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The article discusses a study which analyzed the clinical data of 16 patients with chronic invasive fungal rhinosinusitis (CIFRS) who were diagnosed in the Department of Rhinology of Beijing Tongren Hospital during the period from 2006 to 2014. Topics covered include the pathological features of CIFRS, its insidious onset and gradual progression, and the proposed feasible diagnosis and treatment strategies.

Conclusion:From aspect of fluid dynamics, expanding patients’ nasopharyngeal coronal-sectional area to 48.3–54.7% of normal area will bring the airflow velocity back to normal in adenoidal hypertrophy children. It might provide a suggestion for adenoidectomy range selection and whether total resection is necessary. Objectives:To evaluate the nasopharyngeal airflow characteristics in pediatric OSA patients with adenoidal hypertrophy, and to explore the proper resection range for adenoidectomy Method:Nine OSA patients and four normal children were recruited. The CT scans of their upper airway were collected and used to construct three dimensional models for fluid dynamics analysis. Using computational fluid dynamics, indices such as velocity, pressure, and coronal-sectional area were calculated. Results:Compared with the normal, the OSA children showed three characteristics in nasopharyngeal: the airflow velocity was significantly higher (p < 0.05), the coronal-sectional area was significantly smaller (p < 0.01), while pressure showed no difference (p > 0.05). In a study of the relationship between velocity and coronal-sectional area, this study investigates different coronal-sectional areas from 30–300 mm2. It was found that, when patients’ nasopharyngeal coronal-sectional area was expanded over 155–170 mm2, namely 48.3–54.7% of normal area, airflow velocity in nasopharyngeal showed no difference than normal. [ABSTRACT FROM PUBLISHER]

Aldosterone, which plays a key role in maintaining water and electrolyte balance, is produced by zona glomerulosa cells of the adrenal cortex. Autonomous overproduction of aldosterone from zona glomerulosa cells causes primary hyperaldosteronism. Recent clinical studies have highlighted the pathological role of the KCNJ5 potassium channel in primary hyperaldosteronism. Our objective was to determine whether small-conductance Ca(2+)-activated potassium (SK) channels may also regulate aldosterone secretion in human adrenocortical cells. We found that apamin, the prototypic inhibitor of SK channels, decreased membrane voltage, raised intracellular Ca(2+) and dose dependently increased aldosterone secretion from human adrenocortical H295R cells. By contrast, 1-Ethyl-2-benzimidazolinone, an agonist of SK channels, antagonized apamin's action and decreased aldosterone secretion. Commensurate with an increase in aldosterone production, apamin increased mRNA expression of steroidogenic acute regulatory protein and aldosterone synthase that control the early and late rate-limiting steps in aldosterone biosynthesis, respectively. In addition, apamin increased angiotensin II-stimulated aldosterone secretion, whereas 1-Ethyl-2-benzimidazolinone suppressed both angiotensin II- and high K(+)-stimulated production of aldosterone in H295R cells. These findings were supported by apamin-modulation of basal and angiotensin II-stimulated aldosterone secretion from acutely prepared slices of human adrenals. We conclude that SK channel activity negatively regulates aldosterone secretion in human adrenocortical cells. Genetic association studies are necessary to determine whether mutations in SK channel subtype 2 genes may also drive aldosterone excess in primary hyperaldosteronism. [ABSTRACT FROM AUTHOR]

Background/Aims: Arachidonic acid (AA) and its metabolites are important endogenous lipid messengers. In this study, we test the effect of Leukotriene B4 (LTB4), a 5-lipoxygenase metabolite of AA, on L-type calcium channels in A7r5 rat aortic vascular smooth muscle cells. Methods: L-type calcium channel currents were recorded by a patch-clamp technique. The mRNA expression of CaV1.2 was determined by Real-time RT-PCR. The protein expression of CaV1.2 and p38 activity was determined by Western blot analysis. Results: LTB4 inhibits L-type channel currents in A7r5 cells in a dose-and time- dependent manner. LTB4 reduced the mRNA/protein expression of CaV1.2 channels in A7r5 cells. BLT1 receptor antagonist LY29311 abrogated the inhibitory effect of LTB4, while BLT2 receptor antagonist LY255283 had no effect. 5Z-7-oxozeaenol and SB203580, which block TAK1 and p38 kinase respectively, abrogated the LTB4 inhibitory effect on L-type calcium channels. LTB4 increased p38 activity in A7r5 cells. Blockage of Src, PI3K, JNK and NF-κB kinase had no effects on LTB4 inhibition of L-type calcium channel currents in A7r5 cells. Conclusion: We conclude that LTB4 inhibits L-type calcium channels through BLT1-TAk1-p38 signaling pathway. The LTB4 inhibitory effect on L-type calcium channels may be involved in its pathological processes such as atherosclerosis. © 2015 The Author(s) Published by S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

With deep research into historical gardens as well as the existing ones in both China and Japan, this article compares the gardens' origins and evolution in the two countries, and draws the conclusion that the gardens in each country emerged and developed naturally, and classical Chinese gardens originated earlier than those in Japan, but made their progress in a much slower way. [ABSTRACT FROM AUTHOR]

Abstract: Extremely low-frequency electromagnetic fields (ELF-EMF) causes various biological effects through altering intracellular calcium homeostasis. The role of high voltage-gated (HVA) calcium channels in ELF-EMF induced effects has been extensively studied. However, the effect of ELF-EMF on low-voltage-gated (LVA) T-type calcium channels has not been reported. In this study, we test the effect of ELF-EMF (50Hz) on human T-type calcium channels transfected in HEK293 cells. Conversely to its stimulant effects on HVA channels, ELF-EMF exposure inhibited all T-type (Cav3.1, Cav3.2 and Cav3.3) channels. Neither the protein expression nor the steady-state activation and inactivation kinetics of Cav3.2 channels were altered by ELF-EMF (50Hz, 0.2mT) exposure. Exposure to ELF-EMF increased both arachidonic acid (AA) and leukotriene E4 (LTE4) levels in HEK293 cells. CAY10502 and bestatin, which block the increase of AA and LTE4 respectively, abrogated the ELF-EMF inhibitory effect on Cav3.2 channels. Exogenous LTE4 mimicked the ELF-EMF inhibition of T-type calcium channels. ELF-EMF (50Hz) inhibits native T-type calcium channels in primary cultured mouse cortical neurons via LTE4. We conclude that 50Hz ELF-EMF inhibits T-type calcium channels through AA/LTE4 signaling pathway. [Copyright &y& Elsevier]

The slow inactivation of voltage-gated potassium (Kv) channels plays an important role in controlling cellular excitability. Recently, the two hydrogen bonds (H-bonds) formed by W434-D447 and T439-Y445 have been reported to control the slow inactivation in Shaker potassium channels. The four residues are highly conserved among Kv channels. Our objective was to find the roles of the two H-bonds in controlling the slow inactivation of mammalian Kv2.1, Kv2.2, and Kv1.2 channels by point mutation and patch-clamp recording studies. We found that mutations of the residues equivalent to W434 and T439 in Shaker did not change the slow inactivation of the Kv2.1, Kv2.2, and Kv1.2 channels. Surprisingly, breaking of the inter-subunit H-bond formed by W366 and Y376 (Kv2.1 numbering) by various mutations resulted in the complete loss of K+ conductance of the three Kv channels. In conclusion, we found differences in the H-bonds controlling the slow inactivation of the mammalian Kv channels and Shaker channels. Our data provided the first evidence, to our knowledge, that the inter-subunit H-bond formed by W366 and Y376 plays an important role in regulating the K+ conductance of mammalian Kv2.1, Kv2.2, and Kv1.2 channels. [ABSTRACT FROM AUTHOR]

The precise regulation of Ca 2+ signals plays a crucial role in the physiological functions of neurons. Here, we investigated the rapid effect of glucocorticoids on Ca 2+ signals in cultured hippocampal neurons from both female and male rats. In cultured hippocampal neurons, glucocorticoids inhibited the spontaneous somatic Ca 2+ spikes generated by Kv2.1-organized Ca 2+ microdomains. Furthermore, glucocorticoids rapidly reduced the cell surface expressions of Kv2.1 and Ca V 1.2 channels in hippocampal neurons. In HEK293 cells transfected with Kv2.1 alone, glucocorticoids significantly reduced the surface expression of Kv2.1 with little effect on K + currents. In HEK293 cells transfected with Ca V 1.2 alone, glucocorticoids inhibited Ca V 1.2 currents but had no effect on the cell surface expression of Ca V 1.2. Notably, in the presence of wild-type Kv2.1, glucocorticoids caused a decrease in the surface expression of Ca V 1.2 channels in HEK293 cells. However, this effect was not observed in the presence of non-clustering Kv2.1S586A mutant channels. Live cell imaging showed that glucocorticoids rapidly decreased Kv2.1 clusters on the plasma membrane. Correspondingly, western blot results indicated a significant increase in the cytoplasmic level of Kv2.1, suggesting the endocytosis of Kv2.1 clusters. Glucocorticoids rapidly decreased the intracellular cAMP concentration and the phosphorylation level of PKA in hippocampal neurons. The PKA inhibitor H89 mimicked the effect of glucocorticoids on Kv2.1, while the PKA agonist forskolin abrogated the effect. In conclusion, glucocorticoids rapidly suppress Ca V 1.2-mediated Ca 2+ signals in hippocampal neurons by promoting the endocytosis of Kv2.1 channel clusters through reducing PKA activity. Significance Statement Glucocorticoids are well-known stress hormones, but their rapid non-genomic effects on the brain remain unclear. The hippocampus is one of the main effectors of glucocorticoids in the brain. Here, we demonstrate that glucocorticoids rapidly inhibit voltage-gated calcium (Ca V ) channel Ca V 1.2-mediated somatic calcium (Ca 2+ ) spikes in hippocampal neurons. Glucocorticoids reduce the surface expression of Kv2.1 voltage-activated potassium (Kv) channel clusters but do not affect the surface expression of non-clustering Kv2.1. Moreover, glucocorticoids induce the endocytosis of Ca V 1.2 channels through wild-type Kv2.1. However, glucocorticoids cannot induce the endocytosis of Ca V 1.2 channels through non-clustering Kv2.1S586A mutant channels. This study elucidates the complex interaction between glucocorticoids, Kv2.1, and Ca V 1.2 channels, enhancing our understanding of glucocorticoid actions in the brain., (Copyright © 2024 the authors.)

Ischaemic stroke is a common condition that can lead to cerebral ischaemia-reperfusion injury. Phillygenin (PHI), a natural bioactive compound derived from Forsythia suspensa, has been shown to play a crucial role in regulating inflammation across various diseases. However, its specific regulatory effects in ischaemic stroke progression remain unclear. In this study, we established a middle cerebral artery occlusion (MCAO) rat model. Treatment with PHI (50 or 100 mg/kg) significantly reduced cerebral infarction in MCAO rats. PHI treatment also mitigated the increased inflammatory response observed in these rats. Additionally, PHI suppressed microglial activation by reducing iNOS expression, a marker of M1-type polarization of microglia, and attenuated increased brain tissue apoptosis in MCAO rats. Furthermore, PHI's anti-inflammatory effects in MCAO rats were abrogated upon co-administration with GW9662, a peroxisome proliferator-activated receptor γ (PPARγ) inhibitor. In summary, PHI attenuated microglial activation and apoptosis in cerebral ischaemia-reperfusion injury through PPARγ activation, suggesting its potential as a therapeutic agent for mitigating cerebral ischaemia-reperfusion injury., (© 2024 John Wiley & Sons Australia, Ltd.)

Extensive use of renewable and clean energy is one of the promising ways to solve energy/environmental problems and promote the sustainable development of our society. As inexhaustible energy sources, the photothermal (PT) and radiative cooling (RC) energy from the sun and outer space have recently attracted tremendous interest. However, these two kinds of energy utilization have distinctly opposite spectral properties, especially in the infrared range, making it extremely difficult to integrate these two energy harvesting modes within a fixed device for continuous energy collection. Thus, in the current study, we have proposed a spectrally self-adaptive broadband absorber/emitter (SSBA/E) based on vanadium dioxide (VO 2 ), a typical phase transition material, to achieve continuous energy harvesting via collecting solar thermal energy in PT mode during the day and obtaining cool energy in wide-band RC mode at night. Experimental results show that owing to the phase transition property of the VO 2 layer, these two energy collection modes can be adaptively switched. Specifically, the VO 2 -based device shows a broadband infrared emissivity modulation from 0.21 to 0.75 and low critical temperatures (58.4 and 49.2 °C) during the phase transition, leading to continuous energy harvesting with high efficiency. Due to the broadband infrared emission, the RC maximum power of the SSBA/E device was estimated to be 58 W m -2 . The proposed VO 2 smart coatings are also applicable for many other applications such as thermal management of spacecraft, infrared camouflage, or adaptive optical devices.

The electrochromic WO 3 smart window based on an aqueous electrolyte shows an excellent liquid/solid interface and thus can achieve a fast electrochromic response, while the aqueous electrolyte has a limited electrochemical window, which probably induces the H + reduction and degrades the practical application. Here, we propose a strategy to modify the traditional Li + acidic aqueous electrolyte by adding some selective inert metal ions, which not only improve the electrochromic performance but also avoid the possible production of hydrogen bubbles due to the broadened electrochemical window. Furthermore, reversible electroplating of inert metal ions will occur, leading to an enhanced optical transmission change of up to 77.5% at 500 nm and 70.4% at 700 nm. This combination of Li-ion insertion and metal electroplating in the ESW device makes it superior to all of the previous reports. The device also demonstrates high stability and high electrochromic efficiency after 1000 cycles. The current study not only emphasizes the rational design for aqueous electrolytes but also demonstrates a practical way to realize an excellent electrochromic window for practical applications.

As a typical correlated metal oxide, vanadium dioxide (VO 2 ) shows specific metal-insulator transition (MIT) properties and demonstrates great potential applications in ultrafast optoelectronic switch, resistive memory, and neuromorphic devices. Effective control of the MIT process is essential for improving the device performance. In the current study, we have first proposed a photoassisted ion-doping method to modulate the phase transition of the VO 2 layer based on the photovoltaic effect and electron-ion synergic doping in acid solution. Experimental results show that, for the prepared n-VO 2 /p-GaN nanojunction, this photoassisted strategy can effectively dope the n-VO 2 layer by H + , Al 3+ , or Mg 2+ ions under light radiation and trigger consecutive insulator-metal-insulator transitions. If combined with standard lithography or electron beam etching processes, selective doping with nanoscale size area can also be achieved. This photoassisted doping method not only shows a facile route for MIT modulation via a doping route under ambient conditions but also supplies some clues for photosensitive detection in the future.

Ca V 3.2 calcium channels play important roles in both neural excitability and aldosterone secretion. Recent clinical studies found four germline mutations (S196 L, M1549I, V1951E and P2083 L) in Ca V 3.2 channels. All four mutations caused primary aldosteronism (PA), while only the M1549I mutation resulted in obvious neural malfunctions besides PA. In human, there are two major Ca V 3.2 channel gene (CACNA1H) splice variants, either with or without exon 26. In this study, we tested the expression of the two CACNA1H splice variants in zona glomerulosa (ZG) cells of human adrenal cortex and the possibility that Ca V 3.2 (-26) and Ca V 3.2 (+26) channels have different functional responses to the four PA mutations. We found that human ZG cells only express long form Ca V 3.2(+26) channels. The M1549I mutation slowed the inactivation of Ca V 3.2(+26) more than 5 fold, and Ca V 3.2(-26) more than 2 fold. The S196 L, V1951E and P2083 L mutations accelerated channel recovery from inactivation for Ca V 3.2(+26), but not Ca V 3.2(-26) channels. All four mutations resulted in gain of function of Ca V 3.2(+26) channels, leading to overproduction of aldosterone. In conclusion, the four PA mutations caused more profound changes on Ca V 3.2 (+26) currents than on Ca V 3.2 (-26) currents, and except the M1549I mutation, the S196 L, V1951E and P2083 L have little effect on the electrophysiological properties of Ca V 3.2(-26) currents, which may partially explain the limitation of the phenotype associated with the V1951E, S196 L and P2083 L germline mutations to PA., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Aldosterone, which plays a key role in maintaining water and electrolyte balance, is produced by zona glomerulosa cells of the adrenal cortex. Autonomous overproduction of aldosterone from zona glomerulosa cells causes primary hyperaldosteronism. Recent clinical studies have highlighted the pathological role of the KCNJ5 potassium channel in primary hyperaldosteronism. Our objective was to determine whether small-conductance Ca(2+)-activated potassium (SK) channels may also regulate aldosterone secretion in human adrenocortical cells. We found that apamin, the prototypic inhibitor of SK channels, decreased membrane voltage, raised intracellular Ca(2+) and dose dependently increased aldosterone secretion from human adrenocortical H295R cells. By contrast, 1-Ethyl-2-benzimidazolinone, an agonist of SK channels, antagonized apamin's action and decreased aldosterone secretion. Commensurate with an increase in aldosterone production, apamin increased mRNA expression of steroidogenic acute regulatory protein and aldosterone synthase that control the early and late rate-limiting steps in aldosterone biosynthesis, respectively. In addition, apamin increased angiotensin II-stimulated aldosterone secretion, whereas 1-Ethyl-2-benzimidazolinone suppressed both angiotensin II- and high K(+)-stimulated production of aldosterone in H295R cells. These findings were supported by apamin-modulation of basal and angiotensin II-stimulated aldosterone secretion from acutely prepared slices of human adrenals. We conclude that SK channel activity negatively regulates aldosterone secretion in human adrenocortical cells. Genetic association studies are necessary to determine whether mutations in SK channel subtype 2 genes may also drive aldosterone excess in primary hyperaldosteronism., (© 2016 American Heart Association, Inc.)

Objective: To investigate the relationship between the maxillary sinus flow field, temperature field and the maxillary sinus ostium size, and to provide a reference for endoscopic surgery according to the maxillary sinus scope., Methods: One case of adult female CT image data was obtained, and used to build a three-dimensional model of nasal cavity and maxillary sinus. Computational fluid dynamics method was used to study the airflow and temperature of the maxillary sinus, as well as the physiological function of the maxillary sinus. Simulation surgery by means of different maxillary sinus diameters (normal, 8 mm, 10 mm, 12 mm and 15 mm) was used to describe the maxillary sinus airflow and temperature change., Results: It was found that by numerical simulation the airflow of maxillary sinus and nasal cavity showed lower speed (average speed 0.062 m/s) than that in the middle nasal meatus (average speed of 3.260 m/s), and the average temperature in the normal maxillary sinus was 34°C, which was higher than that in the middle nasal meatus (temperature 28.7°C). With the increase of the diameter of the maxillary sinus, the air temperature change was not obvious., Conclusions: The physiological function of the maxillary sinus can be studied through the numerical simulation. With the increase of the ostia diameter of maxillary sinus, the sinus temperature and ventilation is not affected. It provides a reference for quantification of clinical endoscopic maxillary sinus surgery.