scholarly journals Elevated serum transaminase activities were associated with increased serum levels of iron regulatory hormone hepcidin and hyperferritinemia risk

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Peng An ◽  
Hao Wang ◽  
Qian Wu ◽  
Xin Guo ◽  
Aimin Wu ◽  
...  



1986 ◽  
Vol 155 (2) ◽  
pp. 390-392 ◽  
Author(s):  
Frederik K. Lotgering ◽  
Jan Lind ◽  
Frans J.M. Huikeshoven ◽  
Henk C.S. Wallenburg


PEDIATRICS ◽  
1990 ◽  
Vol 86 (1) ◽  
pp. 87-90
Author(s):  
Halim M. Hennes ◽  
Douglas S. Smith ◽  
Kathleen Schneider ◽  
Mary A. Hegenbarth ◽  
Michael A. Duma ◽  
...  

The medical records of 43 hemodynamically stable children with elevated serum transaminase levels (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) who underwent abdominal computed tomographic (CT) scan for blunt abdominal trauma were reviewed. Nineteen patients (44.2%) had AST levels >450 IU/L and ALT levels >250 IU/L, and 17 of these 19 patients had hepatic injury identified on abdominal CT scan. Of the 43 patients, 25 (58.1%) had AST and ALT levels of less than 450 IU/L and 250 IU/L, respectively, and none of these patients had evidence of hepatic injury on CT scan. Elevated serum transaminase levels (AST >450 IU/L and ALT >250 IU/L) identified all of the patients with hepatic injury visible on abdominal CT scan. The sensitivity and specificity of elevated serum transaminase levels were 100% and 92.3%, respectively, for predicting hepatic injury. It is recommended that hemodynamically stable pediatric patients with blunt abdominal trauma and AST levels >450 IU/L and/or ALT levels >250 IU/L undergo abdominal CT scan to determine the presence and extent of hepatic injury. Children with serum transaminase levels below these values are at decreased risk of liver injury.



Author(s):  
Minae KOBAYASHI ◽  
Nobuo YAMADA ◽  
Hisao SHIBATA ◽  
Takashi NISHIKAWA


Author(s):  
Bianca Mages ◽  
Thomas Fuhs ◽  
Susanne Aleithe ◽  
Alexandra Blietz ◽  
Constance Hobusch ◽  
...  

AbstractIn the setting of ischemic stroke, the neurofilament subunit NF-L and the microtubule-associated protein MAP2 have proven to be exceptionally ischemia-sensitive elements of the neuronal cytoskeleton. Since alterations of the cytoskeleton have been linked to the transition from reversible to irreversible tissue damage, the present study investigates underlying time- and region-specific alterations of NF-L and MAP2 in different animal models of focal cerebral ischemia. Although NF-L is increasingly established as a clinical stroke biomarker, MAP2 serum measurements after stroke are still lacking. Therefore, the present study further compares serum levels of MAP2 with NF-L in stroke patients. In the applied animal models, MAP2-related immunofluorescence intensities were decreased in ischemic areas, whereas the abundance of NF-L degradation products accounted for an increase of NF-L-related immunofluorescence intensity. Accordingly, Western blot analyses of ischemic areas revealed decreased protein levels of both MAP2 and NF-L. The cytoskeletal alterations are further reflected at an ultrastructural level as indicated by a significant reduction of detectable neurofilaments in cortical axons of ischemia-affected areas. Moreover, atomic force microscopy measurements confirmed altered mechanical properties as indicated by a decreased elastic strength in ischemia-affected tissue. In addition to the results from the animal models, stroke patients exhibited significantly elevated serum levels of MAP2, which increased with infarct size, whereas serum levels of NF-L did not differ significantly. Thus, MAP2 appears to be a more sensitive stroke biomarker than NF-L, especially for early neuronal damage. This perspective is strengthened by the results from the animal models, showing MAP2-related alterations at earlier time points compared to NF-L. The profound ischemia-induced alterations further qualify both cytoskeletal elements as promising targets for neuroprotective therapies.



2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Danielle Perez-Bercoff ◽  
Hélène Laude ◽  
Morgane Lemaire ◽  
Oliver Hunewald ◽  
Valérie Thiers ◽  
...  

AbstractAPOBEC3 (A3) enzymes are best known for their role as antiviral restriction factors and as mutagens in cancer. Although four of them, A3A, A3B, A3F and A3G, are induced by type-1-interferon (IFN-I), their role in inflammatory conditions is unknown. We thus investigated the expression of A3, and particularly A3A and A3B because of their ability to edit cellular DNA, in Systemic Lupus Erythematosus (SLE), a chronic inflammatory disease characterized by high IFN-α serum levels. In a cohort of 57 SLE patients, A3A and A3B, but also A3C and A3G, were upregulated ~ 10 to 15-fold (> 1000-fold for A3B) compared to healthy controls, particularly in patients with flares and elevated serum IFN-α levels. Hydroxychloroquine, corticosteroids and immunosuppressive treatment did not reverse A3 levels. The A3AΔ3B polymorphism, which potentiates A3A, was detected in 14.9% of patients and in 10% of controls, and was associated with higher A3A mRNA expression. A3A and A3B mRNA levels, but not A3C or A3G, were correlated positively with dsDNA breaks and negatively with lymphopenia. Exposure of SLE PBMCs to IFN-α in culture induced massive and sustained A3A levels by 4 h and led to massive cell death. Furthermore, the rs2853669 A > G polymorphism in the telomerase reverse transcriptase (TERT) promoter, which disrupts an Ets-TCF-binding site and influences certain cancers, was highly prevalent in SLE patients, possibly contributing to lymphopenia. Taken together, these findings suggest that high baseline A3A and A3B levels may contribute to cell frailty, lymphopenia and to the generation of neoantigens in SLE patients. Targeting A3 expression could be a strategy to reverse cell death and the generation of neoantigens.



Endocrinology ◽  
2016 ◽  
Vol 158 (2) ◽  
pp. 419-430 ◽  
Author(s):  
Zhaofei Wu ◽  
M. Elena Martinez ◽  
Donald L. St. Germain ◽  
Arturo Hernandez

Abstract The role of thyroid hormones (THs) in the central regulation of energy balance is increasingly appreciated. Mice lacking the type 3 deiodinase (DIO3), which inactivates TH, have decreased circulating TH levels relative to control mice as a result of defects in the hypothalamic-pituitary-thyroid axis. However, we have shown that the TH status of the adult Dio3−/− brain is opposite that of the serum, exhibiting enhanced levels of TH action. Because the brain, particularly the hypothalamus, harbors important circuitries that regulate metabolism, we aimed to examine the energy balance phenotype of Dio3−/− mice and determine whether it is associated with hypothalamic abnormalities. Here we show that Dio3−/− mice of both sexes exhibit decreased adiposity, reduced brown and white adipocyte size, and enhanced fat loss in response to triiodothyronine (T3) treatment. They also exhibit increased TH action in the hypothalamus, with abnormal expression and T3 sensitivity of genes integral to the leptin-melanocortin system, including Agrp, Npy, Pomc, and Mc4r. The normal to elevated serum levels of leptin, and elevated and repressed expression of Agrp and Pomc, respectively, suggest a profile of leptin resistance. Interestingly, Dio3−/− mice also display elevated locomotor activity and increased energy expenditure. This occurs in association with expanded nighttime activity periods, suggesting a disrupted circadian rhythm. We conclude that DIO3-mediated regulation of TH action in the central nervous system influences multiple critical determinants of energy balance. Those influences may partially compensate each other, with the result likely contributing to the decreased adiposity observed in Dio3−/− mice.



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