult Leydig cells, in which it stimulates basal and LH-induced cAMP formation and steroidogenesis. In other studies cAMP production in Sertoli cells was found to be stimulated by GHRH. In the present report, we describe a potential paracrine action of GHRH in the Sertoli cell, with stimulation of cAMP formation in cultured adult and pubertal Sertoli cells. GHRH increased FSH-stimulated cAMP production in adult and pubertal cultures in a time-dependent manner. GHRH stimulation of basal and FSH-induced extracellular cAMP formation was more prominent in pubertal than in adult cultures. Immunocytochemical studies demonstrated the presence of GHRH-like immunoreactivity in rat interstitial cells from day 4 to adult life and in the acrosomal region of early and intermediate spermatids at stages III-VI of the seminiferous epithelium cycle. Immunoreactive GHRH was not observed in late spermatids and mature sperm or in Sertoli cells at any age. These results indicate that GHRH acts synergistically with FSH to promote cAMP production in Sertoli cells in culture. Testicular GHRH of Leydig and germ cell origin may be an important paracrine regulator of Sertoli cell function. Alternatively, GHRH present in germ cells may exert stage-specific intracrine functions.
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- 1995
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7. Growth hormone-releasing hormone is produced by rat Leydig cell in culture and acts as a positive regulator of Leydig cell function.
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Ciampani T, Fabbri A, Isidori A, and Dufau ML
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- Animals, Chorionic Gonadotropin pharmacology, Chromatography, High Pressure Liquid, Cyclic AMP biosynthesis, Growth Hormone-Releasing Hormone pharmacology, Kinetics, Leydig Cells drug effects, Male, Rats, Receptors, Gastrointestinal Hormone physiology, Receptors, Vasoactive Intestinal Peptide, Testosterone biosynthesis, Vasoactive Intestinal Peptide metabolism, Growth Hormone-Releasing Hormone biosynthesis, Leydig Cells metabolism
- Abstract
Rat GH-releasing hormone (GHRH), mainly contained in hypothalamic neurons, has also been identified in several extraneural tissues, including the gastrointestinal tract, placenta, ovary, and testis. In the testis, GHRH mRNA is ontogenically regulated, and GHRH immunoreactivity can be observed in interstitial cells and tubules, suggesting an intratesticular role for the peptide. Leydig cells in culture are able to produce hypothalamic releasing hormones, i.e. CRH, which acts as an autocrine negative regulator of Leydig cell function. In this study we investigated whether GHRH is present in Leydig cells and evaluated the role of the peptide in Leydig cell function. Adult Leydig cells in culture produced considerable amounts of immunoreactive GHRH [23.9 +/- 2.1 (+/- SE) pg/10(6) cells.30 min], and the release of the peptide was acutely stimulated by hCG. HPLC analysis of GHRH in media from basal and hCG-treated cultures showed the presence of a single peak eluting at the same retention time as that of hypothalamic rat GHRH. Radioligand binding and activation studies revealed a common receptor for vasoactive intestinal peptide (VIP) and rat GHRH in Leydig cell membrane. Specific binding of [125I]VIP to Leydig cell membranes showed the presence of a single site, with high affinity and low binding capacity. The relative potencies of VIP-related peptides for inhibition of radioligand binding were: VIP > rat GHRH > secretin > human GHRH. In cultured Leydig cells, GHRH and VIP stimulated cAMP production, consistent with coupling of the receptor to the adenylate cyclase system. VIP displayed a lower ED50 than GHRH in stimulating cAMP production (P < 0.01), comparable with the higher binding potency of this peptide. No additive effects of VIP- and GHRH-stimulated cAMP generation were observed, suggesting that both peptides compete for the same receptor protein. GHRH and VIP had no effect on basal steroidogenesis, indicating a lack of tonic actions and compartmentalization of the peptides' effect. On the other hand, GHRH acted as a potentiator of the acute gonadotropin stimulation of testosterone production and cAMP generation. [125I]hCG binding to the Leydig cells in culture showed that GHRH was unable to affect the number or affinity of binding sites for hCG, indicating that the GHRH-sensitizing effect on LH action is beyond the level of gonadotropin binding and possibly is through the facilitation of LH receptor coupling functions.(ABSTRACT TRUNCATED AT 400 WORDS)
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- 1992
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8. Rat Leydig cells bind platelet-derived growth factor through specific receptors and produce platelet-derived growth factor-like molecules.
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Gnessi L, Emidi A, Farini D, Scarpa S, Modesti A, Ciampani T, Silvestroni L, and Spera G
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- Animals, Binding, Competitive, Cells, Cultured, Male, Platelet-Derived Growth Factor biosynthesis, Rats, Rats, Inbred Strains, Receptors, Platelet-Derived Growth Factor, Leydig Cells metabolism, Platelet-Derived Growth Factor metabolism, Receptors, Cell Surface metabolism
- Abstract
The platelet-derived growth factor (PDGF) is a major mitogen for cells of mesenchymal origin. Because Leydig cells arise from mesenchymal precursors, we tested the hypothesis that these cells might be a target for PDGF. We also investigated a possible production of a PDGF-like substance by Leydig cells in culture and the distribution of PDGF-like material in the rat testis using immunohistochemistry. PDGF was found to bind specifically to high affinity receptors on the surface of purified adult rat Leydig cells. Conditioned medium from cultured Leydig cells competed with 125I-labeled PDGF for binding to the Leydig cells. The secretion of PDGF receptor-competing activity was stimulated in a dose-dependent manner by the trophic hormone hCG. Immunohistochemical studies revealed specific staining for PDGF in the Leydig cells of adult rat testis. Taken together these observations suggest that PDGF may play a role in the local control mechanisms of testicular function.
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- 1992
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