A novel enzymatic method for isolation of plastic particles from human blood.

Microplastic particles have been detected in the human body. This study aimed to develop a blood digestion method that preserves microplastics during analysis. Acidic and alkaline reagents, commonly used for isolating plastic particles from organic materials, were tested on human blood samples and microplastics.

A Coupled Global Atmosphere-Ocean Model for Air-Sea Exchange of Mercury: Insights into Wet Deposition and Atmospheric Redox Chemistry.

Air-sea exchange of mercury (Hg) is the largest flux between Earth system reservoirs. Global models simulate air-sea exchange based either on an atmospheric or ocean model simulation and treat the other media as a boundary condition. Here we develop a new modeling capability (NJUCPL) that couples GEOS-Chem (atmospheric model) and MITgcm (ocean model) at the native hourly model time step.

Familial Sinus Node Disease Caused by a Gain of GIRK (G-Protein Activated Inwardly Rectifying K Channel) Channel Function.

Background: Inherited forms of sinus node dysfunction (SND) clinically include bradycardia, sinus arrest, and chronotropic incompetence and may serve as disease models to understand sinus node physiology and impulse generation. Recently, a gain-of-function mutation in the G-protein gene GNB2 led to enhanced activation of the GIRK (G-protein activated inwardly rectifying K channel). Thus, human cardiac GIRK channels are important for heart rate regulation and subsequently, genes encoding their subunits Kir3.

The Impact of the Major Baltic Inflow of December 2014 on the Mercury Species Distribution in the Baltic Sea.

The Baltic Sea is a marginal sea characterized by stagnation periods of several years. Oxygen consumption in its deep waters leads to the buildup of sulfide from sulfate reduction. Some of the microorganisms responsible for these processes also transform reactive ionic mercury to neurotoxic methylmercury.

A Mutation in the G-Protein Gene Causes Familial Sinus Node and Atrioventricular Conduction Dysfunction.

Rationale: Familial sinus node and atrioventricular conduction dysfunction is a rare disorder that leads to paroxysmal dizziness, fatigue, and syncope because of a temporarily or permanently reduced heart rate. To date, only a few genes for familial sinus and atrioventricular conduction dysfunction are known, and the majority of cases remain pathogenically unresolved.

Objective: We aim to identify the disease gene in a large 3-generation family (n=25) with autosomal dominant sinus node dysfunction (SND) and atrioventricular block (AVB) and to characterize the mutation-related pathomechanisms in familial SND+AVB.