11 research outputs found
Author Correction: AHR is a Zika virus host factor and a candidate target for antiviral therapy
No full textFil: Giovannoni, Federico. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Estrategias Antivirales; Argentina. CONICET-Instituto de Química Biológica; Argentina.Fil: Bosch, Irene. Massachusetts Institute of Technology. Institute for Medical Engineering and Science; Estados Unidos. Mount Sinai School of Medicine. Department of Medicine; Estados Unidos.Fil: Manganeli Polonio, Carolina. University of São Paulo. Immunology Department-ICB IV. Neuroimmune Interactions Laboratory; Brasil. University of São Paulo. Scientific Platform Pasteur-USP; Brasil.Fil: Torti, María F. University of São Paulo. Immunology Department-ICB IV. Neuroimmune Interactions Laboratory; Brasil. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Estrategias Antivirales; Argentina. CONICET-Instituto de Química Biológica; Argentina.Fil: Wheeler, Michael A. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Li, Zhaorong. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Romorini, Leonardo. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina.Fil: Rodríguez Varela, María Soledad. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina.Fil: Rothhammer, Veit. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Barroso, Andreia. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Tjon, Emily C. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Sanmarco, Liliana M. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Takenaka, Maisa C. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Sadegh Modaresi, Seyed Mohamad. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Gutiérrez-Vázquez, Cristina. Harvard Medical School. Brigham and Women's Hospital. Ann Romney Center for Neurologic Diseases; Estados Unidos.Fil: Ghabdan Zanluqui, Nágela. University of São Paulo. Scientific Platform Pasteur-USP; Brasil. University of São Paulo. School of Medicine. Immunopathology and Allergy Post Graduate Program; Brasil.Fil: Barreto Dos Santos, Nilton. University of São Paulo. Institute of Biomedical Science. Department of Pharmacology; Brasil.Fil: Demarchi Munhoz, Carolina. University of São Paulo. Institute of Biomedical Science. Department of Pharmacology; Brasil.Fil: Wang, Zhongyan. Boston University School of Public Health. Dept. of Environmental Health; Estados Unidos.Fil: Damonte, Elsa B. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Estrategias Antivirales; Argentina. CONICET-Instituto de Química Biológica; Argentina
Author Correction: Control of tumor-associated macrophages and T cells in glioblastoma via AHR and CD39
No full textRecruitment of the multiple sclerosis cohort within the European Mobilise-D clinical validation study—lessons learnt, baseline demographics and clinical characteristics
No full text\ua9 The Author(s) 2026. Background: Multiple sclerosis (MS) is a common cause of disability in working age adults. Current clinical assessments are inadequate at disability assessment or predicting clinically relevant outcomes. Loss of mobility is an important functional disability to people with MS. Mobilise-D aims to develop, validate, and implement a digital mobility solution which measures unsupervised mobility performance across several chronic conditions, including MS, using a single wearable device. Methods: Six hundred two adults with MS, an Expanded Disability Status Scale (EDSS) score of 3.0–6.5, documented disability worsening over the previous 2 years and a 30-day freedom from relapses, were recruited across four European centres. Results: Of 1416 invited, 602 participants (42%) were recruited. Primary recruitment sources were clinicians (42%) and local registries (42%). Among 616 who declined screening, the main reasons were a lack of interest (44%), the time commitment (25%) or the travel involved (13%). Participants had a mean age of 52 years; 64% were female, with a median EDSS score of 5.0. Of those, 56% had relapsing-remitting MS, 33% secondary progressive MS and 10% primary progressive MS. Falls occurred in 58% of participants in the 12 months prior to recruitment. Of those recruited, 556 (93%) participants had valid mobility data recorded. Conclusions: The longitudinal collection of clinical and unsupervised mobility assessments will provide a comprehensive dataset, allowing for the determination of digital mobility assessments’ construct validity, predictive capacity, responsiveness, and clinical meaningfulness. Novel insights into real-world mobility that describe both walking activity and gait outcomes will be gained. Trial registration: The study was registered at the ISRCTN registry on 12/10/2020, titled “Clinical validation of a mobility monitor to measure and predict health outcomes” (ISRCTN Number: 12051706)
Update on the diagnosis and treatment of neuromyelitis optica spectrum disorders (NMOSD) – revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part II: Attack therapy and long-term management
No full textInternational audienceThis manuscript presents practical recommendations for managing acute attacks and implementing preventive immunotherapies for neuromyelitis optica spectrum disorders (NMOSD), a rare autoimmune disease that causes severe inflammation in the central nervous system (CNS), primarily affecting the optic nerves, spinal cord, and brainstem. The pillars of NMOSD therapy are attack treatment and attack prevention to minimize the accrual of neurological disability. Aquaporin-4 immunoglobulin G antibodies (AQP4-IgG) are a diagnostic marker of the disease and play a significant role in its pathogenicity. Recent advances in understanding NMOSD have led to the development of new therapies and the completion of randomized controlled trials. Four preventive immunotherapies have now been approved for AQP4-IgG-positive NMOSD in many regions of the world: eculizumab, ravulizumab - most recently-, inebilizumab, and satralizumab. These new drugs may potentially substitute rituximab and classical immunosuppressive therapies, which were as yet the mainstay of treatment for both, AQP4-IgG-positive and -negative NMOSD. Here, the Neuromyelitis Optica Study Group (NEMOS) provides an overview of the current state of knowledge on NMOSD treatments and offers statements and practical recommendations on the therapy management and use of all available immunotherapies for this disease. Unmet needs and AQP4-IgG-negative NMOSD are also discussed. The recommendations were developed using a Delphi-based consensus method among the core author group and at expert discussions at NEMOS meetings
Correction to: Mobilise-D insights to estimate real-world walking speed in multiple conditions with a wearable device (Scientific Reports, (2024), 14, 1, (1754), 10.1038/s41598-024-51766-5)
No full text\ua9 The Author(s) 2024.Correction to: Scientific Reportshttps://doi.org/10.1038/s41598-024-51766-5, published online 19 January 2024 The original version of this Article contained an error in Figure 7 where an incorrect reference was cited for one of the recommended algorithms for Gait Speed Detection (GSD). The original Figure 7 and accompanying legend appear below. (Figure presented.) Overview over the diferent algorithmic steps of the analytical pipeline with short explanations of the intermediate and fnal outputs of each of the algorithmic blocks; gait sequence detection (GSD), initial contact detection (ICD), cadence estimation (CAD) and stride length estimation (SL). Te algorithm column indicates the used algorithms for the two pipelines P1 (HA, COPD, CHF). (MS, PD, PFF) and P2 (MS, PD, PFF) Short citations for the algorithms are provided below the fgure. For more details see Table 1 in26. In addition, the Supplementary Information 1 file published with this Article contained errors in Tables 1 and 2. The Intraclass Correlation Coefficients (ICCs) for walking speed were incorrectly reported instead of the correct ICC values for stride length and cadence. The original Supplementary Information 1 file is provided below. The original Article and the Supplementary Information 1 file that accompanies the original Article have been corrected
Cutaneous malignant melanoma: Update on diagnostic and prognostic biomarkers
No full textThe incidence of cutaneous malignant melanoma has rapidly increased in recent years in all parts of the world, and melanoma is a leading cause of cancer death. As even relatively small melanomas may have metastatic potential, accurate assessment of progression is critical. Although diagnosis of cutaneous malignant melanoma is usually based on histopathologic criteria, these criteria may at times be inadequate in differentiating melanoma from certain types of benign nevi. As for prognosis, tumor (Breslow) thickness, mitotic rate, and ulceration have been considered the most important prognostic indicators among histopathologic criteria. However, there are cases of thin primary melanomas that have ultimately developed metastases despite complete excision. Given this, an accurate assessment of melanoma progression is critical, and development of molecular biomarkers that identify high-risk melanoma in its early phase is urgently needed. Large-scale genomic profiling has identified considerable heterogeneity in melanoma and suggests subgrouping of tumors by patterns of gene expression and mutation will ultimately be essential to accurate staging. This subgrouping in turn may allow for more targeted therapy. 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The Transcriptomic and Genomic Analysis of Lamin A/C Expression in the Colon and in Colorectal Cancer
No full textLamins A and C, also known as A-type lamins, are type V nuclear intermediate filament proteins which form an interlacing meshwork of filaments subjacent to the inner nuclear membrane termed the nuclear lamina. A-type lamins have been implicated in DNA replication, gene transcription regulation, apoptosis, regulation of growth promoters and nuclear migration. Traditionally, expression of A-type lamins has been associated with differentiated cells. As such, mutations in A-type lamins have been associated with a diverse range of genetic diseases, including premature ageing syndromes and with increased proliferation, especially in tumours.
In colorectal cancer, expression of A-type lamins, have been shown to impart an adverse prognosis. In order to understand the underlying biological processes responsible for this adverse outcome in patients with colorectal cancer, I sought to clarify the expression profile of A-type lamins and their binding partners in normal colonic/rectal mucosa, prior to investigating the expression of A-type lamins in colorectal cancers. I used fresh tissue specimens obtained from patients with colorectal cancer for my experiments. A unique finding was the expression of lamin A in the putative stem cell niche of colonic / rectal mucosal crypts.
Further studies in the form of a microarray analysis, revealed a very complex picture of up regulation involving various signalling cascades in the cancer samples expressing A-type lamins. There was no evidence to suggest a direct involvement of A-type lamins influencing the Wnt signalling cascade, however, direct involvement of other signalling cascades, such as the IGF signalling cascade, Shh signalling cascade and TGF-β signalling cascades were noted. These signalling cascades were known to influence the Wnt signalling cascades and hence could play a crucial role in the pathogenesis of colorectal cancers expressing A-type lamins.
In addition to these important signalling cascades, other key genes involved in apoptosis, growth promoters, cell adhesion, stem cell regulation, oncogenes and tumour suppression, were noted to have a unique expression profile in the cancer sample expressing A-type lamins, not observed in the cancer sample lacking A-type lamin expression. These observations were suggestive of A-type lamins having a diverse range of actions via, as yet, undefined pathways. It would appear that A-type lamins were imparting a more motile, less adherent phenotype with stem cell like features in colorectal cancers expressing A-type lamins. This could explain the observed poor prognosis of patients with colorectal cancers expressing A-type lamins.
Creatine kinase brain (CKB), was also identified as an additional, potential, prognostic indicator in the Duke’s B group of patients with colorectal cancer expressing A-type lamins. This potential marker, in conjunction with A-type lamin expression could be used to identify a sub group of Duke’s B patients at high risk. Whether adjuvant therapy in this group would help improve their long term survival is unknown since no study has been done to assess this
Nonrandom Factors In Modern Human Morphological Diversification: A Study Of Craniofacial Variation In Southern South American Populations
No full textThe causes of craniofacial variation among human populations have been the subject of controversy. In this work, we studied aboriginal populations from southern South America, the last continental region peopled by humans and with a wide range of ecological conditions. Because of these characteristics, southern South America provides a unique opportunity to study the relative importance of random and nonrandom factors in human diversification. Previous craniometric studies recognized remarkable differences among populations from this region, usually resorting to random factors as the main explanation. In contrast, here we suggest, using tests based on quantitative genetic models, that: (1) the rate of craniofacial divergence among these populations is too high and (2) the patterns of variation within and between populations are too different to be explained by genetic drift alone. In addition, the among-sample craniofacial variation is correlated with climate and diet but not with mtDNA variation. We suggest that the influence of nonrandom factors (e.g., plasticity, selection) on human craniofacial diversification in regions with large ecological variation is more important than generally acknowledged and capable to generate large craniofacial divergence in a short period of time. These results bring nonrandom factors into focus for the interpretation of human craniofacial variation. © 2009 The Author(s).634978993Ackermann, R.R., Cheverud, J.M., Discerning evolutionary processes in patterns of tamarin (genus Saguinus) craniofacial variation (2002) Am. J. Phys. Anthropol., 117, pp. 260-271Ackermann, R.R., Cheverud, J.M., Detecting genetic drift versus selection in human evolution (2004) Proc. Natl. Acad. Sci. USA, 101, pp. 17946-17951Adams, D.C., Rohlf, F.J., Slice, D.E., Geometric morphometrics: Ten years of progress following the 'revolution.' (2004) Ital. J. 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Correction to: Update on the diagnosis and treatment of neuromyelitis optica spectrum disorders (NMOSD) – revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part II: Attack therapy and long-term management
No full textDyadic Coping of NMOSD and MOGAD patients and their partners: a sociological and psychological examination of strategies (CoMMOnsense-Study)
No full textBackground Neuromyelitis optica spectrum disorders (NMOSD) and myelin oligodendrocyte glycoprotein antibody-associated diseases (MOGAD) impose psychological burdens on patients. Chronic illnesses create challenges for both patients and their partners, who also play a crucial role in managing disease-related stress. Despite its relevance, little is known about the role of dyadic coping (DC) in these conditions. This study investigates DC in NMOSD and MOGAD, aiming to provide clinical recommendations.Methods The CoMMOnsense-Study is a cross-sectional, prospective study of 59 NMOSD and 50 MOGAD patients and their respective partners, recruited from 15 centres of the German Neuromyelitis Optica Study Group registry. Participants completed self-report questionnaires on DC, depression, anxiety and quality of relationship. Correlation analyses were performed to compare findings based on antibody status. Subsequently, multivariate regression analyses were conducted to identify relevant predictors of DC.Results Patients with NMOSD and MOGAD demonstrated higher levels of depressive symptoms (NMOSD: p=0.007; MOGAD: p=0.023) and stress communication scores (NMOSD: p=0.022; MOGAD: p=0.013) than their partners. Negative coping was low across all subgroups (Stanine 1). Despite high DC and relationship quality, discrepancies were observed in the coping perceptions between partners.Conclusions Coping is highly shared within partnerships affected by NMOSD and MOGAD, while discrepancies in coping perceptions and protective buffering suggest the presence of unfavourable coping mechanisms. Reducing protective buffering and illness-related distortions shows potential areas for enhancing DC
