Simple and Rapid HPLC-ICP-MS Method for the Simultaneous Determination of Cr(III) and Cr(VI) by Combining a 2,6-Pyridinedicarboxylic Acid Pre-Complexation Treatment.

A simple and rapid analytical method was developed for the simultaneous determination of two chromium species, Cr(III) and Cr(VI), in the environmental waters by high-performance liquid chromatography-inductively coupled plasma-mass spectrometry (HPLC-ICP-MS). This study incorporated a chelating pretreatment with 2,6-pyridinedicarboxylic acid (PDCA) to convert Cr(III) species into a stable Cr(III)-PDCA anion complex, which was then separated from Cr(VI) oxyanion using an anion exchange column. Building on the fundamental analytical approach proposed by Shigeta .

High-fat/high-sucrose diet results in a high rate of MASH with HCC in a mouse model of human-like bile acid composition.

Background: Wild-type (WT) mice fed a conventional high-fat/high-sucrose diet (HFHSD) rarely develop metabolic dysfunction-associated steatohepatitis (MASH) with HCC. Because mouse bile acid (BA) is highly hydrophilic, we hypothesized that making it hydrophobic would lead to MASH with HCC.

Methods: Eleven-week-old WT and Cyp2a12/Cyp2c70 double knockout (DKO) mice were divided into two groups, including one which was fed a normal chow diet, and one which was fed an HFHSD.

Cord Blood Transplantation Using Myeloablative Conditioning for Pediatric Advanced Myelodysplastic Syndrome in AMeD Syndrome With a Novel ADH5 Variant.

Aplastic anemia, mental retardation, and dwarfism syndrome (AMeDS) is a rare inherited bone marrow failure syndrome. Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only possible treatment option for hematological complications in AMeDS; however, there are no reports addressing allo-HSCT for AMeDS. A 6-year-old female diagnosed with AMeDS accompanying myelodysplastic syndrome with increased blast was successfully treated with cord blood transplantation followed by myeloablative conditioning (MAC).

Dopamine release and dopamine-related gene expression in the amygdala are modulated by the gastrin-releasing peptide in opposite directions during stress-enhanced fear learning and extinction.

Fear extinction leads to a decrease of originally acquired fear responses after the threat is no longer present. Fear extinction is adaptive and critical for organism's survival, but deficits in extinction may lead to exaggerated fear in animals or post-traumatic stress disorder (PTSD) in humans. Dopamine has recently emerged as essential for fear extinction and PTSD, however the neural circuits serving this dopamine function are only beginning to be investigated, and the dopamine intracellular signaling pathways are unknown.