Vacciniumchaozhouense (Ericaceae), a new species from East Guangdong, China.

Vacciniumchaozhouense (Ericaceae), a new species from East Guangdong Province, China is described and illustrated. This new species is morphologically similar to V.wrightii by having flowers with persistent and leaf-like bracts, long pedicels, and white spherical-urceolate corollas, but is distinguished by having glandular trichomes on the abaxial surface of the leaf blade, shorter pedicels, sparsely pilose corolla ridges, and anther thecae longer than the tubules. A key to the new species and morphologically similar species is also provided.

Estrogen regulates duodenal glucose absorption by affecting estrogen receptor-α on glucose transporters.

The mechanisms of estrogen in glucose metabolism are well established; however, its role in glucose absorption remains unclear. In this study, we investigated the effects of estrogen on glucose absorption in humans, mice, and SCBN intestinal epithelial cells. We first observed a correlation between estrogen and blood glucose in young women and found that glucose tolerance was significantly less in the premenstrual phase than in the preovulatory phase. Similarly, with decreased serum estradiol levels in ovariectomized mice, estrogen receptors alpha (ERα) and beta (ERß) in the duodenum were reduced, and weight and abdominal fat increased significantly. The expression of sodium/glucose cotransporter 1 (SGLT1) and glucose transporter 2 (GLUT2) and glucose absorption in the duodenum decreased significantly. Estrogen significantly upregulated SGLT1 and GLUT2 expression in SCBN cells. Silencing of ERα, but not ERß, reversed this trend, suggesting that ERα may be key to estrogen-regulating glucose transporters. A mechanistic study revealed that downstream, estrogen regulates the protein kinase C (PKC) pathway. Overall, our findings indicate that estrogen promotes glucose absorption, and estrogen and ERα deficiency can inhibit SGLT1 and GLUT2 expression through the PKC signaling pathway, thereby reducing glucose absorption.

The role of Nod-like receptor protein 3 inflammasome activated by ion channels in multiple diseases.

The inflammasome is a multimeric protein complex located in the cytoplasm that is activated by many factors and subsequently promotes the release of proinflammatory factors such as interleukin (IL)-1ß and IL-18, resulting in a series of inflammatory responses that ultimately lead to the occurrence of various diseases. The Nod-like receptor protein 3 (NLRP3) inflammasome is the most characteristic type and the most widely studied among many inflammasomes. Activation of the NLRP3 inflammasome is closely related to the occurrence of many diseases, such as Alzheimer's disease. At present, a large number of studies have focused on the mechanisms underlying the activation of the NLRP3 inflammasome. Plenty of articles have reported the activation of the NLRP3 inflammasome by various ions, such as K+ and Na+ reflux and Ca2+ influx. However, few articles have reviewed the effects of various ion channels on the activation of the NLRP3 inflammasome and the relationship between the diseases caused by these proteins. This article mainly summarizes the relationship between intracellular and extracellular ion activities and ion channels and the activation of the NLRP3 inflammasome. We also provide a general summary of the diseases of each system caused by NLRP3 activation. We hope that more research will provide options for the treatment of diseases driven by the NLRP3 inflammasome.

The role of Chemerin in human diseases.

Chemerin is a protein encoded by the Rarres2 gene that acts through endocrine or paracrine regulation. Chemerin can bind to its receptor, regulate insulin sensitivity and adipocyte differentiation, and thus affect glucose and lipid metabolism. There is growing evidence that it also plays an important role in diseases such as inflammation and cancer. Chemerin has been shown to play a role in the pathogenesis of inflammatory and metabolic diseases caused by leukocyte chemoattractants in a variety of organs, but its biological function remains controversial. In conclusion, the exciting findings collected over the past few years clearly indicate that targeting Chemerin signaling as a biological target will be a major research goal in the future. This article reviews the pathophysiological roles of Chemerin in various systems and diseases,and expect to provide a rationale for its role as a clinical therapeutic target.

The role of ion channels in immune-related diseases.

Ion channel is an integral membrane protein that allows the permeation of charge ions across hydrophobic phospholipid membranes, including plasma membranes and organelle membranes (such as mitochondria, endoplasmic reticulum and vacuoles), which are widely distributed in various cells and tissues, such as cardiomyocytes, smooth muscle cells, and nerve cells. Ion channels establish membrane potential by regulating ion concentration and membrane potential. Membrane potential plays an important role in cells. Studies have shown that ion channels play a role in a number of immune-related diseases caused by functional defects in ion channels on immune or non-immune cells in major human organs, usually affecting specific organs or multiple organs. The present review discusses the relationship between ion channels and immune diseases in major organs of the human body.

Effects of Ion-Transporting Proteins on the Digestive System Under Hypoxia.

Hypoxia refers to a state of oxygen limitation, which mainly mediates pathological processes in the human body and participates in the regulation of normal physiological processes. In the hypoxic environment, the main regulator of human body homeostasis is the hypoxia-inducible factor family (HIF). HIF can regulate the expression of many hypoxia-induced genes and then participate in various physiological and pathological processes of the human body. Ion-transporting proteins are extremely important types of proteins. Ion-transporting proteins are distributed on cell membranes or organelles and strictly control the inflow or outflow of ions in cells or organelles. Changes in ions in cells are often closely related to extensive physiological and pathological processes in the human body. Numerous studies have confirmed that hypoxia and its regulatory factors can regulate the transcription and expression of ion-transporting protein-related genes. Under hypoxic stress, the regulation and interaction of ion-transporting proteins by hypoxia often leads to diseases of various human systems and even tumors. Using ion-transporting proteins and hypoxia as targets to explore the mechanism of digestive system diseases and targeted therapy is expected to become a new breakthrough point.

Exosome-mediated effects and applications in inflammatory diseases of the digestive system.

Exosomes are membranous vesicles containing RNA and proteins that are specifically secreted in vivo. Exosomes have many functions, such as material transport and signal transduction between cells. Many studies have proven that exosomes can not only be used as biomarkers for disease diagnosis but also as carriers to transmit information between cells. Exosomes participate in a variety of physiological and pathological processes, including the immune response, antigen presentation, cell migration, cell differentiation, and tumour development. Differences in exosome functions depend on cell type. In recent years, exosome origin, cargo composition, and precise regulatory mechanisms have been the focus of research. Although exosomes have been extensively reported in digestive tumours, few articles have reviewed their roles in inflammatory diseases of the digestive system, especially inflammatory-related diseases (such as reflux oesophagitis, gastritis, inflammatory bowel disease, hepatitis, and pancreatitis). This paper briefly summarizes the roles of exosomes in inflammatory diseases of the digestive system to provide a basis for research on the mechanism of inflammatory diseases of the digestive system targeted by exosomes.

Beneficial effects of dietary capsaicin in gastrointestinal health and disease.

Chili pepper and its major active compound capsaicin have long been used not only a daily food additive but also medication worldwide. Like in other human organs and systems, capsaicin has multiple actions in gastrointestinal (GI) physiology and pathology. Numerous studies have revealed that capsaicin acts on GI tract in TRPV1-dependent and -independent manners, mostly depending on its consumption concentrations. In this review, we will focus on the beneficial role of capsaicin in GI tract, a less highlighted aspect, in particular how dietary capsaicin affects GI health, the mechanisms of actions and its preventive/therapeutic potentials to several GI diseases. Dietary capsaicin affects GI tract not only via TRPV1-derpendent and independent manners, but also via acute and chronic effects. Although high dose intake of dietary capsaicin is harmful to human health sometimes, current literatures suggest that appropriate dose intake is likely beneficial to GI health and is preventive/therapeutic to GI disease in most cases as well. With extensive and intensive studies on its GI actions, capsaicin, as a daily consumed food additive, has potential to become a safe drug for the treatment of several GI diseases.

Sensitization of Mn2+ luminescence via efficient energy transfer to suit the application of high color rendering WLEDs.

Developing novel luminescent materials with ideal properties is an endless project, urged by growing requirements of advances in energy saving, healthy lighting and environmental friendliness. Herein, a series of ScCaOBO3:Ce3+,Mn2+ phosphors with excellent luminescence properties were synthesized by the high temperature solid state method. X-ray diffraction was applied to analyse the phase composition of the obtained phosphors. The morphology and dopant distribution were observed by scanning electron microscopy (SEM) and energy dispersive spectrometry (EDS), respectively. The Rietveld refinements and luminescence spectra indicate that Ce3+ preferentially occupies the Sc3+ site and produces a blue emission band at around 460 nm, which originates from the characteristic 5d-4f transitions, while Mn2+ preferentially occupies the Ca2+ site and emits red light due to its characteristic 4T1(4G)-6A1(6S) transitions. Upon excitation at 354 nm, both Ce3+ and Mn2+ emissions can be obtained and further investigations evidenced that the broad and intense light emission of Mn2+ located in the red spectral region is the result of energy transfer from Ce3+ to Mn2+. Theoretical calculations reveal that the energy transfer process from Ce3+ to Mn2+ is of the resonance type and is governed by electric dipole-dipole interactions. Since the ScCaOBO3:Ce3+,Mn2+ phosphors are capable of producing broadband emissions that widely cover the blue and red spectral regions, the introduction of a green light-emitting phosphor CMA:Tb3+ can conveniently generate high quality white light. Therefore, a white light-emitting diode device with extremely high color rendering indices, Ra = 93.7 and R9 = 91.9, was successfully obtained.

Radiofrequency ablation of intubation granulomas.

OBJECTIVE: We explored the outcomes and voice parameters of patients undergoing plasma radiofrequency (RF) ablation to treat intubation granulomas. STUDY DESIGN: Prospective case series. METHODS AND MATERIALS: Patients with intubation granulomas who met the inclusion criteria underwent RF ablation. The complete remission rate and voice function were evaluated preoperatively and at 6 months postoperatively. RESULTS: We enrolled 13 patients with 25 intubation granulomas. The mean time between intubation and initial diagnosis was 38.6 days and that between intubation and surgical diagnosis was 2.7 months. All 25 granulomas were successfully removed and histologically confirmed. No surgical remnant was evident on the vocal folds and complete glottal closure was observed at 2 weeks postoperatively. No recurrence or RF ablation-related complications were observed during the 6-month follow-up. The complete remission rate was 100% (13/13). In addition, the mean hoarseness, roughness, breathiness, asthenia, and strain (GRBAS) scores, and the maximum phonation time (MPT), improved significantly after treatment (all P < 0.05). CONCLUSIONS: RF ablation is effective and safe for patients with intubation granulomas who failed medical management or request the procedure. In this study, the complete resolution rate was high and voice restoration outcomes were good.

Pathophysiologic Role of Neurotransmitters in Digestive Diseases.

Neurotransmitters are special molecules that serve as messengers in chemical synapses between neurons, cells, or receptors, including catecholamines, serotonin, dopamine, and other neurotransmitters, which play an important role in both human physiology and pathology. Compelling evidence has indicated that neurotransmitters have an important physiological role in various digestive diseases. They act as ligands in combination with central or peripheral receptors, and transmits signals through chemical synapses, which are involved in regulating the physiological and pathological processes of the digestive tract organs. For instance, neurotransmitters regulate blood circulation and affect intestinal movement, nutrient absorption, the gastrointestinal innate immune system, and the microbiome. In this review, we will focus on the role of neurotransmitters in the pathogenesis of digestive tract diseases to provide novel therapeutic targets for new drug development in digestive diseases.

Effects of calcium­permeable ion channels on various digestive diseases in the regulation of autophagy (Review).

Autophagy is a process of degradation and catabolism in cells. By removing damaged or dysfunctional organelles, autophagy interacts with the ubiquitin­proteasome degradation system to jointly regulate cell function and energy homeostasis. Since autophagy plays a key role in physiology, disorders of the autophagy mechanism are associated with various diseases. Therefore, thorough understanding of the autophagy regulatory mechanism are crucially important in the diagnosis and treatment of diseases. To date, ion channels may affect the development and treatment of diseases by regulating autophagy, especially calcium­permeable ion channels, in the process of digestive system diseases. However, the mechanism by which calcium ions and their channels regulate autophagy is still poorly understood, thus emphasizing the need for further research in this field. The present review intends to discuss the association, mechanism and application of calcium ions, their channels and autophagy in the occurrence and development of digestive system diseases.

Disorder-Induced Broadband Near-Infrared Persistent and Photostimulated Luminescence in Mg2SnO4:Cr3.

Materials with near-infrared (NIR) persistent luminescence (PersL) and NIR-to-NIR photostimulated luminescence (PSL) properties are attractive platforms for photonic energy harvesting and release. In this work, we develop Mg2SnO4:Cr as a broadband NIR PersL and NIR-to-NIR PSL material (luminescence maxima at ∼800 nm) and reveal the origin of the PersL and PSL properties. The material has an inverse spinel structure with the Mg2+ and Sn4+ disorder at the Wyckoff 16d site based on the Rietveld refinement. Cr K-edge X-ray absorption near-edge structure (XANES) spectra uncover that the doped Cr ions have a +3 valence state and occupy the disordered (Mg,Sn) site with octahedral coordination. The disorder results in multiple Cr3+ centers, and the broadband luminescence originates from the 4T2(4F) → 4A2 transition of Cr3+ at sites with intermediate crystal field strength. The distribution of trap depths is continuous according to the analysis of thermoluminescence (TL) spectra using the initial rising method, which relates to the random distribution of Mg2+ and Sn4+ at the second coordination sphere of the Cr3+ centers rather than the oxygen-related defects. Stimulating the material with a NIR laser, the NIR PersL gets significantly enhanced due to a PSL process. The broadband PersL and PSL are detectable beyond 100 h and have good tissue penetrability and therefore the developed Mg2SnO4:Cr3+ has potential in applications of optical information storage/reading and autofluorescence-free bioimaging. Finally, three crystal and electronic structure factors are proposed for screening new Cr3+-activated PersL and PSL materials.

Characterization of intestinal microbiota and fecal cortisol, T3, and IgA in forest musk deer (Moschus berezovskii) from birth to weaning.

Analysis of the intestinal microbiota and physiological parameters in mammalian infancy can reveal health status. In this study, we used a combination of molecular and immunochemical approaches to assess fecal microbiota as well as Cortisol (Cor), Triiodothyronine (T3), and immunoglobulin A (IgA) levels of young forest musk deer (FMD), from birth to one month after weaning (7 days of age-110 days of age). During development as the diet of FMD changes from consuming milk to eating plants, the richness and diversity of intestinal microbiota of young FMD increased significantly. Cor levels remained unchanged throughout early development while significantly increased after weaning, T3 and IgA initially were derived from milk during lactation, significantly decreased after weaning. Correlation network analysis showed that the community of food-oriented microbes were highly structured and that many genera were correlated. Overall, this study provides scientific insights into effective management strategies for the protection of FMD population.

Pathophysiological Role of Purinergic P2X Receptors in Digestive System Diseases.

P2X receptors (P2XRs) are trimeric, non-selective cation channels activated by extracellular ATP and widely distributed in the digestive system. P2XRs have an important role in the physiological function of the digestive system, such as neurotransmission, ion transports, proliferation and apoptosis, muscle contraction, and relaxation. P2XRs can be involved in pain mechanisms both centrally and in the periphery and confirmed the association of P2XRs with visceral pain. In the periphery, ATP can be released as a result of tissue injury, visceral distension, or sympathetic activation and can excite nociceptive primary afferents by acting at homomeric P2X(3)R or heteromeric P2X(2/3)R. Thus, peripheral P2XRs, and homomeric P2X(3) and/or heteromeric P2X(2/3)R in particular, constitute attractive targets for analgesic drugs. Recently studies have shown that P2XRs have made significant advances in inflammation and cancer. P2X7R mediates NLRP3 inflammasome activation, cytokine and chemokine release, T lymphocyte survival and differentiation, transcription factor activation, and cell death. The P2X7R is a potent stimulant of inflammation and immunity and a promoter of cancer cell growth. This makes P2X7R an appealing target for anti-inflammatory and anti-cancer therapy. It is believed that with the further study of P2XRs and its subtypes, P2XRs and its specific antagonists will be expected to be widely used in the treatment of human digestive diseases in the future.

Role of gut microbiota via the gut-liver-brain axis in digestive diseases.

The gut-brain axis is a bidirectional information interaction system between the central nervous system (CNS) and the gastrointestinal tract, in which gut microbiota plays a key role. The gut microbiota forms a complex network with the enteric nervous system, the autonomic nervous system, and the neuroendocrine and neuroimmunity of the CNS, which is called the microbiota-gut-brain axis. Due to the close anatomical and functional interaction of the gut-liver axis, the microbiota-gut-liver-brain axis has attracted increased attention in recent years. The microbiota-gut-liver-brain axis mediates the occurrence and development of many diseases, and it offers a direction for the research of disease treatment. In this review, we mainly discuss the role of the gut microbiota in the irritable bowel syndrome, inflammatory bowel disease, functional dyspepsia, non-alcoholic fatty liver disease, alcoholic liver disease, cirrhosis and hepatic encephalopathy via the gut-liver-brain axis, and the focus is to clarify the potential mechanisms and treatment of digestive diseases based on the further understanding of the microbiota-gut- liver-brain axis.

Advances in Ca2+ modulation of gastrointestinal anion secretion and its dysregulation in digestive disorders (Review).

Intracellular calcium (Ca2+) is a critical cell signaling component in gastrointestinal (GI) physiology. Cytosolic calcium ([Ca2+]cyt), as a secondary messenger, controls GI epithelial fluid and ion transport, mucus and neuropeptide secretion, as well as synaptic transmission and motility. The key roles of Ca2+ signaling in other types of secretory cell (including those in the airways and salivary glands) are well known. However, its action in GI epithelial secretion and the underlying molecular mechanisms have remained to be fully elucidated. The present review focused on the role of [Ca2+]cyt in GI epithelial anion secretion. Ca2+ signaling regulates the activities of ion channels and transporters involved in GI epithelial ion and fluid transport, including Cl- channels, Ca2+-activated K+ channels, cystic fibrosis (CF) transmembrane conductance regulator and anion/HCO3 - exchangers. Previous studies by the current researchers have focused on this field over several years, providing solid evidence that Ca2+ signaling has an important role in the regulation of GI epithelial anion secretion and uncovering underlying molecular mechanisms. The present review is largely based on previous studies by the current researchers and provides an overview of the currently known molecular mechanisms of GI epithelial anion secretion with an emphasis on Ca2+-mediated ion secretion and its dysregulation in GI disorders. In addition, previous studies by the current researchers demonstrated that different regulatory mechanisms are in place for GI epithelial HCO3 - and Cl- secretion. An increased understanding of the roles of Ca2+ signaling and its targets in GI anion secretion may lead to the development of novel strategies to inhibit GI diseases, including the enhancement of fluid secretion in CF and protection of the GI mucosa in ulcer diseases.

Dynamic changes in intestinal microbiota in young forest musk deer during weaning.

Weaning is an important event for all mammals, including young forest musk deer. However, weaning stress may cause intestinal microbiota-related disorders. Therefore, high-throughput 16S rRNA gene sequencing was applied to study the dynamic changes in intestinal microbiota during pre-weaning (10 days before weaning) and post-weaning (10 days after weaning) in 15 young forest musk deer. We saw that intestinal microbiota diversity in the post-weaning period was significantly higher than that in the pre-weaning period. The most dominant bacterial phyla were similar in the two groups (Firmicutes, Bacteroidetes and Verrucomicrobia). Meanwhile, we applied Linear discriminant analysis effect size (LefSe) to identify the most differentially microbial taxa in the pre-weaning and post-weaning groups. In the post-weaning forest musk deer, the relative abundance of Actinobacteria, Spirochaetes, Ruminococcaceae_UCG-005, Treponema and Prevotella was higher than in the pre-weaning group. However, higher relative abundance of the phyla Bacteroidetes was found in the pre-weaning group compared with that in the post-weaning group. In summary, this research provides a theoretical foundation for the dynamics of young forest musk deer intestinal microbiota during the weaning transition, which may benefit in understanding the growth and health of forest musk deer.

Plasma membrane Ca2+-permeable channels and sodium/calcium exchangers in tumorigenesis and tumor development of the upper gastrointestinal tract.

The upper gastrointestinal (GI) tumors are multifactorial diseases associated with a combination of oncogenes and environmental factors. Currently, surgery, chemotherapy, radiotherapy and immunotherapy are relatively effective treatment options for the patients with these tumors. However, the asymptomatic phenotype of these tumors during the early stages poses as a significant limiting factor to diagnosis and often renders treatments ineffective. Therefore, new early diagnosis and effective therapy for upper GI tumors are urgently needed. Ca2+ is a pivotal intracellular second messenger and plays a crucial role in living cells by regulating several processes from cell division to death. The aberrant Ca2+ homeostasis is related to many human pathological conditions and diseases, including cancer, and thus the changes in the expression and function of plasma membrane Ca2+ permeable channels and sodium/calcium exchangers are frequently described in tumorigenesis and tumor development of the upper GI tract, including voltage-gated Ca2+ channels (VGCC), transient receptor potential (TRP) channels, store-operated channels (SOC) and Na+/Ca2+ exchanger (NCX). This review will summarize the current knowledge about plasma membrane Ca2+ permeable channels and sodium/calcium exchangers in the upper GI tumors and provide a synopsis of recent advancements on the role and involvement of these channels in upper GI tumors as well as a discussion of the possible strategies to target these channels and exchangers for diagnosis and therapy of the upper GI tumors.

A simple and selective UHPLC-MS/MS method for quantification of plantagoguanidinic acid in rat plasma and its application to a pharmacokinetic study.

A simple, sensitive and specific UHPLC-MS/MS method for quantification of plantagoguanidinic acid (PGA) in rat plasma was applied to investigate the pharmacokinetic behavior in vivo, using protopine as internal standard. The chromatography was separated on a Phenomenex® Luna-C18 column (2.1 × 150 mm, 3.0 µm) within 7.0 min using a mobile phase consisting of acetonitrile-0.1% formic acid solution under gradient elution at a flow rate of 0.4 mL/min. Prepared samples were monitored by multiple reaction monitoring mode, with the target fragmentions m/z 226.2 → 84.2 for PGA and m/z 354.2 → 188.9 for IS in positive electrospray ionization. The calibration curve of PGA was linear throughout the range 1-1000 ng/mL (r = 0.9962). The lower limit of quantitation in plasma for PGA was 0.1 ng/mL, and the recovery was >88.6%. Intra- and interday accuracy ranged from -8.6 to 4.9%. Furthermore, this validated method was successfully used for a pre-clinical pharmacokinetic study of PGA at a single dose of 20 and 5 mg/kg in rats via oral and intravenous administration. The study showed that PGA was absorpted rapidly and eliminated gradually with a greater absolute oral bioavailability of 70.1% in rats.