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Dysregulated macrophage responses and changes in tissue metabolism are hallmarks of chronic inflammation in the skin. However, the metabolic cues that direct and support macrophage functions in the skin are poorly understood. Here, we show that during sterile skin inflammation, the epidermis and macrophages uniquely depend on glycolysis and the TCA cycle, respectively. This compartmentalisation is initiated by ROS-induced HIF-1α stabilization leading to enhanced glycolysis in the epidermis. The end-product of glycolysis, lactate, is then exported by epithelial cells and utilized by the dermal macrophages to induce their M2-like fates through NF-κB pathway activation. In addition, we show that psoriatic skin disorder is also driven by such lactate metabolite-mediated crosstalk between the epidermis and macrophages. Notably, small-molecule inhibitors of lactate transport in this setting attenuate sterile inflammation and psoriasis disease burden, and suppress M2-like fate acquisition in dermal macrophages. Our study identifies an essential role for the metabolite lactate in regulating macrophage responses to inflammation, which may be effectively targeted to treat inflammatory skin disorders such as psoriasis. Synopsis: Inflammation alters skin tissue metabolism, however, the consequences for immune cell effector function remain unclear. Here, in vivo work in mice uncovers a ROS/HIF-1α-induced metabolic crosstalk between epidermal cells and macrophages during sterile inflammation, which aggravates disease progression. Induced skin inflammation shifts metabolic preferences to glycolysis and the TCA cycle in the epidermis and in macrophages, respectively. Inflammation-induced metabolic compartmentalisation is bridged by lactate secreted from the epidermis. Inhibition of lactate transport leads to reduced macrophage-mediated ECM degradation and in turn, inflammation. Inhibition of lactate transfer attenuates psoriasis symptoms in a imiquimod-induced mouse model. Lactate produced via glycolysis in epidermal cells activates NF-κB signaling and M2-like pro-remodeling phenotypes in dermal macrophages. [ABSTRACT FROM AUTHOR]

The perception regarding lactate has changed over the past decades, and some of its physiological roles have gradually been revealed. However, the effects of exogenous lactate on skeletal muscle synthesis remain unclear. This study aimed to confirm the effects of a 5‐week lactate administration and post‐exercise lactate administration on skeletal muscle synthesis. Thirty‐two Institute of Cancer Research mice were randomly assigned to non‐trained + placebo, non‐trained + lactate, trained + placebo, and trained + lactate groups. Furthermore, 3 g/kg of lactate or an equivalent volume of saline was immediately administered after exercise training (maximum oxygen uptake: 70%). Lactate administration and/or exercise training was performed 5 days/week for 5 weeks. After the experimental period, it was observed that lactate administration tended to elevate skeletal muscle weight, increased protein kinase B (p < 0.05) and mammalian target of rapamycin (p < 0.05) mRNA levels, and decreased muscle ring‐finger protein‐1 expression (p < 0.05). Lactate administration after exercise training significantly enhanced plantaris muscle weight; however, it had no additional effects on most signaling factors. This study demonstrated that a 5‐week lactate administration could stimulate skeletal muscle synthesis, and lactate administration after exercise training may provide additional effects, such as increasing skeletal muscle. [ABSTRACT FROM AUTHOR]

Under the long‐term pressure overload stimulation, the heart experiences embryonic gene activation, leading to myocardial hypertrophy and ventricular remodelling, which can ultimately result in the development of heart failure. Identifying effective therapeutic targets is crucial for the prevention and treatment of myocardial hypertrophy. Histone lysine lactylation (HKla) is a novel post‐translational modification that connects cellular metabolism with epigenetic regulation. However, the specific role of HKla in pathological cardiac hypertrophy remains unclear. Our study aims to investigate whether HKla modification plays a pathogenic role in the development of cardiac hypertrophy. The results demonstrate significant expression of HKla in cardiomyocytes derived from an animal model of cardiac hypertrophy induced by transverse aortic constriction surgery, and in neonatal mouse cardiomyocytes stimulated by Ang II. Furthermore, research indicates that HKla is influenced by glucose metabolism and lactate generation, exhibiting significant phenotypic variability in response to various environmental stimuli. In vitro experiments reveal that exogenous lactate and glucose can upregulate the expression of HKla and promote cardiac hypertrophy. Conversely, inhibition of lactate production using glycolysis inhibitor (2‐DG), LDH inhibitor (oxamate) and LDHA inhibitor (GNE‐140) reduces HKla levels and inhibits the development of cardiac hypertrophy. Collectively, these findings establish a pivotal role for H3K18la in pathological cardiac hypertrophy, offering a novel target for the treatment of this condition. [ABSTRACT FROM AUTHOR]

Increasing numbers of studies have shown that tumor cells prefer fermentative glycolysis over oxidative phosphorylation to provide a vast amount of energy for fast proliferation even under oxygen‐sufficient conditions. This metabolic alteration not only favors tumor cell progression and metastasis but also increases lactate accumulation in solid tumors. In addition to serving as a byproduct of glycolytic tumor cells, lactate also plays a central role in the construction of acidic and immunosuppressive tumor microenvironment, resulting in therapeutic tolerance. Recently, targeted drug delivery and inherent therapeutic properties of nanomaterials have attracted great attention, and research on modulating lactate metabolism based on nanomaterials to enhance antitumor therapy has exploded. In this review, the advanced tumor therapy strategies based on nanomaterials that interfere with lactate metabolism are discussed, including inhibiting lactate anabolism, promoting lactate catabolism, and disrupting the "lactate shuttle". Furthermore, recent advances in combining lactate metabolism modulation with other therapies, including chemotherapy, immunotherapy, photothermal therapy, and reactive oxygen species‐related therapies, etc., which have achieved cooperatively enhanced therapeutic outcomes, are summarized. Finally, foreseeable challenges and prospective developments are also reviewed for the future development of this field. [ABSTRACT FROM AUTHOR]

The incorporation of isolated Sn (IV) and Zr (IV) ions into silica frameworks is attracting widespread attention, which exhibits remarkable catalytic performance (conversion, selectivity, and stability) in a broad range of reactions, especially in the field of biomass catalytic conversion. As a representative example, the conversion route of carbohydrates into valuable platform and commodity chemicals such as lactic acid and alkyl lactates, has already been established. The zeotype materials also possess water‐tolerant ability and are capable to be served as promising heterogeneous catalysts for aqueous reactions. Therefore, dozens of Sn‐ and Zr‐containing silica materials with various channel systems have been prepared successfully in the past decades, containing 8 membered rings (MR) small pore CHA zeolite, 10‐MR medium pore zeolites (FER, MCM‐56, MEL, MFI, MWW), 12‐MR large pore zeolites (Beta, BEC, FAU, MOR, MSE, MTW), and 14‐MR extra‐large pore UTL zeolite. This review about Sn‐ and Zr‐containing metallosilicate materials focuses on their synthesis strategy, catalytic applications for diverse reactions, and the effect of zeolite characteristics on their catalytic performances. [ABSTRACT FROM AUTHOR]

The article investigates how tumor cells use acetate to support their growth and evade the immune system. It shows that acetate is abundant in the tumor microenvironment and contributes to tumor cell proliferation and immune evasion by enhancing the acetylation of c-Myc, a key oncogenic protein. Topics include acetate's role in tumor metabolism, its impact on c-Myc acetylation and stabilization, and its effects on immune cell infiltration and tumor growth.

Since assessing aerobic capacity is key to enhancing swimming performance, a simple and widely applicable technology should be developed. Therefore, we aimed to noninvasively visualize real‐time changes in sweat lactate (sLA) levels during swimming and investigate the relationship between lactate thresholds in sweat (sLT) and blood (bLT). This prospective study included 24 university swimmers (age: 20.7 s ± 1.8 years, 58% male) who underwent exercise tests at incremental speeds with or without breaks in a swimming flume to measure heart rate (HR), bLT, and sLT based on sLA levels using a waterproof wearable lactate sensor attached to the dorsal upper arm on two different days. The correlation coefficient and Bland–Altman methods were used to verify the similarities of the sLT with bLT and personal performance. In all tests, dynamic changes in sLA levels were continuously measured and projected onto the wearable device without delay, artifacts, or contamination. Following an initial minimal current response, with increasing speed the sLA levels increased substantially, coinciding with a continuous rise in HR. The speed at sLT strongly correlated with that at bLT (p < 0.01 and r = 0.824). The Bland–Altman plot showed a strong agreement (mean difference: 0.08 ± 0.1 m/s). This prospective study achieved real‐time sLA monitoring during swimming, even with vigorous movement. The sLT closely approximated bLT; both were subsequently validated for their relevance to performance. Highlights: A new technique using a wearable device can measure sweat lactate (sLA) levels during swimming without artifacts or contamination.Lactate threshold assessed using sLA dynamics is consistent with that calculated from blood samples.The current novel measurement method is expected to promote a personalized training regimen and simultaneous multi‐person measurements. [ABSTRACT FROM AUTHOR]

Modulation of testing conditions such as resting lactate (Larest) levels or carbohydrate intake may affect the calculation of the maximal glycolytic rate (νLa.max). To evaluate the impact of elevated Larest as well as reduced and increased carbohydrate availability on νLa.max in running sprints (RST), twenty‐one participants completed five 15‐s RST tests on a running track under five different conditions: (I). baseline: Larest ≤1.5 mmol·L−1; (II). Lactate+: Larest ≥2.5 mmol·L−1; (III). CHO−: carbohydrate intake: ≤ 1 g·kg−1 BW d−1 for 3 days; (IV). CHO+: carbohydrate intake: ≥ 9 g·kg−1 BW d−1 for one day; and (V). acuteCHO: 500 mL glucose containing beverage consumed before RST. νLa.max was significantly reduced in lactate+ and CHO− conditions compared to the baseline RST, due to a reduction in the arithmetic mean delta (∆) between Lapeak and Larest lactate concentration (Lapeak, mmol · L−1). AcuteCHO led to an increase in Larest compared to baseline, CHO− and CHO+ with a high interindividual variability but did not significantly reduce νLa.max. Therefore, avoiding low carbohydrate nutrition before νLa.max testing, along with carefully adjusting Larest to below ≤1.5 mmol·L‐1, is crucial to prevent the unintentional underestimation of νLa.max. [ABSTRACT FROM AUTHOR]

We examine the impact of the acute manipulation of oxygen availability during discrete phases (active and passive) of a repeated‐sprint cycling protocol on performance, physiological, and perceptual responses. On separate days, twelve trained males completed four sets of five 5‐s 'all out' cycle sprints (25‐s inter‐sprint recovery and 5‐min interset rest) in four randomized conditions: normobaric hypoxia (inspired oxygen fraction of 12.9%) applied continuously (C‐HYP), intermittently during only the sets of sprints (I‐HYPSPRINT) or between‐sets recovery periods (I‐HYPRECOVERY), or not at all (C‐NOR). Peak and mean power output, peripheral oxygen saturation, heart rate, blood lactate concentration, exercise‐related sensations, and vastus lateralis muscle oxygenation using near‐infrared spectroscopy were assessed. Peak and mean power output was ∼4%–5% lower for C‐HYP compared to C‐NOR (P ≤ 0.050) and I‐HYPRECOVERY (P ≤ 0.027). Peripheral oxygen saturation was lower during C‐HYP and I‐HYPSPRINT compared with C‐NOR and I‐HYPRECOVERY during sets of sprints (∼83–85 vs. ∼95%–97%; P < 0.001), while lower values were obtained for C‐HYP and I‐HYPRECOVERY than C‐NOR and I‐HYPSPRINT during between‐sets rest period (∼84–85 vs. ∼96%; P < 0.001). Difficulty in breathing was ∼21% higher for C‐HYP than C‐NOR (P = 0.050). Ratings of perceived exertion (P = 0.435), limb discomfort (P = 0.416), heart rate (P = 0.605), blood lactate concentration (P = 0.976), and muscle oxygenation‐derived variables (P = 0.056 to 0.605) did not differ between conditions. In conclusion, the method of hypoxic exposure application (continuous vs. intermittent) affects mechanical performance, while internal demands remained essentially comparable during repeated cycle sprints. Highlights: Continuous hypoxic exposure resulted in reduced repeated sprint performance compared to both normoxia and intermittent hypoxia during recoveries.Cardiovascular solicitation and glycolytic contribution showed no significant differences between ambient air and hypoxic conditions regardless of the timing of hypoxic gas administration (entire session, sprints only, or recovery only).The method of applying hypoxic exposure significantly affected mechanical performance, while internal physiological demands remained essentially comparable between conditions during repeated cycle sprints. [ABSTRACT FROM AUTHOR]

Objectives: Reflecting the need for an effective support for the daily oral hygiene routine of patients experiencing (symptoms of) gum inflammation, a new mouthwash has been developed containing an amine + zinc lactate + fluoride system. The in vitro efficacy of this product was assessed using traditional laboratory methods, as well as novel experimentation. Materials and Methods: This mouthwash has been evaluated in a series of laboratory tests including two short interval kill tests (SIKTs), a 12‐h (longer term) biofilm regrowth assay, a plaque glycolysis assay, and an aerobic, repeated exposure biofilm model, as well as tests for soft tissue uptake and LPS neutralization. Results: Several laboratory studies demonstrate that a mouthwash containing an amine + zinc lactate + fluoride system provides short‐term and long‐term antibacterial activity. While the immediate efficacy of this formula has been shown to be driven by the presence of the amine, zinc lactate provides a long‐term antibacterial effect, as well as is able to inhibit bacterial metabolism. Conclusions: This research provides the basis for understanding the mode of action of this new mouthwash formulation and explains the previously observed clinical efficacy of this formula against plaque and gingivitis. [ABSTRACT FROM AUTHOR]

To investigate the effect of forced even pacing through virtual pacing assistance and an opponent in a competitive setting on end‐spurt behaviour in freestyle swimmers, including related physiological underpinnings. Twenty‐seven competitive swimmers and triathletes were recruited. There were four 1500 m freestyle trials: (i) familiarisation time trial, (ii) self‐paced time trial (STT), (iii) head‐to‐head competition time trial (CTT) and (iv) forced even pacing through virtual pacing assistance time trial (FET). Eventually, 12 swimmers met the criteria for the CTT and FET to be included in the analysis. Changes in end‐spurt behaviour, finishing time and physiological parameters (lactate, cortisol, noradrenaline and heart rate) were analysed using a linear mixed model with fixed effects for trials and a random effect for swimmer identity. A separate linear model was computed for competition outcome. The end‐spurt for each race was determined by means of an end‐spurt indicator (ESI; ESI > 0 greater end‐spurt). Swimmers demonstrated a significantly greater ESI in FET (+2.6; p < 0.001) and CTT (+1.4; p = 0.022) compared to STT. Blood lactate concentration in FET (+1.0 mmol L−1; p < 0.001) and CTT (+1.6 mmol L−1; p < 0.001) was significantly higher than in STT. Winners had a significantly greater ESI than losers in CTT (+1.6 and p = 0.005). Swimmers utilised a greater end‐spurt through metabolically optimal forced even pacing by virtual pacing assistance and in a head‐to‐head competition due a larger mobilisation of anaerobic reserves as indicated by greater blood lactate concentrations. Winners had a significantly greater end‐spurt than losers despite similar metabolic disturbances. Highlights: Compared to a self‐paced time trial, swimmers in a forced even pacing trial by virtual pacing assistance and in a head‐to‐head competition execute a greater end‐spurt.The larger end‐spurt is associated with larger mobilisation of anaerobic reserves as indicated by greater blood lactate concentrations.Winners had a significantly greater end‐spurt than losers despite similar metabolic disturbances. [ABSTRACT FROM AUTHOR]

Citrulline malate (CM) is purported to be an ergogenic aid during various types of exercise performance. However, the effects of CM on repeated sprint performance (RSP) are under‐explored. In a placebo‐controlled, double‐blind, counterbalanced cross‐over design, male university‐level team sport athletes (n = 13) performed two familiarization trials, after which CM or placebo (PLA) (8 × 1 g tablets each day) were taken on the 2 days prior to, and with breakfast on the morning of, each main experimental trial. The main experimental trials employed a RSP protocol consisting of 10 repetitions of 40 m maximal shuttle run test (MST) with a 30 s interval between the start of each sprint. Sprint times and heart rate were recorded throughout the MST, and blood lactate concentrations were measured before, immediately after, and 5 min after completing the MST. CM resulted in better RSP compared to PLA, as indicated by a lower sprint performance decrement (Sdec: CM, 4.68% ± 1.82% vs. PLA, 6.10% ± 1.83%; p = 0.03; ES = 0.77), which was possibly influenced by the fastest sprint time being faster in CM (CM, 8.16 ± 0.34 s vs. PLA, 8.29 ± 0.39 s; p = 0.011; ES = 0.34). There were no differences between CM and PLA in average sprint time (p = 0.54), slowest sprint time (p = 0.48), blood lactate concentrations (p = 0.73) or heart rate (p = 0.18), nor was there a condition × time interaction effect across the 10 sprints (p = 0.166). Three days of CM supplementation (8 g daily) attenuated the sprint performance decrement during short‐duration high‐intensity exercise in the form of running RSP in male university‐level team sport athletes. Highlights: This study addresses a knowledge gap around the ergogenic potential of citrulline malate (CM) in repeated sprint running performance.Three days of CM supplementation (8 g daily) was observed to improve short‐duration (5 min) high‐intensity exercise performance in male university‐level team sport athletes when measured by the sprint performance decrement in a 10 repetition 40 m maximal shuttle run test.The attenuation in the sprint performance decrement was not associated with any differences compared to the placebo condition in heart rate or blood lactate concentrations.The outcomes of this study suggest that short‐term CM supplementation could be beneficial for team sport athletes who perform short‐duration high‐intensity efforts, such as soccer, Gaelic games, field hockey, and rugby. [ABSTRACT FROM AUTHOR]

We investigated the effect of ischemic preconditioning (IPC) with and without caffeine supplementation on mean power output (MPO) during a 4‐min cycling time‐trial (TT). In a double‐blinded, randomized, crossover‐design, 11 trained men performed a TT on 4 days separated by ∼1 week. One hour before TT, participants ingested either caffeine (3 mg kg bw−1) or placebo pills, after which femoral blood‐flow was either restricted with occlusion cuffs inflated to ∼180 mmHg (IPC), or sham‐restricted (0–10 mmHg; Sham) during 3 × 2‐min low‐intensity cycling (10% of incremental peak power output). Then, participants performed a standardized warm‐up followed by the TT. Plasma lactate and K+ concentrations and ratings of perceived exertion (RPE) were measured throughout trials. TT MPO was 382 ± 17 W in Placebo + Sham and not different from Placebo + IPC (−1 W; 95% CI: −9 to 7; p = 0.848; d: 0.06), whereas MPO was higher with Caffeine + Sham (+6W; 95% CI: −2 to 14; p = 0.115; d: 0.49) and Caffeine + IPC (+8 W; 95% CI: 2–13; p = 0.019; d: 0.79) versus Placebo + Sham. MPO differences were attributed to caffeine (caffeine main‐effect: +7 W; 95% CI: 2–13; p = 0.015; d: 0.54. IPC main‐effect: 0 W; 95% CI: −6 to 7; p = 0.891; d: 0.03; caffeine × IPC interaction‐effect: p = 0.580; d: 0.17). TT RPE and plasma variables were not different between treatments. In conlcusion, IPC with co‐ingestion of placebo does not improve short‐term high‐intensity performance in trained men versus a double‐placebo control (Placebo + Sham) and does not additively enhance performance with caffeine. These data do not support IPC as a useful strategy for athletes prior to competition but confirms caffeine's performance‐enhancing effect. Highlights: Active ischemic preconditioning (IPC) prior to exercise has been proposed as a strategy to enhance short‐term exercise performance.However, the effect of combined IPC and caffeine ingestion on short‐term high‐intensity exercise performance in trained individuals remains unclear.Active IPC with co‐ingestion of placebo pills did not improve short‐term high‐intensity exercise performance in trained men and its use cannot be recommended over caffeine to improve subsequent short‐term maximal performanceIngestion of caffeine (3 mg kg bw−1) prior to short‐term high‐intensity exercise is an effective ergogenic strategy which athletes may benefit from. [ABSTRACT FROM AUTHOR]

Heart Rate (HR) is widely used for erobic exercise intensity prescriptions and/or studies of exercise training. It is often assumed that exercising at a given HR results in similar physiological response, regardless of exercise modality. This study aimed to gauge cellular immune mobilization to submaximal exercise at a given target HR on a cycle ergometer (CE) and treadmill (TM). Thirteen healthy male adults (23.2 ± 3.5 y.o) completed 4 laboratory visits. Participants performed two graded exercise tests to exhaustion on CE and TM and two 30‐min constant exercise challenges at 70% HR reserve on CE or TM in random order. Rating of Perceived Exertion (RPE) was recorded every 5 min, and blood was drawn before and after exercise to measure leukocytes subpopulation levels, lactate, and IL‐6. HR was successfully "clamped" during the exercise in CE and TM (CE 156.7 ± 1.1; TM 159.3 ± 1.6 bpm). Cycling was perceived as more strenuous than running and was accompanied by a greater increase in lactate post‐exercise (p < 0.0001; 6.2 ± 0.3 vs. 2.9 ± 0.3 mmol/L). IL‐6 and leukocytes subpopulations were significantly elevated post‐exercise (p < 0.003) with no difference between exercise modalities (monocytes; CE 57.6% TM 61.2%, granulocytes; CE 41.37%, TM 50.1%, lymphocytes; CE 91.03%, TM 78.8%). The findings revealed that HR is not sufficient in and of itself to fully assess the metabolic stress associated with a given exercise modality. However, despite different metabolic and subjective stress, the IL‐6 and leukocyte counts relative changes were similar in the two modalities. Highlights: These findings provide valuable insights into the leukocytes and lactate responses to cycling and running at the same target heart rate. The study further elaborates on the shared patterns and distinctions in physiological and metabolic responses and their implications for designing targeted training programs.At the same target heart rate, running resulted in significantly lower lactate levels and subjective rate of perceived exertion (RPE) while yielding higher VO2 levels compared to cycling.Leukocytes and IL‐6 increases post‐exercise were not different between running and cycling, indicating that they did not reflect the distinct metabolic and subjective perceived loads associated with cycling and running.Since heart rate in and of itself is not sufficient to fully characterize the metabolic stress induced by a specific exercise modality, it is important to consider the modality of exercise when prescribing training programs for improving cardiovascular fitness or achieving target energy expenditure through heart rate monitoring. [ABSTRACT FROM AUTHOR]

Background: Cervical cancer is one of the most common gynecological cancers. Accumulated evidence shows that long non‐coding RNAs (lncRNAs) play essential roles in cervical cancer occurrence and progression, but their specific functions and mechanisms remain to be further explored. Methods: The RT‐qPCR assay was used to detect the expression of NEAT1 in cervical cancer tissues and cell lines. CCK‐8, colony formation, flow cytometry, western blotting, and Transwell assays were used to evaluate the impact of NEAT1 on the malignant behavior of cervical cancer cells. Glucose consumption, lactate production, ATP levels, ROS levels, MMP levels, and the mRNA expressions of glycolysis‐related genes and tricarboxylic acid cycle‐related genes were detected to analyze the effect of NEAT1 on metabolism reprograming in cervical cancer cells. The expressions of PDK1, β‐catenin and downstream molecules of the WNT/β‐catenin signaling pathway in cervical cancer cells and tissues were detected by western blotting, RT‐qPCR, immunofluorescence and immunohistochemistry assays. Results: This study investigated the role and possible molecular mechanism of lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) in cervical cancer. Our results showed that NEAT1 was highly expressed in cervical cancer tissues and cell lines. Downregulation of NEAT1 inhibited the proliferation, migration, invasion and glycolysis of cervical cancer cells, while overexpression of NEAT1 led to the opposite effects. Mechanistically, NEAT1 upregulated pyruvate dehydrogenase kinase (PDK1) through the WNT/β‐catenin signaling pathway, which enhanced glycolysis and then facilitated cervical cancer metastasis. Furthermore, NEAT1 maintained the protein stability of β‐catenin but did not affect its mRNA level. We also excluded the direct binding of NEAT1 to the β‐catenin protein via RNA pull‐down assay. The suppressive impact of NEAT1 knockdown on cell proliferation, invasion, and migration was rescued by β‐catenin overexpression. The WNT inhibitor iCRT3 attenuated the carcinogenic effect induced by NEAT1 overexpression. Conclusion: In summary, these findings indicated that NEAT1 may contribute to the progression of cervical cancer by activating the WNT/β‐catenin/PDK1 signaling axis. [ABSTRACT FROM AUTHOR]

Biopreservation refers to the use of natural or controlled microbial single strains or consortia, and/or their metabolites such as short-chain carboxylic acids (SCCA), to improve the shelf-life of foods. This study aimed at establishing a novel Lactobacillaceae-driven bioprocess that led to the production of the SCCA propionate through the cross-feeding on 1,2-propanediol (1,2-PD) derived from the deoxyhexoses rhamnose or fucose. When grown as single cultures in Hungate tubes, strains of Lacticaseibacillus rhamnosus preferred fucose over rhamnose and produced 1,2-PD in addition to lactate, acetate, and formate, while Limosilactobacillus reuteri metabolized 1,2-PD into propionate, propanol and propanal. Loigolactobacillus coryniformis used fucose to produce 1,2-PD and only formed propionate when supplied with 1,2-PD. Fermentates collected from batch fermentations in bioreactor using two-strain consortia (L. rhamnosus and L. reuteri) or fed-batch fermentations of single strain cultures of L. coryniformis with rhamnose contained mixtures of SCCA consisting of mainly lactate and acetate and also propionate. Synthetic mixtures that contained SCCA at concentrations present in the fermentates were more antimicrobial against Salmonella enterica if propionate was present. Together, this study (i) demonstrates the potential of single strains and two-strain consortia to produce propionate in the presence of deoxyhexoses extending the fermentation metabolite profile of Lactobacillaceae, and (ii) emphasizes the potential of applying propionate-containing fermentates as biopreservatives., (© 2024 The Authors. Microbial Biotechnology published by Applied Microbiology International and John Wiley & Sons Ltd.)

Lactate is now considered an additional fuel or signaling molecule in the brain. In this study, using an oxygen–glucose deprivation (OGD) model, we found that treatment with lactate inhibited the global increase in intracellular calcium ion concentration ([Ca2+]) in neurons and astrocytes, decreased the percentage of dying cells, and caused a metabolic shift in astrocytes and neurons toward aerobic oxidation of substrates. OGD resulted in proinflammatory changes and increased expression of cytokines and chemokines, whereas incubation with lactate reduced these changes. Pure astrocyte cultures were less sensitive than neuroglia cultures during OGD. Astrocytes exposed to lipopolysaccharide (LPS) also showed pro‐inflammatory changes that were reduced by incubation with lactate. Our study suggests that lactate may have neuroprotective effects under ischemic and inflammatory conditions. [ABSTRACT FROM AUTHOR]

This study compared physiological and perceptual responses between cycling prescribed using fixed‐power (PWR) and fixed rating of perceived exertion (RPE), when performed with blood flow restricted (BFRPWR and BFRRPE) and unrestricted (CONPWR and CONRPE). Endurance cyclists/triathletes cycled for 10 min in four separate randomized conditions; that is, two methods of prescribed exercise intensity (power at the first ventilatory threshold or RPE matched to CONPWR) combined with two occlusion levels (with BFR or without). Cardiorespiratory and perceptual variables were recorded every 2 min. Blood lactate concentration was measured pre‐, immediately and 2‐min postexercise. Power output during BFRRPE was lower than CONRPE (−13 ± 13%). The greatest physiological and perceptual responses were achieved during BFRPWR. Heart rate during BFRRPE was not different compared with CONPWR, yet was greater than CONRPE (+4 ± 11%). Muscular discomfort during BFRRPE was greater than CONPWR (+43 ± 18%) and CONRPE (+65 ± 58%). Cuff pain was greater during BFRPWR than BFRRPE (+14 ± 21%). Blood lactate concentration was not different between BFRRPE, CONPWR, and CONRPE at any timepoint. The reduction in power (fixed‐RPE trials; BFR minus unrestricted) correlated with changes in the respiratory rate (r = 0.85, confidence intervals [CI] = 0.51, 0.96) and postexercise lactate (r = 0.75, CI = 0.27, 0.93) but not muscular discomfort (r = 0.18, CI = −0.47, 0.71). Cardiorespiratory and metabolic stress, muscular discomfort, and cuff pain likely mediated self‐regulating fixed‐RPE cycling with BFR. While cycling with BFR at a fixed‐RPE resulted in less physiological stress compared to BFRPWR, it still provided a heightened level of physiological stress, with less pain and discomfort. As such, fixed‐RPE can be a suitable alternative for prescribing BFR to trained cyclists. Highlights: Applying BFR at the fixed‐power associated with the first ventilatory threshold can increase the heart rate from the moderate to high exercise intensity domain for some individuals, indicating BFR exercise may not necessarily be low intensity.Fixed‐power cycling with BFR can be used at low work rates, perhaps following injury, yet practitioners should consider the balance between the physiological demands, discomfort, and pain at any given work rate.Discomfort and pain associated with BFR is alleviated in a fixed‐RPE model, which presents a suitable method of prescribing aerobic BFR cycling, yet physiological stress is lower compared to BFR cycling at a fixed‐power. [ABSTRACT FROM AUTHOR]

Background: Breast cancer (BC) is a common malignancy which threatens the health of women. Circular RNAs (circRNAs) are critical factors in multiple cancers, including BC. The aim of this experiment was to investigate the molecular mechanisms of circRNA Septin 9 (circSEPT9) in the progression of BC. Methods: CircSEPT9, microRNA-625-5p (miR-625-5p) and polypyrimidine tractbinding protein 3 (PTBP3) levels were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was performed to detect the protein levels of PTBP3, E-cadherin and vimentin. Cell counting kit-8 assay (CCK8) and thymidine analog 5-ethynyl-20-deoxyuridine (EDU) was utilized for proliferation examination. Flow cytometry was conducted to measure apoptosis. Transwell assay and wound healing assay to investigate the migration of BC cells. Glucose uptake and lactate production were determined by specific kits. Additionally, dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were utilized to verify the interaction. A murine xenograft model was established to investigate the function of circSEPT9 in BC in vivo. Results: Overexpression of circSEPT9 was found in BC tissues and cells. Silencing circSEPT9 impeded BC cell proliferation, migration, epithelial-mesenchymal transition (EMT) and glycolytic metabolism but facilitated cell apoptosis in vitro. Meanwhile, circSEPT9 knockdown constrained tumor growth in vivo. MiR-625-5p was targeted by circSEPT9. The influence of silencing circSEPT9 on BC cell function was regained by miR-625-5p inhibitor. Furthermore, miR-625-5p regulated BC cell malignant phenotypes via downregulating PTBP3. Conclusion: circSEPT9 contributed to the malignant progression of BC by upregulating PTBP3 via sponging miR-625-5p. [ABSTRACT FROM AUTHOR]

Cardiac function is a major determinant of cardiopulmonary fitness. This study aimed to determine if novel echocardiographic myocardial function and efficiency parameters at rest can predict exercise performance during different types of prolonged high‐intensity endurance exercise. Echocardiography was performed before exercise in 40 healthy (75% males) 50.3 ± 9.1‐year‐old recreational athletes. Echocardiographic parameters at rest were compared with exercise performance assessed by power output during two different exercises: A lactate threshold and cardiopulmonary exercise test (La‐CPET) and a 91‐km mountain bike sport cycling race. The La‐CPET had a median duration of 43 (40, 45) minutes and a mean power output of 2.9 ± 0.5 W/kg. The race had a median duration of 236 (214, 268) minutes and a mean power output of 2.1 ± 0.5 W/kg. There was moderate left ventricular (LV) dilatation in individuals with the highest performance. The myocardial efficiency parameter, global wasted work (GWW), was positively correlated with race duration (rho = 0.42, p = 0.008) and negatively correlated with mean power output during both the La‐CPET (rho = −0.43, p = 0.007) and the race (rho = −0.44, p = 0.005). In multivariable models, including LV volumes, left GWW remained an independent predictor of race duration (beta = 0.40, p = 0.007) and of mean power output during the La‐CPET (beta = −0.40, p = 0.006) and the race (beta = −0.43, p = 0.003). The novel echocardiographic myocardial efficiency parameter, GWW, measured at rest, is an independent predictor of prolonged high‐intensity endurance exercise performance in healthy middle‐aged athletes. These findings suggest that resting myocardial efficiency parameters may aid the identification of exercise‐induced LV dilatation. Highlights: What is new? The novel echocardiographic parameter global wasted work represents a measure of myocardial efficiencyThis is the first study to demonstrate that global wasted work at rest is a marker of exercise‐induced cardiac remodeling and a predictor of exercise performance What are the clinical implications? Global wasted work at rest may be used to predict exercise performance levelGWW may aid in separating exercise‐induced from pathological left ventricular dilatation [ABSTRACT FROM AUTHOR]

Hypoxic exercise, which can induce arterial and tissue deoxygenation, promotes physiological adaptations. However, reduced oxygen availability can lower the absolute training intensity (i.e., mechanical stress). Adding normoxic recovery to sprint interval exercise (SIE) is one potential approach to strike a balance between providing a hypoxic stimulus and maintaining the absolute training intensity. However, the effects of adding normoxic recovery to SIE on performance and physiological responses are uncertain. We tested the hypothesis that hypoxic SIE with normoxic recovery enhances arterial deoxygenation and muscle deoxygenation levels without impeding performance compared to an entirely normoxic condition. On separate days, seven male sprinters performed 4 × 30‐s 'all‐out' cycle sprints with 4.5‐min recovery with hypoxic exposure (FiO2: 12.7%O2) applied continuously (hypoxia, HYP), intermittently during sprint periods only (intermittent, INT), or not at all (normoxia, NOR). Power output, oxygen saturation, muscle oxygenation, surface electromyography (EMG) activity, heart rate, blood lactate concentration, and ratings of perceived exertion were measured. The total work significantly decreased in HYP than NOR (p < 0.05) and INT (p < 0.01). The aTrterial oxygen saturation was lower during HYP than NOR (∼86% vs. ∼97%; p < 0.001), while lower values were also obtained for INT than NOR during sprint periods (∼85% vs. ∼97%; p < 0.001) but not during recovery periods (∼96% vs. ∼97%). The heart rate differed (p < 0.05) between conditions (NOR: ∼164 bpm; INT: ∼160 bpm; HYP: ∼156 bpm). No other variables demonstrated significant differences between conditions. Adding hypoxia during exercise while recovering in normoxia did not compromise exercise capacity during SIE, despite inducing larger arterial deoxygenation levels compared to normoxia. Highlights: Utilizing severe hypoxia during exercise and normoxia during recovery induces a substantial hypoxic stimulus while safeguarding mechanical performance in sprinters.This approach maintains neuromuscular, metabolic, and perceptual parameters without any detrimental effects, ensuring athletes can perform at their best.Alternating hypoxia and normoxia during active and passive phases shows potential for optimizing hypoxic training, striking an ideal balance between the hypoxic stimulus and training intensity and load. [ABSTRACT FROM AUTHOR]

Colon cancer is a common cancer with high mortality globally. The role of chondroitin polymerizing factor (CHPF) has been elucidated in various cancers. However, its role and mechanism remain unknown in colon cancer. CHPF expression was examined by GEPIA database, reverse transcription‐quantitative polymerase chain reaction and western blot. The relationship between CHPF expression and the clinicopathologic characteristics as well as miR‐214‐3p level was determined in colon cancer patients. The role and mechanism of CHPF in the growth, ferroptosis, and glycolysis of colon cancer cells were evaluated by cell counting kit‐8, biochemical detections, luciferase, and western blot experiments. Additionally, the role of CHPF was explored in xenografted mice. CHPF expression was increased and was related to advanced TNM stage, poor differentiation and shorter overall survival in patients with colon cancer. Knockdown of CHPF inhibited colon cancer cell growth, and downregulated the expression of proteins involving in ferroptosis and glycolysis both in vitro and in vivo. Besides, CHPF silencing increased the levels of ferrous iron and ROS, but decreased glucose uptake, lactate product, and ATP level in vitro. Mechanically, miR‐214‐3p directly targeted CHPF and negatively regulated its expression. Upregulation of miR‐214‐3p reduced cell viability, glucose uptake, lactate product, and ATP level, but increased the levels of ferrous iron and ROS, which were reversed by the overexpression of CHPF. Upregulation of CHPF predicted poor prognosis, and miR‐214‐3p/CHPF axis inhibited growth, downregulated the levels of glycolysis‐related indexes, and promoted ferroptosis in colon cancer cells. [ABSTRACT FROM AUTHOR]

The brain possesses intricate mechanisms for monitoring sodium (Na) levels in body fluids. During prolonged dehydration, the brain detects variations in body fluids and produces sensations of thirst and aversions to salty tastes. At the core of these processes Nax, the brain's Na sensor, exists. Specialized neural nuclei, namely the subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT), which lack the blood--brain barrier, play pivotal roles. Within the glia enveloping the neurons in these regions, Nax collaborates with Na+/K+-ATPase and glycolytic enzymes to drive glycolysis in response to elevated Na levels. Lactate released from these glia cells activates nearby inhibitory neurons. The SFO hosts distinct types of angiotensin II- sensitive neurons encoding thirst and salt appetite, respectively. During dehydration, Nax-activated inhibitory neurons suppress salt-appetite neuron's activity, whereas salt deficiency reduces thirst neuron's activity through cholecystokinin. Prolonged dehydration increases the Na sensitivity of Nax via increased endothelin expression in the SFO. So far, patients with essential hypernatremia have been reported to lose thirst and antidiuretic hormone release due to Naxtargeting autoantibodies. Inflammation in the SFO underlies the symptoms. Furthermore, Nax activation in the OVLT, driven by Na retention, stimulates the sympathetic nervous system via acid-sensing ion channels, contributing to a blood pressure elevation. [ABSTRACT FROM AUTHOR]

Metastasis is an important contributor to increased mortality rates in non‐small cell lung cancer (NSCLC). The TGF‐β signalling pathway plays a crucial role in facilitating tumour metastasis through epithelial‐mesenchymal transition (EMT). Glycolysis, a key metabolic process, is strongly correlated with NSCLC metastasis. Pirfenidone (PFD) has been shown to safely and effectively inhibit TGF‐β1 in patients with lung diseases. Furthermore, TGF‐β1 and glycolysis demonstrate an interdependent relationship within the tumour microenvironment. Our previous study demonstrated that PFD effectively inhibited glycolysis in NSCLC cells, prompting further investigation into its potential antitumour effects in this context. Therefore, the present study aims to investigate the potential antitumour effect of PFD in NSCLC and explore the relationship among TGF‐β1, glycolysis and EMT through further experimentation. The antitumour effects of PFD were evaluated using five different NSCLC cell lines and a xenograft tumour model. Notably, PFD demonstrated a significant antitumour effect specifically in highly glycolytic H1299 cells. To elucidate the underlying mechanism, we compared the efficacy of PFD after pretreatment with either TGF‐β1 or a TGF‐β receptor inhibitor (LY2109761). The energy metabolomics analysis of tumour tissue demonstrated that PFD, a chemosensitizing agent, reduced lactate and ATP production, thereby inhibiting glycolysis and exerting synergistic antineoplastic effects. Additionally, PFD combined with cisplatin targeted TGF‐β1 to inhibit glycolysis during EMT and enhanced the chemosensitization of A549 and H1299 cells. The magnitude of the anticancer effect exhibited by PFD was intricately linked to its metabolic properties. [ABSTRACT FROM AUTHOR]

Purpose: Inflammation is commonly considered a mechanism underlying contrast‐associated acute kidney injury (CA‐AKI). This study aimed to explore the predictive capability of the novel inflammatory marker lactate dehydrogenase‐to‐albumin ratio (LAR) for CA‐AKI following percutaneous coronary intervention (PCI), and further compare it with other common inflammatory biomarkers. Methods: This study enrolled 5,435 patients undergoing elective PCI. The primary outcome was CA‐AKI, and the secondary outcome was all‐cause mortality. All patients were grouped into three groups based on the LAR tertiles. Results: Three hundred fifteen patients (5.8%) experienced CA‐AKI during hospitalization. The fully adjusted logistic regression suggested a significant increase in the risk of CA‐AKI in LAR Tertile 3 (odds ratio [OR]: 2.51, 95% confidence interval [CI]: 1.68−3.83, p <.001) and Tertile 2 (OR: 2.11, 95% CI: 1.42−3.20, p <.001) compared to Tertile 1. Additionally, receiver operating characteristic (ROC) analysis demonstrated that LAR exhibited significantly superior predictive capability for CA‐AKI compared to other inflammatory biomarkers. Regarding the secondary outcome, multivariate COX regression analysis showed a positive correlation between elevated LAR levels and all‐cause mortality. Conclusion: In patients undergoing elective PCI, LAR was significantly independently associated with CA‐AKI, and it stood out as the optimal inflammatory biomarker for predicting CA‐AKI. [ABSTRACT FROM AUTHOR]

This document is a correction to a published paper titled "Increased resting lactate levels and reduced carbohydrate intake cause νLa.max underestimation by reducing net lactate accumulation—A pilot study in young adults." The correction addresses two mistakes in the original paper. The first mistake is in Figure 1, where the text "Larest ≤ 1.8 mmol · L‐1" should have read "Larest ≤ 1.5 mmol · L‐1." The second mistake is in paragraph 7 of the "Discussion" section, where the text incorrectly stated a rise of 79% in glucose and 42% in lactate levels, when it should have been a rise of 42% in glucose and 79% in lactate levels. The correction does not change the conclusion of the study. [Extracted from the article]

Different interventions can independently improve athletic performance via different central or peripheral mechanisms, but little is known about their potential combination. We tested the effects of seven combined interventions (enhanced recovery package [ERP]) on performance during intermittent high‐intensity cycling compared with placebo. Sixteen trained men (maximal power output: 5.0 ± 0.5 W･kg−1) completed six 30‐s cycling sprints with 3‐min breaks in‐between under ERP, placebo, and control conditions. The ERP combined neck cooling, carbohydrate and caffeine mouth rinsing, carbohydrate and water ingestion, hyperventilation, hyperoxia, and potentiation maneuvers. Power output, heart rate, blood lactate concentration, rate of perceived exertion, and gas exchange were compared between the ERP and placebo conditions. Mean power output was higher during ERP compared with placebo (570 ± 74 W vs. 560 ± 71 W, p < 0.001, dz = 1.15). Heart rate was higher (+3 ± 4 bpm, p = 0.012) during ERP, as was breathing frequency (+2.4 ± 4.0 breaths･min−1, p = 0.028) and respiratory exchange ratio (+0.12 ± 0.06, p < 0.001). Oxygen uptake was 80 ± 109 mL･min−1 lower (p = 0.013) for ERP. No differences were found with regards to the rate of perceived exertion or blood lactate concentration. Performance gains with ERP were small in magnitude but consistent across individuals. The ERP might have prevented a loss of aerobic efficiency or increased reliance on anaerobic energy. Testing combined interventions might increase the chances to see beyond daily variability in practice. Highlights: Combining seven different ergogenic interventions boosted repeated sprint performance by approximately 1.8% compared with placebo in trained individuals, suggesting that gains from single interventions are not cumulative.Fifteen out of 16 participants showed improved performance with the combined interventions, suggesting that the benefit of the combination might reside in the consistency of the gains obtained across individuals.The increase in power output with the ergogenic interventions took place despite lower oxygen uptake, suggesting either a maintenance of aerobic efficiency or increased reliance on anaerobic energy.A top‐down approach might be interesting for coaches and athletes trying to identify a set of interventions that improve performance, which can then be tailored to remove the ones that are least practical or least appreciated. [ABSTRACT FROM AUTHOR]

Background: Cardiogenic shock (CS) is associated with high in‐hospital mortality. Objective assessment of its severity and prognosis is paramount for timely therapeutic interventions. This study aimed to evaluate the efficacy of the shock index (SI) and its variants as prognostic indicators for in‐hospital mortality. Methods: A retrospective study involving 1282 CS patients were evaluated. Baseline patient characteristics, clinical trajectory, hospital outcomes, and shock indices were collected and analysed. Receiver operating characteristic (ROC) curves were employed to determine the predictive accuracy of shock indices in predicting in‐hospital mortality. Results: Of those evaluated, 866 (67.6%) survived until discharge. Non‐survivors were older (66.0 ± 13.7 vs. 57.4 ± 16.2, P < 0.001), had a higher incidence of cardiac risk factors, and were more likely to present with acute coronary syndrome (33.4% vs. 16.1%, P < 0.001) and out‐of‐hospital cardiac arrest (11.3% vs. 5.3%, P < 0.001). All mean shock indices were significantly higher in non‐survivors compared with survivors. ROC curves demonstrated that adjusted shock index (ASI), age‐modified shock index (AMSI), and shock index‐C (SIC) had the highest predictive accuracy for in‐hospital mortality, with AUC values of 0.654, 0.667, and 0.659, respectively. Subgroup analysis revealed that SIC had good predictive ability in patients with STEMI (AUC: 0.714) and ACS (AUC: 0.696) while AMSI and ASI were notably predictive in the OHCA group (AUC: 0.707 and 0.701, respectively). Conclusions: Shock index and its variants, especially ASI, AMSI, and SIC, may be helpful in predicting in‐hospital mortality in CS patients. Their application could guide clinicians in upfront risk stratification. SIC, ASI, and AMSI show potential in predicting in‐hospital mortality in specific CS subsets (STEMI and OHCA). This is the first study to evaluate SI and its variants in CS patients. [ABSTRACT FROM AUTHOR]

Adaptive metabolic responses and innate metabolites hold promising therapeutic potential for stroke, while targeted interventions require a thorough understanding of underlying mechanisms. Adiposity is a noted modifiable metabolic risk factor for stroke, and recent research suggests that it benefits neurological rehabilitation. During the early phase of experimental stroke, the lipidomic results showed that fat depots underwent pronounced lipolysis and released fatty acids (FAs) that feed into consequent hepatic FA oxidation and ketogenesis. Systemic supplementation with the predominant ketone beta‐hydroxybutyrate (BHB) is found to exert discernible effects on preserving blood‐brain barrier (BBB) integrity and facilitating neuroinflammation resolution. Meanwhile, blocking FAO‐ketogenesis processes by administration of CPT1α antagonist or shRNA targeting HMGCS2 exacerbated endothelial damage and aggravated stroke severity, whereas BHB supplementation blunted these injuries. Mechanistically, it is unveiled that BHB infusion is taken up by monocarboxylic acid transporter 1 (MCT1) specifically expressed in cerebral endothelium and upregulated the expression of tight junction protein ZO‐1 by enhancing local β‐hydroxybutyrylation of H3K9 at the promoter of TJP1 gene. Conclusively, an adaptive metabolic mechanism is elucidated by which acute lipolysis stimulates FAO‐ketogenesis processes to restore BBB integrity after stroke. Ketogenesis functions as an early metabolic responder to restrain stroke progression, providing novel prospectives for clinical translation. [ABSTRACT FROM AUTHOR]

Background: Dilated cardiomyopathy (DCM) is characterized by dilatation of the left ventricle, systolic dysfunction, and normal or reduced thickness of the left ventricular wall. It is a leading cause of heart failure and cardiac death at a young age. Cases with neonatal onset DCM were correlated with severe clinical presentation and poor prognosis. A monogenic molecular etiology accounts for nearly half of cases. Family description: Here, we report a family with three deceased offspring at the age of 1 year old. The autopsy of the first deceased infant revealed a DCM. The second infant presented a DCM phenotype with a severely reduced Left Ventricular Ejection Fraction (LVEF) of 10%. Similarly, the third infant showed a severe DCM phenotype with LVEF of 30% as well, in addition to eccentric mitral insufficiency. Results: Exome sequencing was performed for the trio (the second deceased infant and her parents). Data analysis following the autosomal dominant and recessive patterns of inheritance was carried out along with a mitochondrial pathways‐based analysis. We identified a homozygous frameshift variant in the TNNI3 gene (c.204delG; p.(Arg69AlafsTer8)). This variant has been recently reported in the ClinVar database in association with cardiac phenotypes as pathogenic or likely pathogenic and classified as pathogenic according to ACMG. Conclusion: Genetic counseling was provided for the family and a prenatal diagnosis of choronic villus was proposed in the absence of pre‐implantation genetic diagnosis possibilities. Our study expands the case series of early‐onset DCM patients with a protein‐truncating variant in the TNNI3 gene by reporting three affected infant siblings. [ABSTRACT FROM AUTHOR]

Introduction: Since the 1970s, fetal scalp blood sampling (FSBS) has been used as a second‐line test of the acid–base status of the fetus to evaluate fetal well‐being during labor. The commonly employed thresholds that delineate normal pH (>7.25), subnormal (7.20–7.25), and pathological pH (<7.20) guide clinical decisions. However, these experienced‐based thresholds, based on observations and common sense, have yet to be confirmed. The aim of the study was to investigate if pH drop rate accelerates at the common thresholds (7.25 and 7.20) and to explore the possibility of identifying more accurate thresholds. Material and methods: A retrospective study was conducted at a tertiary maternity hospital between June 2017 and July 2021. Patients with at least one FSBS during labor for category II fetal heart rate and delivery of a singleton cephalic infant were included. The rate of change in pH value between consecutive samples for each patient was calculated and plotted as a function of pH value. Linear regression models were used to model the evolution of the pH drop rate estimating slope and standard errors across predefined pH intervals. Exploration of alternative pH action thresholds was conducted. To explore the independence of the association between pH value and pH drop rate, multiple linear regression adjusted on age, body mass index, parity, oxytocin stimulation and suspected small for gestational age was performed. Results: We included 2047 patients with at least one FSBS (total FSBS 3467); with 2047 umbilical cord blood pH, and a total of 5514 pH samples. Median pH values were 7.29 1 h before delivery, 7.26 30 min before delivery. The pH drop was slow between 7.40 and 7.30, then became more pronounced, with median rates of 0.0005 units/min at 7.25 and 0.0013 units/min at 7.20. Out of the alternative pH thresholds, 7.26 and 7.20 demonstrated the best alignment with our dataset. Multiple linear regression revealed that only pH value was significantly associated to the rate of pH change. Conclusions: Our study confirms the validity and reliability of current guideline thresholds for fetal scalp pH in category II fetal heart rate. [ABSTRACT FROM AUTHOR]

The 16th European College of Equine Internal Medicine (ECEIM) Congress took place in Lyon, France and featured research on various topics related to equine medicine. Some of the topics discussed included trigeminal nerve asymmetry in horses with headshaking, the detection of Equine Hepacivirus RNA in stable flies, and the role of insulin clearance in hyperinsulinemia and non-alcoholic fatty liver disease in horses. Another study investigated an outbreak of Equine Herpesvirus 1 Myeloencephalopathy in Valencia, Spain and evaluated risk factors and outcomes. Other studies examined equine health topics such as equine herpesvirus infections, equine recurrent urticaria, hypothalamic-pituitary-adrenal gland axis response, equine malignant lymphoma, equine glandular gastric disease, sepsis biomarkers, subpalpebral lavage systems, severe equine asthma, obesity in Connemara ponies, eosinophilic keratoconjunctivitis, and Equine Proliferative Enteropathy. Lastly, a study evaluated the diagnostic and prognostic potential of the Delta Neutrophil Index in equine neonatal sepsis. These studies provide valuable insights into various aspects of equine health and highlight the need for further research. [Extracted from the article]

Aims: Evidence for the effectiveness of left ventricular (LV) unloading in patients who received venoaterial extracorporeal membrane oxygenation (VA‐ECMO) for acute myocardial infarction (AMI) or non‐AMI induced cardiogenic shock (CS) is limited. The aim of the present study was to compare the effect of LV unloading in AMI‐induced and non‐AMI‐induced CS. Methods and results: This is a single‐centre retrospective observational study of patients with CS undergoing VA‐ECMO from January 2011 to March 2019. Patients were classified as AMI‐induced and non‐AMI‐induced CS. The association of LV unloading with 90‐day mortality in both groups was analysed using Cox proportional hazard regression analysis. Results: Of the 128 CS patients, 71 (55.5%) patients received VA‐ECMO due to AMI‐induced CS, and the remaining 57 (44.5%) received VA‐ECMO due to non‐AMI‐induced CS. The modality of LV unloading was predominantly with IABP (94.5%). In the AMI‐induced CS group, LV unloading did not reduce 90‐day mortality (adjusted hazard ratio 1.96, 95% confidence interval 0.90–4.27, P = 0.089). However, in the non‐AMI‐induced CS group, LV unloading combined with VA‐ECMO significantly reduced 90‐day mortality (adjusted hazard ratio 0.37, 95% confidence interval 0.14–0.96, P = 0.041; P for interaction = 0.029) as compared with those who received VA‐ECMO alone. Conclusions: LV unloading with VA‐ECMO may reduce 90‐day mortality compared with VA‐ECMO alone in patients with non‐AMI‐induced CS, but not in AMI‐induced CS. [ABSTRACT FROM AUTHOR]