Objective: To observe the changes in plasma S-100 beta and neuron-specific enolase (NSE) and to study their relationship with encephalopathy after orthotopic liver transplantation (OLT).
Methods: Thirty patients without neurological disease undergoing OLT were studied. Plasma S-100 beta and NSE were examined at three time points: after induction of anesthesia (T1), at the end of operation (T2) and 24 hours after reperfusion of the transplant (T3). The difference of plasma S-100 beta and NSE between encephalopathy group and non-encephalopathy group was analyzed.
Results: Eleven patients were complicated with encephalopathy after OLT. In 30 patients, S-100 beta at T2 [(3.715+/-1.523) microg/L] was higher than that at T1 [(1.478+/-0.809) microg/L, P<0.01]; S-100 beta at T3 [(1.765+/-0.894) microg/L] decreased to normal level (T1). NSE at T2 [(26.684+/-7.973) microg/L] was higher than that at T1 [(14.012+/-4.612) microg/L, P<0.01]. At T3, the level of plasma NSE [(18.105+/-7.345) microg/L] was decreased, but higher than that at T1. Plasma S-100 beta and NSE in encephalopathy group (11 cases) and non-encephalopathy group (19 cases) showed the same tendency of change as all of the patients. Plasma S-100 beta at T3 in encephalopathy group [(2.007+/-0.854)microg/L] was higher than that in non-encephalopathy group [(1.468+/-0.903) microg/L, P<0.05], and it was correlated with the presence of encephalopathy (r=0.385, P=0.039), but not at T1 and T2. Plasma NSE at three time points showed no relationship to the presence of encephalopathy.
Conclusion: The increase in plasma S-100 beta and NSE during OLT indicates the occurrence of damage to the brain. But plasma S-100 beta and NSE cannot predict encephalopathy after OLT.
Download full-text PDF |
Source |
---|
Int J Mol Sci
January 2025
School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.
The Receptor for Advanced Glycation End Products (RAGE), part of the immunoglobulin superfamily, plays a significant role in various essential functions under both normal and pathological conditions, especially in the progression of Alzheimer's disease (AD). RAGE engages with several damage-associated molecular patterns (DAMPs), including advanced glycation end products (AGEs), beta-amyloid peptide (Aβ), high mobility group box 1 (HMGB1), and S100 calcium-binding proteins. This interaction impairs the brain's ability to clear Aβ, resulting in increased Aβ accumulation, neuronal injury, and mitochondrial dysfunction.
View Article and Find Full Text PDFFluids Barriers CNS
January 2025
Sanders-Brown Center on Aging, College of Medicine, University of Kentucky, 760 Press Ave, 124 HKRB, Lexington, KY, 40536-0679, USA.
Background: Blood-brain barrier dysfunction is one characteristic of Alzheimer's disease (AD) and is recognized as both a cause and consequence of the pathological cascade leading to cognitive decline. The goal of this study was to assess markers for barrier dysfunction in postmortem tissue samples from research participants who were either cognitively normal individuals (CNI) or diagnosed with AD at the time of autopsy and determine to what extent these markers are associated with AD neuropathologic changes (ADNC) and cognitive impairment.
Methods: We used postmortem brain tissue and plasma samples from 19 participants: 9 CNI and 10 AD dementia patients who had come to autopsy from the University of Kentucky AD Research Center (UK-ADRC) community-based cohort; all cases with dementia had confirmed severe ADNC.
Arch Dermatol Res
January 2025
Department of Dermatology, Father Muller Medical College, Mangalore, India.
Vitiligo is a depigmenting disorder characterized by melanocyte loss, which results in pigment dilution of the skin. Vitiligo is commonly associated with thyroid disorders and thyroid stimulating hormone (TSH) is a sensitive marker to detect thyroid disorders. S100B is damage associated molecular pattern (DAMP) molecule released when there is melanocyte damage.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
January 2025
State Key Laboratory of Organ Failure Research, National Clinical Research Center of Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangdong Provincial Key Laboratory of Renal Failure Research, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China; Biobank of Peking University First Hospital, Peking University First Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University Health Science Center, Peking University, Beijing 100034, China. Electronic address:
A couple of S100 family proteins (S100s) have been reported to exert pro-inflammatory functions in the progression of renal fibrosis (RF). Unlike some S100s which are expressed by both epithelial and stromal inflammatory cells, S100A7 is restricted expressed in epithelium. Persistent S100A7 expression occurs in some invasive carcinomas and is associated with poor prognostic factors.
View Article and Find Full Text PDFBiomedicines
December 2024
Department of Clinical and Experimental Medicine, School and Operative Unit of Allergy and Clinical Immunology, University of Messina, 98125 Messina, Italy.
: In the world, approximately 1% of the population suffers from chronic spontaneous urticaria (CSU), burdening patients' quality of life and challenging clinicians in terms of treatment. Recent scientific evidence has unveiled the potential role of a family of molecules known as "alarmins" in the pathogenesis of CSU. : Papers focusing on the potential pathogenetic role of alarmins in CSU with diagnostic (as biomarkers) and therapeutic implications, in English and published in PubMed, Scopus, Web of Science, as well as clinical studies registered in ClinicalTrials.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!