Activity

The change in α-l-fucosidase activity in COVID-19 preceded the IgM and SAA and showed a preferable relation with glucometabolic disorders, which may be conducive to virus invasion or invoke an immune response against SARS-CoV-2.

The change in α-l-fucosidase activity in COVID-19 preceded the IgM and SAA and showed a preferable relation with glucometabolic disorders, which may be conducive to virus invasion or invoke an immune response against SARS-CoV-2.

We report a unique case of transient hyperphosphatasemia in a pediatric patient with a history of hepatic and skeletal abnormalities.

A 2-month old male was diagnosed with progressive familial intrahepatic cholestasis type-2 and osteoporosis after marked increases in liver function tests were noted at 1month of age. He underwent a second liver transplantation at 1 y. The increased liver function test trend resolved a few weeks post-transplantation. Four months after successful liver transplantation, unexplained significant increases in alkaline phosphatase (ALP) were observed, and they persisted for almost 9months. Among the etiologies under consideration for the isolated increased ALP activity were viral infections and macro-ALP.

A persistent trend in abnormally increased ALP for 9months was investigated leading to a confirmed diagnosis of transient hyperphosphatasemia (TH).

Pediatric post-liver transplant patients with skeletal and hepatic abnormalities including isolated markedly increased ALP activities represent a previously undescribed TH patient population. The 4.3% prevalence of TH in pediatric liver transplant recipients within our healthcare system is considerably higher than the previously reported prevalence of 2.1% for patients within the United States.

Pediatric post-liver transplant patients with skeletal and hepatic abnormalities including isolated markedly increased ALP activities represent a previously undescribed TH patient population. The 4.3% prevalence of TH in pediatric liver transplant recipients within our healthcare system is considerably higher than the previously reported prevalence of 2.1% for patients within the United States.

Mitochondrial DNA (mtDNA) resembles bacterial DNA and potentially triggers local and systemic inflammation. We evaluate the prognostic implications of PD effluent mtDNA level in peritoneal dialysis (PD) patients.

We measured mtDNA in the PD effluent (PDE) sediment and supernatant of 168 incident PD patients. All patients were followed for hospitalization, technique and overall survival.

The median PD effluent supernatant and sediment mtDNA levels were 255.4 unit (interquartile range [IQR] 157.5-451.3) and 201.6 unit (IQR 147.8-267.3), respectively. Serum C-reactive protein level closely with PDE sediment mtDNA level (r=0.471, p<0.001) and less with supernatant mtDNA level (r=0.156, p=0.044). PDE supernatant mtDNA level correlates with dialysate-to-plasma creatinine ratio at 4h (D/P4) (r=0.361, p<0.001) but not with any clinical outcome. PDE sediment mtDNA was an independent predictor of technique survival (p=0.011) and the duration of hospitalization (p=0.044) after adjusting for clinical confounding factors.

PDE sediment mtDNA level significantly correlated with systemic inflammation, while PDE supernatant mtDNA level correlated with peritoneal transport. PDE sediment mtDNA level also independently predicted technique survival and duration of hospitalization. GS-4997 manufacturer The mechanism of the different implications between PDE sediment and supernatant mtDNA levels deserves further investigations.

PDE sediment mtDNA level significantly correlated with systemic inflammation, while PDE supernatant mtDNA level correlated with peritoneal transport. PDE sediment mtDNA level also independently predicted technique survival and duration of hospitalization. The mechanism of the different implications between PDE sediment and supernatant mtDNA levels deserves further investigations.

Staphylococcus aureus (S. aureus) is the most common causative bacterial pathogen involved in promoting infection-induced osteomyelitis, a disease resulting in severe bone degradation. In this study, we aimed to identify the mechanism behind inhibition of osteoclast survival and differentiation by CHI3L1, a lectin previously reported to regulate S. aureus-induced osteomyelitis.

The role of CHI3L1 in osteoclast survival, proliferation, and differentiation was studied ex vivo using primary human bone marrow derived stem cells (HBMSCs) and transducing them with lentiviral expression vectors or shRNA knockdown constructs. Cell apoptosis was analyzed by flow cytometry using annexin V-fluorescein isothiocyanate/propidium iodide staining. Cell proliferation was assessed using alkaline phosphatase, Alcian Blue, and TRAP staining. The qRT-PCR was used to measure mRNA levels of osteoclast maturation markers, and western blotting was used to analyze protein expression. An in vivo murine model for osteomyelitis and mteomyelitis.This work presents a detailed and complete review of publications on pupillary light reflex (PLR) used to aid diagnoses. These are computational techniques used in the evaluation of pupillometry, as well as their application in computer-aided diagnoses (CAD) of pathologies or physiological conditions that can be studied by observing the movements of miosis and mydriasis of the human pupil. A careful survey was carried out of all studies published over the last 10 years which investigated, electronic devices, recording protocols, image treatment, computational algorithms and the pathologies related to PLR. We present the frontier of existing knowledge regarding methods and techniques used in this field of knowledge, which has been expanding due to the possibility of performing diagnoses with high precision, at a low cost and with a non-invasive method.Behçet disease (BD) is a complex, multi-systemic inflammatory condition mainly hallmarked by oral and genital ulcers which can also affect the vessels, gastrointestinal tract, central nervous system and even the axial skeleton. Without a clear classification among autoimmune or autoinflammatory conditions, BD has been recently classified as a MHC-I-opathy. BD aetiology is still obscure, but it is thought that certain microorganisms can elicit an aberrant adaptive immune response in the presence of a permissive genetic background. Altered T-cell homeostasis, mostly Th1/Th17 expansion and Treg impairment, could lead to an overactivation of the innate immunity, which underlies tissue damage and thus, signs and symptoms. Immunosuppression and/or immunomodulation are central to the BD management. A complex armamentarium ranging from classical synthetic disease-modifying antirrheumatic drugs to new-era biologic agents or small molecules is available in BD, with different therapeutic outcomes depending on disease manifestations.