LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 28

Search options

  1. Article ; Online: Pitt Hopkins-Like Syndrome 1 with Novel CNTNAP2 Mutation in Siblings.

    Mittal, Rea / Kumar, Ashutosh / Ladda, Roger / Mainali, Gayatra / Aliu, Ermal

    Child neurology open

    2021  Volume 8, Page(s) 2329048X211055330

    Abstract: Pitt Hopkins-like syndrome 1 (PTHLS1, OMIM # 610042) is an ultra-rare autosomal recessive condition with a prevalence of <1/1,000,000. Intragenic deletions of CNTNAP2 has been implicated in PTHLS1, however to our knowledge a compound heterozygous ... ...

    Abstract Pitt Hopkins-like syndrome 1 (PTHLS1, OMIM # 610042) is an ultra-rare autosomal recessive condition with a prevalence of <1/1,000,000. Intragenic deletions of CNTNAP2 has been implicated in PTHLS1, however to our knowledge a compound heterozygous deletion of exon 4 and a c.1977_1989del13; p.V660Ffsx9 frameshift variant have not been published previously. In this case report, the proband is a seven year old female with PTHLS1, developmental delay, autism spectrum disorder, focal epilepsy, hypotonia, refractory errors, strabismus, and obstructive sleep apnea. Whole exome sequencing analysis revealed biallelic pathogenic variants of the CNTNAP2 gene. Proband has a three year old sister who has who has a similar phenotype including, developmental delay, epilepsy, gait abnormality, refractory errors, strabismus. Family variants were tested and she shared the same CNTNAP2 variants as her sister. The sisters described highlight two novel variants leading to PTHLS1. Genetic workup is essential in identification and management guidance in these populations.
    Language English
    Publishing date 2021-11-10
    Publishing country United States
    Document type Case Reports
    ZDB-ID 2785453-X
    ISSN 2329-048X ; 2329-048X
    ISSN (online) 2329-048X
    ISSN 2329-048X
    DOI 10.1177/2329048X211055330
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Book: Clinical Genodermatology

    Butterworth, Thomas / Ladda, Roger L.

    1981  

    Author's details Thomas Butterworth ; ROGER L. LADDA
    Keywords SKIN DISEASES / GENETICS
    Size VOL. 1-2.
    Publisher PRAEGER
    Publishing place NEW YORK
    Document type Book
    HBZ-ID HT002629772
    ISBN 0-03-056127-2 ; 978-0-03-056127-6
    Database Catalogue ZB MED Medicine, Health

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    1982 A 1595 -1- order for loan Magazin
    1982 A 1595 -2- order for loan Magazin

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: Börjeson-Forssman-Lehmann syndrome: delineating the clinical and allelic spectrum in 14 new families.

    Jain, Vani / Foo, Seow Hoong / Chooi, Stephen / Moss, Celia / Goodwin, Richard / Berland, Siren / Clarke, Angus J / Davies, Sally J / Corrin, Sian / Murch, Oliver / Doyle, Samantha / Graham, Gail E / Greenhalgh, Lynn / Holder, Susan E / Johnson, Diana / Kumar, Ajith / Ladda, Roger L / Sell, Susan / Begtrup, Amber /
    Lynch, Sally A / McCann, Emma / Østern, Rune / Pottinger, Caroline / Splitt, Miranda / Fry, Andrew E

    European journal of human genetics : EJHG

    2023  Volume 31, Issue 12, Page(s) 1421–1429

    Abstract: Börjeson-Forssman-Lehmann syndrome (BFLS) is an X-linked intellectual disability syndrome caused by variants in the PHF6 gene. We ascertained 19 individuals from 15 families with likely pathogenic or pathogenic PHF6 variants (11 males and 8 females). One ...

    Abstract Börjeson-Forssman-Lehmann syndrome (BFLS) is an X-linked intellectual disability syndrome caused by variants in the PHF6 gene. We ascertained 19 individuals from 15 families with likely pathogenic or pathogenic PHF6 variants (11 males and 8 females). One family had previously been reported. Six variants were novel. We analysed the clinical and genetic findings in our series and compared them with reported BFLS patients. Affected males had classic features of BFLS including intellectual disability, distinctive facies, large ears, gynaecomastia, hypogonadism and truncal obesity. Carrier female relatives of affected males were unaffected or had only mild symptoms. The phenotype of affected females with de novo variants overlapped with the males but included linear skin hyperpigmentation and a higher frequency of dental, retinal and cortical brain anomalies. Complications observed in our series included keloid scarring, digital fibromas, absent vaginal orifice, neuropathy, umbilical hernias, and talipes. Our analysis highlighted sex-specific differences in PHF6 variant types and locations. Affected males often have missense variants or small in-frame deletions while affected females tend to have truncating variants or large deletions/duplications. Missense variants were found in a minority of affected females and clustered in the highly constrained PHD2 domain of PHF6. We propose recommendations for the evaluation and management of BFLS patients. These results further delineate and extend the genetic and phenotypic spectrum of BFLS.
    MeSH term(s) Male ; Humans ; Female ; Intellectual Disability/genetics ; Mental Retardation, X-Linked/genetics ; Hypogonadism/genetics ; Hypogonadism/complications ; Hypogonadism/diagnosis ; Obesity/genetics
    Language English
    Publishing date 2023-09-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1141470-4
    ISSN 1476-5438 ; 1018-4813
    ISSN (online) 1476-5438
    ISSN 1018-4813
    DOI 10.1038/s41431-023-01447-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 3589: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article: Failure to Thrive: An Expanded Differential Diagnosis.

    Lazzara, Alexandra / Daymont, Carrie / Ladda, Roger / Lull, Jordan / Ficicioglu, Can / Cohen, Jennifer L / Aprile, Justen

    Journal of pediatric genetics

    2018  Volume 8, Issue 1, Page(s) 27–32

    Abstract: The patient is a term 6-month-old male, who presented with failure to thrive since birth. History was remarkable for suspected milk and soy protein allergy, gastroesophageal reflux, constipation, and abdominal distension that was present since birth. He ... ...

    Abstract The patient is a term 6-month-old male, who presented with failure to thrive since birth. History was remarkable for suspected milk and soy protein allergy, gastroesophageal reflux, constipation, and abdominal distension that was present since birth. He was losing weight despite oral intake of over 100 kcal/kg per day. Prior workup including laboratory studies, abdominal X-ray, upper gastrointestinal series with fluoroscopy, barium enema, and abdominal ultrasound were all within normal limits. The patient's history, diagnostic evaluation, and final diagnosis are revealed. This case highlights a rare condition presenting as failure to thrive, a common problem with a wide differential diagnosis.
    Language English
    Publishing date 2018-08-31
    Publishing country Germany
    Document type Case Reports
    ISSN 2146-4596
    ISSN 2146-4596
    DOI 10.1055/s-0038-1669445
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  5. Article ; Online: Case Report: Genetic analysis and anesthetic management of a child with Niemann-Pick disease Type A.

    Dalal, Priti G / Coleman, Melissa / Horst, Meagan / Rocourt, Dorothy / Ladda, Roger L / Janicki, Piotr K

    F1000Research

    2015  Volume 4, Page(s) 1423

    Abstract: A 14-month-old child, recently diagnosed with Niemann-Pick disease type A, presented for a laparoscopic placement of a gastrostomy tube under general anesthesia. The disease was confirmed and further characterized by genetic testing, which revealed ... ...

    Abstract A 14-month-old child, recently diagnosed with Niemann-Pick disease type A, presented for a laparoscopic placement of a gastrostomy tube under general anesthesia. The disease was confirmed and further characterized by genetic testing, which revealed evidence of the presence of two known pathogenic mutations in the SMPD1 gene, and enzyme studies showed a corresponding very low level of enzymatic activity of acidic sphingomyelinase. The anesthetic management involved strategies to manage an anticipated difficult intubation and avoid post-operative ventilation.
    Language English
    Publishing date 2015
    Publishing country England
    Document type Journal Article
    ZDB-ID 2699932-8
    ISSN 2046-1402 ; 2046-1402
    ISSN (online) 2046-1402
    ISSN 2046-1402
    DOI 10.12688/f1000research.7470.1
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: "Mosaic trachea" in a child with trisomy 9 mosaicism.

    Gniady, John P / Isaacson, Glenn / Ladda, Roger L

    International journal of pediatric otorhinolaryngology

    2010  Volume 74, Issue 10, Page(s) 1193–1195

    Abstract: Humans with mosaic karyotypes may present with milder forms of birth defects than one would see in non-mosaic individuals. Mosaicism may also affect tissues, resulting in different parts of an organ manifesting varied phenotypes. We present the case of a ...

    Abstract Humans with mosaic karyotypes may present with milder forms of birth defects than one would see in non-mosaic individuals. Mosaicism may also affect tissues, resulting in different parts of an organ manifesting varied phenotypes. We present the case of a child born with mosaic trisomy 9 and multiple congenital anomalies. Her trachea displays segmental abnormalities that suggest tissue mosaicism. We describe the endoscopic and cytogenetic findings in this child and propose a possible genetic mechanism to account for the unusual malformations.
    MeSH term(s) Abnormalities, Multiple/genetics ; Abnormalities, Multiple/pathology ; Chromosomes, Human, Pair 9/genetics ; Female ; Humans ; Infant, Newborn ; Mosaicism ; Trachea/abnormalities ; Trisomy/diagnosis
    Language English
    Publishing date 2010-10
    Publishing country Ireland
    Document type Case Reports ; Journal Article
    ZDB-ID 754501-0
    ISSN 1872-8464 ; 0165-5876
    ISSN (online) 1872-8464
    ISSN 0165-5876
    DOI 10.1016/j.ijporl.2010.07.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1507: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 134: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  7. Article ; Online: Clinical features, functional consequences, and rescue pharmacology of missense GRID1 and GRID2 human variants.

    Allen, James P / Garber, Kathryn B / Perszyk, Riley / Khayat, Cara T / Kell, Steven A / Kaneko, Maki / Quindipan, Catherine / Saitta, Sulagna / Ladda, Roger L / Hewson, Stacy / Inbar-Feigenberg, Michal / Prasad, Chitra / Prasad, Asuri N / Olewiler, Leah / Mu, Weiyi / Rosenthal, Liana S / Scala, Marcello / Striano, Pasquale / Zara, Federico /
    McCullock, Tyler W / Jauss, Robin-Tobias / Lemke, Johannes R / MacLean, David M / Zhu, Cheng / Yuan, Hongjie / Myers, Scott J / Traynelis, Stephen F

    Human molecular genetics

    2023  Volume 33, Issue 4, Page(s) 355–373

    Abstract: GRID1 and GRID2 encode the enigmatic GluD1 and GluD2 proteins, which form tetrameric receptors that play important roles in synapse organization and development of the central nervous system. Variation in these genes has been implicated in ... ...

    Abstract GRID1 and GRID2 encode the enigmatic GluD1 and GluD2 proteins, which form tetrameric receptors that play important roles in synapse organization and development of the central nervous system. Variation in these genes has been implicated in neurodevelopmental phenotypes. We evaluated GRID1 and GRID2 human variants from the literature, ClinVar, and clinical laboratories and found that many of these variants reside in intolerant domains, including the amino terminal domain of both GRID1 and GRID2. Other conserved regions, such as the M3 transmembrane domain, show different intolerance between GRID1 and GRID2. We introduced these variants into GluD1 and GluD2 cDNA and performed electrophysiological and biochemical assays to investigate the mechanisms of dysfunction of GRID1/2 variants. One variant in the GRID1 distal amino terminal domain resides at a position predicted to interact with Cbln2/Cbln4, and the variant disrupts complex formation between GluD1 and Cbln2, which could perturb its role in synapse organization. We also discovered that, like the lurcher mutation (GluD2-A654T), other rare variants in the GRID2 M3 domain create constitutively active receptors that share similar pathogenic phenotypes. We also found that the SCHEMA schizophrenia M3 variant GluD1-A650T produced constitutively active receptors. We tested a variety of compounds for their ability to inhibit constitutive currents of GluD receptor variants and found that pentamidine potently inhibited GluD2-T649A constitutive channels (IC50 50 nM). These results identify regions of intolerance to variation in the GRID genes, illustrate the functional consequences of GRID1 and GRID2 variants, and suggest how these receptors function normally and in disease.
    MeSH term(s) Humans ; Central Nervous System/metabolism ; Mutation ; Protein Domains ; Receptors, Glutamate/metabolism
    Chemical Substances glutamate receptor delta 2 ; Receptors, Glutamate ; GLUD1 protein, human (EC 1.4.1.3)
    Language English
    Publishing date 2023-11-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddad188
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 3469: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  8. Article ; Online: Tethered cord, corpus callosum abnormalities, and periventricular cysts in Wolf-Hirschhorn syndrome. Report of two cases and review of the literature.

    Verbrugge, Joel / Choudhary, Arabinda Kumar / Ladda, Roger

    American journal of medical genetics. Part A

    2009  Volume 149A, Issue 10, Page(s) 2280–2284

    Abstract: Wolf-Hirschhorn syndrome (4p-) is a rare disorder with characteristic physical findings. Neuroimaging findings are relatively scarce. We performed a literature search and found 22 reports of neuroimaging findings. We present findings in our two cases, ... ...

    Abstract Wolf-Hirschhorn syndrome (4p-) is a rare disorder with characteristic physical findings. Neuroimaging findings are relatively scarce. We performed a literature search and found 22 reports of neuroimaging findings. We present findings in our two cases, each with the previously unreported finding of a tethered cord. The most common abnormalities were of the corpus callosum, occurring in 71% of all cases. There appears to be a high association in the syndrome between corpus callosal abnormalities and periventricular cysts formation in the first year of life. These cysts eventually fuse with the frontal horns during late infancy with enlargement of the frontal horns. Absence of other causes for periventricular cyst formation, such as perinatal distress, prematurity, or cytomegalovirus infection, appears to strengthen the association. With further studies, neuroimaging findings may eventually assist in the diagnosis of patients with Wolf-Hirschhorn syndrome.
    MeSH term(s) Abnormalities, Multiple/diagnosis ; Agenesis of Corpus Callosum ; Brain Diseases/complications ; Brain Diseases/diagnosis ; Cysts/complications ; Cysts/diagnosis ; Female ; Humans ; Infant, Newborn ; Pregnancy ; Spinal Diseases/complications ; Spinal Diseases/diagnosis ; Umbilical Cord/abnormalities ; Wolf-Hirschhorn Syndrome/complications ; Wolf-Hirschhorn Syndrome/diagnosis
    Language English
    Publishing date 2009-09-11
    Publishing country United States
    Document type Case Reports ; Journal Article ; Review
    ZDB-ID 1493479-6
    ISSN 1552-4833 ; 1552-4825
    ISSN (online) 1552-4833
    ISSN 1552-4825
    DOI 10.1002/ajmg.a.33022
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  9. Article: Failure to Thrive: An Expanded Differential Diagnosis

    Lazzara, Alexandra / Daymont, Carrie / Ladda, Roger / Lull, Jordan / Ficicioglu, Can / Cohen, Jennifer L. / Aprile, Justen

    Journal of Pediatric Genetics

    2018  Volume 08, Issue 01, Page(s) 27–32

    Abstract: The patient is a term 6-month-old male, who presented with failure to thrive since birth. History was remarkable for suspected milk and soy protein allergy, gastroesophageal reflux, constipation, and abdominal distension that was present since birth. He ... ...

    Abstract The patient is a term 6-month-old male, who presented with failure to thrive since birth. History was remarkable for suspected milk and soy protein allergy, gastroesophageal reflux, constipation, and abdominal distension that was present since birth. He was losing weight despite oral intake of over 100 kcal/kg per day. Prior workup including laboratory studies, abdominal X-ray, upper gastrointestinal series with fluoroscopy, barium enema, and abdominal ultrasound were all within normal limits. The patient's history, diagnostic evaluation, and final diagnosis are revealed. This case highlights a rare condition presenting as failure to thrive, a common problem with a wide differential diagnosis.
    Keywords Wolman's disease ; failure to thrive
    Language English
    Publishing date 2018-08-31
    Publisher Georg Thieme Verlag KG
    Publishing place Stuttgart ; New York
    Document type Article
    ISSN 2146-460X ; 2146-4596
    ISSN (online) 2146-460X
    ISSN 2146-4596
    DOI 10.1055/s-0038-1669445
    Database Thieme publisher's database

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  10. Article ; Online: POLR1A variants underlie phenotypic heterogeneity in craniofacial, neural, and cardiac anomalies.

    Smallwood, Kelly / Watt, Kristin E N / Ide, Satoru / Baltrunaite, Kristina / Brunswick, Chad / Inskeep, Katherine / Capannari, Corrine / Adam, Margaret P / Begtrup, Amber / Bertola, Debora R / Demmer, Laurie / Demo, Erin / Devinsky, Orrin / Gallagher, Emily R / Guillen Sacoto, Maria J / Jech, Robert / Keren, Boris / Kussmann, Jennifer / Ladda, Roger /
    Lansdon, Lisa A / Lunke, Sebastian / Mardy, Anne / McWalters, Kirsty / Person, Richard / Raiti, Laura / Saitoh, Noriko / Saunders, Carol J / Schnur, Rhonda / Skorvanek, Matej / Sell, Susan L / Slavotinek, Anne / Sullivan, Bonnie R / Stark, Zornitza / Symonds, Joseph D / Wenger, Tara / Weber, Sacha / Whalen, Sandra / White, Susan M / Winkelmann, Juliane / Zech, Michael / Zeidler, Shimriet / Maeshima, Kazuhiro / Stottmann, Rolf W / Trainor, Paul A / Weaver, K Nicole

    American journal of human genetics

    2023  Volume 110, Issue 5, Page(s) 809–825

    Abstract: Heterozygous pathogenic variants in POLR1A, which encodes the largest subunit of RNA Polymerase I, were previously identified as the cause of acrofacial dysostosis, Cincinnati-type. The predominant phenotypes observed in the cohort of 3 individuals were ... ...

    Abstract Heterozygous pathogenic variants in POLR1A, which encodes the largest subunit of RNA Polymerase I, were previously identified as the cause of acrofacial dysostosis, Cincinnati-type. The predominant phenotypes observed in the cohort of 3 individuals were craniofacial anomalies reminiscent of Treacher Collins syndrome. We subsequently identified 17 additional individuals with 12 unique heterozygous variants in POLR1A and observed numerous additional phenotypes including neurodevelopmental abnormalities and structural cardiac defects, in combination with highly prevalent craniofacial anomalies and variable limb defects. To understand the pathogenesis of this pleiotropy, we modeled an allelic series of POLR1A variants in vitro and in vivo. In vitro assessments demonstrate variable effects of individual pathogenic variants on ribosomal RNA synthesis and nucleolar morphology, which supports the possibility of variant-specific phenotypic effects in affected individuals. To further explore variant-specific effects in vivo, we used CRISPR-Cas9 gene editing to recapitulate two human variants in mice. Additionally, spatiotemporal requirements for Polr1a in developmental lineages contributing to congenital anomalies in affected individuals were examined via conditional mutagenesis in neural crest cells (face and heart), the second heart field (cardiac outflow tract and right ventricle), and forebrain precursors in mice. Consistent with its ubiquitous role in the essential function of ribosome biogenesis, we observed that loss of Polr1a in any of these lineages causes cell-autonomous apoptosis resulting in embryonic malformations. Altogether, our work greatly expands the phenotype of human POLR1A-related disorders and demonstrates variant-specific effects that provide insights into the underlying pathogenesis of ribosomopathies.
    MeSH term(s) Humans ; Mice ; Animals ; Mandibulofacial Dysostosis/genetics ; Apoptosis ; Mutagenesis ; Ribosomes/genetics ; Phenotype ; Neural Crest/pathology ; Craniofacial Abnormalities/genetics ; Craniofacial Abnormalities/pathology
    Language English
    Publishing date 2023-04-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 219384-x
    ISSN 1537-6605 ; 0002-9297
    ISSN (online) 1537-6605
    ISSN 0002-9297
    DOI 10.1016/j.ajhg.2023.03.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 107: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top