A high-throughput method for the determination of 14 UV-filters in human plasma by LC-MS/MS: Minimize interferences from proteins and phospholipids in the matrix.

Accurate monitoring of UV-filters exposure levels in human plasma is a challenge because of the significant differences in the physicochemical properties of UV-filters, as well as the matrix effect caused by abundant proteins and phospholipids in plasma. Therefore, an effective and rapid method for simultaneous determination of 14 UV-filters in human plasma using protein precipitation-solid phase extraction (SPE) coupled with liquid chromatography tandem mass spectrometry (LC-MS/MS) was developed. Acetonitrile with 0.1 % formic acid and 10 % isopropanol (v/v) were used as mobile phases. A gradient elution on an ACQUITY UPLC BEH-C18 column at 30 °C and 0.3 mL/min flow rate was applied for separation. The electrospray ionization positive or negative modes were selected to determine the corresponding analyte to increase selectivity and sensitivity. Results showed that acetonitrile-tetrahydrofuran (v/v, 8:2) as the extraction solvent can effectively precipitate protein in plasma and improve the solubility of UV-filters. The HybridSPE cartridge improved the removal efficiency of phospholipids, while 1 mL of methanol elution increased the extraction recoveries of targets. Fourteen UV-filters achieved good linearities, low detection limits (0.050 to 0.10 µg/L) and quantification limits (0.10 to 1.0 µg/L). Method accuracy and precision, extraction recoveries, and storage stabilities of all analytes met the criterion of 80-120 %. Moreover, this method was successfully applied for the determination of UV-filters in plasma randomly collected from adults. Nine of 14 UV-filters were determined and their concentrations were distributed widely, suggesting a big variation of individual UV-filters exposure.

The Pathogenesis and Treatment of Cardiovascular Autonomic Dysfunction in Parkinson's Disease: What We Know and Where to Go.

Cardiovascular autonomic dysfunctions (CAD) are prevalent in Parkinson's disease (PD). It contributes to the development of cognitive dysfunction, falls and even mortality. Significant progress has been achieved in the last decade. However, the underlying mechanisms and effective treatments for CAD have not been established yet. This review aims to help clinicians to better understand the pathogenesis and therapeutic strategies. The literatures about CAD in patients with PD were reviewed. References for this review were identified by searches of PubMed between 1972 and March 2021, with the search term "cardiovascular autonomic dysfunctions, postural hypotension, orthostatic hypotension (OH), supine hypertension (SH), postprandial hypotension, and nondipping". The pathogenesis, including the neurogenic and non-neurogenic mechanisms, and the current pharmaceutical and non-pharmaceutical treatment for CAD, were analyzed. CAD mainly includes four aspects, which are OH, SH, postprandial hypotension and nondipping, among them, OH is the main component. Both non-neurogenic and neurogenic mechanisms are involved in CAD. Failure of the baroreflex circulate, which includes the lesions at the afferent, efferent or central components, is an important pathogenesis of CAD. Both non-pharmacological and pharmacological treatment alleviate CAD-related symptoms by acting on the baroreflex reflex circulate. However, pharmacological strategy has the limitation of failing to enhance baroreflex sensitivity and life quality. Novel OH treatment drugs, such as pyridostigmine and atomoxetine, can effectively improve OH-related symptoms via enhancing residual sympathetic tone, without adverse reactions of supine hypertension. Baroreflex impairment is a crucial pathological mechanism associated with CAD in PD. Currently, non-pharmacological strategy was the preferred option for its advantage of enhancing baroreflex sensitivity. Pharmacological treatment is a second-line option. Therefore, to find drugs that can enhance baroreflex sensitivity, especially via acting on its central components, is urgently needed in the scientific research and clinical practice.

Tumor-forming plasmacytoid dendritic cells in acute myelocytic leukemia: a report of three cases and literature review.

Plasmacytoid dendritic cells (PDCs), through their production of type I interferons (IFNs) and other pro-inflammatory cytokines, link the innate and adaptive immunity, and provide anti-viral resistance. It is reported PDCs accumulated in inflammatory and human neoplasms, including hematopoietic malignancies. To date, the clinical significance of tumor-forming PDCs (TF-PDCs) in AML is largely unknown. Here, we designed an integral scheme using flow cytometry, by which we accurately have detected the TF-PDCs in cases of AML. Combined the case characters and progress, we suggested that: TF-PDCs in AML maybe originate from the bone marrow mononuclear precursor cells, so it often associated with mononuclear line-related myeloid tumors; the accumulation of PDCs indicated highly aggressive tumor with poor progress and probably potential myelodysplasia or dysplasia.