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Recently, the number of high-resolution Earth-observing satellite sensors has been increasing owing to the growing needs of intelligence, mapping, and environmental monitoring. An acquired satellite image should be processed for analysis-ready data (ARD) that can be used for many applications. An important step among the processing is georeferencing that assigns geographic coordinates to each image pixel. These days, georeferencing is directly carried out using onboard sensors to produce sensor model information such as rational polynomial coefficients (RPCs). However, postprocessing is required to increase the positional accuracy of RPCs through bias compensation. Recently, bias compensation has been carried out on the basis of an automated process using ground control point (GCP) image chips. Image matching is carried out between the chips and the target satellite image to model the bias over the entire image. However, if the dissimilarity between the chip and the target satellite image increases owing to large differences in acquisition time and seasonal differences, the image matching often fails. Therefore, in this study, we utilized both intensity-based matching and edge-based matching to overcome these issues. We selected normalized cross-correlation (NCC) for intensity-based matching and relative edge cross-correlation (RECC) for edge-based matching. First, GCP chips were projected onto the target satellite images to align the two datasets. Then, both image matching methods were carried out in a pyramid image matching scheme, and their results were merged before RPC bias compensation with outlier removal. The experiments were carried out for two Kompsat-3A strips consisting of 9 and 7 scenes. NCC and RECC showed different matching results per scene, but RECC tended to show better results. NCC + RECC could derive most matching points, but the accuracy was between NCC and RECC. However, NCC + RECC shows potential to suppress a matching outlier. By applying automated bias compensation, 1.1-1.2 pixels of accuracy in root mean square error (RMSE) could be obtained. [ABSTRACT FROM AUTHOR]

This review highlights the molecular basis of salt sensitivity in hypertension, with a focus on the regulation of sodium transport in the distal nephron. Sodium reabsorption in this region is often linked to the actions of aldosterone, although in recent years numerous findings have been reported on the aldosterone-independent pathway of acquiring salt sensitivity by potassium deficiency or potassium loading. The key to this discussion is the interplay, through extracellular potassium concentration, between the first part of the tubules expressing the Na+-Cl− cotransporter (NCC) and the second part expressing the epithelial Na+ channel (ENaC). The molecular pathways such as with-no-lysine 1 (WNK)-STE20/SPS1-related proline-alanine-rich kinase (SPAK)/oxidative stress-responsive kinase 1 (OSR1) signaling, Kelch-like family member 3 (KLHL3)-cullin 3 (CUL3) complex, protein phosphatases, and mechanistic target of rapamycin complex 2 (mTORC2)-Nedd4L pathway are described as the mechanism by which salt sensitivity on blood pressure is acquired in response to changes in physiological conditions including potassium depletion or loading. This review highlights the potential for targeting these molecular pathways to develop novel therapeutic strategies for the treatment of salt-sensitive hypertension, the mechanism of which remains to be elucidated. [ABSTRACT FROM AUTHOR]

We have previously observed that prolonged administration of rapamycin, an inhibitor targeting the mammalian target of rapamycin complex (mTORC)1, partially reduced hypertension and alleviated kidney inflammation in Dahl salt-sensitive (SS) rats. In contrast, treatment with PP242, an inhibitor affecting both mTORC1/mTORC2, not only completely prevented hypertension but also provided substantial protection against kidney injury. Notably, PP242 exhibited potent natriuretic effects that were not evident with rapamycin. The primary objective of this study was to pinpoint the specific tubular sites responsible for the natriuretic effect of PP242 in SS rats subjected to either 0.4% NaCl (normal salt) or 4.0% NaCl (high salt) diet. Acute effects of PP242 on natriuretic, diuretic, and kaliuretic responses were determined in unanesthetized SS rats utilizing benzamil, furosemide, or hydrochlorothiazide [inhibitors of epithelial Na+ channel (ENaC), Na-K-2Cl cotransporter (NKCC2), or Na-Cl cotransporter (NCC), respectively] either administered alone or in combination. The findings indicate that the natriuretic effects of PP242 in SS rats stem predominantly from the inhibition of NCC and a reduction of ENaC open probability. Molecular analysis revealed that mTORC2 regulates NCC activity through protein phosphorylation and ENaC activity through proteolytic cleavage in vivo. Evidence also indicated that PP242 also prevents the loss of K+ associated with the inhibition of NCC. These findings suggest that PP242 may represent an improved therapeutic approach for antihypertensive intervention, potentially controlling blood pressure and mitigating kidney injury in salt-sensitive human subjects. NEW & NOTEWORTHY: This study explored mechanisms underlying the natriuretic effects of mammalian target of rapamycin protein complex 2 inhibition using PP242 and revealed both epithelial Na+ channel and Na-Cl cotransporter in the distal tubular segments were potentially inhibited. These observations, with prior lab evidence, indicate that PP242 prevents hypertension via its potent inhibitory effects on these specific sodium transporters and by reducing renal immune responses. This dual action, coupled with potassium sparing effects, suggests an improved approach for managing hypertension and associated kidney damage. [ABSTRACT FROM AUTHOR]

Calcineurin, protein phosphatase 2B (PP2B) or protein phosphatase 3 (PP3), is a calcium‐dependent serine/threonine protein phosphatase. Calcineurin is widely expressed in the kidney and regulates renal Na+ and K+ transport. In the thick ascending limb, calcineurin plays a role in inhibiting NKCC2 function by promoting the dephosphorylation of the cotransporter and an intracellular sorting receptor, called sorting‐related‐receptor‐with‐A‐type repeats (SORLA), is involved in modulating the effect of calcineurin on NKCC2. Calcineurin also participates in regulating thiazide‐sensitive NaCl‐cotransporter (NCC) in the distal convoluted tubule. The mechanisms by which calcineurin regulates NCC include directly dephosphorylation of NCC, regulating Kelch‐like‐3/CUL3 E3 ubiquitin–ligase complex, which is responsible for WNK (with‐no‐lysin‐kinases) ubiquitination, and inhibiting Kir4.1/Kir5.1, which determines NCC expression/activity. Finally, calcineurin is also involved in regulating ROMK (Kir1.1) channels in the cortical collecting duct and Cyp11 2 expression in adrenal zona glomerulosa. In summary, calcineurin is involved in the regulation of NKCC2, NCC, and inwardly rectifying K+ channels in the kidney, and it also plays a role in modulating aldosterone synthesis in adrenal gland, which regulates epithelial‐Na+‐channel expression/activity. Thus, application of calcineurin inhibitors (CNIs) is expected to abrupt calcineurin‐mediated regulation of transepithelial Na+ and K+ transport in the kidney. Consequently, CNIs cause hypertension, compromise renal K+ excretion, and induce hyperkalemia. [ABSTRACT FROM AUTHOR]

Hypertension affects approximately one in two United States adults and sex plays an important role in the pathogenesis of hypertension. The Na+-Cl− cotransporter (NCC), regulated by a kinase network including with-no-lysine kinase (WNK)1 and WNK4, STE20/SPS1-related proline alanine-rich kinase (SPAK), and oxidative stress response 1 (OxSR1), is critical to Na+ reabsorption and blood pressure regulation. Dietary salt differentially modulates NCC in salt-sensitive and salt-resistant rats, in part by modulation of WNK/SPAK/OxSR1 signaling. In this study, we tested the hypothesis that sex-dependent differences in NCC regulation contribute to the development of the salt sensitivity of blood pressure using male and female Sprague-Dawley (SD), Dahl salt-resistant (DSR), and Dahl salt-sensitive (DSS) rats. In normotensive salt-resistant SD and DSR rats, a high-salt diet evoked significant decreases in NCC activity, expression, and phosphorylation. In males, these changes were associated with no change in WNK1 expression, a decrease in WNK4 levels, and suppression of SPAK/OxSR1 expression and phosphorylation. In contrast, in females, there was decreased NCC activity associated with suppression of SPAK/OxSR1 expression and phosphorylation. In hypertensive DSS rats, the ability of females to suppress NCC (in opposition to males) via a SPAK/OxSR1 mechanism likely contributes to their lower magnitude of salt-sensitive hypertension. Collectively, our findings support the existence of sex differences in male versus female rats with NCC regulation during dietary salt intake involving suppression of WNK4 expression in male rats only and the involvement of SPAK/OxSR1 signaling in both males and females. NEW & NOTEWORTHY: NCC regulation is sex dependent. In normotensive male and female Sprague-Dawley and Dahl salt-resistant rats, which exhibit dietary Na+-evoked NCC suppression, male rats exhibit decreased WNK4 expression and decreased SPAK and OxSR1 levels, whereas female rats only suppress SPAK and OxSR1. In hypertensive Dahl salt-sensitive rats, the ability of females to suppress NCC (in opposition to males) via a SPAK/OxSR1 mechanism likely contributes to their lower magnitude of salt-sensitive hypertension. [ABSTRACT FROM AUTHOR]

The dietary approach to stop hypertension (DASH) diet combines the antihypertensive effect of a low sodium and high potassium diet. In particular, the potassium component of the diet acts as a switch in the distal convoluted tubule to reduce sodium reabsorption, similar to a diuretic but without the side effects. Previous trials to understand the mechanism of the DASH diet were based on animal models and did not characterize changes in human ion channel protein abundance. More recently, protein cargo of urinary extracellular vesicles (uEVs) has been shown to mirror tissue content and physiological changes within the kidney. We designed an inpatient open label nutritional study transitioning hypertensive volunteers from an American style diet to DASH diet to examine physiological changes in adults with stage 1 hypertension otherwise untreated (Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER 3rd, Simons-Morton DG, Karanja N, Lin PH; DASH-Sodium Collaborative Research Group. N Engl J Med 344: 3–10, 2001). Urine samples from this study were used for proteomic characterization of a large range of pure uEVs (small to large) to reveal kidney epithelium changes in response to the DASH diet. These samples were collected from nine volunteers at three time points, and mass spectrometry identified 1,800 proteins from all 27 samples. We demonstrated an increase in total SLC12A3 [sodium-chloride cotransporter (NCC)] abundance and a decrease in aquaporin-2 (AQP2) in uEVs with this mass spectrometry analysis, immunoblotting revealed a significant increase in the proportion of activated (phosphorylated) NCC to total NCC and a decrease in AQP2 from day 5 to day11. This data demonstrates that the human kidney's response to nutritional interventions may be captured noninvasively by uEV protein abundance changes. Future studies need to confirm these findings in a larger cohort and focus on which factor drove the changes in NCC and AQP2, to which degree NCC and AQP2 contributed to the antihypertensive effect and address if some uEVs function also as a waste pathway for functionally inactive proteins rather than mirroring protein changes. NEW & NOTEWORTHY: Numerous studies link DASH diet to lower blood pressure, but its mechanism is unclear. Urinary extracellular vesicles (uEVs) offer noninvasive insights, potentially replacing tissue sampling. Transitioning to DASH diet alters kidney transporters in our stage 1 hypertension cohort: AQP2 decreases, NCC increases in uEVs. This aligns with increased urine volume, reduced sodium reabsorption, and blood pressure decline. Our data highlight uEV protein changes as diet markers, suggesting some uEVs may function as waste pathways. We analyzed larger EVs alongside small EVs, and NCC in immunoblots across its molecular weight range. [ABSTRACT FROM AUTHOR]

Sodium-glucose cotransporter-2 inhibitors (SGLT2i) reduce blood pressure (BP) in patients with hypertension, yet the precise molecular mechanisms remain elusive. SGLT2i inhibits proximal tubule (PT) NHE3-mediated sodium reabsorption in normotensive rodents, yet no hypotensive effect is observed under this scenario. This study examined the effect of empagliflozin (EMPA) on renal tubular sodium transport in normotensive and spontaneously hypertensive rats (SHRs). It also tested the hypothesis that EMPA-mediated PT NHE3 inhibition in normotensive rats is associated with upregulation of distal nephron apical sodium transporters. EMPA administration for 14 days reduced BP in 12-wk-old SHRs but not in age-matched Wistar rats. PT NHE3 activity was inhibited by EMPA treatment in both Wistar and SHRs. In Wistar rats, EMPA increased NCC activity, mRNA expression, protein abundance, and phosphorylation levels, but not in SHRs. SHRs showed higher NKCC2 activity and an abundance of cleaved ENaC α and γ subunits compared with Wistar rats, none of which were affected by EMPA. Another set of male Wistar rats was treated with EMPA, the NCC inhibitor hydrochlorothiazide (HCTZ), and EMPA combined with HCTZ or vehicle for 14 days. In these rats, BP reduction was observed only with combined EMPA and HCTZ treatment, not with either drug alone. These findings suggest that NCC upregulation counteracts EMPA-mediated inhibition of PT NHE3 in male normotensive rats, maintaining their baseline BP. Moreover, the reduction of NHE3 activity without further upregulation of major apical sodium transporters beyond the PT may contribute to the BP-lowering effect of SGLT2i in experimental models and patients with hypertension. NEW & NOTEWORTHY: This study suggests that reduced NHE3-mediated sodium reabsorption in the renal proximal tubule may account, at least in part, for the BP-lowering effect of SGLT2 inhibitors in the setting of hypertension. It also demonstrates that chronic treatment with SGLT2 inhibitors upregulates NCC activity, phosphorylation, and expression in the distal tubule of normotensive but not hypertensive rats. SGLT2 inhibitor-mediated upregulation of NCC seems crucial to counteract proximal tubule natriuresis in subjects with normal BP. [ABSTRACT FROM AUTHOR]

Abstract Previous research on the neural correlates of consciousness (NCC) in visual perception revealed an early event-related potential (ERP), the visual awareness negativity (VAN), to be associated with stimulus awareness. However, due to the use of brief stimulus presentations in previous studies, it remains unclear whether awareness-related negativities represent a transient onset-related response or correspond to the duration of a conscious percept. Studies are required that allow prolonged stimulus presentation under aware and unaware conditions. The present ERP study aimed to tackle this challenge by using a novel stimulation design. Male and female human participants (n = 62) performed a visual task while task-irrelevant line stimuli were presented in the background for either 500 or 1000 ms. The line stimuli sometimes contained a face, which needed so-called visual one-shot learning to be seen. Half of the participants were informed about the presence of the face, resulting in faces being perceived by the informed but not by the uninformed participants. Comparing ERPs between the informed and uninformed group revealed an enhanced negativity over occipitotemporal electrodes that persisted for the entire duration of stimulus presentation. Our results suggest that sustained visual awareness negativities (SVAN) are associated with the duration of stimulus presentation.

The mineralization within the North China Craton (NCC) is intricately linked to Mesozoic large-scale extension in eastern China and is a consequence of a unified geodynamic tectonic background. Despite previous attempts to elucidate the relationship between large-scale mineralization and magmatic activity in the NCC, a lack of systematic research has hindered the identification of connections among deposits with inconsistent metallogenic ages. This study focuses on the coal measures of the Huanghebei Coalfield (HHBC) in western Shandong, presenting a regional magmatic–hydrothermal metallogenic system with a genetic connection. It delves into the intricate interplay between the multi-mineral enrichment mechanism, metallogenic regularity, and the NCC's destruction. The findings reveal that: (1) Various stages of magmatic intrusion during the Yanshanian period significantly influenced the Late Paleozoic coal measures in the HHBC. The coal measures exhibit distinct ranks, ranging from medium-rank bituminous C to A and high-rank anthracite C, resulting in noticeable differences in gas generation among different coal ranks. The shale between the coal seams C5 and C7 emerges as excellent with a good hydrocarbon-generating capacity during the middle-maturity stage. (2) The "Intrusion along the rock layer type" proves most conducive to shale gas enrichment, while the "laccolith type" is more favorable for shale gas enrichment compared to "dike type" intrusions, which have a limited impact on shale gas enrichment. (3) The mineralization process of CBM, shale gas, and iron ore is influenced by Yanshanian-period magma. The enrichment degree of CBM and shale gas exhibits an inverse correlation with the distance from the magmatic intrusion. Iron deposits demonstrate a close association with the magmatic intrusion, with enhanced enrichment along the rock layer. The results indicate that the destruction of the NCC triggered intense metasomatism in the deep cratonic fluids, serving as the primary driving mechanism for large-scale mineralization during the Yanshanian period. Magmatic intrusions bring hydrothermal fluids conducive to mineralization, and the heat release from these intrusions promotes thermal evolution, hydrocarbon generation, and the enrichment of organic-rich strata. [ABSTRACT FROM AUTHOR]

Aldosterone is responsible for maintaining volume and potassium homeostasis. Although high salt consumption should suppress aldosterone production, individuals with hyperaldosteronism lose this regulation, leading to a state of high aldosterone despite dietary sodium consumption. The present study examines the effects of elevated aldosterone, with or without high salt consumption, on the expression of key Na+ transporters and remodelling in the distal nephron. Epithelial sodium channel (ENaC) α‐subunit expression was increased with aldosterone regardless of Na+ intake. However, ENaC β‐ and γ‐subunits unexpectedly increased at both a transcript and protein level with aldosterone when high salt was present. Expression of total and phosphorylated Na+Cl− cotransporter (NCC) significantly increased with aldosterone, in association with decreased blood [K+], but the addition of high salt markedly attenuated the aldosterone‐dependent NCC increase, despite equally severe hypokalaemia. We hypothesized this was a result of differences in distal convoluted tubule length when salt was given with aldosterone. Imaging and measurement of the entire pNCC‐positive tubule revealed that aldosterone alone caused a shortening of this segment, although the tubule had a larger cross‐sectional diameter. This was not true when salt was given with aldosterone because the combination was associated with a lengthening of the tubule in addition to increased diameter, suggesting that differences in the pNCC‐positive area are not responsible for differences in NCC expression. Together, our results suggest the actions of aldosterone, and the subsequent changes related to hypokalaemia, are altered in the presence of high dietary Na+. Key points: Aldosterone regulates volume and potassium homeostasis through effects on transporters in the kidney; its production can be dysregulated, preventing its suppression by high dietary sodium intake.Here, we examined how chronic high sodium consumption affects aldosterone's regulation of sodium transporters in the distal nephron.Our results suggest that high sodium consumption with aldosterone is associated with increased expression of all three epithelial sodium channel subunits, rather than just the alpha subunit.Aldosterone and its associated decrease in blood [K+] lead to an increased expression of Na‐Cl cotransporter (NCC); the addition of high sodium consumption with aldosterone partially attenuates this NCC expression, despite similarly low blood [K+].Upstream kinase regulators and tubule remodelling do not explain these results. [ABSTRACT FROM AUTHOR]

BACKGROUND: KDM6A (Lysine-Specific Demethylase 6A) is a specific demethylase for histone 3 lysine (K) 27 trimethylation (H3K27me3). The purpose of this study is to investigate whether KDM6A in renal tubule cells plays a role in the regulation of kidney function and blood pressure. METHODS: We first crossed Ksp-Cre+/− and KDM6Aflox/flox mice for generating inducible kidney-specific deletion of KDM6A gene. RESULTS: Notably, conditional knockout of KDM6A gene in renal tubule cells (KDM6A-cKO) increased H3K27me3 levels which leads to a decrease in Na excretion and elevation of blood pressure. Further analysis showed that the expression of NKCC2 (Na-K-2Cl cotransporter 2) and NCC (Na-Cl cotransporters) was upregulated which contributes to impaired Na excretion in KDM6A-cKO mice. The expression of AQP2 (aquaporin 2) was also increased in KDM6A-cKO mice, which may facilitate water reabsorption in KDM6A-cKO mice. The expression of Klotho was downregulated while expression of aging markers including p53, p21, and p16 was upregulated in kidneys of KDM6A-cKO mice, indicating that deletion of KDM6A in the renal tubule cells promotes kidney aging. Interestingly, KDM6A-cKO mice developed salt-sensitive hypertension which can be rescued by treatment with Klotho. KDM6A deficiency induced salt-sensitive hypertension likely through downregulation of the Klotho/ERK (extracellular signal-regulated kinase) signaling and upregulation of the WNK (with-no-lysine kinase) signaling. CONCLUSIONS: This study provides the first evidence that KDM6A plays an essential role in maintaining normal tubular function and blood pressure. Renal tubule cell specific KDM6A deficiency causes hypertension due to increased H3K27me3 levels and the resultant downregulation of Klotho gene expression which disrupts the Klotho/ERK/NCC/NKCC2 signaling. [ABSTRACT FROM AUTHOR]

Ancient orogens within the supercontinent like Columbia can remain stable evolution as long as the cratons. What kind of lithospheric mantle was beneath those orogens and how it evolved into a stable state are still enigmatic. The Trans‐North China orogen (TNCO) is one of the typical collisional orogens within the Columbia supercontinent and was formed at ca. 1.85 Ga. Our work reveals that a cluster of kimberlites intruded the orogenic belt at ca. 1.54 Ga. These rocks were originally generated under a thick lithosphere (>200 km). Their entrained olivine cores show a composition of overlapping olivines from refractory mantle peridotites. The results suggest a thick and refractory lithospheric mantle beneath the TNCO at ca. 1.54 Ga. Such craton‐like property may result from large volume melt extraction from the lithospheric mantle, possibly caused by the ca. 1.78 Ga large igneous event, which eventually induces the long‐term stability of the TNCO during the subsequent supercontinent cycle. [ABSTRACT FROM AUTHOR]

The mineralization within the North China Craton (NCC) is intricately linked to Mesozoic large-scale extension in eastern China and is a consequence of a unified geodynamic tectonic background. Despite previous attempts to elucidate the relationship between large-scale mineralization and magmatic activity in the NCC, a lack of systematic research has hindered the identification of connections among deposits with inconsistent metallogenic ages. This study focuses on the coal measures of the Huanghebei Coalfield (HHBC) in western Shandong, presenting a regional magmatic–hydrothermal metallogenic system with a genetic connection. It delves into the intricate interplay between the multi-mineral enrichment mechanism, metallogenic regularity, and the NCC’s destruction. The findings reveal that: (1) Various stages of magmatic intrusion during the Yanshanian period significantly influenced the Late Paleozoic coal measures in the HHBC. The coal measures exhibit distinct ranks, ranging from medium-rank bituminous C to A and high-rank anthracite C, resulting in noticeable differences in gas generation among different coal ranks. The shale between the coal seams C5 and C7 emerges as excellent with a good hydrocarbon-generating capacity during the middle-maturity stage. (2) The “Intrusion along the rock layer type” proves most conducive to shale gas enrichment, while the “laccolith type” is more favorable for shale gas enrichment compared to “dike type” intrusions, which have a limited impact on shale gas enrichment. (3) The mineralization process of CBM, shale gas, and iron ore is influenced by Yanshanian-period magma. The enrichment degree of CBM and shale gas exhibits an inverse correlation with the distance from the magmatic intrusion. Iron deposits demonstrate a close association with the magmatic intrusion, with enhanced enrichment along the rock layer. The results indicate that the destruction of the NCC triggered intense metasomatism in the deep cratonic fluids, serving as the primary driving mechanism for large-scale mineralization during the Yanshanian period. Magmatic intrusions bring hydrothermal fluids conducive to mineralization, and the heat release from these intrusions promotes thermal evolution, hydrocarbon generation, and the enrichment of organic-rich strata.

Background & Aims: In Wilson disease (WD), copper accumulation and increased non-ceruloplasmin-bound copper in plasma lead to liver and brain pathology. To better understand the fate of non-ceruloplasmin-bound copper, we used PET/CT to examine the whole-body distribution of intravenously injected 64-copper (64Cu). Methods: Eight patients with WD, five heterozygotes, and nine healthy controls were examined by dynamic PET/CT for 90 min and static PET/CT up to 20 h after injection. We measured 64Cu activity in blood and tissue and quantified the kinetics by compartmental analysis. Results: Initially, a large fraction of injected 64Cu was distributed to extrahepatic tissues, especially skeletal muscle. Thus, across groups, extrahepatic tissues accounted for 45-58% of the injected dose (%ID) after 10 min, and 45-55% after 1 h. Kinetic analysis showed rapid exchange of 64Cu between blood and muscle as well as adipose tissue, with 64Cu retention in a secondary compartment, possibly mitochondria. This way, muscle and adipose tissue may protect the brain from spikes in non-ceruloplasmin-bound copper. Tiny amounts of cerebral 64Cu were detected (0.2%ID after 90 min and 0.3%ID after 6 h), suggesting tight control of cerebral copper in accordance with a cerebral clearance that is 2-3-fold lower than in muscle. Compared to controls, patients with WD accumulated more hepatic copper 6-20 h after injection, and also renal copper at 6 h. Conclusion: Non-ceruloplasmin-bound copper is initially distributed into a number of tissues before being redistributed slowly to the eliminating organ, the liver. Cerebral uptake of copper is extremely slow and likely highly regulated. Our findings provide new insights into the mechanisms of copper control. Impact and implications: Maintaining non-ceruloplasmin-bound copper within the normal range is an important treatment goal in WD as this “free” copper is considered toxic to the liver and brain. We found that intravenously injected non-ceruloplasmin-bound copper quickly distributed to a number of tissues, especially skeletal muscle, subcutaneous fat, and the liver, while uptake into the brain was slow. This study offers new insights into the mechanisms of copper control, which may encourage further research into potential new treatment targets. Clinical trial number: 2016–001975-59.

The goal of this study was to investigate the neurophysiological correlates of visual awareness, with a specific focus on its event‐related spectral perturbation (ERSP) features. To this aim, we tried to disentangle the proper neural correlates of consciousness (NCC) from other prerequisite and post‐perceptual processing. To do so, we administered an orientation discrimination task, inducing a response bias through task instructions. EEG results showed that different frequency bands are involved in this kind of task, with different spectral and temporal dynamics. In particular, alpha and beta bands seem to be particularly engaged, especially in the aware‐unaware contrast, showing a main power suppression for aware trials and replicating previous literature. Moreover, we demonstrated that the process of visual awareness is orchestrated by a complex interaction of different frequencies (i.e., theta, alpha, beta and gamma) being involved as prerequisites and post‐perceptual processes. [ABSTRACT FROM AUTHOR]

In the Late Neoarchaean, the lithosphere of the North China Craton (NCC) experienced a strong extensional event, which is of great significance for understanding the evolution of the continental crust in the Precambrian. In this study, a suite of mafic dykes from Shandong province in the northeastern NCC were investigated to determine the nature, timing and source of rift-related magma activities using zircon U–Pb data, whole-rock geochemistry and Nd–Hf isotopes. Zircon U–Pb dating of four dolerites by laser ablation – inductively coupled plasma – mass spectrometry (LA-ICP-MS) yielded weighted mean 207Pb/206Pb ages in the range 2509 ± 6.1 to 2537 ± 6.2 Ma (2σ, 95 % confidence interval). The mafic dykes are classified as alkaline rocks based on their K2O + Na2O contents (6.78–7.21 wt %) and belong to the shoshonitic series according to their K2O contents (3.23–3.36 wt %). The dolerites show low concentrations of light rare earth elements ((La/Yb)N between 7.17 and 8.55), positive Eu anomalies (Eu/Eu* between 1.12 and 1.27), positive Ba, K, Pb, Sr, Eu, Dy and Lu anomalies, and depleted U, Nb, Pr, Ta, P, Nd and Ti anomalies. The dykes are characterized by low initial (87Sr/86Sr)i (∼0.6969), positive ε Nd(t) values (0.2–0.8) and ε Hf(t) values (0.5–8.6) and relatively old mean Nd and Hf model age (2.73 Ga). Collectively, the data suggest that the mafic dykes were derived from the partial melting (10–20 %) of an isotope-depleted garnet–lherzolite mantle source that was hybridized through interaction with subducted lower crustal material. The parental magmas of these dykes underwent a certain number of crustal contaminations during magma ascent. The mafic magmatism represented in the form of the dyke swarms is considered to be a response to widespread lithospheric extension which affected the NCC at c. 2.5 Ga during the Neoarchaean. [ABSTRACT FROM AUTHOR]

This study assessed how Nigerian Communications Commission’s media activities helped to create meaningful positive awakening on the knowledge, attitude and perception (KAP) of telecoms users’ rights among mobile phone users in Calabar, Nigeria. It adopted the descriptive survey research method and used Perception Theory and Uses and Gratifications Theory to lend theoretical support to it. Out of 400 copies of a questionnaire distributed, 385 were retrieved. Findings included that NCC’s media activities on telecoms users’ rights were intensive and helped to create positive awakening on the knowledge of telecoms users’ rights in Calabar, thus leading them to exhibit positive attitude and perception towards the overall awareness campaign on their rights. It was recommended that NCC should carry out more independent studies in other localities across Nigeria with a view to ascertaining the extent of telecoms consumers’ knowledge of their rights, particularly among rural dwellers. [ABSTRACT FROM AUTHOR]

The case describes an 82-year-old right-handed Hispanic male with multiple chronic comorbidities complaining of upper and lower extremity weakness as well as paresthesias that had been worsening over the last two weeks. He had bilateral upper and lower extremity weakness that was worse on the right and he complained of not being able to walk on his own with several falls preceding admission because of this. There were no overt signs of spinal cord compression or cauda equina syndrome. Laboratory work-up was unremarkable with exception to mildly elevated acute phase reactants. Computed tomography (CT) and magnetic resonance (MR) imaging later showed critical cervical compressive myelopathy at the C3-C4 level and multiple parenchymal and extra-axial enhancing lesions in the frontal lobes with associated calcifications suspicious for neurocysticercosis. Antihelminthic therapy was started and the patient underwent spinal fusion surgery with neurosurgery with an uncomplicated post-operative course - also lacking seizure activity of any kind.

To enhance the conventional LSB technique of digital image watermarking, the paper introduces a novel approach of LSB technique based on matrix multiplication process. This technique selects the non-consecutive matrix of pixels to replace the last three bits of each RGB components of cover image by watermark image. The filtering process is applied on each block of matrix to select the suitable block for embedding process. Extraction process of watermark is just the reverse of the embedding process. The non-uniform substitution of bits makes the system more vigorous in terms of robustness, imperceptibility and security. Although the proposed method is non blind type of digital watermarking, the original image is required at destination side for the extraction process. MATLAB tool is used for the evaluation of the proposed system. The strength of the given methodology is highlighted by experimental results and tabulated for statistical attacks. This technique is suitable for content authentication and copyright protection applications.

Neurocysticercosis (NCC)—a parasitic CNS infection endemic to developing nations—has been called the leading global cause of acquired epilepsy yet remains understudied. It is currently unknown why a large proportion of patients develop recurrent seizures, often following the presentation of acute seizures. Furthermore, the presentation of NCC is heterogenous and the features that predispose to the development of an epileptogenic state remain uncertain. Perilesional factors (such as oedema and gliosis) have been implicated in NCC-related ictogenesis, but the effects of cystic factors, including lesion load and location, seem not to play a role in the development of habitual epilepsy. In addition, the cytotoxic consequences of the cyst's degenerative stages are varied and the majority of research, relying on retrospective data, lacks the necessary specificity to distinguish between acute symptomatic and unprovoked seizures. Previous research has established that epileptogenesis can be the consequence of abnormal network connectivity, and some imaging studies have suggested that a causative link may exist between NCC and aberrant network organisation. In wider epilepsy research, network approaches have been widely adopted; studies benefiting predominantly from the rich, multimodal data provided by advanced MRI methods are at the forefront of the field. Quantitative MRI approaches have the potential to elucidate the lesser-understood epileptogenic mechanisms of NCC. This review will summarise the current understanding of the relationship between NCC and epilepsy, with a focus on MRI methodologies. In addition, network neuroscience approaches with putative value will be highlighted, drawing from current imaging trends in epilepsy research. [Display omitted] [ABSTRACT FROM AUTHOR]

The kidney regulates blood pressure through salt/water reabsorption affected by tubular sodium transporters. Expanding our prior research on placental cluster of differentiation 81 (CD81), this study explores the interaction of renal CD81 with sodium transporters in preeclampsia (PE). Effects of renal CD81 with sodium transporters were determined in lipopolysaccharide (LPS)‐induced PE rats and immortalized mouse renal distal convoluted tubule cells. Urinary exosomal CD81, sodium potassium 2 chloride cotransporter (NKCC2), and sodium chloride cotransporter (NCC) were measured in PE patients. LPS‐PE rats had hypertension from gestational days (GD) 6 to 18 and proteinuria from GD9 to GD18. Urinary CD81 in both groups tented to rise during pregnancy. Renal CD81, not sodium transporters, was higher in LPS‐PE than controls on GD14. On GD18, LPS‐PE rats exhibited higher CD81 in kidneys and urine exosomes, higher renal total and phosphorylated renal NKCC2 and NCC with elevated mRNAs, and lower ubiquitinated NCC than controls. CD81 was co‐immunoprecipitated with NKCC2 or NCC in kidney homogenates and co‐immunostained with NKCC2 or NCC in apical membranes of renal tubules. In plasma membrane fractions, LPS‐PE rats had greater amounts of CD81, NKCC2, and NCC than controls with enhanced co‐immunoprecipitations of CD81 with NKCC2 or NCC. In renal distal convoluted tubule cells, silencing CD81 with siRNA inhibited NCC and prevented LPS‐induced NCC elevation. Further, PE patients had higher CD81 in original urines, urine exosomes and higher NKCC2 and NCC in urine exosomes than controls. Thus, the upregulation of renal CD81 on NKCC2 and NCC may contribute to the sustained hypertension observed in LPS‐PE model. Urine CD81 with NKCC2 and NCC may be used as biomarkers for PE. [ABSTRACT FROM AUTHOR]

The Paleoproterozoic Khondalite Belt, located in the northwestern segment of North China Craton (NCC), is characterized by widespread high-temperature/ultrahigh-temperature (UHT) granulite/gneiss and large-scale magmatic activity. The tectonic evolution is still controversial. Here, we report new geochronological, elemental, and Hf-O-Sr-Nd isotopic data for a Paleoproterozoic layered complex in the Jining terrane to constrain the tectonic evolution of the Khondalite Belt. In situ zircon U-Pb dating indicates that the Sanchakou gabbros were emplaced between ~1.94 Ga and ~1.82 Ga, which might be the heat source of UHT metamorphism. The elemental and Hf-O-Sr-Nd isotopic analysis shows that the formation of Sanchakou gabbros is consistent with the assimilation and fractional crystallization (AFC) process. The magma originates from the 10%~20% partial melting of the spinel + garnet lherzolite mantle. The Sanchakou gabbros are magmatic crystallization products mixed with crustal wallrocks in the magma chamber. We have established a tectonic evolution model involving asthenosphere upwelling after the amalgamation of the Ordos and Yinshan Blocks at ~1.95 Ga. [ABSTRACT FROM AUTHOR]

The gills are the major organ for Na+ uptake in teleosts. It was proposed that freshwater (FW) teleosts adopt Na+/H+ exchanger 3 (Nhe3) as the primary transporter for Na+ uptake and Na+-Cl− co-transporter (Ncc) as the backup transporter. However, convincing molecular physiological evidence to support the role of Ncc in branchial Na+ uptake is still lacking due to the limitations of functional assays in the gills. Thus, this study aimed to reveal the role of branchial Ncc in Na+ uptake with an in vivo detection platform (scanning ion-selective electrode technique, SIET) that has been recently established in fish gills. First, we identified that Ncc2-expressing cells in zebrafish gills are a specific subtype of ionocyte (NCC ionocytes) by using single-cell transcriptome analysis and immunofluorescence. After a long-term low-Na+ FW exposure, zebrafish increased branchial Ncc2 expression and the number of NCC ionocytes and enhanced gill Na+ uptake capacity. Pharmacological treatments further suggested that Na+ is indeed taken up by Ncc, in addition to Nhe, in the gills. These findings reveal the uptake roles of both branchial Ncc and Nhe under FW and shed light on osmoregulatory physiology in adult fish. [ABSTRACT FROM AUTHOR]

The thiazide sensitive Na+:Cl- cotransporter (NCC) is the principal via for salt reabsorption in the apical membrane of the distal convoluted tubule (DCT) in mammals and plays a fundamental role in managing blood pressure. The cotransporter is targeted by thiazide diuretics, a highly prescribed medication that is effective in treating arterial hypertension and edema. NCC was the first member of the electroneutral cation-coupled chloride cotransporter family to be identified at a molecular level. It was cloned from the urinary bladder of the Pseudopleuronectes americanus (winter flounder) 30 years ago. The structural topology, kinetic and pharmacology properties of NCC have been extensively studied, determining that the transmembrane domain (TM) coordinates ion and thiazide binding. Functional and mutational studies have discovered residues involved in the phosphorylation and glycosylation of NCC, particularly on the N-terminal domain, as well as the extracellular loop connected to TM7-8 (EL7-8). In the last decade, single-particle cryogenic electron microscopy (cryo-EM) has permitted the visualization of structures at high atomic resolution for six members of the SLC12 family (NCC, NKCC1, KCC1-KCC4). Cryo-EM insights of NCC confirm an inverted conformation of the TM1-5 and TM6-10 regions, a characteristic also found in the amino acid-polyamine-organocation (APC) superfamily, in which TM1 and TM6 clearly coordinate ion binding. The high-resolution structure also displays two glycosylation sites (N-406 and N-426) in EL7-8 that are essential for NCC expression and function. In this review, we briefly describe the studies related to the structure-function relationship of NCC, beginning with the first biochemical/functional studies up to the recent cryo-EM structure obtained, to acquire an overall view enriched with the structural and functional aspects of the cotransporter. [ABSTRACT FROM AUTHOR]

The thiazide sensitive Na+:Cl− cotransporter (NCC) is the principal via for salt reabsorption in the apical membrane of the distal convoluted tubule (DCT) in mammals and plays a fundamental role in managing blood pressure. The cotransporter is targeted by thiazide diuretics, a highly prescribed medication that is effective in treating arterial hypertension and edema. NCC was the first member of the electroneutral cation-coupled chloride cotransporter family to be identified at a molecular level. It was cloned from the urinary bladder of the Pseudopleuronectes americanus (winter flounder) 30 years ago. The structural topology, kinetic and pharmacology properties of NCC have been extensively studied, determining that the transmembrane domain (TM) coordinates ion and thiazide binding. Functional and mutational studies have discovered residues involved in the phosphorylation and glycosylation of NCC, particularly on the N-terminal domain, as well as the extracellular loop connected to TM7-8 (EL7-8). In the last decade, single-particle cryogenic electron microscopy (cryo-EM) has permitted the visualization of structures at high atomic resolution for six members of the SLC12 family (NCC, NKCC1, KCC1-KCC4). Cryo-EM insights of NCC confirm an inverted conformation of the TM1-5 and TM6-10 regions, a characteristic also found in the amino acid-polyamine-organocation (APC) superfamily, in which TM1 and TM6 clearly coordinate ion binding. The high-resolution structure also displays two glycosylation sites (N-406 and N-426) in EL7-8 that are essential for NCC expression and function. In this review, we briefly describe the studies related to the structure-function relationship of NCC, beginning with the first biochemical/functional studies up to the recent cryo-EM structure obtained, to acquire an overall view enriched with the structural and functional aspects of the cotransporter.

With-no-lysine (K) (WNK) kinases have been identified as the causal genes for pseudohypoaldosteronism type II (PHAII), a rare hereditary hypertension condition characterized by hyperkalemia, hyperchloremic metabolic acidosis, and thiazide-hypersensitivity. We thought that clarifying the link between WNK and NaCl cotransporter (NCC) would bring us new mechanism(s) of NCC regulation. For the first time, we were able to produce a knock-in mouse model of PHAII and anti-phosphorylated NCC antibodies against the putative NCC phosphorylation sites and discover that constitutive activation of NCC and increased phosphorylation of NCC are the primary pathogenesis of the disease in vivo. We have since demonstrated that this regulatory mechanism is mediated by the kinases oxidative stress-response protein 1 (OSR1) and STE20/SPS1- related proline/alanine-rich kinase (SPAK) (WNK-OSR1/SPAK-NCC signaling cascade) and that the signaling is not only important in the pathological condition of PHAII but also plays a crucial physiological role in the regulation of NCC. [ABSTRACT FROM AUTHOR]

Traditional contrastive analysis has been the foundation of consciousness science, but its limitations due to the lack of a reliable method for measuring states of consciousness have prompted the exploration of alternative approaches. Structuralist theories have gained attention as an alternative that focuses on the structural properties of phenomenal experience and seeks to identify their neural encoding via structural similarities between quality spaces and neural state spaces. However, the intertwining of philosophical assumptions about structuralism and structuralist methodology may pose a challenge to those who are skeptical of the former. In this paper, I offer an analysis and defense of structuralism as a methodological approach in consciousness science, which is partly independent of structuralist assumptions on the nature of consciousness. By doing so, I aim to make structuralist methodology more accessible to a broader scientific and philosophical audience. I situate methodological structuralism in the context of questions concerning mental representation, psychophysical measurement, holism, and functional relevance of neural processes. At last, I analyze the relationship between the structural approach and the distinction between conscious and unconscious states. [ABSTRACT FROM AUTHOR]

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The standard treatment guidelines of neurocysticercosis have been described as per computed tomography (CT)–based studies. We aimed to prospectively study if posttreatment magnetic resonance imaging (MRI) clearance rates of neurocysticercosis were like those reported in literature using CT.A prospective observational study in newly diagnosed children with neurocysticercosis was undertaken. Children were treated with antihelminthics and steroids and followed up after 6 months. The primary objective was to study the proportion of children with single-lesion neurocysticercosis who were in radiologic resolution at 6 months and clinical remission (seizure-free for the preceding 3 months).Eighty of 128 consecutive children screened were included (single lesion, 65; multiple lesions, 15). Seventy-two children were evaluated at 6 months. Seizure recurrence was seen in 5 (6.2%). Brain MRI showed an overall clearance of lesions in 10 (14%) children. In the children with single-lesion neurocysticercosis (65), 59 were followed up at 6 months, and lesions resolved in 9 (15.3%, 95% confidence interval of 6.1-24.4).In children with single-lesion neurocysticercosis treated with antihelminthics and corticosteroids, the lesion resolution rate is only 15% at 6 months. Thus, there is a need to review old recommendations and use MRI as a standard outcome measure. [ABSTRACT FROM AUTHOR]

How teleosts take up Na+ from the surrounding freshwater (FW) as well as the underlying mechanisms associated with this process have received considerable attention over the past 85 years. Owing to an enormous ion gradient between hypotonic FW and fish body fluids, teleosts gills have to actively absorb Na+ (via ionocytes) to compensate for the passive loss of Na+. To date, three models have been proposed for Na+ uptake in teleost ionocytes, including Na+/H+ exchanger (NHE)-mediated, acid-sensing ion channel (ASIC)-mediated, Na+-Cl- co-transporter (NCC)-mediated pathways. However, some debates regarding these models and unclear mechanisms still remain. To better understand how teleosts take up Na+ from FW, this mini-review summarizes the main progress and related regulatory mechanisms of Na+ uptake, and discusses some of the challenges to the current models.

Basolateral potassium channels in the distal convoluted tubule (DCT) are composed of inwardly-rectifying potassium channel 4.1 (Kir4.1) and Kir5.1. Kir4.1 interacts with Kir5.1 to form a 40 pS K+ channel which is the only type K+ channel expressed in the basolateral membrane of the DCT. Moreover, Kir4.1/Kir5.1 heterotetramer plays a key role in determining the expression and activity of thiazide-sensitive Na-Cl cotransport (NCC). In addition to Kir4.1/Kir5.1, Kir1.1 (ROMK) is expressed in the apical membrane of the late DCT (DCT2) and plays a key role in mediating epithelial Na+ channel (ENaC)-dependent K+ excretion. High dietary-K+-intake (HK) stimulates ROMK and inhibits Kir4.1/Kir5.1 in the DCT. Inhibition of Kir4.1/Kir5.1 is essential for HK-induced suppression of NCC whereas the stimulation of ROMK is important for increasing ENaC-dependent K+ excretion during HK. We have nowused the patch-clamp-technique to examine whether gender and Cl- content of K+-diet affect HK-induced inhibition of basolateral Kir4.1/Kir5.1 and HK-induced stimulation of ROMK. Single-channelrecording shows that basolateral 40 pS K+ channel (Kir4.1/Kir5.1) activity of the DCT defined by NPo was 1.34 (1% KCl, normal K, NK), 0.95 (5% KCl) and 1.03 (5% K+- citrate) in male mice while it was 1.47, 1.02 and 1.05 in female mice. The whole-cell recording shows that Kir4.1/Kir5.1-mediated-K+ current of the early-DCT (DCT1) was 1,170 pA (NK), 725 pA (5% KCl) and 700 pA (5% K+-citrate) inmalemicewhereas it was 1,125 pA, 674 pA and 700 pA in female mice. Moreover, K+-currents (IK) reversal potential of DCT (an index of membrane potential) was -63 mV (NK), -49 mV (5% KCl) and -49 mV (5% K-citrate) in the male mice whereas it was -63 mV, -50 mV and -50 mV in female mice. Finally, TPNQ-sensitive wholecell ROMK-currents in the DCT2/initial-connecting tubule (CNT)were 910 pA (NK), 1,520 pA (5% KCl) and 1,540 pA (5% K+-citrate) in male mice whereas the ROMKmediated K+ currents were 1,005 pA, 1,590 pA and 1,570 pA in female mice. We conclude that the effect of HK intake on Kir4.1/Kir5.1 of the DCT and ROMK of DCT2/CNT is similar between male and female mice. Also, Cl- content in HK diets has no effect on HK-induced inhibition of Kir4.1/Kir5.1 of the DCT and HK-induced stimulation of ROMK in DCT2/CNT. [ABSTRACT FROM AUTHOR]

Over ten years of Visible Infrared Imaging Radiometer Suite (VIIRS) Environmental Data Records (EDR) Imagery Team activities have included primarily imagery validation, but also product generation and display and user interactions. VIIRS imagery validation starts with pre-launch preparations leading up to producing first-light imagery shortly after the launch of each Joint Polar Satellite System (JPSS) satellite. Imagery quality is scrutinized for typical imagery visualization problems, as well as the overall ability to utilize VIIRS imagery for analysis and forecasting purposes. Then, long-term monitoring of imagery continues through the lifetime of each VIIRS instrument. The VIIRS EDR Imagery Team has undertaken four major ground system code changes. The first of these code changes was needed in 2013 when Near Constant Contrast (NCC) Imagery at night was not routinely being generated from the Day-Night Band (DNB) due to incorrect sensitivity limits. The second applied Terrain Correction to the VIIRS EDR Imagery in 2020. The third, in 2021, was needed to fix an imagery banding anomaly in the NCC, which was masked for years by the natural variability of most NCC Imagery. The fourth was the increase from 6 M-band EDRs to all 16 M-band EDRs in 2021, allowing for the display of true-color and other multi-band imagery products from VIIRS Imagery EDRs. Here, we summarize the efforts of the VIIRS EDR Imagery Team which have resulted in a valuable suite of quality-controlled imagery products for the user community. [ABSTRACT FROM AUTHOR]

To enhance the conventional LSB technique of digital image watermarking, the paper introduces a novel approach of LSB technique based on matrix multiplication process. This technique selects the non-consecutive matrix of pixels to replace the last three bits of each RGB components of cover image by watermark image. The filtering process is applied on each block of matrix to select the suitable block for embedding process. Extraction process of watermark is just the reverse of the embedding process. The non-uniform substitution of bits makes the system more vigorous in terms of robustness, imperceptibility and security. Although the proposed method is non blind type of digital watermarking, the original image is required at destination side for the extraction process. MATLAB tool is used for the evaluation of the proposed system. The strength of the given methodology is highlighted by experimental results and tabulated for statistical attacks. This technique is suitable for content authentication and copyright protection applications. [ABSTRACT FROM AUTHOR]

The with-no-lysine (WNK) kinase family, comprising four serine-threonine protein kinases (WNK1-4), were first linked to hypertension due to their mutations in association with pseudohypoaldosteronism type II (PHAII). WNK kinases regulate crucial blood pressure regulators, SPAK/OSR1, to mediate the post-translational modifications (PTMs) of their downstream ion channel substrates, such as sodium chloride co-transporter (NCC), epithelial sodium chloride (ENaC), renal outer medullary potassium channel (ROMK), and Na/K/2Cl co-transporters (NKCCs). In this review, we summarize the molecular pathways dysregulating the WNKs and their downstream target renal ion transporters. We summarize each of the genetic variants of WNK kinases and the small molecule inhibitors that have been discovered to regulate blood pressure via WNK-triggered PTM cascades. [ABSTRACT FROM AUTHOR]

Background The proposed watermarking framework is based on the multi-resolution Walsh-Hadamard Transform (MR-WHT) along with Schur factorization. For embedding, the cover image is converted into a frequency domain using MR-WHT before Schur factorization is applied. Methods The upper triangle's highest stable eigenvalues in the Schur factorization are employed as reliable embedding locations for the watermark. The singular values of these coefficients are updated with the singular values of the watermark, and the matrix array generated by the biggest eigenvalues is further factorised by singular value decomposition using multiple scaling factors and Differential evolution (DE). Later, an inverse SVD, inverse Schur, and inverse multiresolution Walsh-Hadamard transform is executed to obtain a watermarked image. Results The simulation results show that the proposed method is imperceptible and robust against existing watermarking algorithms used in the literature.

Basolateral potassium channels in the distal convoluted tubule (DCT) are composed of inwardly-rectifying potassium channel 4.1 (Kir4.1) and Kir5.1. Kir4.1 interacts with Kir5.1 to form a 40 pS K+ channel which is the only type K+ channel expressed in the basolateral membrane of the DCT. Moreover, Kir4.1/Kir5.1 heterotetramer plays a key role in determining the expression and activity of thiazide-sensitive Na-Cl cotransport (NCC). In addition to Kir4.1/Kir5.1, Kir1.1 (ROMK) is expressed in the apical membrane of the late DCT (DCT2) and plays a key role in mediating epithelial Na+ channel (ENaC)-dependent K+ excretion. High dietary-K+-intake (HK) stimulates ROMK and inhibits Kir4.1/Kir5.1 in the DCT. Inhibition of Kir4.1/Kir5.1 is essential for HK-induced suppression of NCC whereas the stimulation of ROMK is important for increasing ENaC-dependent K+ excretion during HK. We have now used the patch-clamp-technique to examine whether gender and Cl− content of K+-diet affect HK-induced inhibition of basolateral Kir4.1/Kir5.1 and HK-induced stimulation of ROMK. Single-channel-recording shows that basolateral 40 pS K+ channel (Kir4.1/Kir5.1) activity of the DCT defined by NPo was 1.34 (1% KCl, normal K, NK), 0.95 (5% KCl) and 1.03 (5% K+-citrate) in male mice while it was 1.47, 1.02 and 1.05 in female mice. The whole-cell recording shows that Kir4.1/Kir5.1-mediated-K+ current of the early-DCT (DCT1) was 1,170 pA (NK), 725 pA (5% KCl) and 700 pA (5% K+-citrate) in male mice whereas it was 1,125 pA, 674 pA and 700 pA in female mice. Moreover, K+-currents (IK) reversal potential of DCT (an index of membrane potential) was -63 mV (NK), −49 mV (5% KCl) and −49 mV (5% K-citrate) in the male mice whereas it was -63 mV, −50 mV and −50 mV in female mice. Finally, TPNQ-sensitive whole-cell ROMK-currents in the DCT2 /initial-connecting tubule (CNT) were 910 pA (NK), 1,520 pA (5% KCl) and 1,540 pA (5% K+−citrate) in male mice whereas the ROMK-mediated K+ currents were 1,005 pA, 1,590 pA and 1,570 pA in female mice. We conclude that the effect of HK intake on Kir4.1/Kir5.1 of the DCT and ROMK of DCT2/CNT is similar between male and female mice. Also, Cl− content in HK diets has no effect on HK-induced inhibition of Kir4.1/Kir5.1 of the DCT and HK-induced stimulation of ROMK in DCT2/CNT.

Manufacturing companies using CPSS integrate multiple data in organizational production and present the data in the form of data visualization with the help of a big screen data visualization. In order to help the manufacturing enterprises using the data visualization screen to understand the data trend of the whole production process more conveniently, this paper proposes a method to establish the connection and interaction between the visualization screen and the mobile terminal based on the positive octagon K-value template matching algorithm, match the pre-processed mobile phone pictures with the visual large screen image, determine the area where the captured image is located in the large screen image, and return the detailed information of chart components contained in the visual large screen area to the mobile phone for users' observation and analysis. This matching algorithm has good matching accuracy and time efficiency. Application cases and related investigations in enterprises also prove the practicability of this method to a certain extent. [ABSTRACT FROM AUTHOR]

Effects of 2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPO) oxidation were evaluated for magnetic bio-nanocomposites of nanocrystalline cellulose (NCC). The magnetic bio-nanocomposites were prepared using NCC and nanomagnetite (NM) to produce organic compounds. The NCC was oxidized by sodium bromide (NaBr), sodium hypochlorite (NaOCl), and TEMPO. The oxidized NCC (ONCC) was characterized by Fouriertransform infrared spectroscopy (FTIR) and conductometry. The bionanocomposite particles from the NCC and the ONCC were prepared via in situ precipitation of iron salts from alkaline solution. The resultant bionanocomposites were coated on the surface of kraft paper. The magnetic bio-nanocomposite and coated papers were characterized using scanning electron microscopy (SEM), atomic force microscopy (AFM), X-ray diffraction (XRD), and vibrating sample magnetometry (VSM). The results revealed that the carboxyl groups were introduced successfully on the NCC surface. The bio-nanocomposite particles showed good dispersion in the surface of the papers. The saturation magnetizations of the coated papers with magnetic bio-nanocomposites of NCC and ONCC were 10.9 and 14.57 emu/g, respectively. The magnetic coated papers exhibited a superparamagnetic behavior. The strengths, apparent density, and air resistance of the coated paper with the ONCC bio-nanocomposites increased in comparison to the NCC coated sample, while the water absorption diminished due to the TEMPO-oxidation. [ABSTRACT FROM AUTHOR]