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We examined the extent to which apnoea‐induced extremes of oxygen demand/carbon dioxide production impact redox regulation of cerebral bioenergetic function. Ten ultra‐elite apnoeists (six men and four women) performed two maximal dry apnoeas preceded by normoxic normoventilation, resulting in severe end‐apnoea hypoxaemic hypercapnia, and hyperoxic hyperventilation designed to ablate hypoxaemia, resulting in hyperoxaemic hypercapnia. Transcerebral exchange of ascorbate radicals (by electron paramagnetic resonance spectroscopy) and nitric oxide metabolites (by tri‐iodide chemiluminescence) were calculated as the product of global cerebral blood flow (by duplex ultrasound) and radial arterial (a) to internal jugular venous (v) concentration gradients. Apnoea duration increased from 306 ± 62 s during hypoxaemic hypercapnia to 959 ± 201 s in hyperoxaemic hypercapnia (P ≤ 0.001). Apnoea generally increased global cerebral blood flow (all P ≤ 0.001) but was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose (P = 0.015–0.044). This was associated with a general net cerebral output (v > a) of ascorbate radicals that was greater in hypoxaemic hypercapnia (P = 0.046 vs. hyperoxaemic hypercapnia) and coincided with a selective suppression in plasma nitrite uptake (a > v) and global cerebral blood flow (P = 0.034 to <0.001 vs. hyperoxaemic hypercapnia), implying reduced consumption and delivery of nitric oxide consistent with elevated cerebral oxidative–nitrosative stress. In contrast, we failed to observe equidirectional gradients consistent with S‐nitrosohaemoglobin consumption and plasma S‐nitrosothiol delivery during apnoea (all P ≥ 0.05). Collectively, these findings highlight a key catalytic role for hypoxaemic hypercapnia in cerebral oxidative–nitrosative stress. Key points: Local sampling of blood across the cerebral circulation in ultra‐elite apnoeists determined the extent to which severe end‐apnoea hypoxaemic hypercapnia (prior normoxic normoventilation) and hyperoxaemic hypercapnia (prior hyperoxic hyperventilation) impact free radical‐mediated nitric oxide bioavailability and global cerebral bioenergetic function.Apnoea generally increased the net cerebral output of free radicals and suppressed plasma nitrite consumption, thereby reducing delivery of nitric oxide consistent with elevated oxidative–nitrosative stress.The apnoea‐induced elevation in global cerebral blood flow was insufficient to prevent a reduction in the cerebral metabolic rates of oxygen and glucose.Cerebral oxidative–nitrosative stress was greater during hypoxaemic hypercapnia compared with hyperoxaemic hypercapnia and coincided with a lower apnoea‐induced elevation in global cerebral blood flow, highlighting a key catalytic role for hypoxaemia.This applied model of voluntary human asphyxia might have broader implications for the management and treatment of neurological diseases characterized by extremes of oxygen demand and carbon dioxide production. [ABSTRACT FROM AUTHOR]

Aim: How the cerebral metabolic rates of oxygen and glucose utilization (CMRO2 and CMRGlc, respectively) are affected by alterations in arterial PCO2 (PaCO2) is equivocal and therefore was the primary question of this study. Methods: This retrospective analysis involved pooled data from four separate studies, involving 41 healthy adults (35 males/6 females). Participants completed stepwise steady‐state alterations in PaCO2 ranging between 30 and 60 mmHg. The CMRO2 and CMRGlc were assessed via the Fick approach (CBF × arterial‐internal jugular venous difference of oxygen or glucose content, respectively) utilizing duplex ultrasound of the internal carotid artery and vertebral artery to calculate cerebral blood flow (CBF). Results: The CMRO2 was altered by 0.5 mL × min−1 (95% CI: −0.6 to −0.3) per mmHg change in PaCO2 (p < 0.001) which corresponded to a 9.8% (95% CI: −13.2 to −6.5) change in CMRO2 with a 9 mmHg change in PaCO2 (inclusive of hypo‐ and hypercapnia). The CMRGlc was reduced by 7.7% (95% CI: −15.4 to −0.08, p = 0.045; i.e., reduction in net glucose uptake) and the oxidative glucose index (ratio of oxygen to glucose uptake) was reduced by 5.6% (95% CI: −11.2 to 0.06, p = 0.049) with a + 9 mmHg increase in PaCO2. Conclusion: Collectively, the CMRO2 is altered by approximately 1% per mmHg change in PaCO2. Further, glucose is incompletely oxidized during hypercapnia, indicating reductions in CMRO2 are either met by compensatory increases in nonoxidative glucose metabolism or explained by a reduction in total energy production. [ABSTRACT FROM AUTHOR]

Despite elite human free divers achieving incredible feats in competitive free diving, there has yet to be a study that compares consummate divers, (i.e. northern elephant seals) to highly conditioned free divers (i.e., elite competitive free-diving humans). Herein, we compare these two diving models and suggest that hematological traits detected in seals reflect species-specific specializations, while hematological traits shared between the two species are fundamental mammalian characteristics. Arterial blood samples were analyzed in elite human free divers (n = 14) during a single, maximal volitional apnea and in juvenile northern elephant seals (n = 3) during rest-associated apnea. Humans and elephant seals had comparable apnea durations (∼6.5 min) and end-apneic arterial P o 2 [humans: 40.4 ± 3.0 mmHg (means ± SE); seals: 27.1 ± 5.9 mmHg; P = 0.2]. Despite similar increases in arterial P co 2 (humans: 33 ± 5%; seals: 16.3 ± 5%; P = 0.2), only humans experienced reductions in pH from baseline (humans: 7.45 ± 0.01; seals: 7.39 ± 0.02) to end apnea (humans: 7.37 ± 0.01; seals: 7.38 ± 0.02; P < 0.0001). Hemoglobin P50 was greater in humans compared to elephant seals (29.9 ± 1.5 and 28.7 ± 0.6 mmHg, respectively; P = 0.046). Elephant seals overall had higher carboxyhemoglobin (COHb) levels (5.9 ± 2.6%) compared to humans (0.8 ± 1.2%; P < 0.0001); however, following apnea, COHb was reduced in seals (baseline: 6.1 ± 0.3%; end apnea: 5.6 ± 0.3%) and was slightly elevated in humans (baseline: 0.7 ± 0.1%; end apnea: 0.9 ± 0.1%; P < 0.0002, both comparisons). Our data indicate that during static apnea, seals have reduced hemoglobin P50, greater pH buffering, and increased COHb levels. The differences in hemoglobin P50 are likely due to the differences in the physiological environment between the two species during apnea, whereas enhanced pH buffering and higher COHb may represent traits selected for in elephant seals. NEW & NOTEWORTHY: This study uses similar methods and protocols in elite human free divers and northern elephant seals. Using highly conditioned divers (elite free-diving humans) and highly adapted divers (northern elephant seals), we explored which hematological traits are fundamentally mammalian and which may have been selected for. We found differences in P50, which may be due to different physiological environments between species, while elevated pH buffering and carbon monoxide levels might have been selected for in seals. [ABSTRACT FROM AUTHOR]

Aim: Plants distributed between southern Taiwan and the north of the Philippines are spread among numerous small islands in an area crossed by the powerful Kuroshio current. Oceanic currents can be effective seed-dispersal agents for coastal plant species. Moreover, the Luzon Strait is an area prone to tropical cyclones. The aim of this study is to look at the dispersal capability of an endangered coastal plant species, the Mearns fig (Ficus pedunculosa var. mearnsii), using both experimental and population genetics methods. Location: Southern Taiwan, the Philippines, and the islands between Luzon and Taiwan Island. Methods: This study combined two types of analysis, i.e., buoyancy experiments on syconia and double digest restriction-associated DNA sequencing (ddRAD), to analyze the population genetics of the Mearns fig. Results: We first discovered that mature Mearns fig syconia could float in seawater. They have a mean float duration of 10 days to a maximum of 21 days. Germination rates varied significantly between Mearns fig seeds that had undergone different durations of flotation treatment. Population genetic analysis shows a high degree of inbreeding among various Mearns fig populations. Moreover, no isolation by distance was found between the populations and individuals. Main conclusions: From our analysis of the genetic structure of the Mearns fig populations, we can clearly highlight the effect of the Kuroshio oceanic current on the seed dispersal of this fig tree. Comprehensive analysis has shown that Mearns fig seeds are still viable before the mature syconium sinks into the seawater, and so they could use the Kuroshio Current to float to the current population locations in Taiwan. [ABSTRACT FROM AUTHOR]

This article discusses the role of Notch1 as a potential mechanosensor in the vascular system. Mechanosensors are responsible for detecting changes in hemodynamic forces and play a crucial role in maintaining vascular health. The article highlights the complex mechanisms of vascular mechanotransduction, including various techniques used to analyze mechanosignaling and the different mechanosensors involved. It also explores the Notch1 pathway and its interaction with other mechanosensory factors. The authors suggest that understanding the role of Notch1 in mechanosensing could have implications for vascular therapies. However, further research is needed to fully understand the extent of Notch1's role in vascular mechanotransduction. [Extracted from the article]

This paper proposes a novel data fusion technique for a wearable multi-sensory patch that integrates an accelerometer and a flexible resistive pressure sensor to accurately capture breathing patterns. It utilizes an accelerometer to detect breathing-related diaphragmatic motion and other body movements, and a flex sensor for muscle stretch detection. The proposed sensor data fusion technique combines inertial and pressure sensors to eliminate nonbreathing body motion-related artifacts, ensuring that the filtered signal exclusively conveys information pertaining to breathing. The fusion technique mitigates the limitations of relying solely on one sensor's data, providing a more robust and reliable solution for continuous breath monitoring in clinical and home environments. The sensing system was tested against gold-standard spirometry data from multiple participants for various breathing patterns. Experimental results demonstrate the effectiveness of the proposed approach in accurately monitoring breathing rates, even in the presence of nonbreathing-related body motion. The results also demonstrate that the multi-sensor patch presented in this paper can accurately distinguish between varying breathing patterns both at rest and during body movements. [ABSTRACT FROM AUTHOR]

The genus Ficus is unique in that it has a closed inflorescence (fig) holding all of the flowers inside its cavity, which is isolated from the outside world by a fleshy barrier: the fig wall. The fig wall is the main structure of the fig, giving its shape, but the wall has also important ecological functions such as protection of fig seeds and fig wasp larvae. Nevertheless, the fig wall anatomy is poorly understood. This study aims to examine the fig wall anatomy of 22 Ficus taxa (21 species, one species having two varieties) in Taiwan to reveal the diversity in anatomy of the fig wall. We found that these 21 fig species exhibited a great variety in fig wall anatomy, from the simplest parenchymatic wall to complex fig walls. The walls of the figs from 12 sampled taxa developed aerenchyma and sclerenchyma formations whereas seven taxa had fig walls containing tanniferous cells. Five anatomical types of fig walls have been identified according to the presence or absence of the different differentiated tissues. These types are distributed among the Ficus subgenera. Further studies on tissue differentiations of the fig wall should be investigated in other Ficus species as well as the ecological functions of the fig wall. Key words: comparative anatomy, Ficus, histology, inflorescence. Le genre Ficus est unique par son inflorescence fermée (figue) qui garde toutes les fleurs à l'intérieur de sa cavité, laquelle est isolée du monde extérieur par une barrière charnue, la paroi de la figue. La paroi de la figue constitue la structure principale de la figue qui lui donne sa forme, mais la paroi exerce aussi des fonctions écologiques importantes telles que la protection des graines de figue et des larves de la guêpe du figuier. Malgré cela, l'anatomie de la paroi de la figue est peu comprise. Cette étude vise à examiner l'anatomie de la paroi de la figue de 22 taxons de Ficus (21 espèces, une espèce comportant deux variétés) à Taiwan afin de révéler la diversité de l'anatomie de la paroi de la figue. Les auteurs ont trouvé que ces 21 espèces de figuiers présentaient une grande variété en ce qui concerne l'anatomie de la paroi de la figue, allant de parois de parenchyme simple à des parois complexes. Les parois des figues de 12 taxons échantillonnés développaient des formations d'aérenchyme et de sclérenchyme alors que sept taxons avaient des parois contenant des cellules tannifères. Cinq types anatomiques de parois ont été identifiés en fonction de la présence ou de l'absence de certains tissus différenciés. Ces types sont distribués entre les sous-genres de Ficus. Des études supplémentaires sur la différenciation des tissus de la paroi de la figue devraient être réalisées sur d'autres espèces de Ficus, de même des études sur les fonctions écologiques de la paroi de la figue. [Traduit par la Rédaction] Mots-clés : anatomie comparée, Ficus, histologie, inflorescence., Introduction The Moraceae family comprises about 38 genera and 1180 species (Christenhusz and Byng 2016) displaying a great diversity of life-history traits with a few synapomorphic characters such as laticifers, [...]

Passive hyperthermia causes cerebral hypoperfusion primarily from heat‐induced respiratory alkalosis. However, despite the cerebral hypoperfusion, it is possible that the mild alkalosis might help to attenuate cerebral inflammation. In this study, the cerebral exchange of extracellular vesicles (microvesicles), which are known to elicit pro‐inflammatory responses when released in conditions of stress, were examined in hyperthermia with and without respiratory alkalosis. Ten healthy male adults were heated passively, using a warm water‐perfused suit, up to core temperature + 2°C. Blood samples were taken from the radial artery and internal jugular bulb. Microvesicle concentrations were determined in platelet‐poor plasma via cells expressing CD62E (activated endothelial cells), CD31+/CD42b− (apoptotic endothelial cells), CD14 (monocytes) and CD45 (pan‐leucocytes). Cerebral blood flow was measured via duplex ultrasound of the internal carotid and vertebral arteries to determine cerebral exchange kinetics. From baseline to poikilocapnic (alkalotic) hyperthermia, there was no change in microvesicle concentration from any cell origin measured (P‐values all >0.05). However, when blood CO2 tension was normalized to baseline levels in hyperthermia, there was a marked increase in cerebral uptake of microvesicles expressing CD62E (P = 0.028), CD31+/CD42b− (P = 0.003) and CD14 (P = 0.031) compared with baseline, corresponding to large increases in arterial but not jugular venous concentrations. In a subset of seven participants who underwent hypercapnia and hypocapnia in the absence of heating, there was no change in microvesicle concentrations or cerebral exchange, suggesting that hyperthermia potentiated the CO2/pH‐mediated cerebral uptake of microvesicles. These data provide insight into a potential beneficial role of respiratory alkalosis in heat stress. Key points: The hyperthermia‐induced hyperventilatory response is observed in most humans, despite causing potentially harmful reductions in cerebral blood flow.We tested the hypothesis that the respiratory‐induced alkalosis is associated with lower circulating microvesicle concentrations, specifically in the brain, despite the reductions in blood flow.At core temperature + 2°C with respiratory alkalosis, microvesicles derived from endothelial cells, monocytes and leucocytes were at concentrations similar to baseline in the arterial and cerebral venous circulation, with no changes in cross‐brain microvesicle kinetics.However, when core temperature was increased by 2°C with CO2/pH normalized to resting levels, there was a marked cerebral uptake of microvesicles derived from endothelial cells and monocytes. The CO2/pH‐mediated alteration in cerebral microvesicle uptake occurred only in hyperthermia.These new findings suggest that the heat‐induced hyperventilatory response might serve a beneficial role by preventing potentially inflammatory microvesicle uptake in the brain. [ABSTRACT FROM AUTHOR]

The role of cerebral blood flow (CBF) on a maximal breath-hold (BH) in ultra-elite divers was examined. Divers (n = 7) performed one control BH, and one BH following oral administration of the non-selective cyclooxygenase inhibitor indomethacin (1.2 mg/kg). Arterial blood gases and CBF were measured prior to (baseline), and at BH termination. Compared to control, indomethacin reduced baseline CBF and cerebral delivery of oxygen (CDO2) by about 26% (p < 0.01). Indomethacin reduced maximal BH time from 339 ± 51 to 319 ± 57 seconds (p = 0.04). In both conditions, the CDO2 remained unchanged from baseline to the termination of apnea. At BH termination, arterial oxygen tension was higher following oral administration of indomethacin compared to control (4.05 ± 0.45 vs. 3.44 ± 0.32 kPa). The absolute increase in CBF from baseline to the termination of apnea was lower with indomethacin (p = 0.01). These findings indicate that the impact of CBF on maximal BH time is likely attributable to its influence on cerebral H+ washout, and therefore central chemoreceptive drive to breathe, rather than to CDO2.

Brewster, L. Madden, Anthony R. Bain, Vinicius P. Garcia, Noah M. DeSouza, Michael M. Tymko, Jared J. Greiner, and Philip N. Ainslie. Global REACH 2018: high altitude-related circulating extracellular microvesicles promote a proinflammatory endothelial phenotype in vitro. High Alt Med Biol. 24:223–229, 2023. Introduction: Ascent to high altitude (HA) can induce vascular dysfunction by promoting a proinflammatory endothelial phenotype. Circulating microvesicles (MVs) can mediate the vascular endothelium and inflammation. It is unclear whether HA-related MVs are associated with endothelial inflammation. Objectives: We tested the hypothesis that MVs derived from ascent to HA induce a proinflammatory endothelial phenotype. Methods: Ten healthy adults (8 M/2 F; age: 28 ± 2 years) residing at sea level (SL) were studied before and 4–6 days after rapid ascent to HA (4,300 m). MVs were isolated and enumerated from plasma by centrifugation and flow cytometry. Human umbilical vein endothelial cells were treated with MVs collected from each subject at SL (MV-SL) and at HA (MV-HA). Results: Circulating MV number significantly increased at HA (26,637 ± 3,315 vs. 19,388 ± 1,699). Although intracellular expression of total nuclear factor kappa beta (NF-κB; 83.4 ± 6.7 arbitrary units [AU] vs. 90.2 ± 6.9 AU) was not affected, MV-HA resulted in ∼55% higher (p < 0.05) active NF-κB (129.6 ± 19.8 AU vs. 90.7 ± 10.5 AU) expression compared with MV-SL. In addition, MV-HA induced higher interleukin (IL)-6 (63.9 ± 3.9 pg/ml vs. 53.3 ± 3.6 pg/ml) and IL-8 (140.2 ± 3.6 pg/ml vs. 120.7 ± 3.8 pg/ml) release compared with MV-SL, which was blunted with NF-κB blockade. Conclusions: Circulating extracellular MVs increase at HA and induce endothelial inflammation, potentially contributing to altitude-related vascular dysfunction. [ABSTRACT FROM AUTHOR]