Characteristics of white matter alterations along fibres in patients with bulimia nervosa: A combined voxelwise and tractography study.

Accumulating evidence supports the hypothesis that white matter (WM) abnormalities are involved in the pathophysiology of bulimia nervosa (BN); however, findings from in vivo neuroimaging studies have been inconsistent. We aimed to investigate the possible brain WM alterations, including WM volume and microstructure, in patients with BN. We recruited 43 BN patients and 31 healthy controls (HCs). All participants underwent structural and diffusion tensor imaging. Differences in WM volume and microstructure were evaluated using voxel-based morphometry, tract-based spatial statistics, and automated fibre quantification analysis. Compared with HCs, BN patients showed significantly decreased fractional anisotropy in the middle part of the corpus callosum (nodes 31-32) and increased mean diffusivity in the right cranial nerve V (CN V) (nodes 27-33 and nodes 55-88) and vertical occipital fasciculus (VOF) (nodes 58-85). Moreover, we found decreased axial diffusivity in the right inferior fronto-occipital fasciculus (node 67) and increased radial diffusivity in the CN V (nodes 22-34 and nodes 52-89) and left VOF (nodes 60-66 and nodes 81-85). Meanwhile, WM microstructural changes were correlated with patients' clinical manifestations. We did not find any significant differences in WM volume and the main WM fibre bundle properties between BN patients and HCs. Taken together, these findings provide that BN shows significant brain WM reorganization, but primarily in microstructure (part of WM fibre bundle), which is not sufficient to cause changes in WM volume. The automated fibre quantification analysis could be more sensitive to detect the subtle pathological changes in a point or segment of the WM fibre bundle.

Uncovering neural pathways underlying bulimia nervosa: resting-state neural connectivity disruptions correlate with maladaptive eating behaviors.

PURPOSE: Bulimia nervosa (BN) is characterized by recurrent binge-eating episodes and inappropriate compensatory behaviors. This study investigated alterations in resting-state surface-based neural activity in BN patients and explored correlations between brain activity and eating behavior. METHODS: A total of 26 BN patients and 28 healthy controls were enrolled. Indirect measurement of cerebral cortical activity and functional connectivity (FC) analyses were performed in Surfstat. A principal component analysis (PCA) model was used to capture the commonalities within the behavioral questionnaires from the BN group. RESULTS: Compared with the healthy control group, the BN group showed decreased surface-based two-dimensional regional homogeneity in the right superior parietal lobule (SPL). Additionally, the BN group showed decreased FC between the right SPL and the bilateral lingual gyrus and increased FC between the right SPL and the left caudate nucleus and right putamen. In the FC-behavior association analysis, the second principal component (PC2) was negatively correlated with FC between the right SPL and the left caudate nucleus. The third principal component (PC3) was negatively correlated with FC between the right SPL and the left lingual gyrus and positively correlated with FC between the right SPL and the right lingual gyrus. CONCLUSION: We revealed that the right SPL undergoes reorganization with respect to specific brain regions at the whole-brain level in BN. In addition, our results suggest a correlation between brain reorganization and maladaptive eating behavior. These findings may provide useful information to better understand the neural mechanisms of BN. LEVEL OF EVIDENCE: V, descriptive study.

Divergent Syntheses of Spiroindanones and 2-Substituted 1-Indanones by Ruthenium-Catalyzed Tandem Coupling and Cyclization of Aromatic Acids with α,ß-Unsaturated Ketones.

The one-step strategy for the facile syntheses of structurally diverse 1-indanones in moderate to good isolated yields was developed via a ruthenium-catalyzed tandem coupling and cyclization of simple aromatic acids with α,ß-unsaturated ketones. The tandem cyclization involves one-pot sequential reactions of C-H activation, conjugate addition, Dieckmann condensation, Michael addition, intramolecular Aldol reaction, or hydrolysis. Switchable access to spiroindanones and 2-substituted 1-indanones could be achieved by manganese additive and H2O. Mn(II) additive is found to play an important role in this transformation, and a trace amount of water can promote the formation of 2-substituted 1-indanones. This process features the one-pot efficient construction of multiple C-C bonds, high step-economy, commercially available starting materials, and a broad substrate scope.

Silencing of COL1A2, COL6A3, and THBS2 inhibits gastric cancer cell proliferation, migration, and invasion while promoting apoptosis through the PI3k-Akt signaling pathway.

This study explores the effect of COL1A2, COL6A3, and THBS2 gene silencing on proliferation, migration, invasion, and apoptosis of gastric cancer cells through the PI3K-Akt signaling pathway. The gastric cancer microarray expression data (GSE19826, GSE79973, and GSE65801) was analyzed. Gastric cancer tissues and corresponding adjacent normal tissues were extracted from patients. Positive expression rate of PI3K, Akt, and p-Akt was measured with immunohistochemistry. Two cell lines, BGC-823 and SGC-7901, were transfected and cells were grouped into blank, negative control, COL1A2-shRNA, COL6A3-shRNA, and THBS2-shRNA groups. Expressions of COL1A2, COL6A3, and THBS2 in gastric cancer cells transfected with corresponding silencing sequences were evaluated by RT-qPCR and Western blot. MTT assay, Transwell, and cell scratch tests were conducted to evaluate cell proliferation, invasion, and migration capacity, respectively. Flow cytometry was used to evaluate cell cycle distribution and apoptosis. The positive expression of PI3K, Akt, and p-Akt was higher in gastric cancer tissues compared with adjacent normal tissues, and the mRNA expression of COL1A2, COL6A3, and THBS2 was increased in gastric cancer tissues. Akt, p-Akt, and PI3K expression drastically decreased in cells transfected with COL1A2, COL6A3, and THBS2 silencing sequences. Cells transfected with COL1A2, COL6A3, and THBS2 silencing sequences exhibited promoted apoptosis but inhibited proliferation, migration, and invasion. This study demonstrates that COL1A2, COL6A3, and THBS2 gene silencing inhibits gastric cancer cell proliferation, migration, and invasion while promoting apoptosis through the PI3K-Akt signaling pathway.

Effects of PKM2 Gene Silencing on the Proliferation and Apoptosis of Colorectal Cancer LS-147T and SW620 Cells.

BACKGROUND/AIMS: This paper aims to explore the effects of pyruvate kinase (PK) M2 gene silencing on the proliferation and apoptosis of colorectal cancer (CRC) LS-147T and SW620 cells. METHODS: CRC LS-147T and SW620 cells highly expressing PKM2 were randomly selected by quantitative real-time polymerase chain reaction (qRT-PCR) and then assigned into the blank (no transfection), PKM2-shRNA (transfection with shRNA) and empty plasmid (transfection with empty plasmid) groups. Immunofluorescence was applied to detect PKM2 protein expression. qRT-PCR and Western blotting were conducted to assess mRNA and protein expression of PKM2, p53 and p21. The cell counting kit-8 (CCK-8) assay was used to assess cell proliferation. Flow cytometry was used to assess the cell cycle and apoptosis rate, and a senescence-associated ß-galactosidase staining kit was used to assess cell senescence. RESULTS: PKM2 exhibited high mRNA expression among CRC LS-147T and SW620 cells with remarkable protein expression noted in the cytoplasm and nucleus. The PKM2-shRNA group exhibited reduced PKM2 mRNA and protein expression, whereas p53 and p21 expression was increased compared with the blank and empty plasmid groups. Cell proliferation in PKM2-shRNA cells decreased significantly compared with the blank group and empty plasmid groups. The PKM2-shRNA group exhibited more cells in the G1 phase and fewer cells in the G2/M phase compared with the blank and empty plasmid groups. In addition, the PKM2-shRNA group exhibited significantly increased apoptosis rates and ß-galactosidase activity compared with the blank and empty plasmid groups. CONCLUSION: Our study demonstrates that PKM2 gene silencing suppresses proliferation and promotes apoptosis in LS-147T and SW620 cells.

Effects of hepatitis C virus infection on the safety of chemotherapy for breast cancer patients.

PURPOSE: Hepatitis C virus (HCV) is one of the major pathogens of chronic viral hepatitis, and approximately 38 million patients are infected with HCV in China. However, little information is available on the effect of HCV infection during chemotherapy for breast cancer and the impact of HCV infection on the toxicity of chemotherapy and targeted therapy. METHODS: We performed a retrospective survey of 835 patients who were diagnosed with breast cancer between January 2010 and December 2015 at our institution. All patients had been screened for HCV infection at the time of breast cancer diagnosis. We retrospectively investigated the toxicities of chemotherapy and the changes in HCV load based on a review of the medical records. RESULTS: A total of 21 patients with positive anti-HCV antibody tests received chemotherapy. The median patient age was 46.3 ± 11.2 years. Four (19.0%) patients exhibited abnormal liver function at baseline. The morbidity of abnormal liver function at baseline was higher in HCV-infected patients (19.0% vs. 0, P = 0.000). Four patients received trastuzumab therapy. Five (23.8%) patients who received chemotherapy developed hepatitis. No patients presented with HCV reactivation. The morbidity of hepatitis and the rate of disruption of chemotherapy were not significantly different between breast cancer patients without HCV infection and those with HCV infection (23.8 vs. 14.2% P = 0.342, 9.5 vs. 5.0% P = 0.619, respectively). CONCLUSION: HCV infection had no adverse impact on chemotherapy in breast cancer patients. However, consulting a gastroenterologist and closely monitoring liver function during the course of chemotherapy may benefit patients.

Downregulation of SATB1 increases the invasiveness of Jurkat cell via activation of the WNT/ß-catenin signaling pathway in vitro.

Special AT-rich sequence-binding protein-1 (SATB1) is critical for genome organizer that reprograms chromatin organization and transcription profiles, and associated with tumor growth and metastasis in several cancer types. Many studies suggest that SATB1 overexpression is an indicator of poor prognosis in various cancers, such as breast cancer, malignant cutaneous melanoma, and liver cancer. However, their expression patterns and function values for adult T cell leukemia (ATL) are still largely unknown. The aim of this study is to examine the levels of SATB1 in ATL and to explore its function and mechanisms in Jurkat cell line. Here, we reported that SATB1 expressions were decreased in ATL cells (p < 0.001) compared with normal controls. Knockdown of SATB1 expression significantly enhanced invasion of Jurkat cell in vitro. Furthermore, knockdown of SATB1 gene enhances ß-catenin nuclear accumulation and transcriptional activity and thus may increase the invasiveness of Jurkat cell through the activation of Wnt/ß-catenin signaling pathway in vitro.

[All-trans retinoic acid effectively inhibits breast cancer stem cells growth in vitro].

OBJECTIVE: To detect the inhibitory effect of all-trans retinoic acid(ATRA) on breast cancer stem cells (CSCs). METHODS: The inhibitory effect of ATRA on MCF-7 and SK-BR-3 cell lines was analyzed using a Cell Counting Kit-8 (CCK-8). The proportion of CD44(+)CD24(-) tumor cells of the two cell lines were measured before and after the ATRA treatment, and the role of ATRA in the regulation of CSC self-renewing ability was evaluated with a tumor sphere assay. The tumor spheres were grown in an adherent culture to evaluate the ATRA-induced differentiation of breast cancer stem cells. RESULTS: ATRA effectively inhibited the unsorted cells and stem cells, but the CSCs were more sensitive to ATRA. At a concentration of 10(-6) mol/L, the inhibitory rate of MCF-7 unsorted cells and stem cells were (8.66 ± 1.06)% and (21.09 ± 3.25)%, respectively (P = 0.004). For SK-BR-3 cells, the rates were (39.19 ± 1.47)% and (51.22 ± 2.80)%, respectively (P = 0.005). The self-renewing ability of the CSCs was impaired by ATRA at a concentration of 10(-6) mol/L. The rate of MCF-7 and SK-BR-3 stem cells to form tumor sphere was 5.2% (5/96) and 13.5% (13/96), respectively. For the control group, it was 86.5% (83/96) and 93.8% (90/96), respectively (P < 0.001). ATRA also promoted the CD44(+)CD24(-) subpopulation to differentiate. SK-BR-3 stem cells were grown in an adherent culture. After using ATRA, the proportion of CD44(+)CD24(-) cells was (48.1 ± 2.5)% and that of the control group was (86.6 ± 2.5)% (P < 0.001). CONCLUSIONS: ATRA effectively inhibits breast NCSCs and CSCs, but CSCs are more sensitive to ATRA. ATRA impairs the self-renewing ability of CSCs and promotes CSCs to differentiate.

[Advances in the pathogenesis and treatment of neurosurgical emergency with coagulation disorders].

Neurosurgical emergencies including intracranial hemorrhage and head trauma have high mortality and morbidity rates and meanwhile are often accompanied with coagulation disorders. On one hand, coagulation disorder follows traumatic brain injury;on the other hand, the increasing use of anticoagulant and antiplatelet treatment for cardiovascular diseases increases the risk of death among patients with brain trauma or bleeding. Once the intracranial pressure increases, such patients need emergency surgical intervention, but coagulation disorder is a relative contraindication. This article reviews the pathogenesis and treatment of coagulation disorders in patients with neurosurgical emergency. It also analyzes clinical monitoring indices for such patients and their variations and summarizes the strategies and measures of perioperative management.

M2 macrophages mediate fibrotic scar formation in the early stages after cerebral ischemia in rats.

In the central nervous system, the formation of fibrotic scar after injury inhibits axon regeneration and promotes repair. However, the mechanism underlying fibrotic scar formation and regulation remains poorly understood. M2 macrophages regulate fibrotic scar formation after injury to the heart, lung, kidney, and central nervous system. However, it remains to be clarified whether and how M2 macrophages regulate fibrotic scar formation after cerebral ischemia injury. In this study, we found that, in a rat model of cerebral ischemia induced by middle cerebral artery occlusion/reperfusion, fibrosis and macrophage infiltration were apparent in the ischemic core in the early stage of injury (within 14 days of injury). The number of infiltrated macrophages was positively correlated with fibronectin expression. Depletion of circulating monocyte-derived macrophages attenuated fibrotic scar formation. Interleukin 4 (IL4) expression was strongly enhanced in the ischemic cerebral tissues, and IL4-induced M2 macrophage polarization promoted fibrotic scar formation in the ischemic core. In addition, macrophage-conditioned medium directly promoted fibroblast proliferation and the production of extracellular matrix proteins in vitro. Further pharmacological and genetic analyses showed that sonic hedgehog secreted by M2 macrophages promoted fibrogenesis in vitro and in vivo, and that this process was mediated by secretion of the key fibrosis-associated regulatory proteins transforming growth factor beta 1 and matrix metalloproteinase 9. Furthermore, IL4-afforded functional restoration on angiogenesis, cell apoptosis, and infarct volume in the ischemic core of cerebral ischemia rats were markedly impaired by treatment with an sonic hedgehog signaling inhibitor, paralleling the extent of fibrosis. Taken together, our findings show that IL4/sonic hedgehog/transforming growth factor beta 1 signaling targeting macrophages regulates the formation of fibrotic scar and is a potential therapeutic target for ischemic stroke.

Turn-on luminescent sensing of metal cations via quencher displacement: rational design of a highly selective chemosensor for chromium(III).

A highly selective luminescent chemosensor for Cr(3+) in aqueous solution was assembled by a low-selectivity luminogenic receptor with Cu(2+) as a metal quencher. Three tetranitrogen chelating sites were integrated into the multichannel receptor with a tris(1,10-phenanthroline)ruthenium(II) luminophore at the core. This receptor (2) exhibits chelating affinity for many transition-metal cations, among which Cu(2+) efficiently quenches the emission. The further addition of Cr(3+) into the Cu(2+)-titrated solution of 2 results in a metal-exchange reaction and a sensitive turn-on luminescence response highly selective over other metal cations. The quencher displacement sensing strategy in this design can be a simple but efficient approach for OFF-ON luminescent sensing of metal cations that inherently lack selective ligands.

[Adsorption of Mn2+ by Modified Biochar Fixed Bed in Simulated Lakes and Reservoir Waters].

Lakes and reservoirs are important water resources for human survival and sustainable development. The seasonal excess of manganese ions (Mn2+) in drinking water in lakes and reservoirs has become an important factor threatening human life in health and social safety in production. Firstly, a batch study of NaOH-modified biochar was carried out. The effects of pyrolysis temperature (400, 500, and 600℃) and modification conditions (unmodified, pre-alkali modified, and post-alkali modified) on the adsorption performance of biochar were investigated. The results showed that the alkali pretreatment could improve the adsorption capacity of biochar, and the maximum adsorption capacity of the modified biochar obtained by alkali pretreatment at 400℃ was 41.06 mg·g-1. Additionally, the dynamic adsorption characteristics of Mn2+in the application on the fixed bed were investigated. The results showed that the stronger the adsorption capacity of biochar in the batch experiment, the longer its breakthrough point (ct/c0=0.1) and saturation point (ct/c0=0.9) in the dynamic adsorption process. In addition, when the initial concentration of Mn2+ and the influent flow rate were increased, the breakthrough point of the fixed bed was shortened from 360 min to 160 min and 200 min, respectively, and the saturation point was shortened from 865 min to 700 min and 600 min, respectively. The Thomas model could better fit the adsorption process of the fixed bed, indicating that the removal of Mn2+ by biochar was also dominated by chemical adsorption. This outcome can provide theoretical guidance for actual operations.

Altered gray matter volume and functional connectivity in medial orbitofrontal cortex of bulimia nervosa patients: A combined VBM and FC study.

Brain structural and functional abnormalities have been shown to be involved in the neurobiological underpinnings of bulimia nervosa (BN), while the mechanisms underlying this dysregulation are unclear. The main goal of this investigation was to explore the presence of brain structural alterations and relevant functional changes in BN. We hypothesized that BN patients had regional gray matter volume abnormalities and corresponding resting-state functional connectivity (rsFC) changes compared with healthy controls. Thirty-one BN patients and twenty-eight matched healthy controls underwent both high-resolution T1-weighted magnetic resonance imaging (MRI) and resting-state functional MRI. Structural analysis was performed by voxel-based morphometry (VBM), with subsequent rsFC analysis applied by a seed-based, whole-brain voxelwise approach using the abnormal gray matter volume (GMV) region of interest as the seed. Compared with the controls, the BN patients showed increased GMV in the left medial orbitofrontal cortex (mOFC). The BN patients also exhibited significantly increased rsFC between the left mOFC and the right superior occipital gyrus (SOG) and decreased rsFC between the left mOFC and the left precentral gyrus, postcentral gyrus, and supplementary motor area (SMA). Furthermore, the z values of rsFC between the left mOFC and right SOG was positively correlated with the Dutch Eating Behavior Questionnaire-external eating scores. Findings from this investigation further suggest that the mOFC plays a crucial role in the neural pathophysiological underpinnings of BN, which may lead to sensorimotor and visual regions reorganization and be related to representations of body image and the drive behind eating behavior. These findings have important implications for understanding neural mechanisms in BN and developing strategies for prevention.

Regional Neural Activity Abnormalities and Whole-Brain Functional Connectivity Reorganization in Bulimia Nervosa: Evidence From Resting-State fMRI.

The management of eating behavior in bulimia nervosa (BN) patients is a complex process, and BN involves activity in multiple brain regions that integrate internal and external functional information. This functional information integration occurs in brain regions involved in reward, cognition, attention, memory, emotion, smell, taste, vision and so on. Although it has been reported that resting-state brain activity in BN patients is different from that of healthy controls, the neural mechanisms remain unclear and need to be further explored. The fractional amplitude of low-frequency fluctuation (fALFF) analyses are an important data-driven method that can measure the relative contribution of low-frequency fluctuations within a specific frequency band to the whole detectable frequency range. The fALFF is well suited to reveal the strength of interregional cooperation at the single-voxel level to investigate local neuronal activity power. FC is a brain network analysis method based on the level of correlated dynamics between time series, which establishes the connection between two spatial regions of interest (ROIs) with the assistance of linear temporal correlation. Based on the psychological characteristics of patients with BN and the abnormal brain functional activities revealed by previous neuroimaging studies, in this study, we investigated alterations in regional neural activity by applying fALFF analysis and whole-brain functional connectivity (FC) in patients with BN in the resting state and to explore correlations between brain activities and eating behavior. We found that the left insula and bilateral inferior parietal lobule (IPL), as key nodes in the reorganized resting-state neural network, had altered FC with other brain regions associated with reward, emotion, cognition, memory, smell/taste, and vision-related functional processing, which may have influenced restrained eating behavior. These results could provide a further theoretical basis and potential effective targets for neuropsychological treatment in patients with BN.

Near-infrared chromogenic sensing of organotin species by a cyclopalladated azo dye.

A simple cyclopalladated complex of 4-(2-thiazolylazo)resorcinol showed a specific red-to-green colour change upon addition of organotin species in the acetonitrile-water medium.

Anti-tumor effect of oncolytic herpes simplex virus G47delta on human nasopharyngeal carcinoma.

Oncolytic herpes simplex virus (HSV) can replicate in and kill cancer cells without harming normal tissue. G47delta is a third-generation HSV vector. In this study, the therapeutic effects of G47delta on human nasopharyngeal carcinoma (NPC) were determined in vitro and in vivo. The human NPC cell lines CNE-2 and SUNE-1, primary normal nasopharyngeal epithelial cells (NPECs), and immortalized nasopharyngeal cells NP-69 and NPEC2/Bmi1 were infected with G47delta at different multiplicities of infection (MOIs). The survival of infected cells was observed daily. Two subcutaneous models of NPC were established with CNE-2 and SUNE-1 in Balb/c nude mice. G47delta or virus buffer as control was injected into the subcutaneous tumors. Tumor size was measured twice a week, and animals were euthanized when the diameter of their tumors exceeded 18 mm or when the animals appeared moribund. For the NPC cell lines CNE-2 and SUNE-1, more than 85% and 95% of cells were killed on day 5 after G47delta infection at MOI = 0.01 and MOI = 0.1, respectively. Similar results were observed for an immortalized cell line NPEC2/Bmi-1. A moderate effect of G47delta was also found on another immortalized cell line NP-69, of which only 27.7% and 75.9% of cells were killed at MOI = 0.01 and MOI = 0.1, respectively. On the contrary, there was almost no effect observed on NPECs. The in vivo experiments showed that tumors in mice in the G47delta-treated group regressed completely, and the mice exhibited much longer survival time than those in the control groups. Our results suggest that the potential therapeutic effects of G47delta would be applicable for treatment of NPC patients in the future.

[Profiling of Antibiotic Resistance Genes in Different Croplands].

Soil is the primary interface of Earth's critical zone and plays an important role in food security and sustaining environmental balance. Antibiotic resistance genes (ARGs) pose significant threat to human health and ecosystems, with croplands being intensively affected via planting patterns and the application of fertilizers. The transmission of ARGs in croplands remains largely unknown. Using high throughput quantitative Polymerase Chain Reaction (HT-qPCR) techniques, we investigated the occurrence and diversity of ARGs and their association with heavy metals in different croplands in China. A total of 187 ARGs were identified, ranging from 89 to 159 in agricultural soils. The abundance of ARGs ranged from 6.47×109 to 1.41×1010 copies·g-1 with multidrug resistance genes being the most abundant. Heavy metals including As, Co, Cr, Mo, Ni, and Pb were correlated with ARGs using the R package 'evnfit'. Furthermore, redundancy analysis (RDA) revealed that the heavy metals explained 59.3% of the variability of ARGs in the different croplands, indicating that heavy metals might exert an important influence on the composition and transmission of ARGs. Croplands soils act as a vital reservoir and reaction media for ARGs. Different crop cultivation coupled with selection pressure of heavy metals from fertilizers could have potential impacts on the prevalence, diversity, and distribution of ARGs.

Pingchuan formula attenuates airway mucus hypersecretion via regulation of the PNEC-GABA-IL13-Muc5ac axis in asthmatic mice.

BACKGROUND/AIMS: Asthma is a common chronic respiratory disease. It has been reported that Pingchuan formula (PCF) can control asthma attacks by reducing airway inflammation, muscle spasm and mucus secretion. However, PCF's mechanism for reducing airway mucus hypersecretion remains unclear. This study aimed to investigate the effect of PCF on airway mucus secretion in asthmatic mice and to explore changes in the PNEC-GABA-IL13-Muc5ac axis. METHODS: Male Babl/c mice were used to establish the asthma model via sensitisation with OVA. Mice were randomly divided into Normal, OVA, DEX, and PCF groups. After treatment, lung histopathology was observed with H&E and PAS staining. BALF levels of IL-5 and IL-13 were detected using ELISA. The levels of mRNA and protein expression for GAD1, GABAARß1, GABAARα1 and Muc5ac in the lung tissue were measured by RT-PCR and Western blot assays. PNECs were observed with AgNOR staining. RESULTS: PCF treatment effectively reduced goblet cell (P < 0.01) and PNEC (P < 0.05) proliferation, lung tissue inflammation and airway mucus hypersecretion. In addition, PCF also markedly downregulated mRNA and protein expression of GAD1, GABAARß1, GABAARα1 and Muc5ac (P < 0.05, compared with OVA), thus inhibiting the GABA-IL-13 pathway in the lung tissue of asthmatic mice. CONCLUSION: These findings suggest that PCF controls asthma attacks by reducing airway inflammation and mucus hypersecretion via the PNEC-GABA-IL13-Muc5ac axis.

Pingchuan formula improves allergic asthma in mice through inhibiting nuclear factor-kappa B / mitogen-activated protein kinase signaling pathway.

OBJECTIVE: To examine the role and decipher the mechanism of Pingchuan formula (PCF) in treating allergic asthma. METHODS: The mice were treated with saline, dexamethasone (DXM) and PCF for 1 week after the asthma model was established and their respiratory function including respiratory resistance (RI), pulmonary dynamic compliance (Cdyn) and maximum voluntary ventilation (MVV) were measured. In addition, cellular changes in bronchoalveolar lavage fluid (BALF) and pathological changes in lung biopsy as well as the expression level of -smooth muscle actin (α-SMA), transforming growth factor-beta1 (TGF-α1) in BALF and interleukin-5 (IL-5), interleukin-13 (IL-13), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), nuclear factor-kappa B-p65 (NF-κBp65), inhibitor-α of nuclear transcription factor κB (IκBα), p38 mitogen-activated protein kinase (p38MAPK), c-jun n-terminal kinase (JNK) and its phosphorylated proteins in lung tissue were also examined and compared among different groups. RESULTS: Our data suggested that the respiratory functions were significantly improved and the pathological changes ameliorated in the DXM group and the PCF group compared to the model group. Both DXM and PCF effectively decreased the number of eosinophils, lymphocytes, and neutrophils in BAL as well as the secretion of α-SMA and TGF-α1, IL-5, IL-13, while increased the expression of TNF-α and IFN-γ. Furthermore, our study indicated that the NF-κBp65, IκBα, p38MAPK and JNK pathways were inhibited under the treatment of PCF. CONCLUSION: Our data indicated that PCF can attenuate the inflammatory response in asthma through inhibiting the NF-κB/MAPK signaling pathway. This study not only supported the use of PCF in allergic asthma in clinic but also shed light upon afurther understanding of thediseasepathogenesis.

Acute Kidney Injury in Oncology Patients.

With rapid progress in cancer diagnosis and treatment in the last two decades, outcomes in oncological patients have improved significantly. However, the incidence of acute kidney injury (AKI) in this population has also increased significantly. AKI complicates many aspects of patients' care and adversely affects their prognoses; thus, accurately diagnosing the risk factors for AKI ensures appropriate management. AKI may be caused by pre-renal, intrinsic renal, and post-renal reasons, as well as for combined reasons. This review summarizes the potential etiologies of AKI according to the three classifications. For each underlying cause of AKI, the cancer itself and/or cancer treatment may contribute to a patient developing AKI. Therefore, we present disease- and treatment-related factors for each cause category, with special focus on immune checkpoint inhibitors, which are being used increasingly more often. It is important for nephrology services to be knowledgeable to provide the best level of care.