Unexpected antibody against the high-prevalence P antigen before cardiac surgery.

P is a high-prevalence antigen present in 99.9 percent of the population and is fully developed at birth. P- individuals form naturally occurring antibodies against P, which are often of immunoglobulin (Ig)M and/or IgG type, very potent in complement activation, and able to cause serious intravascular hemolytic transfusion reactions.

Soluble mannose receptor induces proinflammatory macrophage activation and metaflammation.

Proinflammatory activation of macrophages in metabolic tissues is critically important in the induction of obesity-induced metaflammation. Here, we demonstrate that the soluble mannose receptor (sMR) plays a direct functional role in both macrophage activation and metaflammation. We show that sMR binds CD45 on macrophages and inhibits its phosphatase activity, leading to an Src/Akt/NF-κB-mediated cellular reprogramming toward an inflammatory phenotype both in vitro and in vivo.

Prevalence of viral hepatitis B and C in Sierra Leone-current knowledge and knowledge gaps: a narrative review.

There are no comprehensive data on viral hepatitis from Sierra Leone; however, a huge disease burden has been observed in different subpopulations. This review summarizes available data on hepatitis B and C virus (HBV and HCV) prevalence in Sierra Leone and identifies knowledge gaps. Despite the non-uniformity of the studies and the lack of systematic case recording, different reports published in recent decades yielded a hepatitis B prevalence of 8.

The helminth glycoprotein omega-1 improves metabolic homeostasis in obese mice through type 2 immunity-independent inhibition of food intake.

Type 2 immunity plays an essential role in the maintenance of metabolic homeostasis and its disruption during obesity promotes meta-inflammation and insulin resistance. Infection with the helminth parasite Schistosoma mansoni and treatment with its soluble egg antigens (SEA) induce a type 2 immune response in metabolic organs and improve insulin sensitivity and glucose tolerance in obese mice, yet, a causal relationship remains unproven. Here, we investigated the effects and underlying mechanisms of the T2 ribonuclease omega-1 (ω1), one of the major S mansoni immunomodulatory glycoproteins, on metabolic homeostasis.

Schistosoma haematobium infection is associated with lower serum cholesterol levels and improved lipid profile in overweight/obese individuals.

Infection with parasitic helminths has been reported to improve insulin sensitivity and glucose homeostasis, lowering the risk for type 2 diabetes. However, little is known about its impact on whole-body lipid homeostasis, especially in obese individuals. For this purpose, a cross-sectional study was carried out in lean and overweight/obese adults residing in the Lambaréné region of Gabon, an area endemic for Schistosoma haematobium.

Focused Assessment with Sonography for Urinary Schistosomiasis (FASUS)-pilot evaluation of a simple point-of-care ultrasound protocol and short training program for detecting urinary tract morbidity in highly endemic settings.

Background: Urogenital schistosomiasis (UGS) causes inflammation and fibrosis of the urinary tract. In resource-limited settings, affordable tools for morbidity assessment in clinical care are needed. Point-of-care ultrasound has not yet been validated for UGS-related pathology.

Determination of Adenine Nucleotide Concentrations in Cells and Tissues by High-Performance Liquid Chromatography.

The serine/threonine AMP-activated protein kinase (AMPK) is a central player in the regulation of energy homeostasis, and its activity is tightly controlled, among other mechanisms, by subtle changes in cellular adenine nucleotide levels. In this chapter, we describe a step-by-step protocol for rapid, highly sensitive, reproducible, and simultaneous determination of ATP, ADP, and AMP concentrations in cell or tissue samples by reversed-phase high-performance liquid chromatography (HPLC).

Chronic helminth infection and helminth-derived egg antigens promote adipose tissue M2 macrophages and improve insulin sensitivity in obese mice.

Chronic low-grade inflammation associated with obesity contributes to insulin resistance and type 2 diabetes. Helminth parasites are the strongest natural inducers of type 2 immune responses, and short-lived infection with rodent nematodes was reported to improve glucose tolerance in obese mice. Here, we investigated the effects of chronic infection (12 weeks) with Schistosoma mansoni, a helminth that infects millions of humans worldwide, on whole-body metabolic homeostasis and white adipose tissue (WAT) immune cell composition in high-fat diet-induced obese C57BL/6 male mice.

The insulin sensitizing effect of topiramate involves KATP channel activation in the central nervous system.

Background And Purpose: Topiramate improves insulin sensitivity, in addition to its antiepileptic action. However, the underlying mechanism is unknown. Therefore, the present study was aimed at investigating the mechanism of the insulin-sensitizing effect of topiramate both in vivo and in vitro.

A novel dominant hyperekplexia mutation Y705C alters trafficking and biochemical properties of the presynaptic glycine transporter GlyT2.

Hyperekplexia or startle disease is characterized by an exaggerated startle response, evoked by tactile or auditory stimuli, producing hypertonia and apnea episodes. Although rare, this orphan disorder can have serious consequences, including sudden infant death. Dominant and recessive mutations in the human glycine receptor (GlyR) α1 gene (GLRA1) are the major cause of this disorder.

Cell surface turnover of the glutamate transporter GLT-1 is mediated by ubiquitination/deubiquitination.

The main glutamate transporter in the brain, GLT-1, mediates glutamatergic neurotransmission in both physiological and pathological conditions. GLT-1 activity is controlled by both constitutive and regulated trafficking, and although recent evidence indicates that the turnover of this protein in the plasma membrane is accelerated by protein kinase C via an ubiquitin-dependent process, the mechanisms driving the constitutive trafficking of GLT-1 remain unexplored. Here, we used a heterologous system and primary astrocytes to investigate the turnover of GLT-1 and the role of ubiquitin attachment in this process.

Protein kinase C (PKC)-promoted endocytosis of glutamate transporter GLT-1 requires ubiquitin ligase Nedd4-2-dependent ubiquitination but not phosphorylation.

Glutamate transporter-1 (GLT-1) is the main glutamate transporter in the central nervous system, and its concentration severely decreases in neurodegenerative diseases. The number of transporters in the plasma membrane reflects the balance between their insertion and removal, and it has been reported that the regulated endocytosis of GLT-1 depends on its ubiquitination triggered by protein kinase C (PKC) activation. Here, we identified serine 520 of GLT-1 as the primary target for PKC-dependent phosphorylation, although elimination of this serine did not impair either GLT-1 ubiquitination or endocytosis in response to phorbol esters.

Splice variants of the glutamate transporter GLT1 form hetero-oligomers that interact with PSD-95 and NMDA receptors.

The glutamate transporter GLT1 is expressed in at least two isoforms, GLT1a and GLT1b, which differ in their C termini. As GLT1 is an oligomeric protein, we have investigated whether GLT1a and GLT1b might associate as hetero-oligomers. Differential tagging (HA-GLT1a and YFP-GLT1b) revealed that these isoforms form complexes that could be immunoprecipitated when co-expressed in heterologous systems.

PKC-dependent endocytosis of the GLT1 glutamate transporter depends on ubiquitylation of lysines located in a C-terminal cluster.

The activity of the main glutamate transporter in the CNS, GLT1, can be regulated by protein kinase C (PKC). It is known that activation of PKC by phorbol esters promotes the clathrin-dependent internalization of the transporter, followed by its lysosomal degradation. However, the molecular mechanisms that link PKC activation and the internalization of GLT1 are not fully understood.

The glutamate transporter GLT1b interacts with the scaffold protein PSD-95.

The glutamate transporter (GLT1) regulates glutamate concentrations in glutamatergic synapses and it is expressed in at least two isoforms, GLT1a and GLT1b. In this work, we show that the C-terminus of GLT1b is able to interact with the PDZ domains of a number of proteins. Notably, one of them might be the scaffold protein post-synaptic density (PSD-95).