المؤلفون: Benvenuto, Monica, Ciuffa, Sara, Focaccetti, Chiara, Sbardella, Diego, Fazi, Sara, Scimeca, Manuel, Tundo, Grazia Raffaella, Barillari, Giovanni, Segni, Maria, Bonanno, Elena, Manzari, Vittorio, Modesti, Andrea, Masuelli, Laura, Coletta, Massimo, Bei, Roberto

المساهمون: Benvenuto, M, Ciuffa, S, Focaccetti, C, Sbardella, D, Fazi, S, Scimeca, M, Tundo, Gr, Barillari, G, Segni, M, Bonanno, E, Manzari, V, Modesti, A, Masuelli, L, Coletta, M, Bei, R

مصطلحات موضوعية: Settore MED/04 - PATOLOGIA GENERALE, Settore MED/05 - PATOLOGIA CLINICA, Settore MED/08 - ANATOMIA PATOLOGICA, Settore BIO/10 - BIOCHIMICA

الوصف: Head and neck cancer (HNC) has frequently an aggressive course for the development of resistance to standard chemotherapy. Thus, the use of innovative therapeutic drugs is being assessed. Bortezomib is a proteasome inhibitor with anticancer effects. In vitro antitumoral activity of Bortezomib was investigated employing human tongue (SCC-15, CAL-27), pharynx (FaDu), salivary gland (A-253) cancer cell lines and a murine cell line (SALTO-5) originated from a salivary gland adenocarcinoma arising in BALB-neuT male mice transgenic for the oncogene neu. Bortezomib inhibited cell proliferation, triggered apoptosis, modulated the expression and activation of pro-survival signaling transduction pathways proteins activated by ErbB receptors and inhibited proteasome activity in vitro. Intraperitoneal administration of Bortezomib delayed tumor growth of SALTO-5 cells transplanted in BALB-neuT mice, protracted mice survival and adjusted tumor microenvironment by increasing tumor-infiltrating immune cells (CD4+ and CD8+ T cells, B lymphocytes, macrophages, and Natural Killer cells) and by decreasing vessels density. In addition, Bortezomib modified the expression of proteasome structural subunits in transplanted SALTO-5 cells. Our findings further support the use of Bortezomib for the treatment of HNC and reveal its ineffectiveness in counteracting the activation of deregulated specific signaling pathways in HNC cell lines when resistance to proteasome inhibition is developed.

العلاقة: info:eu-repo/semantics/altIdentifier/pmid/34561494; info:eu-repo/semantics/altIdentifier/wos/WOS:000698985300044; volume:11; issue:1; numberofpages:23; journal:SCIENTIFIC REPORTS; http://hdl.handle.net/2108/279465Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85115687575

الإتاحة: https://doi.org/10.1038/s41598-021-98450-6Test
http://hdl.handle.net/2108/279465Test

المؤلفون: Apellaniz-Ruiz, Maria, Segni, Maria, Kettwig, Matthias, Glüer, Sylvia, Pelletier, Dylan, Nguyen, Van-Hung, Wagener, Rabea, López, Cristina, Muchantef, Karl, Bouron-Dal Soglio, Dorothée, Foulkes, William D.

المساهمون: Apellaniz-Ruiz, Maria, Segni, Maria, Kettwig, Matthias, Glüer, Sylvia, Pelletier, Dylan, Nguyen, Van-Hung, Wagener, Rabea, López, Cristina, Muchantef, Karl, Bouron-Dal Soglio, Dorothée, Foulkes, William D.

العلاقة: https://resolver.sub.uni-goettingen.de/purl?gro-2/134325Test

الإتاحة: https://doi.org/10.1056/NEJMoa1812169Test
https://resolver.sub.uni-goettingen.de/purl?gro-2/134325Test

المؤلفون: SANTAGUIDA, MARIA GIULIA, GATTO, ILENIA, MANGINO, GIORGIO, VIRILI, CAMILLA, Stramazzo, Ilaria, Fallahi, Poupak, Antonelli, Alessandro, SEGNI, Maria, ROMEO, Giovanna, CENTANNI, Marco

المساهمون: Santaguida, MARIA GIULIA, Gatto, Ilenia, Mangino, Giorgio, Virili, Camilla, Stramazzo, Ilaria, Fallahi, Poupak, Antonelli, Alessandro, Segni, Maria, Romeo, Giovanna, Centanni, Marco

مصطلحات موضوعية: Breg cell, cellular immunity, hashimoto's thyroiditi, polyglandular autoimmune syndrome, thyroid autoimmunity

الوصف: Hashimoto thyroiditis (HT) may occur isolated or associated with other non-endocrine autoimmune disorders (NEAD). No data are available about Breg cells in these disorders and this represented the aim of the study. Th17 and Breg cells subset were characterized on peripheral blood mononuclear cells isolated from 18 healthy donors (HD), 19 patients with isolated HT and 26 patients with HT+NEAD. Th17 were higher in patients with isolated HT than in HD but no further changes were seen in patients with HT+NEAD. CD24(hi)CD38(hi) unstimulated Breg cells were similar in HT patients and in HD, but significantly higher in patients with HT+NEAD than in both HT and in HD. CD19(+)CD24(hi)CD27(+) Breg memory phenotype was similar in HD and in HT patients, but decreased in patients with HT+NEAD (23.4%vs38.5%). Upon CpG-stimulation, CD24(hi)CD38(hi) IL-10(+) Breg cells were higher in HT patients than in HD (3.9%vs1.8%) but similar in patients with HT+NEAD (2.4%).

وصف الملف: STAMPA

العلاقة: info:eu-repo/semantics/altIdentifier/pmid/28461108; info:eu-repo/semantics/altIdentifier/wos/WOS:000414888300005; volume:184; firstpage:42; lastpage:47; numberofpages:6; journal:CLINICAL IMMUNOLOGY; http://hdl.handle.net/11573/953877Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85018985338

الإتاحة: https://doi.org/10.1016/j.clim.2017.04.012Test
http://hdl.handle.net/11573/953877Test

المؤلفون: Chen, Jian Hua, SEGNI, Maria, Payne, Felicity, Huang Doran, Isabel, Sleigh, Alison, Adams, Claire, Durbin, Richard, Muddyman, Dawn, Soranzo, Nicole, Timpson, Nic, Spector, Tim, Richards, Bren, Palotie, Aarno, Owen, Michael, Barrett, Jeff, Geschwind, Daniel, Hurles, Matt, Fitzpatrick, David, Barroso, Inês, Farooqi, Sadaf, Zeggini, Eleftheria, Kaye, Jane, Kennedy, Karen, Mccarthy, Shane, Stalker, Jim, Langford, Cordelia, Keane, Thomas, Savage, David B., O’Rahilly, Stephen, Semple, Robert K.

المساهمون: Chen, Jian Hua, Segni, Maria, Payne, Felicity, Huang Doran, Isabel, Sleigh, Alison, Adams, Claire, Durbin, Richard, Muddyman, Dawn, Soranzo, Nicole, Timpson, Nic, Spector, Tim, Richards, Bren, Palotie, Aarno, Owen, Michael, Barrett, Jeff, Geschwind, Daniel, Hurles, Matt, Fitzpatrick, David, Barroso, Inê, Farooqi, Sadaf, Zeggini, Eleftheria, Kaye, Jane, Kennedy, Karen, Mccarthy, Shane, Stalker, Jim, Langford, Cordelia, Keane, Thoma, Savage, David B., O’Rahilly, Stephen, Semple, Robert K.

مصطلحات موضوعية: POC1A, centriole, centrosome, diabete, dyslipidaemia, insulin resistance, primary cilium, short stature, skeletal dysplasia

الوصف: We describe a female proband with primordial dwarfism, skeletal dysplasia, facial dysmorphism, extreme dyslipidaemic insulin resistance and fatty liver associated with a novel homozygous frameshift mutation in POC1A, predicted to affect two of the three protein products of the gene. POC1A encodes a protein associated with centrioles throughout the cell cycle and implicated in both mitotic spindle and primary ciliary function. Three homozygous mutations affecting all isoforms of POC1A have recently been implicated in a similar syndrome of primordial dwarfism, although no detailed metabolic phenotypes were described. Primary cells from the proband we describe exhibited increased centrosome amplification and multipolar spindle formation during mitosis, but showed normal DNA content, arguing against mitotic skipping, cleavage failure or cell fusion. Despite evidence of increased DNA damage in cells with supernumerary centrosomes, no aneuploidy was detected. Extensive centrosome clustering both at mitotic spindles and in primary cilia mitigated the consequences of centrosome amplification, and primary ciliary formation was normal. Although further metabolic studies of patients with POC1A mutations are warranted, we suggest that POC1A may be added to ALMS1 and PCNT as examples of centrosomal or pericentriolar proteins whose dysfunction leads to extreme dyslipidaemic insulin resistance. Further investigation of links between these molecular defects and adipose tissue dysfunction is likely to yield insights into mechanisms of adipose tissue maintenance and regeneration that are critical to metabolic health.

العلاقة: info:eu-repo/semantics/altIdentifier/pmid/26336158; info:eu-repo/semantics/altIdentifier/wos/WOS:000365033300009; volume:55; issue:2; firstpage:147; lastpage:158; numberofpages:12; journal:JOURNAL OF MOLECULAR ENDOCRINOLOGY; http://hdl.handle.net/11573/891593Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84944314739; http://jme.endocrinology-journals.org/content/55/2/147.full.pdfTest

الإتاحة: https://doi.org/10.1530/JME-15-0090Test
http://hdl.handle.net/11573/891593Test
http://jme.endocrinology-journals.org/content/55/2/147.full.pdfTest

المؤلفون: Elli, Francesca Marta, Bordogna, Paolo, de Sanctis, Luisa, Giachero, Federica, Verrua, Elisa, Segni, Maria, Mazzanti, Laura, Boldrin, Valentina, Toromanovic, Alma, Spada, Anna, Mantovani, Giovanna

المساهمون: Ministero della Salute

المصدر: Journal of Bone and Mineral Research ; volume 31, issue 6, page 1215-1224 ; ISSN 0884-0431 1523-4681

مصطلحات موضوعية: Orthopedics and Sports Medicine, Endocrinology, Diabetes and Metabolism

الوصف: The cyclic adenosine monophosphate (cAMP) intracellular signaling pathway mediates the physiological effects of several hormones and neurotransmitters, acting by the activation of G-protein coupled receptors (GPCRs) and several downstream intracellular effectors, including the heterotrimeric stimulatory G-protein (Gs), the cAMP-dependent protein kinase A (PKA), and cAMP-specific phosphodiesterases (PDEs). Defective G-protein–mediated signaling has been associated with an increasing number of disorders, including Albright hereditary osteodistrophy (AHO) and pseudohypoparathyroidism (PHP), a heterogeneous group of rare genetic metabolic disorders resulting from molecular defects at the GNAS locus. Moreover, mutations in PRKAR1A and PDE4D genes have been recently detected in patients with acrodysostosis (ACRDYS), showing a skeletal and endocrinological phenotype partially overlapping with AHO/PHP. Despite the high detection rate of molecular defects by currently available molecular approaches, about 30% of AHO/PHP patients still lack a molecular diagnosis, hence the need to screen patients negative for GNAS epi/genetic defects also for chromosomal regions and genes associated with diseases that undergo differential diagnosis with PHP. According to the growing knowledge on Gsα-cAMP signaling-linked disorders, we investigated our series of patients (n = 81) with a clinical diagnosis of PHP/AHO but negative for GNAS anomalies for the presence of novel genetic variants at PRKAR1A and PDE4D genes. Our work allowed the detection of 8 novel missense variants affecting genes so far associated with ACRDYS in 9 patients. Our data further confirm the molecular and clinical overlap among these disorders. We present the data collected from a large series of patients and a brief review of the literature in order to compare our findings with already published data; to look for PRKAR1A/PDE4D mutation spectrum, recurrent mutations, and mutation hot spots; and to identify specific clinical features associated with ACRDYS ...

الإتاحة: https://doi.org/10.1002/jbmr.2785Test
https://academic.oup.com/jbmr/article-pdf/31/6/1215/56649375/jbmr2785.pdfTest

المؤلفون: Chen, Jian-Hua, Segni, Maria, Payne, Felicity, Huang-Doran, Isabel, Sleigh, Alison, Adams, Claire, UK10K Consortium, Savage, David B, O'Rahilly, Stephen, Semple, Robert K, Barroso, Inês

مصطلحات موضوعية: POC1A, centriole, centrosome, diabetes, dyslipidaemia, insulin resistance, primary cilium, short stature, skeletal dysplasia, Adult, Amino Acid Sequence, Body Height, Cell Cycle, Cell Cycle Proteins, Centrioles, Cytoskeletal Proteins, Dwarfism, Facies, Fatty Liver, Female, Frameshift Mutation, Humans, Mitosis, Molecular Sequence Data, Protein Isoforms, Proteins, Sequence Alignment, Spindle Apparatus

الوصف: We describe a female proband with primordial dwarfism, skeletal dysplasia, facial dysmorphism, extreme dyslipidaemic insulin resistance and fatty liver associated with a novel homozygous frameshift mutation in POC1A, predicted to affect two of the three protein products of the gene. POC1A encodes a protein associated with centrioles throughout the cell cycle and implicated in both mitotic spindle and primary ciliary function. Three homozygous mutations affecting all isoforms of POC1A have recently been implicated in a similar syndrome of primordial dwarfism, although no detailed metabolic phenotypes were described. Primary cells from the proband we describe exhibited increased centrosome amplification and multipolar spindle formation during mitosis, but showed normal DNA content, arguing against mitotic skipping, cleavage failure or cell fusion. Despite evidence of increased DNA damage in cells with supernumerary centrosomes, no aneuploidy was detected. Extensive centrosome clustering both at mitotic spindles and in primary cilia mitigated the consequences of centrosome amplification, and primary ciliary formation was normal. Although further metabolic studies of patients with POC1A mutations are warranted, we suggest that POC1A may be added to ALMS1 and PCNT as examples of centrosomal or pericentriolar proteins whose dysfunction leads to extreme dyslipidaemic insulin resistance. Further investigation of links between these molecular defects and adipose tissue dysfunction is likely to yield insights into mechanisms of adipose tissue maintenance and regeneration that are critical to metabolic health. ; This work was supported by the Wellcome Trust [grant numbers WT098498, WT098051,WT095515, and WT091310]; the Medical Research Council [MRC_MC_UU_12012/5]; the United Kingdom National Institute for Health Research (NIHR) Cambridge Biomedical Research Centre. ; This is the final version of the article. It first appeared from Bioscientifica via http://dx.doi.org/10.1530/JME-15-0090Test

وصف الملف: application/pdf

العلاقة: https://www.repository.cam.ac.uk/handle/1810/250316Test

الإتاحة: https://www.repository.cam.ac.uk/handle/1810/250316Test

المؤلفون: PANI, MICHAEL A., REGULLA, KAROLINE, SEGNI, MARIA, HOFMANN, STEFAN, HÜFNER, MICHAEL, PASQUINO, ANNA MARIA, USADEL, KLAUS-H., BADENHOOP, KLAUS

المصدر: Journal of Clinical Endocrinology & Metabolism; Jun2022, Vol. 107 Issue 6, p2564-2567, 4p, 3 Charts

مستخلص: Graves' disease and Hashimoto's thyroiditis are common autoimmune thyroid disorders. Experimentally, 1,25(OH)(2) D(3) prevents Hashimoto's thyroiditis. Vitamin D serum levels in Graves' disease were found to be significantly lower than in nonautoimmune hyperthyroidism. The polymorphic vitamin D-binding protein (DBP) greatly facilitates vitamin D actions, and DBP alleles differ regarding their affinity for 1,25(OH)(2) D(3). Therefore, we investigated polymorphisms of the DBP gene for an association with thyroid autoimmunity. Families with an offspring affected by Graves' disease (95 pedigrees) or by Hashimoto's thyroiditis (92 pedigrees) encompassing 561 individuals of Caucasian origin were genotyped for three DBP polymorphisms [(TAAA)(N) in intron 8; StyI; and HaeIII in exon 11]. Indirect haplotyping and (extended) transmission disequilibrium testing were performed. There was a significant transmission disequilibrium of the intron 8 polymorphism in patients with Graves' disease (P < 0.03) but not of the exon 11 polymorphism. In contrast, neither the intron 8 nor the exon 11 polymorphism was associated with Hashimoto's thyroiditis. Maternal and paternal transmission as well as allele frequencies in DQ2(+) and DQ2(-) patients did not differ in either disease. Therefore, allelic variants of the DBP gene confer susceptibility to Graves' disease but not to Hashimoto's thyroiditis in our population. These findings support a role of the vitamin D endocrine system in thyroid autoimmunity. [ABSTRACT FROM AUTHOR]

: Copyright of Journal of Clinical Endocrinology & Metabolism is the property of Oxford University Press / USA and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

المؤلفون: SEGNI, Maria

المساهمون: De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, Segni, Maria

الوصف: Thyroid disorders in infancy, childhood and adolescence represent common and usually treatable endocrine disorders. Thyroid hormones are essential for normal development and growth of many target tissues, including the brain and the skeleton. Thyroid hormone action on critical genes for neurodevelopment is limited to specific time window, and even a short period of deficiency of TH can cause irreversible brain damage. During the first trimester of pregnancy fetal brain development is totally dependent on maternal thyroid function. Congenital hypothyroidism is one of the most preventable causes of mental retardation, but early diagnosis is needed in order to prevent irreversible SNC damage. Today more than 70% of the babies worldwide are born in areas without an organized screening program. New insights about genetic causes, screening strategies and treatment of congenital hypothyroidism are reported. Hyperthyroidism in newborns is usually a transient consequence of transplacental passage of TSH receptor stimulating antibodies. Hypothyroidism can be detected in infants born to hyperthyroid mothers, due to transplacental passage of TSH receptor antibodies or hypothalamic-pituitary suppression. In childhood and adolescence autoimmune thyroid disease (AITD) as chronic lymphocytic thyroiditis and Graves’ disease account for the main cause of hypothyroidism and hyperthyroidism, respectively. Incidence of AITD increase from infancy to adolescence. Other autoimmune disorders are frequently associated. An increased risk of thyroid nodules and cancer is suggested. Differentiated thyroid cancer and medullary thyroid carcinoma in childhood and adolescence require specific expertise. Follow up programs are advised for high risk patients as long term survivors of childhood cancer. For complete coverage of this and related areas of Endocrinology, please visit our free online textbook

وصف الملف: ELETTRONICO

العلاقة: ispartofbook:Endotext; http://hdl.handle.net/11573/957975Test; www.endotext.org

الإتاحة: http://hdl.handle.net/11573/957975Test

المؤلفون: Penna Martinez, Marissa, Ramos-Lopez, Elizabeth, Robbers, Inka, Kahles, Heinrich, Hahner, Stefanie, Willenberg, Holger S., Reisch, Nicole, Seidl, Christian, Segni, Maria, Badenhoop, Klaus

مصطلحات موضوعية: ddc:610

الوصف: Background: Three genes have been confirmed as major joint susceptibility genes for endocrine autoimmune disease:human leukocyte antigen class II, cytotoxic T-lymphocyte antigen 4 and protein tyrosine phosphatase non-receptor type 22. Recent studies showed that a genetic variation within the interferon induced helicase domain 1 (IFIH1) locus (rs1990760 polymorphism) is an additional risk factor in type 1 diabetes and Graves' disease (GD). Methods: The aim of the present study was to investigate the role of the rs1990760 polymorphism within the IFIH1 gene in German patients with GD (n=258), Hashimoto's thyroiditis (HT,n=106), Addison's disease (AD,n=195) and healthy controls (HC,n=227) as well as in 55 GD families (165 individuals, German) and 100 HT families (300 individuals, Italian). Furthermore, the interaction between rs1990760 polymorphism with human leukocyte antigen (HLA) risk haplotype DQ2(DQA*0501-DQB*0201), the risk haplotypes DQ2/DQ8 (DQA*0301-DQB*0302) and the status of thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb) and TSH receptor antibody (TRAb) in patients and families were analysed. Results:No significant differences were found between the allele and genotype frequencies for rs1990760 IFIH1 polymorphism in patients with GD, HT, AD and HC. Also no differences were observed when stratifying the IFIH1 rs1990760 polymorphism for gender, presence or absence of thyroid antibodies (GD:TRAb and HT:TPOAb/TgAb) and HLA risk haplotypes (DQ2:for GD and HT, DQ2/DQ8:for AD). Furthermore the transmission analysis in GD and HT families revealed no differences in alleles transmission for rs1990760 IFIH1 from parents with or without HLA risk haplotype DQ2 to the affected offspring. In contrast, by dividing the HT parents according to the presence or absence of thyroid Ab titers, mothers and fathers both positive for TPOAb/TgAb overtransmitted the allele A of IFIH1 rs1990760 to their HT affected offspring (61.8% vs 38.2%;p=0.05;corrected p [pc]=0.1). However, these associations did not remain ...

وصف الملف: application/pdf

العلاقة: http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/7362Test; urn:nbn:de:hebis:30-73027; https://nbn-resolving.org/urn:nbn:de:hebis:30-73027Test; https://doi.org/10.1186/1471-2350-10-126Test; http://publikationen.ub.uni-frankfurt.de/files/7362/1471_2350_10_126.pdfTest

الإتاحة: https://doi.org/10.1186/1471-2350-10-126Test
http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/7362Test
https://nbn-resolving.org/urn:nbn:de:hebis:30-73027Test
http://publikationen.ub.uni-frankfurt.de/files/7362/1471_2350_10_126.pdfTest

المؤلفون: Seidl Christian, Reisch Nicole, Willenberg Holger, Hahner Stefanie, Kahles Heinrich, Robbers Inka, Ramos-Lopez Elizabeth, Penna-Martinez Marissa, Segni Maria, Badenhoop Klaus

المصدر: BMC Medical Genetics, Vol 10, Iss 1, p 126 (2009)

مصطلحات موضوعية: Internal medicine, RC31-1245, Genetics, QH426-470

الوصف: Background Three genes have been confirmed as major joint susceptibility genes for endocrine autoimmune disease:human leukocyte antigen class II, cytotoxic T-lymphocyte antigen 4 and protein tyrosine phosphatase non-receptor type 22. Recent studies showed that a genetic variation within the interferon induced helicase domain 1 (IFIH1) locus (rs1990760 polymorphism) is an additional risk factor in type 1 diabetes and Graves' disease (GD). Methods The aim of the present study was to investigate the role of the rs1990760 polymorphism within the IFIH1 gene in German patients with GD (n = 258), Hashimoto's thyroiditis (HT, n = 106), Addison's disease (AD, n = 195) and healthy controls (HC, n = 227) as well as in 55 GD families (165 individuals, German) and 100 HT families (300 individuals, Italian). Furthermore, the interaction between rs1990760 polymorphism with human leukocyte antigen (HLA) risk haplotype DQ2(DQA*0501-DQB*0201), the risk haplotypes DQ2/DQ8 (DQA*0301-DQB*0302) and the status of thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb) and TSH receptor antibody (TRAb) in patients and families were analysed. Results No significant differences were found between the allele and genotype frequencies for rs1990760 IFIH1 polymorphism in patients with GD, HT, AD and HC. Also no differences were observed when stratifying the IFIH1 rs1990760 polymorphism for gender, presence or absence of thyroid antibodies (GD:TRAb and HT:TPOAb/TgAb) and HLA risk haplotypes (DQ2:for GD and HT, DQ2/DQ8:for AD). Furthermore the transmission analysis in GD and HT families revealed no differences in alleles transmission for rs1990760 IFIH1 from parents with or without HLA risk haplotype DQ2 to the affected offspring. In contrast, by dividing the HT parents according to the presence or absence of thyroid Ab titers, mothers and fathers both positive for TPOAb/TgAb overtransmitted the allele A of IFIH1 rs1990760 to their HT affected offspring (61.8% vs 38.2%;p = 0.05;corrected p [pc] = 0.1). However, these ...

العلاقة: http://www.biomedcentral.com/1471-2350/10/126Test; https://doaj.org/toc/1471-2350Test; https://doaj.org/article/4526c66299a749c8b1285f7b85720292Test

الإتاحة: https://doi.org/10.1186/1471-2350-10-126Test
https://doaj.org/article/4526c66299a749c8b1285f7b85720292Test