Journal articles: 'Function'

1

Rathod, Ashok. "Characteristic function and deficiency of algebroid functions on annuli." Ufimskii Matematicheskii Zhurnal 11, no. 1 (2019): 121–32. http://dx.doi.org/10.13108/2019-11-1-121.

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FERNANDES, CLAUDIO, OLEKSIY KARLOVYCH, and M. ARCIO VALENTE. "ON THE DENSITY OF LAGUERRE FUNCTIONS IN SOME BANACH FUNCTION SPACES." Journal of Inequalities and Special Functions 13, no. 2 (June 30, 2022): 37–45. http://dx.doi.org/10.54379/jiasf-2022-2-4.

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Let λ > 0 and Φλ := {ϕ1,λ, ϕ2,λ, . . . } be the system of dilated Laguerre functions. We show that if L1 (R+) ∩ L∞(R+) is embedded into a separable Banach function space X(R+), then the linear span of Φλ is dense in X(R+). This implies that the linear span of Φλ is dense in every separable rearrangement-invariant space X(R+) and in every separable variable Lebesgue space Lp(·) (R+)

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Smer Eker, S., B. �eker, and S. Ece. "On Normalized Rabotnov Function Associated with Certain Subclasses of Analytic Functions." Issues of Analysis 30, no. 2 (June 2023): 97–106. http://dx.doi.org/10.15393/j3.art.2023.12490.

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Carpintero, C., E. Rosas, M. Sallas-Brown, and L. Vasquez. "A unified theory of weakly g-closed sets and weakly g-continuous functions." Sarajevo Journal of Mathematics 9, no. 2 (November 2013): 303–15. http://dx.doi.org/10.5644/sjm.09.2.14.

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Ng, Ka-Lok, Jin-Shuei Ciou, and Chien-Hung Huang. "Prediction of protein functions based on function–function correlation relations." Computers in Biology and Medicine 40, no. 3 (March 2010): 300–305. http://dx.doi.org/10.1016/j.compbiomed.2010.01.001.

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Johansson, Ingvar. "Functions, Function Concepts, and Scales." Monist 87, no. 1 (2004): 96–114. http://dx.doi.org/10.5840/monist20048718.

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Rhodes, Sam, and Jessica Duggan. "Cryptic Functions: Understanding Function Identification." Mathematics Teacher 112, no. 2 (October 2018): 108–13. http://dx.doi.org/10.5951/mathteacher.112.2.0108.

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Abi-Khuzam, Faruk F. "Meromorphic functions with harmonic ∗-function." Complex Variables, Theory and Application: An International Journal 12, no. 1-4 (October 1989): 261–65. http://dx.doi.org/10.1080/17476938908814370.

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Balasubramanian, R., S. Kanemitsu, and K. Ramachandra. "On ideal-function-like functions." Journal of Computational and Applied Mathematics 160, no. 1-2 (November 2003): 27–36. http://dx.doi.org/10.1016/s0377-0427(03)00611-3.

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Thakur, D. S. "Hypergeometric Functions for Function Fields." Finite Fields and Their Applications 1, no. 2 (April 1995): 219–31. http://dx.doi.org/10.1006/ffta.1995.1017.

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Bllaca, Kajtaz H., Jawher Khmiri, Kamel Mazhouda, and Bouchaïb Sodaïgui. "Superzeta functions on function fields." Finite Fields and Their Applications 95 (March 2024): 102367. http://dx.doi.org/10.1016/j.ffa.2024.102367.

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KOTANI, SHINICHI. "Construction of KdV flow I. Tau-Function via Weyl Function." Zurnal matematiceskoj fiziki, analiza, geometrii 14, no. 3 (September 25, 2018): 297–335. http://dx.doi.org/10.15407/mag14.03.297.

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13

RC, Dorca. "Density Function Thermal Scaling and Physical Significance of Shape Functions." Physical Science & Biophysics Journal 1, no. 1 (2017). http://dx.doi.org/10.23880/psbj-16000102.

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14

"A Study of Function Spaces through a Functor." International Journal of Science and Research (IJSR) 5, no. 6 (June 5, 2016): 574–77. http://dx.doi.org/10.21275/v5i6.nov164078.

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"Fixed Coefficients for Certain Subclass of Univalent Functions using Hypergeometric Function." International Journal of Science and Research (IJSR) 5, no. 5 (May 5, 2015): 1072–78. http://dx.doi.org/10.21275/v5i5.11051602.

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Hu, Nengfa. "A Genetic Algorithm for Solving Multimodal Functions Based on Neighborhood Penalty Function." Scholars Journal of Engineering and Technology 4, no. 6 (June 2016). http://dx.doi.org/10.21276/sjet.2016.4.6.4.

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17

Koch, Lauren Gerard, and Steven L. Britton. "Biology: Motion is Function." Function, June 14, 2022. http://dx.doi.org/10.1093/function/zqac030.

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Abstract 1. In 1966 Francis Crick declared that: “The ultimate aim of the modern movement in biology is to explain all biology in terms of physics and chemistry.” This motivated us to contemplate approaches that unify biology at a fundamental level. Exploration led us to consider the features of energy, entropy, and motion. Overall, it can be considered that motion of matter is the feature of life function. No motion. No function. 2. In initial work we evaluated the hypothesis that the scope for biologic function is mediated mechanistically by a differential for energy transfer. Maximal treadmill running capacity served as a proxy for energy transfer. The span for capacity was estimated “biologically” by application of two-way artificial selection in rats for running capacity. Consistent with our “Energy Transfer Hypothesis” (ETH), low physical health and dysfunction segregated with low running capacity and high physical health and function segregated with high running capacity. The high energy yield of aerobic metabolism is also consonant with the ETH; that is, amongst the elements of the universe, oxygen is second only to fluorine in electronegativity. Although we deem these energy findings possibly correct, they are based on correlation and do not illuminate function via fundamental principles. 3. For consideration of life, Entropy (2nd Law of thermodynamics) can be viewed as an open system that exchanges energy with the universe operating via nonequilibrium thermodynamics. The Principle of Maximal Entropy Production (MEP) states that: If a source of free energy is present, complex systems can intercept the free energy flow, and self-organize to enhance entropy production. The development of Benard convection cells in a water heat gradient demonstrate simplistic operation of MEP. 4. A direct step forward would be to explain the mechanism of the obligatory motion of molecules for life function. Motion may be mediated by operation of “action at a distance” for molecules as considered by the Einstein-Podolsky-Rosen Paradox and confirmed by JS Bell. Magnetism, electricity, and gravity are also examples of action at a distance. We propose that some variant of “action at a distance” as directed by the property of Maximal Entropy Production (MEP) underwrites biologic motion.

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Petersen, Ole H. "FUNCTION is now functional." Function 1, no. 1 (January 1, 2020). http://dx.doi.org/10.1093/function/zqaa001.

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Molina, Patricia E. "Thinking through FUNCTION during COVID-19." Function 1, no. 2 (2020). http://dx.doi.org/10.1093/function/zqaa019.

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Brown, Dennis. "Aquaporin Function: Seek and You Shall Find!" Function 2, no. 1 (November 9, 2020). http://dx.doi.org/10.1093/function/zqaa041.

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Shyng, Show-Ling. "KATP Channel Function: More than Meets the Eye." Function 3, no. 1 (2022). http://dx.doi.org/10.1093/function/zqab070.

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"Bifurcation of a Prey-predator System with Holling Type-III Functional Response Function." International Journal of Science and Research (IJSR) 5, no. 3 (March 5, 2016): 1181–83. http://dx.doi.org/10.21275/v5i3.nov162131.

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23

Kroemer, Guido, and Alexei Verkhratsky. "Mitochondrial Localization and Function of the Purinergic Receptor P2X7." Function 2, no. 2 (January 28, 2021). http://dx.doi.org/10.1093/function/zqab006.

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Petersen, Ole H. "FUNCTION Is One Year Old: How Did We Do?" Function 2, no. 3 (March 22, 2021). http://dx.doi.org/10.1093/function/zqab023.

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Noble, Denis. "Function Forms from the Symmetry Between Order and Disorder." Function 2, no. 1 (November 9, 2020). http://dx.doi.org/10.1093/function/zqaa037.

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Harraz, Osama F. "Endothelial cell metabolism and vascular function: A paradigm shift?" Function, January 6, 2023. http://dx.doi.org/10.1093/function/zqad002.

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Pollock, David M. "Physiology Brings Relevance to Biological Research: A Vision for Function." Function, May 6, 2024. http://dx.doi.org/10.1093/function/zqae023.

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Colinas, Olalla, Peter Mombaerts, José López-Barneo, and Patricia Ortega-Sáenz. "Carotid Body Function in Tyrosine Hydroxylase Conditional Olfr78 Knockout Mice." Function, February 22, 2024. http://dx.doi.org/10.1093/function/zqae010.

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Abstract The Olfr78 gene encodes a G-protein coupled receptor that is expressed in olfactory sensory neurons, where it functions as a conventional odorant receptor, and also in several ectopic sites, where its function is not well understood. Olfr78 is one of the most highly expressed mRNA species in glomus cells of the carotid body (CB). These cells are the prototypical oxygen (O2) sensitive arterial chemoreceptors, which, in response to lowered O2 tension (hypoxia), activate the respiratory centers to induce hyperventilation. It has been proposed that Olfr78 is a lactate receptor and that glomus cell activation by the increase in blood lactate mediates the hypoxic ventilatory response (HVR). However, this proposal has been challenged by several groups showing that Olfr78 is not a physiologically relevant lactate receptor and that the O2-based regulation of breathing is not affected in Olfr78 knockout mice. In another study, Olfr78 knockout mice were reported to have altered systemic and CB responses to mild hypoxia. These organismal phenotypes could result from pleiotropic effects of the constitutive Olfr78 knockout mutations in the various CB cell types and/or various organs where this gene is expressed. Therefore, to further characterize the functional role of Olfr78 in CB glomus cells, we here generated a conditional Olfr78 knockout mouse strain and then restricted the knockout to glomus cells and other catecholaminergic cells by crossing with a tyrosine hydroxylase-specific Cre driver strain (TH-Olfr78 KO mice). We find that TH-Olfr78 KO mice have a normal HVR. Interestingly, glomus cells of TH-Olfr78 KO mice exhibit molecular and electrophysiological alterations as well as a reduced dopamine content in secretory vesicles and neurosecretory activity. These functional characteristics resemble those of CB neuroblasts in wild-type mice. We suggest that, although Olfr78 is not essential for CB O2 sensing, activation of Olfr78-dependent pathways is required for the phenotypic specification of mature glomus cells.

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Assmus, Adrienne, Linda Mullins, Mairi Ward, Ross Dobie, Robert Hunter, Neil C. Henderson, and John J. Mullins. "Loss of Adam10 Disrupts Ion Transport in Immortalized Kidney Collecting Duct Cells." Function 2, no. 4 (2021). http://dx.doi.org/10.1093/function/zqab024.

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Abstract The kidney cortical collecting duct (CCD) comprises principal cells (PCs), intercalated cells (IC), and the recently discovered intermediate cell type. Kidney pathology in a mouse model of the syndrome of apparent aldosterone excess revealed plasticity of the CCD, with altered PC:intermediate cell:IC ratio. The self-immortalized mouse CCD cell line, mCCDcl1, shows functional characteristics of PCs, but displays a range of cell types, including intermediate cells, making it ideal to study plasticity. We knocked out Adam10, a key component of the Notch pathway, in mCCDcl1 cells, using CRISPR-Cas9 technology, and isolated independent clones, which exhibited severely affected sodium transport capacity and loss of aldosterone response. Single-cell RNA sequencing revealed significantly reduced expression of major PC-specific markers, such as Scnn1g (γ-ENaC) and Hsd11b2 (11βHSD2), but no significant changes in transcription of components of the Notch pathway were observed. Immunostaining in the knockout clone confirmed the decrease in expression of γ-ENaC and importantly, showed an altered, diffuse distribution of PC and IC markers, suggesting altered trafficking in the Adam10 knockout clone as an explanation for the loss of polarization.

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Abbott, Claire B., Marcus M. Lawrence, Kamil A. Kobak, Erika Barboza Prado Lopes, Frederick F. Peelor, Elizabeth J. Donald, Holly Van Remmen, Timothy M. Griffin, and Benjamin F. Miller. "A Novel Stable Isotope Approach Demonstrates Surprising Degree of Age-Related Decline in Skeletal Muscle Collagen Proteostasis." Function 2, no. 4 (2021). http://dx.doi.org/10.1093/function/zqab028.

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Abstract Age-related deterioration in turnover of collagen proteins accelerates extracellular matrix fibrosis and hinders adaptation to external stimuli. This project sought to understand factors that increase skeletal muscle fibrosis with age by studying what we term the dynamic protein pool. We hypothesized that the dynamic protein pool size of muscle collagen decreases with age, thus indicating a decrease in proteostatic maintenance (ie, ability to maintain proteostasis), and that failure to account for these changes impacts the interpretation of tracer-measured synthesis rates. We used deuterium oxide (D2O) labeling for up to 60 days in adult (6 months) and old (23 months) mice. The dynamic protein pool in adult skeletal muscle was 65% in tibialis anterior (TA), but only 28% in gastrocnemius (Gastroc). In aged muscle, the dynamic protein pool was further decreased to only 35% and 14% for TA and Gastroc, respectively. We showed that this loss in dynamic pool size was associated with increases in markers of fibrosis and decreased proteostatic maintenance. We demonstrate that aged muscle has higher rates of collagen protein synthesis and lower rates of collagen protein breakdown, which causes collagen accumulation. We further demonstrated that the normal assumption of complete protein renewal and the standard practice of taking a single sample with isotope labeling have profound impacts on interpretation of the genesis of fibrosis. Strategies to maintain muscle function with aging should focus on the dynamic protein pool with attention to methodological strategies to assess those changes.

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Rizki-Safitri, Astia, Tamara Traitteur, and Ryuji Morizane. "Bioengineered Kidney Models: Methods and Functional Assessments." Function 2, no. 4 (2021). http://dx.doi.org/10.1093/function/zqab026.

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Abstract Investigations into bioengineering kidneys have been extensively conducted owing to their potential for preclinical assays and regenerative medicine. Various approaches and methods have been developed to improve the structure and function of bioengineered kidneys. Assessments of functional properties confirm the adequacy of bioengineered kidneys for multipurpose translational applications. This review is to summarize the studies performed in kidney bioengineering in the past decade. We identified 84 original articles from PubMed and Mendeley with keywords of kidney organoid or kidney tissue engineering. Those were categorized into 5 groups based on their approach: de-/recellularization of kidney, reaggregation of kidney cells, kidney organoids, kidney in scaffolds, and kidney-on-a-chip. These models were physiologically assessed by filtration, tubular reabsorption/secretion, hormone production, and nephrotoxicity. We found that bioengineered kidney models have been developed from simple cell cultures to multicellular systems to recapitulate kidney function and diseases. Meanwhile, only about 50% of these studies conducted functional assessments on their kidney models. Factors including cell composition and organization are likely to alter the applicability of physiological assessments in bioengineered kidneys. Combined with recent technologies, physiological assessments importantly contribute to the improvement of the bioengineered kidney model toward repairing and refunctioning the damaged kidney.

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Xia, Maosheng, Shanshan Liang, Shuai Li, Ming Ji, Beina Chen, Manman Zhang, Chengyi Dong, et al. "Iatrogenic Iron Promotes Neurodegeneration and Activates Self-Protection of Neural Cells against Exogenous Iron Attacks." Function 2, no. 2 (January 12, 2021). http://dx.doi.org/10.1093/function/zqab003.

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Abstract Metal implants are used worldwide, with millions of nails, plates, and fixtures grafted during orthopedic surgeries. Iron is the most common element of these metal implants. As time passes, implants can be corroded and iron can be released. Ionized iron permeates the surrounding tissues and enters circulation; importantly, iron ions pass through the blood–brain barrier. Can iron from implants represent a risk factor for neurological diseases? This remains an unanswered question. In this study, we discovered that patients with metal implants delivered through orthopedic surgeries have higher incidence of Parkinson’s disease or ischemic stroke compared to patients who underwent similar surgeries but did not have implants. Concentration of serum iron and ferritin was increased in subjects with metal implants. In experiments in vivo, we found that injection of iron dextran selectively decreased the presence of divalent metal transporter 1 (DMT1) in neurons through increasing the expression of Ndfip1, which degrades DMT1 and does not exist in glial cells. At the same time, excess of iron increased expression of DMT1 in astrocytes and microglial cells and triggered reactive astrogliosis and microgliosis. Facing the attack of excess iron, glial cells act as neuroprotectors to accumulate more extracellular iron by upregulating DMT1, whereas neurons limit iron uptake through increasing DMT1 degradation. Cerebral accumulation of iron in animals is associated with impaired cognition, locomotion, and mood. Excess iron from surgical implants thus can affect neural cells and may be regarded as a risk factor for neurodegeneration.

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Von Schulze, Alex T., Fengyan Deng, Kelly N. Z. Fuller, Edziu Franczak, Josh Miller, Julie Allen, Colin S. McCoin, et al. "Heat Treatment Improves Hepatic Mitochondrial Respiratory Efficiency via Mitochondrial Remodeling." Function 2, no. 2 (January 22, 2021). http://dx.doi.org/10.1093/function/zqab001.

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Abstract Nonacholic fatty liver disease, or hepatic steatosis, is the most common liver disorder affecting the western world and currently has no pharmacologic cure. Thus, many investigations have focused on alternative strategies to treat or prevent hepatic steatosis. Our laboratory has shown that chronic heat treatment (HT) mitigates glucose intolerance, insulin resistance, and hepatic steatosis in rodent models of obesity. Here, we investigate the direct bioenergetic mechanism(s) surrounding the metabolic effects of HT on hepatic mitochondria. Utilizing mitochondrial proteomics and respiratory function assays, we show that one bout of acute HT (42°C for 20 min) in male C57Bl/6J mice (n = 6/group) triggers a hepatic mitochondrial heat shock response resulting in acute reductions in respiratory capacity, degradation of key mitochondrial enzymes, and induction of mitophagy via mitochondrial ubiquitination. We also show that chronic bouts of HT and recurrent activation of the heat shock response enhances mitochondrial quality and respiratory function via compensatory adaptations in mitochondrial organization, gene expression, and transport even during 4 weeks of high-fat feeding (n = 6/group). Finally, utilizing a liver-specific heat shock protein 72 (HSP72) knockout model, we are the first to show that HSP72, a protein putatively driving the HT metabolic response, does not play a significant role in the hepatic mitochondrial adaptation to acute or chronic HT. However, HSP72 is required for the reductions in blood glucose observed with chronic HT. Our data are the first to suggest that chronic HT (1) improves hepatic mitochondrial respiratory efficiency via mitochondrial remodeling and (2) reduces blood glucose in a hepatic HSP72-dependent manner.

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Sarti, Alba Clara, Valentina Vultaggio-Poma, Simonetta Falzoni, Sonia Missiroli, Anna Lisa Giuliani, Paola Boldrini, Massimo Bonora, et al. "Mitochondrial P2X7 Receptor Localization Modulates Energy Metabolism Enhancing Physical Performance." Function 2, no. 2 (January 28, 2021). http://dx.doi.org/10.1093/function/zqab005.

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Abstract Basal expression of the P2X7 receptor (P2X7R) improves mitochondrial metabolism, Adenosine 5′-triphosphate (ATP) synthesis, and overall fitness of immune and non-immune cells. We investigated P2X7R contribution to energy metabolism and subcellular localization in fibroblasts (mouse embryo fibroblasts and HEK293 human fibroblasts), mouse microglia (primary brain microglia, and the N13 microglia cell line), and heart tissue. The P2X7R localizes to mitochondria, and its lack (1) decreases basal respiratory rate, ATP-coupled respiration, maximal uncoupled respiration, resting mitochondrial potential, mitochondrial matrix Ca2+ level, (2) modifies expression pattern of oxidative phosphorylation enzymes, and (3) severely affects cardiac performance. Hearts from P2rx7-deleted versus wild-type mice are larger, heart mitochondria smaller, and stroke volume, ejection fraction, fractional shortening, and cardiac output, are significantly decreased. Accordingly, the physical fitness of P2X7R-null mice is severely reduced. Thus, the P2X7R is a key modulator of mitochondrial energy metabolism and a determinant of physical fitness.

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Gaspers, Lawrence D., Andrew P. Thomas, Jan B. Hoek, and Paula J. Bartlett. "Ethanol Disrupts Hormone-Induced Calcium Signaling in Liver." Function 2, no. 2 (January 8, 2021). http://dx.doi.org/10.1093/function/zqab002.

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Abstract Receptor-coupled phospholipase C (PLC) is an important target for the actions of ethanol. In the ex vivo perfused rat liver, concentrations of ethanol >100 mM were required to induce a rise in cytosolic calcium (Ca2+) suggesting that these responses may only occur after binge ethanol consumption. Conversely, pharmacologically achievable concentrations of ethanol (≤30 mM) decreased the frequency and magnitude of hormone-stimulated cytosolic and nuclear Ca2+ oscillations and the parallel translocation of protein kinase C-β to the membrane. Ethanol also inhibited gap junction communication resulting in the loss of coordinated and spatially organized intercellular Ca2+ waves in hepatic lobules. Increasing the hormone concentration overcame the effects of ethanol on the frequency of Ca2+ oscillations and amplitude of the individual Ca2+ transients; however, the Ca2+ responses in the intact liver remained disorganized at the intercellular level, suggesting that gap junctions were still inhibited. Pretreating hepatocytes with an alcohol dehydrogenase inhibitor suppressed the effects of ethanol on hormone-induced Ca2+ increases, whereas inhibiting aldehyde dehydrogenase potentiated the inhibitory actions of ethanol, suggesting that acetaldehyde is the underlying mediator. Acute ethanol intoxication inhibited the rate of rise and the magnitude of hormone-stimulated production of inositol 1,4,5-trisphosphate (IP3), but had no effect on the size of Ca2+ spikes induced by photolysis of caged IP3. These findings suggest that ethanol inhibits PLC activity, but does not affect IP3 receptor function. We propose that by suppressing hormone-stimulated PLC activity, ethanol interferes with the dynamic modulation of [IP3] that is required to generate large, amplitude Ca2+ oscillations.

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Parekh, Anant B. "Opening New Terrain in Intracellular Ca2+ Signaling." Function 2, no. 3 (March 22, 2021). http://dx.doi.org/10.1093/function/zqab016.

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Riedl, Ruth A., Colin M. L. Burnett, Nicole A. Pearson, John J. Reho, Mohamad Mokadem, Robert A. Edwards, Tammy L. Kindel, John R. Kirby, and Justin L. Grobe. "Gut Microbiota Represent a Major Thermogenic Biomass." Function 2, no. 3 (March 22, 2021). http://dx.doi.org/10.1093/function/zqab019.

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Abstract Evidence supports various roles for microbial metabolites in the control of multiple aspects of host energy flux including feeding behaviors, digestive efficiency, and energy expenditure, but few studies have quantified the energy utilization of the biomass of the gut microbiota itself. Because gut microbiota exist in an anoxic environment, energy flux is expected to be anaerobic; unfortunately, commonly utilized O2/CO2 respirometry-based approaches are unable to detect anaerobic energy flux. To quantify the contribution of the gut microbial biomass to whole-animal energy flux, we examined the effect of surgical reduction of gut biomass in C57BL/6J mice via cecectomy and assessed energy expenditure using methods sensitive to anaerobic flux, including bomb and direct calorimetry. First, we determined that cecectomy caused an acceleration of weight gain over several months due to a reduction in combined total host plus microbial energy expenditure, as reflected by an increase in energy efficiency (ie, weight gained per calorie absorbed). Second, we determined that under general anesthesia, cecectomy caused immediate changes in heat dissipation that were significantly modified by short-term pretreatment with dietary or pharmaceutical interventions known to modify the microbiome, and confirmed that these effects were undetectable by respirometry. We conclude that while the cecum only contributes approximately 1% of body mass in the mouse, this organ contributes roughly 8% of total resting energy expenditure, that this contribution is predominantly anaerobic, and that the composition and abundance of the cecal microbial contents can significantly alter its contribution to energy flux.

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Tarran, Robert, R. Graham Barr, Neal L. Benowitz, Aruni Bhatnagar, Hong W. Chu, Pamela Dalton, Claire M. Doerschuk, et al. "E-Cigarettes and Cardiopulmonary Health." Function 2, no. 2 (February 8, 2021). http://dx.doi.org/10.1093/function/zqab004.

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Abstract E-cigarettes have surged in popularity over the last few years, particularly among youth and young adults. These battery-powered devices aerosolize e-liquids, comprised of propylene glycol and vegetable glycerin, typically with nicotine, flavors, and stabilizers/humectants. Although the use of combustible cigarettes is associated with several adverse health effects including multiple pulmonary and cardiovascular diseases, the effects of e-cigarettes on both short- and long-term health have only begun to be investigated. Given the recent increase in the popularity of e-cigarettes, there is an urgent need for studies to address their potential adverse health effects, particularly as many researchers have suggested that e-cigarettes may pose less of a health risk than traditional combustible cigarettes and should be used as nicotine replacements. This report is prepared for clinicians, researchers, and other health care providers to provide the current state of knowledge on how e-cigarette use might affect cardiopulmonary health, along with research gaps to be addressed in future studies.

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Jackson, William F. "Capillary Inward-Rectifying K+ Crippled in a Mouse Model of Alzheimer’s Disease: Phosphatidylinositol 4,5-Bisphosphate to the Rescue!" Function 2, no. 3 (March 22, 2021). http://dx.doi.org/10.1093/function/zqab017.

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Petersen, Ole H. "Different Effects of Alcohol on the Liver and the Pancreas." Function 2, no. 2 (February 10, 2021). http://dx.doi.org/10.1093/function/zqab008.

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Peng, Zhong, and Stephan Kellenberger. "Hydrogen Sulfide Upregulates Acid-sensing Ion Channels via the MAPK-Erk1/2 Signaling Pathway." Function 2, no. 2 (February 10, 2021). http://dx.doi.org/10.1093/function/zqab007.

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Abstract Hydrogen sulfide (H2S) emerged recently as a new gasotransmitter and was shown to exert cellular effects by interacting with proteins, among them many ion channels. Acid-sensing ion channels (ASICs) are neuronal voltage-insensitive Na+ channels activated by extracellular protons. ASICs are involved in many physiological and pathological processes, such as fear conditioning, pain sensation, and seizures. We characterize here the regulation of ASICs by H2S. In transfected mammalian cells, the H2S donor NaHS increased the acid-induced ASIC1a peak currents in a time- and concentration-dependent manner. Similarly, NaHS potentiated also the acid-induced currents of ASIC1b, ASIC2a, and ASIC3. An upregulation induced by the H2S donors NaHS and GYY4137 was also observed with the endogenous ASIC currents of cultured hypothalamus neurons. In parallel with the effect on function, the total and plasma membrane expression of ASIC1a was increased by GYY4137, as determined in cultured cortical neurons. H2S also enhanced the phosphorylation of the extracellular signal-regulated kinase (pErk1/2), which belongs to the family of mitogen-activated protein kinases (MAPKs). Pharmacological blockade of the MAPK signaling pathway prevented the GYY4137-induced increase of ASIC function and expression, indicating that this pathway is required for ASIC regulation by H2S. Our study demonstrates that H2S regulates ASIC expression and function, and identifies the involved signaling mechanism. Since H2S shares several roles with ASICs, as for example facilitation of learning and memory, protection during seizure activity, and modulation of nociception, it may be possible that H2S exerts some of these effects via a regulation of ASIC function.

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Fisher-Wellman, Kelsey H. "Heating Up to Heal—Acute Heat Exposure Increases Hepatic Mitophagy Resulting in Hormetic Improvements in Mitochondrial Bioenergetic Efficiency." Function 2, no. 2 (February 10, 2021). http://dx.doi.org/10.1093/function/zqab011.

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Lee, Seojin, and Gabor G. Kovacs. "Astrocytic-Neuronal Teamwork Against External Iron Attacks: Does It Always Work?" Function 2, no. 2 (February 10, 2021). http://dx.doi.org/10.1093/function/zqab009.

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Mughal, Amreen, Osama F. Harraz, Albert L. Gonzales, David Hill-Eubanks, and Mark T. Nelson. "PIP2 Improves Cerebral Blood Flow in a Mouse Model of Alzheimer’s Disease." Function 2, no. 2 (February 10, 2021). http://dx.doi.org/10.1093/function/zqab010.

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Abstract Alzheimer’s disease (AD) is a leading cause of dementia and a substantial healthcare burden. Despite this, few treatment options are available for controlling AD symptoms. Notably, neuronal activity-dependent increases in cortical cerebral blood flow (CBF; functional hyperemia) are attenuated in AD patients, but the associated pathological mechanisms are not fully understood at the molecular level. A fundamental mechanism underlying functional hyperemia is activation of capillary endothelial inward-rectifying K+ (Kir2.1) channels by neuronally derived potassium (K+), which evokes a retrograde capillary-to-arteriole electrical signal that dilates upstream arterioles, increasing blood delivery to downstream active regions. Here, using a mouse model of familial AD (5xFAD), we tested whether this impairment in functional hyperemia is attributable to reduced activity of capillary Kir2.1 channels. In vivo CBF measurements revealed significant reductions in whisker stimulation (WS)-induced and K+-induced hyperemic responses in 5xFAD mice compared with age-matched controls. Notably, measurements of whole-cell currents in freshly isolated 5xFAD capillary endothelial cells showed that Kir2.1 current density was profoundly reduced, suggesting a defect in Kir2.1 function. Because Kir2.1 activity absolutely depends on binding of phosphatidylinositol 4,5-bisphosphate (PIP2) to the channel, we hypothesized that capillary Kir2.1 channel impairment could be corrected by exogenously supplying PIP2. As predicted, a PIP2 analog restored Kir2.1 current density to control levels. More importantly, systemic administration of PIP2 restored K+-induced CBF increases and WS-induced functional hyperemic responses in 5xFAD mice. Collectively, these data provide evidence that PIP2-mediated restoration of capillary endothelial Kir2.1 function improves neurovascular coupling and CBF in the setting of AD.

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Redolfi, Nelly, Elisa Greotti, Giulia Zanetti, Tino Hochepied, Cristina Fasolato, Diana Pendin, and Tullio Pozzan. "A New Transgenic Mouse Line for Imaging Mitochondrial Calcium Signals." Function 2, no. 3 (February 25, 2021). http://dx.doi.org/10.1093/function/zqab012.

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AbstractMitochondria play a key role in cellular calcium (Ca2+) homeostasis. Dysfunction in the organelle Ca2+ handling appears to be involved in several pathological conditions, ranging from neurodegenerative diseases, cardiac failure and malignant transformation. In the past years, several targeted green fluorescent protein (GFP)-based genetically encoded Ca2+ indicators (GECIs) have been developed to study Ca2+ dynamics inside mitochondria of living cells. Surprisingly, while there is a number of transgenic mice expressing different types of cytosolic GECIs, few examples are available expressing mitochondria-localized GECIs, and none of them exhibits adequate spatial resolution. Here we report the generation and characterization of a transgenic mouse line (hereafter called mt-Cam) for the controlled expression of a mitochondria-targeted, Förster resonance energy transfer (FRET)-based Cameleon, 4mtD3cpv. To achieve this goal, we engineered the mouse ROSA26 genomic locus by inserting the optimized sequence of 4mtD3cpv, preceded by a loxP-STOP-loxP sequence. The probe can be readily expressed in a tissue-specific manner upon Cre recombinase-mediated excision, obtainable with a single cross. Upon ubiquitous Cre expression, the Cameleon is specifically localized in the mitochondrial matrix of cells in all the organs and tissues analyzed, from embryos to aged animals. Ca2+ imaging experiments performed in vitro and ex vivo in brain slices confirmed the functionality of the probe in isolated cells and live tissues. This new transgenic mouse line allows the study of mitochondrial Ca2+ dynamics in different tissues with no invasive intervention (such as viral infection or electroporation), potentially allowing simple calibration of the fluorescent signals in terms of mitochondrial Ca2+ concentration ([Ca2+]).

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Szabo, Csaba. "Hydrogen Sulfide, an Emerging Regulator of Acid-Sensing Ion Channels." Function 2, no. 2 (February 10, 2021). http://dx.doi.org/10.1093/function/zqab014.

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Troia, Angela, Russell H. Knutsen, Carmen M. Halabi, Daniela Malide, Zu Xi Yu, Amanda Wardlaw-Pickett, Elise K. Kronquist, et al. "Inhibition of NOX1 Mitigates Blood Pressure Increases in Elastin Insufficiency." Function 2, no. 3 (March 15, 2021). http://dx.doi.org/10.1093/function/zqab015.

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Abstract Elastin (ELN) insufficiency leads to the cardiovascular hallmarks of the contiguous gene deletion disorder, Williams–Beuren syndrome, including hypertension and vascular stiffness. Previous studies showed that Williams–Beuren syndrome deletions, which extended to include the NCF1 gene, were associated with lower blood pressure (BP) and reduced vascular stiffness. NCF1 encodes for p47phox, the regulatory component of the NOX1 NADPH oxidase complex that generates reactive oxygen species (ROS) in the vascular wall. Dihydroethidium and 8-hydroxyguanosine staining of mouse aortas confirmed that Eln heterozygotes (Eln+/−) had greater ROS levels than the wild-types (Eln+/+), a finding that was negated in vessels cultured without hemodynamic stressors. To analyze the Nox effect on ELN insufficiency, we used both genetic and chemical manipulations. Both Ncf1 haploinsufficiency (Ncf1+/−) and Nox1 insufficiency (Nox1−/y) decreased oxidative stress and systolic BP in Eln+/− without modifying vascular structure. Chronic treatment with apocynin, a p47phox inhibitor, lowered systolic BP in Eln+/−, but had no impact on Eln+/+ controls. In vivo dosing with phenylephrine (PE) produced an augmented BP response in Eln+/− relative to Eln+/+, and genetic modifications or drug-based interventions that lower Nox1 expression reduced the hypercontractile response to PE in Eln+/− mice to Eln+/+ levels. These results indicate that the mechanical and structural differences caused by ELN insufficiency leading to oscillatory flow can perpetuate oxidative stress conditions, which are linked to hypertension, and that by lowering the Nox1-mediated capacity for vascular ROS production, BP differences can be normalized.

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Xie, Zidian, Irfan Rahman, Maciej L. Goniewicz, and Dongmei Li. "Perspectives on Epigenetics Alterations Associated with Smoking and Vaping." Function 2, no. 3 (March 22, 2021). http://dx.doi.org/10.1093/function/zqab022.

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Abstract Epigenetic alterations, including DNA methylation, microRNA, and long noncoding RNA, play important roles in the pathogenesis of numerous respiratory health conditions and diseases. Exposure to tobacco smoking has been found to be associated with epigenetic changes in the respiratory tract. Marketed as a less harmful alternative to combustible cigarettes, electronic cigarette (e-cigarette) has rapidly gained popularity in recent years, especially among youth and young adults. Accumulative evidence from both animal and human studies has shown that e-cigarette use (vaping) is also linked to similar respiratory health conditions as observed with cigarette smoking, including wheezing, asthma, and COPD. This review aims to provide an overview of current studies on associations of smoking and vaping with epigenetic alterations in respiratory cells and provide future research directions in epigenetic studies related to vaping.

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Zubcevic, Jasenka, and Bina Joe. "Ain’t No Sunshine When They’re Gone: Rendering the Gut Microbiota “Homeless” by Cecectomy Reveals Their True Thermogenic Potential." Function 2, no. 3 (March 22, 2021). http://dx.doi.org/10.1093/function/zqab020.

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Sackheim, Adrian M., Nuria Villalba, Maria Sancho, Osama F. Harraz, Adrian D. Bonev, Angelo D’Alessandro, Travis Nemkov, Mark T. Nelson, and Kalev Freeman. "Traumatic Brain Injury Impairs Systemic Vascular Function through Disruption of Inward-Rectifier Potassium Channels." Function 2, no. 3 (March 22, 2021). http://dx.doi.org/10.1093/function/zqab018.

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Abstract Trauma can lead to widespread vascular dysfunction, but the underlying mechanisms remain largely unknown. Inward-rectifier potassium channels (Kir2.1) play a critical role in the dynamic regulation of regional perfusion and blood flow. Kir2.1 channel activity requires phosphatidylinositol 4,5-bisphosphate (PIP2), a membrane phospholipid that is degraded by phospholipase A2 (PLA2) in conditions of oxidative stress or inflammation. We hypothesized that PLA2-induced depletion of PIP2 after trauma impairs Kir2.1 channel function. A fluid percussion injury model of traumatic brain injury (TBI) in rats was used to study mesenteric resistance arteries 24 h after injury. The functional responses of intact arteries were assessed using pressure myography. We analyzed circulating PLA2, hydrogen peroxide (H2O2), and metabolites to identify alterations in signaling pathways associated with PIP2 in TBI. Electrophysiology analysis of freshly-isolated endothelial and smooth muscle cells revealed a significant reduction of Ba2+-sensitive Kir2.1 currents after TBI. Additionally, dilations to elevated extracellular potassium and BaCl2- or ML 133-induced constrictions in pressurized arteries were significantly decreased following TBI, consistent with an impairment of Kir2.1 channel function. The addition of a PIP2 analog to the patch pipette successfully rescued endothelial Kir2.1 currents after TBI. Both H2O2 and PLA2 activity were increased after injury. Metabolomics analysis demonstrated altered lipid metabolism signaling pathways, including increased arachidonic acid, and fatty acid mobilization after TBI. Our findings support a model in which increased H2O2-induced PLA2 activity after trauma hydrolyzes endothelial PIP2, resulting in impaired Kir2.1 channel function.

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Journal articles on the topic 'Function'

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