scholarly journals Role of the clinical immunology laboratory in disease monitoring

2013 ◽  
Vol 3 (2) ◽  
pp. 18 ◽  
Author(s):  
John Maher
1978 ◽  
Vol 16 (1) ◽  
pp. 263-285 ◽  
Author(s):  
H C Young ◽  
J M Prescott ◽  
E E Saari
Keyword(s):  

Gut ◽  
2013 ◽  
Vol 62 (12) ◽  
pp. 1806-1816 ◽  
Author(s):  
Jose-Manuel Benitez ◽  
Marie-Alice Meuwis ◽  
Catherine Reenaers ◽  
Catherine Van Kemseke ◽  
Paul Meunier ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Kai-Uwe Jarr ◽  
Manfred Nelles ◽  
Hugo A. Katus ◽  
Emmanuel Chorianopoulos

Background. TNF-like weak inducer of apoptosis (TWEAK) has been reported to predict mortality in patients with dilated cardiomyopathy. However, whether it can be used as a biomarker for disease monitoring or rather represents a risk factor for disease progression remains unclear.Aim of the Study. To evaluate the potential of sTWEAK as a biomarker in patients with dilated cardiomyopathy.Results. We conducted a serial study of sTWEAK levels in 78 patients with dilated cardiomyopathy. Soluble TWEAK levels predicted not only a combined mortality/heart transplantation endpoint after 4 years (P=0.0001), but also the risk for clinical deterioration (P=0.0001). Compared to NT-proBNP, sTWEAK remained relatively stable in individual patients on follow-up indicating that inter- rather than intraindividual differences in sTWEAK levels predicted outcome. Finally, neither did the scavenger receptor sCD163 correlate with sTWEAK levels nor did its determination add additional information on outcome in patients with dilated cardiomyopathy.Conclusion. Soluble TWEAK levels in patients with dilated cardiomyopathy may not be of value for disease monitoring but may represent a risk factor for disease progression and death. Further research will be necessary to elucidate the exact role of sTWEAK as a potential modulator of immune response in the setting of dilated cardiomyopathy.


2021 ◽  
Vol 27 ◽  
Author(s):  
Adil A. Sayyed ◽  
Piyush Gondaliya ◽  
Palak Bhat ◽  
Mukund Mali ◽  
Neha Arya ◽  
...  

: The discovery of miRNAs has been one of the revolutionary developments and has led to the advent of new diagnostic and therapeutic opportunities for the management of cancer. In this regard, miRNA dysregulation has been shown to play a critical role in various stages of tumorigenesis, including tumor invasion, metastasis as well as angiogenesis. Therefore, miRNA profiling can provide accurate fingerprints for the development of diagnostic and therapeutic platforms. This review discusses the recent discoveries of miRNA-based tools for early detection of cancer as well as disease monitoring in cancers that are common, like breast, lung, hepatic, colorectal, oral and brain cancer. Based on the involvement of miRNA in different cancers as oncogenic miRNA or tumor suppressor miRNA, the treatment with miRNA inhibitors or mimics is recommended. However, the stability and targeted delivery of miRNA remain the major limitations of miRNA delivery. In relation to this, several nanoparticle-based delivery systems have been reported which have effectively delivered the miRNA mimics or inhibitors and showed the potential for transforming these advanced delivery systems from bench to bedside in the treatment of cancer metastasis and chemoresistance. Based on this, we attempted to uncover recently reported advanced nanotherapeutic approaches to deliver the miRNAs in the management of different cancers.


2021 ◽  
pp. 135245852110391
Author(s):  
Gianmarco Abbadessa ◽  
Luigi Lavorgna ◽  
Constantina Andrada Treaba ◽  
Simona Bonavita ◽  
Caterina Mainero

Background: A growing body of evidence has shed light on the role of the hemostatic pathway and its components in the pathogenesis of multiple sclerosis (MS), particularly in enhancing and sustaining neuroinflammation. Objective: To review the clinical, experimental, and neuroimaging evidence supporting the role of different components of the hemostatic pathway in the pathogenesis of neuroinflammation in MS and discuss their translational potential as disease biomarkers and therapeutic targets. Methods: A literature search for most relevant articles from 1956 to 2020 was conducted in PubMed and Scopus. Results: Hemostasis components appear to be involved in different key events of neuroinflammation in MS including mononuclear cell diapedesis, microglia activation, and neuronal damage. Conclusion: The findings on the interplay between hemostatic and thrombotic molecular pathways in the pathogenesis of neuroinflammation in MS open new opportunities for developing novel biomarkers for disease monitoring and prognosis, as well as novel therapeutic targets.


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