Muscle inflammatory pattern in alpha- and gamma-sarcoglycanopathies

2021 ◽  
Author(s):  
Chiara Panicucci ◽  
Serena Baratto ◽  
Lizzia Raffaghello ◽  
Paola Tonin ◽  
Adele D’Amico ◽  
...  
Keyword(s):  
2018 ◽  
Vol Volume 13 ◽  
pp. 591-601 ◽  
Author(s):  
Luis Pérez de Llano ◽  
Borja G Cosío ◽  
Amanda Iglesias ◽  
Natividad de las Cuevas ◽  
Juan Jose Soler-Cataluña ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40523 ◽  
Author(s):  
Carlos Arterio Sorgi ◽  
Stephanie Rose ◽  
Nathalie Court ◽  
Daniela Carlos ◽  
Francisco Wanderley Garcia Paula-Silva ◽  
...  

2018 ◽  
Vol 76 (1) ◽  
pp. 2-5 ◽  
Author(s):  
Mariana Espinola-Nadurille ◽  
Paola Bautista-Gomez ◽  
Jose Flores ◽  
Veronica Rivas-Alonso ◽  
Rodrigo Perez-Esparza ◽  
...  

ABSTRACT Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is a form of autoimmune encephalopathy that presents with a wide variety of symptoms, including neuropsychiatric manifestations. The authors’ aim for this study was to analyze the results of paraclinical studies of patients with a diagnosis of anti-NMDAR encephalitis and the association between symptom onset and diagnosis, and start of immunotherapy. Retrospective data of 29 patients with anti-NMDAR encephalitis were gathered and analyzed. Abnormal EEG was found in 27 patients (93.1%), whereas MRI was abnormal in 19 patients (65.5%). In contrast, an inflammatory pattern on CSF analysis was found in only 13 patients (44.8%). The absence of pleocytosis or increased proteins in the CSF was associated with a longer time from symptom onset to diagnosis and treatment (p = 0.003). The authors conclude that noninflammatory CSF may delay the correct diagnosis and start of immunotherapy in anti-NMDAR encephalitis. In the presence of suggestive clinical features, extensive studies including EEG are recommended.


Author(s):  
Vincenzo Panichi ◽  
Sabrina Paoletti ◽  
Cristina Consani
Keyword(s):  

2014 ◽  
Vol 2 (3) ◽  
pp. 165 ◽  
Author(s):  
In Suk Sol ◽  
Yoon Hee Kim ◽  
Hee Seon Lee ◽  
Min Jung Kim ◽  
Yoon Ki Han ◽  
...  
Keyword(s):  

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Zeinab Shakeri ◽  
Parvin Mirmiran ◽  
Sajjad Khalili-Moghadam ◽  
Firoozeh Hosseini-Esfahani ◽  
Asal Ataie-Jafari ◽  
...  

Author(s):  
Celine Bergeron ◽  
Vasanthi Govindaraju ◽  
Annie Levesque ◽  
Sawsan Al Mot ◽  
Leo Cicoro ◽  
...  
Keyword(s):  

2020 ◽  
Vol 10 ◽  
pp. 204512532093792 ◽  
Author(s):  
Lucas Primo de Carvalho Alves ◽  
Neusa Sica da Rocha

Background Six melancholic features (MFs) of the Hamilton Depression Rating Scale (HAM-D6) represent the construct of melancholia along a continuum of severity (from least to most severe: depressed mood, work and activities, somatic symptoms, psychic anxiety, guilty feelings, psychomotor retardation). We aimed to evaluate the association between these MFs and inflammatory cytokines (IC) in the blood. Methods Each IC [interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), interleukin 2 (IL-2), IL-4, IL-6, IL-10, and IL-17] was associated with the HAM-D6 MFs of 139 severely depressed inpatients, using multiple linear regressions adjusted for covariates. Levels were compared with those of 100 healthy controls. Results Depressed mood was associated with higher levels of IL-4 ( β = 0.167; p = 0.041). Psychic anxiety: lower IL-17 levels ( β = –0.173; p = 0.039). Guilt feelings: lower IL-2 levels ( β = −0.168; p = 0.041) Psychomotor retardation: higher IL-6 levels ( β = 0.195; p = 0.017). Depressed patients’ TNF-α, INF-γ, and IL-4 levels were not significantly different from controls. Depressed patients’ IL-2, IL-6, IL-10, and IL-17 levels were higher than those of controls ( p <0.001). Conclusion Less severe MFs (depressed mood, psychic anxiety, and guilt feelings) were associated with an anti-inflammatory pattern (higher IL-4, lower IL-17 and lower IL-2, respectively). The presence of the most severe MF, psychomotor retardation, was associated with a higher pro-inflammatory response (higher IL-6).


2020 ◽  
Vol 21 (12) ◽  
pp. 4459 ◽  
Author(s):  
Andrea Baragetti ◽  
Alberico Luigi Catapano ◽  
Paolo Magni

Chronic low-grade inflammation, through the specific activation of the NACHT leucine-rich repeat- and PYD-containing (NLRP)3 inflammasome-interleukin (IL)-1β pathway, is an important contributor to the development of atherosclerotic cardiovascular disease (ASCVD), being triggered by intracellular cholesterol accumulation within cells. Within this pathological context, this complex pathway is activated by a number of factors, such as unhealthy nutrition, altered gut and oral microbiota, and elevated cholesterol itself. Moreover, evidence from autoinflammatory diseases, like psoriasis and others, which are also associated with higher cardiovascular disease (CVD) risk, suggests that variants of NLRP3 pathway-related genes (like NLRP3 itself, caspase recruitment domain-containing protein (CARD)8, caspase-1 and IL-1β) may carry gain-of-function mutations leading, in some individuals, to a constitutive pro-inflammatory pattern. Indeed, some reports have recently associated the presence of specific single nucleotide polymorphisms (SNPs) on such genes with greater ASCVD prevalence. Based on these observations, a potential effective strategy in this context may be the identification of carriers of these NLRP3-related SNPs, to generate a genomic score, potentially useful for a better CVD risk prediction, and, possibly, for personalized therapeutic approaches targeted to the NLRP3-IL-1β pathway.


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