Researchers randomly assigned children within weight categories to receive 500 mL of room-temperature tap water, 200 mL of 100% apple juice or no drink. Children remained sedentary for the following hour while completing a questionnaire with a parent or caregiver, and investigators collected unstimulated saliva at baseline and again 45–60 minutes after the assigned treatment. The analysis included 60 children classified as having normal weight, based on an age- and sex-specific body mass index percentile from the 5th through 85th percentile, and 45 classified as having overweight or obesity, above the 85th percentile. All participants were healthy, 91% attended public school and all had Denti-Cal insurance, which the investigators used as a proxy for low income. Although randomization was stratified by weight category, the trial did not reach its original enrollment target of 60 children in each category.

For the main metabolomic comparisons, investigators used orthogonal partial least squares discriminant analysis, or OPLS-DA, to distinguish changes in salivary metabolite profiles after each treatment. They also used permutational multivariate analysis of variance, or PERMANOVA, to test whether the overall treatment-related patterns differed. Among children with normal weight, the change after apple juice differed significantly from the change after water: the validated OPLS-DA model had a predictive Q2 of 0.30 and a permutation p-value of 0.007, while PERMANOVA returned p = 0.04. Among children with overweight or obesity, the change after no drink differed significantly from the change after water, with Q2 = 0.29, a permutation p-value of 0.04 and PERMANOVA p = 0.02. Both significant models explained 94% of the between-group variance, although their predictive performance was described as modest. Baseline metabolomic profiles did not differ significantly among the randomized treatment groups, and the comparison between apple juice and water in children with overweight or obesity and the comparison between no drink and water in children with normal weight were not statistically significant.

The trial detected broad changes extending across hundreds of salivary features. Among children with normal weight, 86 features increased and 46 decreased by at least 1.5-fold after apple juice relative to water, while 111 increased and 61 decreased after no drink relative to water. In the group with overweight or obesity, apple juice was associated with 57 increases and 69 decreases, and no drink with 56 increases and 62 decreases. Identified compounds included amino acids, organic acids, sugars and sugar phosphates, fatty acids, purines, pyrimidines and other small molecules. For example, salivary lactic acid was about 900 times higher after apple juice than after water in the normal-weight group. Some relative changes were also substantial in the other groups, but the study did not establish a statistically significant overall treatment contrast for those comparisons. Because the values describe relative changes in measured abundance rather than whole-body metabolic flux, the researchers treated the pathway findings as hypotheses rather than proof that particular biochemical routes were activated or suppressed.

The metabolomic contrasts coincided with weight-specific patterns in saliva insulin, a marker previously reported to track blood insulin. Following water, 75% of children with normal weight and 47% of those with overweight or obesity had saliva insulin below 170 pg/mL. By comparison, at least 70% in either weight group remained above that threshold after apple juice or no drink. The relative odds of lower insulin after water instead of either comparator were about 10 times greater in the normal-weight group, with an odds ratio of 10.3 and 95% confidence interval of 2.9–36.2, compared with an odds ratio of 4.4 and 95% confidence interval of 1.1–17.7 in the group with overweight or obesity. These findings indicate that baseline weight modified some acute responses, while also showing that the insulin associations were weaker among children with overweight or obesity.

Hydration measurements likewise suggested that weight status may influence the response to water. After water, saliva osmolality was below 70 mmol/kg in 80% of normal-weight children, compared with 50% after apple juice and 45% after no drink. Among children with overweight or obesity, the corresponding proportions were 53%, 80% and 33%. In the normal-weight group, the relative odds of osmolality below 70 mmol/kg after water were significantly higher than after no drink, with an odds ratio of 4.83, 95% confidence interval of 1.05–22.09 and p = 0.042, but the water-versus-apple-juice estimate was not significant. Estimates for children with overweight or obesity were also not statistically significant. At baseline, the overall difference in saliva osmolality between the weight groups was not statistically significant, despite a median of 74 mmol/kg for normal-weight children and 79 mmol/kg for those with overweight or obesity. The trial was not designed to establish insulin or hydration as the mechanism behind every metabolomic difference.

Pathway mapping pointed to several domains that might merit targeted testing in future intervention trials. In both weight groups, metabolites that increased after apple juice or no drink relative to water were associated with starch and sucrose metabolism and with pathways involving bacterial production of aminoglycosides. Metabolites that decreased were linked to alanine, aspartate and glutamate metabolism. In normal-weight children, the results also implicated inositol phosphate metabolism, histidine metabolism, butanoate metabolism and amino-acid pathways, including arginine, proline and phenylalanine metabolism. In children with overweight or obesity, potential effects included the citrate cycle, glycolysis or gluconeogenesis, the pentose phosphate pathway, glycine, serine and threonine metabolism, and galactose metabolism. These descriptive overlaps and differences show that the metabolomic response cannot be summarized as a single universal “water effect”; the detectable contrast depended on what was consumed and on the child’s baseline weight category.

Some differences may reflect the highly concentrated nature of the comparison beverages. The apple juice had an osmolality of 754 mmol/kg and supplied 94 kilocalories and 23 grams of carbohydrate per serving, while water provided no calories and the no-drink group received no fluid. Salivary changes in compounds such as myo-inositol, sorbitol and trehalose could therefore reflect local osmotic responses in the mouth as well as systemic metabolism. The appearance of bacterial aminoglycosides and the large shift in lactic acid also point to possible effects on oral microbial fermentation, particularly after exposure to fructose, glucose and sucrose. Saliva contains both human metabolites and products of oral organisms, making it useful for noninvasive sampling but difficult to interpret as a direct readout of metabolism elsewhere in the body. The investigators therefore proposed that the results might help identify candidate process measures or targets for more focused future studies, rather than establish a biological mechanism on their own.

Several limitations constrain the conclusions. The study followed children for only 45–60 minutes, so it could not determine whether the observed changes persisted, accumulated with repeated exposure or influenced long-term health. The sample was smaller than the researchers’ original enrollment target, and the weight-stratified comparisons had limited power for identifying individual metabolites or pathways. Participants and staff collecting saliva were not blinded to treatment, although the laboratory and epidemiologist analysts were. One child assigned to apple juice declined to drink it, and investigators used an imputed follow-up value in the intention-to-treat analysis. Salivary abundance was reported as relative mass-spectral peak height rather than absolute concentration, and the assay covered mainly hydrophilic, low-molecular-weight compounds rather than the full range of lipids. The trial also did not independently measure pathway flux, so an increased metabolite could reflect greater synthesis, less breakdown or both. Between-batch assay differences and unmeasured influences such as recent oral hygiene, diet, medications and oral microbiota could also affect the metabolomic patterns.

The results do not establish a clinical benefit from replacing juice with water or from drinking water at school, and the researchers did not test weight loss, diabetes prevention or long-term cardiometabolic outcomes. Their immediate contribution is evidence that three specific drink exposures can cause distinct short-term changes in saliva metabolism, with the statistically detectable contrast varying according to the child’s weight status. For public-health researchers, the study offers candidate metabolites and pathways for hypothesis testing in larger, longer trials. It also shows why an intervention’s beverage substitution, dose, baseline weight and hydration status need to be defined precisely rather than treating all drinking-water opportunities as interchangeable. Replication with absolute metabolite measurements, targeted pathway assays, serial samples and repeated exposure will be needed before these acute signatures can be connected to meaningful health outcomes.

Subject of Research: Acute effects of water, apple juice and no drink on salivary metabolomes and insulin in healthy children, stratified by baseline weight status.

Article Title: Acute changes in saliva metabolomic profile after drinking water instead of apple juice or no drink signal improved insulin-related metabolism in healthy children: a randomized controlled trial

Article References: Stookey, J. D., Cholera, M., & Cape, R. (2026). Acute changes in saliva metabolomic profile after drinking water instead of apple juice or no drink signal improved insulin-related metabolism in healthy children: a randomized controlled trial. Frontiers in Nutrition, 13, Article 1812940. https://doi.org/10.3389/fnut.2026.1812940

Image Credits: AI Generated

DOI: 10.3389/fnut.2026.1812940

Keywords: children, drinking water, apple juice, saliva, metabolomics, insulin, randomized trial, weight status, hydration, oral microbiome, Acute, changes

Researchers first integrated 4,646 predicted quercetin targets with 1,602 ICH-associated genes, identifying 657 shared genes that mapped to 642 mouse orthologs. They combined these targets with exploratory differential-expression results from one mouse brain transcriptomic dataset and an endoplasmic-reticulum-stress-related reference set, producing 29 candidate genes. Functional enrichment implicated TNF and IL-17 signaling, leukocyte migration, stress responses and extracellular matrix processes.

A protein-protein interaction analysis ranked the 29 candidates using five centrality methods. Seven genes appeared in all five top-10 lists and were designated consensus hubs: Il1b, Mmp9, Timp1, Myc, Fos, Hmox1 and Socs3. In the discovery dataset, five hubs had higher expression after ICH than in controls and each had an area under the ROC curve greater than 0.9. In an independent dataset, six hubs were differentially expressed and also had AUC values above 0.9, although these exploratory analyses involved only five ICH and five control samples per dataset.

Molecular docking produced putative binding poses between quercetin and all seven hub proteins. The strongest predicted binding scores were reported for Fos, Hmox1, Il1b, Mmp9 and Timp1, while Socs3 and Myc had moderate predicted affinity. These computational estimates were interpreted as hypothesis-generating and do not demonstrate direct biochemical binding or target engagement.

For experimental validation, researchers used male C57BL/6 mice aged 6 to 8 weeks. ICH was induced by injecting collagenase into the striatum, with sham-operated animals receiving saline. Groups of six mice received intraperitoneal quercetin at 25, 50 or 100 mg/kg per administration, twice at 0.5 and 12 hours after hemorrhage, for total 24-hour administered doses of 50, 100 and 200 mg/kg. A separate group received dexamethasone at 2 mg/kg per administration on the same schedule as an anti-inflammatory comparator. The quercetin and dexamethasone regimens were described as literature-informed exploratory designs rather than direct replications.

At 24 hours, brain water content was significantly higher after ICH than in sham-operated mice. Quercetin at 100 mg/kg per administration reduced brain water content compared with untreated ICH, as did dexamethasone; the difference between those two groups was not significant. In perihematomal tissue, quercetin at 50 and 100 mg/kg reduced Il1b expression, while all three doses reduced Mmp9 and Fos expression. Timp1 expression increased after all three doses. Hmox1 increased selectively at the high dose, and Socs3 rose dose-dependently, while Myc was not significantly altered by treatment.

Serum measurements in mice showed increases in IL-1β, IL-6, TNF-α and MMP-9 after ICH. The 25 mg/kg quercetin dose did not significantly reduce any of these markers relative to untreated ICH. At 50 mg/kg, quercetin reduced all four markers, while at 100 mg/kg it produced reductions in all four that were not significantly different from sham levels. Dexamethasone showed a similar pattern, but the study did not establish equivalence between the treatments.

To assess disease relevance in humans, investigators analyzed paired perihematomal and remote non-hemorrhagic brain tissues from six ICH patients undergoing clinically indicated hematoma evacuation. Perihematomal tissue had higher IL1B, MMP9, TIMP1 and HMOX1 messenger RNA than matched remote tissue. Western blotting confirmed higher IL-1β, MMP-9 and TIMP1 proteins, and immunohistochemistry showed greater MMP-9 immunoreactivity and a larger MMP-9-positive area in perihematomal samples. These observations support the relevance of selected targets to human ICH pathology, but the patients did not receive quercetin, so the tissue data do not demonstrate quercetin-specific efficacy or target engagement.

Serum was also collected within 24 hours of symptom onset from six ICH patients and six age- and sex-approximated healthy controls. IL-1β, IL-6, IL-10, IL-17A and TNF-α concentrations were higher in patients. The human cohort was small and observational, while the mouse experiments were limited to males, one collagenase model, small groups of six and a single 24-hour endpoint. Hematoma or lesion volume, neurological and behavioral outcomes, histopathology, blood-brain barrier integrity and cell-specific mechanisms were not assessed. The results therefore support an acute experimental association between quercetin and lower inflammatory, matrix-remodeling and edema-related markers, not clinical benefit in people with ICH.

Subject of Research: Preclinical assessment of quercetin in experimental intracerebral hemorrhage

Article Title: Quercetin attenuates acute inflammation and extracellular matrix remodeling after intracerebral hemorrhage: transcriptomics-informed network pharmacology and experimental validation

Article References: Shu, J., Feng, K., Pan, A., Li, G., Liu, K., & Feng, L. (2026). Quercetin attenuates acute inflammation and extracellular matrix remodeling after intracerebral hemorrhage: transcriptomics-informed network pharmacology and experimental validation. Frontiers in Pharmacology, 17, Article 1930434. https://doi.org/10.3389/fphar.2026.1930434

Image Credits: AI Generated

DOI: 10.3389/fphar.2026.1930434

Keywords: intracerebral hemorrhage, quercetin, neuroinflammation, extracellular matrix, network pharmacology, mouse model, MMP-9, IL-1β, human brain tissue, transcriptomics, attenuates, acute

The investigators consecutively enrolled patients diagnosed with acute myocardial infarction at the Affiliated Hospital of Guangdong Medical University between January 2023 and January 2025. Eligible participants were adults admitted within 72 hours of symptom onset who met expert-consensus diagnostic criteria and had complete clinical data. People with other severe heart disease, infectious disease, malignant tumors, severe liver or kidney dysfunction, mental disorders or cognitive dysfunction that prevented cooperation were excluded. Fifty-nine healthy people who underwent physical examinations during the same period served as the control group. Venous blood was collected and echocardiography performed 24 hours after PCI. The groups did not differ significantly in age, sex, body mass index, smoking history, hypertension, diabetes or four measured lipid indicators. The myocardial infarction group did, however, have higher cTnI, CK-MB and myoglobin concentrations and a lower left ventricular ejection fraction.

CARMN was measured directly in serum by extracting RNA, reverse-transcribing it into complementary DNA and using real-time quantitative polymerase chain reaction. Expression was calculated with the 2−ΔΔCt method relative to β-actin, with the mean healthy-control value used as the calibrator. Each sample was tested in technical triplicate, and inter-assay coefficients of variation for target and reference gene cycle-threshold values were controlled below 5%. The conventional myocardial-injury measures cTnI, CK-MB and myoglobin were quantified with an automated chemiluminescence immunoassay analyzer. Echocardiography used the Simpson two-plane method to measure left ventricular volume and ejection fraction, with measurements taken across three consecutive cardiac cycles and averaged. This design allowed the investigators to test whether circulating CARMN supplied prognostic information beyond laboratory markers of myocardial injury and an echocardiographic measure of ventricular function.

In the case-control comparison, serum CARMN was significantly lower in patients with acute myocardial infarction than in healthy controls. Its receiver operating characteristic curve for distinguishing the two groups had an area under the curve of 0.849. At a reported cutoff of 0.865, sensitivity was 74.36% and specificity was 83.05%. Among patients with myocardial infarction, CARMN was inversely correlated with cTnI, with a Pearson coefficient of −0.623; with CK-MB, at −0.729; and with myoglobin, at −0.747. It was positively correlated with left ventricular ejection fraction, at 0.672. These associations show that lower circulating CARMN accompanied greater biochemical evidence of myocardial injury and lower measured systolic function in this cohort. They do not establish that CARMN causes either injury or subsequent events, and the comparison with healthy controls did not test CARMN in a prospective population of patients suspected of having an infarction.

For prognosis, the researchers divided the 156 infarction patients into two equal groups according to the median CARMN value, with 78 classified as high-expression and 78 as low-expression. Kaplan–Meier analysis showed a higher incidence of major adverse cardiovascular events in the low-expression group, with a log-rank P value below 0.001. Direct group comparisons also found significantly lower CARMN levels among the 60 patients who experienced an event than among the 96 who did not. The composite endpoint consisted of all-cause death, non-fatal myocardial infarction, non-fatal stroke, heart failure or malignant arrhythmia, with any one event meeting the study criterion. During follow-up, the reported components were five deaths, nine non-fatal myocardial infarctions, 13 non-fatal strokes, 18 cases of heart failure and 15 episodes of malignant arrhythmia. The five component counts sum to 60, although the source does not state whether individual patients could experience more than one component.

Univariable and multivariable Cox regression was used to assess whether CARMN retained an association with events after conventional clinical variables were considered. Two nested models were tested. Model A included age, diabetes, cTnI, CK-MB and ejection fraction; Model B added CARMN. In the fully adjusted model, cTnI was associated with a hazard ratio of 4.878, with a 95% confidence interval of 2.026–11.747, and CK-MB with a hazard ratio of 1.823, with a 95% confidence interval of 1.334–2.491. A one-unit increase in ejection fraction was associated with a lower hazard, with a hazard ratio of 0.910 and a 95% confidence interval of 0.868–0.954. Lower CARMN expression was also associated with a higher event hazard, with the fully adjusted model reporting a hazard ratio of 0.049 for the higher-expression category and a 95% confidence interval of 0.012–0.200. Collinearity checks for the four final predictors yielded variance inflation factors from 1.072 to 1.161, which the investigators regarded as evidence against substantial multicollinearity.

In separate receiver operating characteristic analyses for six-month event prediction, CARMN alone had an area under the curve of 0.847, with a reported cutoff of 0.785, 82.46% sensitivity and 72.73% specificity. The corresponding areas under the curve were 0.690 for cTnI, 0.806 for CK-MB and 0.794 for ejection fraction. The researchers then combined CARMN, cTnI, CK-MB and ejection fraction in a nomogram for estimating individual six-month event risk. The full model achieved an area under the curve of 0.867, with a 95% confidence interval of 0.804–0.931. After 1,000 internal bootstrap resamples, its optimism-corrected concordance index was 0.851, and calibration results were consistent with observed event probabilities. Decision-curve analysis indicated greater clinical net benefit for the combined model than for a single indicator across a range of risk thresholds. These analyses evaluate discrimination, calibration and modeled net benefit; they do not show that the nomogram improves treatment selection or patient outcomes.

The incremental analysis compared the full nomogram with a baseline model containing cTnI, CK-MB and ejection fraction but not CARMN. That conventional model had an area under the curve of 0.721, with a 95% confidence interval of 0.639–0.804, and a bootstrap-corrected concordance index of 0.618 after 1,000 resamples. Its calibration suggested acceptable overall performance but a tendency to overestimate risk in the high-risk range. At six months, adding CARMN produced an integrated discrimination improvement of 0.068, with a 95% confidence interval of 0.005–0.119 and P=0.028, and a continuous net reclassification improvement of 0.196, with a 95% confidence interval of 0.023–0.444 and P=0.024. These measures indicate improved discrimination and risk classification relative to the study’s baseline model. They do not, by themselves, demonstrate better clinical outcomes or show that using CARMN would change treatment decisions.

Several limitations constrain the findings. The investigation was retrospective, conducted at one center and limited to 156 infarction patients, with 60 events and 11 censored observations over six months. The nomogram was assessed only by internal bootstrap validation, creating a risk of overfitting, and it was not compared directly with established clinical risk scores such as GRACE or TIMI. The controls were healthy individuals rather than patients with suspected acute myocardial infarction, limiting conclusions about diagnostic performance in a real diagnostic pathway. Time from symptom onset to PCI also varied and could influence biomarker measurements. The study measured circulating CARMN and observed its associations with injury markers, ventricular function and subsequent events, but it did not investigate the molecular mechanisms that might link CARMN to those outcomes. The authors describe the combined model as hypothesis-generating and call for larger multicenter external validation and comparisons with existing risk scores before it could support individualized clinical management.

Subject of Research: Circulating CARMN as a prognostic marker after acute myocardial infarction

Article Title: Circulating CARMN for acute myocardial infarction prognosis and its incremental effect when combined with conventional biomarkers

Article References: Chen, Z., Chen, J., Zhou, J., & Yao, Z. (2026). Circulating CARMN for acute myocardial infarction prognosis and its incremental effect when combined with conventional biomarkers. Frontiers in Cardiovascular Medicine, 13, 1881009. https://doi.org/10.3389/fcvm.2026.1881009

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1881009

Keywords: CARMN, acute myocardial infarction, cardiac biomarkers, prognosis, risk prediction, MACE, cardiac troponin I, left ventricular ejection fraction, long non-coding RNA, retrospective cohort, Circulating, acute

The cohort included 435 adults with confirmed SARS-CoV-2 infection, making it a bi-center observational study rather than an intervention trial. Most acute kidney injury cases were in men, who accounted for 60% of the affected group, and 74.3% of cases occurred among patients older than 60. Severe COVID-19 was present in 70.7% of patients with kidney injury, while 45% required admission to an intensive care unit. The analysis also identified invasive ventilation, higher inflammatory markers, elevated lactate, and increased peak creatinine and blood urea nitrogen as independent mortality predictors. Because the study was retrospective, its regression results identify associations and cannot establish that any of these factors directly caused death.

Kidney injury was graded into three stages: stage 1 occurred in 60% of affected patients, stage 2 in 21.4%, and stage 3 in 18.6%. A higher acute kidney injury stage was associated with poorer renal outcomes and increased mortality, with the relationship reported at p<0.001. The investigators used multivariable logistic regression to assess predictors of acute kidney injury and mortality. Overall, the findings connect the risk of kidney injury during hospitalization with both the clinical severity of COVID-19 and the intensity of organ support, particularly intensive care admission and invasive mechanical ventilation.

For the 140 patients classified as having acute kidney injury, renal recovery was observed in 63.6%, while death occurred in 35.7%. These outcomes indicate that kidney function did not recover in every affected patient, although the abstract does not provide the follow-up duration, definitions used for recovery, or complete clinical characteristics of those who recovered versus died. The study population was restricted to adults admitted to two hospitals in East Jerusalem during the first two years of the pandemic, and the source does not report whether patients were immunized, how viral variants changed over time, or whether the analysis accounted for prior kidney disease and other potential confounders in detail. The findings therefore describe outcomes within this hospitalized Palestinian cohort and may not represent all COVID-19 patients, including those treated outside hospitals or in other health systems.

The results position acute kidney injury as an important complication of severe hospitalized COVID-19 rather than merely a laboratory abnormality. Severity markers and measures of systemic inflammation were closely linked to mortality, but the data do not determine whether inflammatory injury, critical illness, ventilation, kidney dysfunction, or their combination drove the observed risk. What the study does establish is a strong clinical association: among hospitalized adults with COVID-19, acute kidney injury was common, more severe stages accompanied worse outcomes, and the condition was linked to a 3.5-fold increase in the odds of death in the cohort’s multivariable analysis. The authors identified disease severity, intensive care management, and inflammatory load as principal determinants of outcome, providing a detailed account of renal complications in a setting for which regional data had been limited.

Subject of Research: Incidence, predictors, mortality, and renal recovery associated with acute kidney injury in hospitalized COVID-19 patients in Palestine

Article Title: Acute kidney injury in hospitalized COVID-19 patients: predictors, risk factors, mortality, and renal recovery from a bi-center cohort in Palestine

Article References: Abu-Helu, R., Albasha, D. J., Naseef, H. A., & Adwan, G. (2026). Acute kidney injury in hospitalized COVID-19 patients: predictors, risk factors, mortality, and renal recovery from a bi-center cohort in Palestine. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14391-3

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14391-3

Keywords: COVID-19, acute kidney injury, hospitalized patients, mortality, renal recovery, intensive care, Palestine, SARS-CoV-2, Acute, kidney, injury, hospitalized

ARDS is a clinical syndrome of acute hypoxemic respiratory failure and bilateral lung opacities that develops after direct pulmonary insults such as pneumonia or aspiration, or indirect insults such as sepsis, trauma or pancreatitis. Its Berlin definition helps distinguish it from cardiac failure and fluid overload, but the diagnostic criteria do not capture major differences in the injury to alveolar epithelium, pulmonary endothelium, blood vessels and other organs. Even with lung-protective ventilation, prone positioning and neuromuscular blockade, in-hospital mortality remains about 30% to 40%. A patient classified simply as having ARDS may therefore have very different combinations of inflammation, tissue damage, circulatory strain and mechanical vulnerability.

The central hyperinflammatory and hypoinflammatory framework is generated most often through latent class analysis or related data-driven methods using plasma biomarkers, including interleukin-6, interleukin-8, soluble tumor necrosis factor receptor 1 and angiopoietin-2. Hyperinflammatory patients tend to have greater organ dysfunction, shock and metabolic acidosis, with mortality exceeding 40% in several cohorts. The hypoinflammatory group generally has less systemic inflammation and better survival, although its reported outcomes have not been uniform across studies. Hyperinflammatory status is more common early in critical illness, and longitudinal analyses indicate that some patients transition toward a less inflammatory state. That dynamism argues against relying on a single measurement made at admission and supports reassessment as an illness evolves.

At the tissue level, ARDS begins with disruption of the alveolar-capillary barrier, allowing protein-rich fluid to enter the lungs and impairing gas exchange. Angiopoietin-2, high-mobility group box 1 and receptor for advanced glycation end products are among the mediators linked to endothelial and epithelial injury, while mitochondrial dysfunction in alveolar type II cells may connect oxidative stress with impaired surfactant production, defective fluid clearance and fibrosis. Immune differences are similarly complex. Transcriptomic studies associate the hyperinflammatory state with innate immune activation, granulopoiesis, interferon signaling and stress responses, whereas relatively greater expression of adaptive immune genes has been observed in hypoinflammatory profiles. Metabolic studies also associate the more inflammatory group with lipid dysregulation and a shift toward glycolysis.

Those systemic patterns do not necessarily represent what is happening inside the alveoli. Classifications based on bronchoalveolar lavage fluid overlap only partly with those based on plasma, and one study found no significant differences in local inflammatory mediators between plasma-defined “reactive” and “uninflamed” groups. Bronchoalveolar classifications containing interleukin-6, von Willebrand factor, soluble programmed cell-death receptor 1 and neutrophil percentage have instead correlated closely with oxygenation and ventilatory measures. Lung-microbiome findings likewise show limited concordance with circulating inflammatory classes, even though greater bacterial burden, reduced diversity and gut-associated bacterial translocation have been associated with heightened inflammation. The mismatch means that a patient labeled hypoinflammatory in blood may still have substantial pulmonary injury requiring a different therapeutic strategy.

Respiratory mechanics and imaging reveal another axis of heterogeneity. Machine-learning models using compliance, driving pressure, ventilation ratio and mechanical power distinguish restrictive cases with poor distensibility, gas-exchange impairment and elevated risk of ventilator-induced lung injury from more efficient physiological profiles. Rising ventilation ratio or mechanical power can identify worsening trajectories associated with mortality and fewer ventilator-free days. Computed tomography can separate focal disease, characterized by gravity-dependent consolidation, from diffuse disease with widespread ground-glass opacities or consolidation. Focal lungs tend to be less recruitable and may be harmed by indiscriminate increases in positive end-expiratory pressure, or PEEP, whereas diffuse lungs may recruit and improve oxygenation with higher PEEP or prone positioning. Imaging patterns overlap only weakly with inflammatory biomarker classes, indicating that morphology and systemic biology capture different dimensions of injury.

Circulatory complications introduce further distinctions. Analyses combining echocardiography and hemodynamic data have identified four cardiovascular profiles: normal ventricular function, right ventricular dilation with preserved systolic function, right ventricular dilation with impaired contraction and hyperdynamic left ventricular function. Patients with dilation and systolic impairment had 90-day mortality of 78% in one analysis, while a COVID-19 ARDS cohort reported 73% in the corresponding group. Right ventricular strain may reflect pulmonary hypertension, hypoxic vasoconstriction, microthrombi and elevated intrathoracic pressure. In patients receiving venovenous extracorporeal membrane oxygenation, retrospective classifications have separated “wet,” “dry” and “fibrotic” profiles. The fibrotic group had a more prolonged course and elevated risk of intracranial hemorrhage, but these retrospective associations do not establish that phenotype-based anticoagulation or other interventions improve outcomes.

Mechanisms involving regulated cell death add both opportunities and cautions. Ferroptosis has been linked to iron accumulation, lipid peroxidation, glutathione depletion and impaired antioxidant defenses in epithelial, endothelial, macrophage and neutrophil compartments. Ferrostatin-1, liproxstatin-1, melatonin and dipyridamole have reduced ferroptosis-related lung injury in various animal and cellular models, and a nonrandomized dipyridamole study included only five patients with moderate-to-severe ARDS. Pyroptosis, especially in alveolar and recruited macrophages, can amplify cytokine release, damage signals and barrier disruption through inflammasome and gasdermin pathways. Human studies have linked these signals with outcomes, but they do not directly demonstrate active pyroptotic death in vivo, and no clinical trial has established that selectively inhibiting it improves ARDS outcomes. Neither process has yet been validated as a separate clinical subphenotype.

Translation depends first on classification tools that are rapid, inexpensive, reproducible and simple enough for bedside use. The review describes simplified models based on small sets of biomarkers and clinical variables, including angiopoietin-2, soluble tumor necrosis factor receptor 1, procalcitonin and bicarbonate, and a two-marker score using interleukin-8 and soluble ST2 among patients receiving high-flow nasal oxygen. These tools require independent, multicenter prospective validation, including assessment of whether they predict treatment response rather than merely prognosis. Prospective randomized trials would need to assign patients with validated subtypes to targeted interventions or standard care, account for transitions between phenotypes and test whether enrichment improves statistical power. Candidate approaches include immunomodulation for hyperinflammatory disease, morphology-guided PEEP, personalized ventilation and targeted prevention of right ventricular failure, but none should be treated as established subtype-specific therapy on the current evidence.

Future systems may combine clinical observations, continuous ventilator data, imaging, blood biomarkers, transcriptomics, proteomics, metabolomics and microbiome measurements. Artificial intelligence could detect nonlinear patterns across these sources, while longitudinal monitoring could create an evolving digital representation of each patient rather than a fixed label. The review cites early multimodal models that combine CT radiomics with clinical information, and ongoing work is collecting ventilator waveforms, imaging and biospecimens to define biologically grounded endotypes. Major obstacles remain, including standardized data collection, transportability between hospitals, interpretability, privacy and prospective clinical validation. The practical advance is thus not a claim that ARDS has already become a precision-medicine disease, but that its traditional diagnostic label can increasingly be decomposed into testable biological and physiological states that might reveal which patients are likely to benefit from which interventions.

Subject of Research: Biological, physiological and imaging-based subphenotypes of acute respiratory distress syndrome

Article Title: Acute respiratory distress syndrome subphenotypes: the translational path from pathobiology to precision medicine

Article References: Shao, H., Bai, T., Zhang, T., Qiao, Y., & Li, Y. (2026). Acute respiratory distress syndrome subphenotypes: the translational path from pathobiology to precision medicine. Frontiers in Pharmacology, 17, Article 1947054. https://doi.org/10.3389/fphar.2026.1947054

Image Credits: AI Generated

DOI: 10.3389/fphar.2026.1947054

Keywords: acute respiratory distress syndrome, ARDS subphenotypes, precision medicine, hyperinflammation, biomarkers, lung inflammation, mechanical ventilation, right ventricular dysfunction, clinical trials, artificial intelligence, Acute, respiratory

Virtual wards in the review combined hospital-level care delivered at home with remote monitoring of vital signs, clinical variables and symptoms. The model could be used to avoid hospital admission after referral from an emergency department or to support early discharge from a hospital ward. Eligible participants were adults presenting to an emergency department or admitted with an acute condition, including infections, gastrointestinal disorders and pulmonary embolisms. Studies focused exclusively on chronic-care exacerbations, trauma, psychiatry, primary care, hospice care and COVID-19 were excluded.

Investigators searched MEDLINE, Embase, Cochrane, CINAHL, Web of Science and PubMed for peer-reviewed publications through 28 February 2025. Searches combined terms for hospital-at-home care, virtual wards, admission avoidance and early discharge with terms for acute disease, telemedicine and remote monitoring. English-, Dutch-, French- and German-language trials, cohort and pilot studies, letters to editors and qualitative studies were eligible, with no minimum sample size required. Two reviewers independently screened and extracted the data, resolving disagreements by consensus or consultation with a third reviewer.

The search identified 8,562 unique records, of which 217 were considered potentially eligible during title-and-abstract screening. Twenty-two studies were retained after full-text review. The research populations included 11,476 patients receiving virtual-ward care, 17,336 receiving hospital care and 134 receiving non-technology-enabled hospital-at-home care. Most studies were published between 2018 and 2025. Average ages in virtual-ward cohorts ranged from 54 to 80 years, and participants were generally older than comparison groups. Infection, particularly pneumonia and urinary tract infection, was the most common indication and accounted for as much as 100% of patients in some studies.

Virtual-ward delivery varied considerably. Most programs combined physician home visits with remote consultations, although some used remote consultations alone. All programs provided daily physician review, often supplemented by nurse visits and additional clinical review when needed. Communication methods included video calls, telephone calls, text, chat, applications and photographs. Care could include medication administration, intravenous fluids, oxygen, nursing and diagnostics. Patients either actively measured and reported information or used automated devices, and some programs combined both approaches. Monitoring ranged from intermittent measurements, including once-daily checks, to continuous transmission of data, with respiratory rate, oxygen saturation, blood pressure, temperature and weight among the most frequently monitored variables.

Escalation during virtual-ward admission was uncommon in most reports, although rates varied. One study reported emergency-service contact in 4% of patients, while unplanned home visits ranged from 3.7% to 19.0%. Most studies reporting transfer to hospital recorded rates between 0% and 6.5%, although one reported 26%. Hospital readmission during the virtual-ward admission ranged from 0% to 2.1%. In one study, intensive-care transfers occurred in 0% of virtual-ward patients and 4% of hospital patients. These observations do not establish equivalent safety because models, populations and reporting differed.

Post-discharge emergency-department visits and readmissions were also examined. Two randomized trials reported nonsignificantly lower 30-day emergency-department visit rates for virtual wards than for hospital care: 11% versus 18% in one trial and 7% versus 13% in another. The trials also reported nonsignificantly lower 30-day readmission rates, at 11% versus 46% and 7% versus 23%, respectively. Results from nonrandomized studies were mixed. Mortality findings varied, but the two randomized trials reported no mortality difference during admission and comparable 30-day mortality between the groups. The review therefore supports cautious interpretation of these outcome measures rather than a conclusion of equivalence.

Twelve studies reported complications or adverse events. Two randomized trials reported lower adverse-event rates in virtual-ward groups, at 0% versus 9% and 9% versus 15%. A third randomized trial reported more adverse events in a remote virtual-ward arm than in an in-home hospital-at-home arm, with a mean of 6.8 versus 3.9 events per 100 patients and a difference of 2.8 per 100 patients, with a 95% confidence interval of −3.3 to 8.9. Findings from case-control and single-arm studies varied, and differences in underlying illness, medication requirements and other reported factors complicated interpretation.

The review’s principal limitation is that it was designed to map evidence rather than perform a formal assessment of effect size or risk of bias. Only three small randomized trials were included, all conducted at the same study centre, and two additional studies drew participants from those trials, reducing dataset independence. Programs generally selected clinically stable patients and were conducted mainly in well-resourced academic hospitals, limiting generalizability to other settings and higher-risk populations. Inconsistent definitions, differing eligibility rules, varied telemonitoring systems and incomplete outcome reporting also restricted comparisons. The authors concluded that virtual wards may be feasible for selected stable patients with acute conditions, but called for robust randomized trials and comprehensive, standardized cost-effectiveness analyses before wider implementation.

Subject of Research: Scoping review of technology-enabled virtual wards for adults receiving acute care

Article Title: Virtual Wards for Acute Care Patients: A Scoping Review

Article References: van Baar de Knegt, S. M. E., Zelis, N., Kaasjager, K. A. H., & Stassen, P. M. (2026). Virtual Wards for Acute Care Patients: A Scoping Review. Journal of General Internal Medicine. https://doi.org/10.1007/s11606-026-10682-2

Image Credits: AI Generated

DOI: 10.1007/s11606-026-10682-2

Keywords: virtual wards, acute care, hospital at home, telemonitoring, remote monitoring, scoping review, adult patients, hospital admission, patient safety, Virtual, Wards, Acute

The study was designed as a single-center retrospective cohort analysis of treatment-naive patients who had undergone a standardized low-dose bromocriptine test as a marker for dopamine agonist response. Between 2008 and 2017, the test was performed routinely at the Norwegian center as part of the baseline workup for newly diagnosed acromegaly. Of 141 consecutive patients diagnosed during that decade, 71 underwent the test, and 69 were included in the final retrospective analyses after exclusions for logistical reasons, contraindications, acute surgery, hypotension or syncope during testing, prior dopamine agonist treatment, lactose intolerance, pituitary apoplexy, loss to follow-up, or lack of consent.

The bromocriptine test itself is elegantly simple. After an overnight fast, three baseline growth hormone samples are drawn 30 minutes apart and averaged. The patient then swallows a single 2.5 mg oral dose of bromocriptine, and growth hormone is measured again at 2, 4, and 6 hours. A positive response was defined as more than a 50 percent reduction in the nadir growth hormone concentration compared with the baseline mean. In the cohort, responders showed a median growth hormone decline of 74 percent, while non-responders declined only 37 percent. This acute hormonal snapshot served as the surrogate for longer-term dopamine agonist effectiveness, a concept rooted in clinical studies from the 1970s and 1980s that linked early bromocriptine-induced growth hormone suppression with later therapeutic benefit.

To probe the biology behind variable responsiveness, the researchers combined several complementary approaches. Baseline serum hormones, including growth hormone, prolactin, and insulin-like growth factor 1 (IGF1), were measured with standard immunoassays and calibrators. Magnetic resonance images were evaluated retrospectively for tumor size, volume, and invasiveness using the Knosp criteria for cavernous sinus invasion. Immunohistochemical staining of tumor tissue assessed growth hormone, prolactin, thyroid-stimulating hormone, cytokeratin 8, estrogen receptor alpha, and somatostatin receptor subtypes 1, 2, and 5, with staining intensity scored using the immunoreactive score system. Slides were evaluated by an investigator and a senior pathologist, both blinded to clinical data.

A key technical challenge emerged with the dopamine receptor D2 protein itself. Immunohistochemistry using two different commercial antibodies failed repeatedly: on postmortem central nervous system tissue, both showed distinct intracellular granular labeling, but background staining was high and could not be reduced, and on surgical pituitary specimens the staining was diffuse and nonspecific. The team therefore turned to gene expression analysis. Tumor tissue collected during surgery was snap-frozen and stored at minus 80 degrees Celsius, RNA was extracted with a column-based kit after TRIzol homogenization, and dopamine receptor D2 mRNA was quantified by real-time quantitative PCR normalized to two validated reference genes, GAPDH and PSMC4. Gene expression data were available in 54 patients.

The central result was striking. Dopamine agonist test response correlated with higher tumor dopamine receptor D2 gene expression, with a Spearman correlation coefficient of 0.53 and a p-value below 0.001. Patients with a positive test had significantly higher receptor expression than those with a negative test. Crucially, this association remained statistically significant after statistical adjustment for gender, age, tumor volume, growth hormone and prolactin concentrations, and their staining intensities, indicating that the receptor expression carried independent information about drug responsiveness. Higher receptor expression also tracked with higher serum prolactin, stronger tumor prolactin staining, and lower IGF1 levels relative to the age-adjusted upper limit of normal.

Prolactin emerged as a clinically accessible indirect marker. Stronger tumor prolactin expression correlated with better test response, and when prolactin staining was dichotomized as positive or negative, the association with test outcome was significant, with a phi coefficient of 0.39. Notably, 57 of 66 tumors showed prolactin expression by immunohistochemistry, a far higher proportion than the 20 to 30 percent hyperprolactinemia typically reported in acromegaly, reflecting that many tumors secrete prolactin histologically without elevating serum levels beyond normal. When prolactin staining was used as the marker and test response as the outcome, sensitivity was 97 percent, meaning nearly all responders stained positive, while specificity was only 30 percent, since many non-responders also stained positive. The negative predictive value of 89 percent suggests that a prolactin-negative tumor is a strong signal that dopamine agonist therapy will fail.

The statistical architecture of the analysis clarified the causal chain. When the correlation between prolactin and test response was adjusted for dopamine receptor D2 expression, it disappeared, implying that the drug effect is mediated through the receptor itself and that prolactin expression serves as an indirect proxy for receptor abundance and responsiveness. This mechanistic interpretation aligns with known pharmacology: activation of the D2 receptor reduces hormone release and can induce apoptosis in pituitary tumor cells, with the short receptor isoform appearing to exert stronger effects. Somatostatin receptor staining showed no correlation with test response, and the hypothesized link between somatostatin receptor 1 and dopamine receptor D2 expression was not borne out in this cohort.

Estrogen receptor alpha added a second layer of tumor biology. Its expression correlated with prolactin expression, and both were associated with smaller tumor volume and lower invasiveness by Knosp grade. Patients whose tumors stained negative for prolactin were older and had higher IGF1 levels relative to normal. These findings echo the 2022 World Health Organization classification, which distinguishes pure somatotroph tumors from those with combined somatotroph and lactotroph differentiation marked by growth hormone, prolactin, and estrogen receptor alpha positivity. However, the authors caution that the clinical applicability of the estrogen receptor findings remains unclear, as previous studies on estrogen receptor alpha and tumor aggressiveness in acromegaly have yielded conflicting results.

The study has limitations that temper enthusiasm. Gene expression does not necessarily reflect protein abundance, cellular localization, or receptor function, and the analysis did not distinguish between the long and short isoforms of the D2 receptor, which may differ in mechanism. The bromocriptine test is a surrogate for acute response and cannot replace studies of long-term dopamine agonist effectiveness. The 70 patients who did not undergo testing had lower prolactin concentrations and greater growth hormone excess, potentially introducing bias, although age, sex, and tumor size were comparable. Still, the large well-characterized cohort with standardized dynamic testing, supported by molecular and histological analyses, represents a methodological strength over registry-based studies. The authors conclude that readily available prolactin staining of tumor tissue may add valuable information for individualized pharmaceutical management, potentially sparing non-responders from ineffective therapy while guiding responders toward optimized treatment regimens.

Subject of Research: Acromegaly treatment markers

Article Title: Tumor expression of dopamine receptor and prolactin is associated with acute dopamine agonist response in acromegaly

Article References: Atai, S., Abusdal, M., Wessel, M. I., Casar-Borota, O., Øystese, K. A., Winther, J., Bollerslev, J., & Heck, A. (2026). Tumor expression of dopamine receptor and prolactin is associated with acute dopamine agonist response in acromegaly. Frontiers in Endocrinology, 17, Article 1930467. https://doi.org/10.3389/fendo.2026.1930467

Image Credits: AI Generated

DOI: 10.3389/fendo.2026.1930467

Keywords: acromegaly, dopamine agonist, prolactin, pituitary tumor, personalized medicine, Tumor, expression, dopamine, receptor, associated, acute, agonist

The study was conducted as a cross-sectional investigation across selected health facilities in Addis Ababa, running from September 2023 to August 2025. Researchers collected a total of 400 stool samples from children under five presenting with acute diarrheal illness. Each sample was tested for the presence of rotavirus alphagastroenteritidis, the formally designated species name for the classic human rotavirus, and positive specimens were then subjected to genotypic analysis using the TaqMan Array Card, a real-time PCR platform that allows simultaneous detection and typing of multiple viral gene targets in a single reaction.

The results showed that rotavirus was detected in 79 of the 400 samples, corresponding to a prevalence of 19.8 percent. Of these positive specimens, 76 could be genotyped based on the viral VP7 and/or VP4 genes, the two outer capsid proteins that define the G and P genotype systems respectively. The VP7 glycoprotein determines the G genotype, while the VP4 protease-sensitive protein determines the P genotype, and the combination of the two, written as G-P, constitutes the standard nomenclature used by the global rotavirus surveillance community.

What the genotyping revealed was remarkable. Fifteen distinct G-P genotype combinations were identified among the 76 genotyped samples, a level of diversity that underscores the complex molecular ecology of rotavirus in the region. The predominant circulating genotypes were G3P[8] at 11.8 percent (9 of 76 samples), G1P[4] at 10.6 percent (8 of 76), G12P[6] at 7.9 percent (6 of 76), and G2P[4] at 7.9 percent (6 of 76). No single genotype dominated overwhelmingly, suggesting that multiple viral lineages are co-circulating simultaneously within the pediatric population of Addis Ababa.

Perhaps the most significant finding of the study was the detection of three genotypes, G8P[4], G10P[8], and G4P[8], for the first time in Ethiopia. These genotypes had not been previously reported in the country, and their identification raises important questions about viral evolution, zoonotic reservoirs, and the possible introduction of novel strains from neighboring regions. G8 and G10 genotypes are often associated with bovine rotaviruses, and their detection in human clinical specimens can indicate reassortment events between animal and human viral strains, a phenomenon that has been increasingly documented across Africa.

Ethiopia introduced the Rotarix rotavirus vaccine in 2013, adding the monovalent G1P[8] vaccine to its routine immunization schedule. Rotarix contains a single attenuated human strain, and its widespread use has been associated in many settings with a reduction in severe rotavirus disease. However, the continued detection of rotavirus in nearly 20 percent of children with acute diarrhea in Addis Ababa, more than a decade after vaccine introduction, highlights the ongoing burden of disease and the importance of understanding which strains are circulating in the post-vaccine era.

The molecular epidemiology of rotavirus is shaped by the segmented nature of its double-stranded RNA genome, which consists of eleven segments encoding six viral proteins and six nonstructural proteins. This segmented architecture allows reassortment, a process by which co-infecting viral strains can exchange gene segments and generate novel genotype combinations. Reassortment is a key driver of rotavirus diversity and is thought to contribute to the emergence of strains that may partially escape vaccine-induced immunity, making continued strain surveillance an essential component of public health planning.

The study’s findings carry particular relevance for Sub-Saharan Africa, which bears the greatest burden of rotavirus disease globally. The wide diversity of genotypes identified in Addis Ababa, including unusual genotypes not previously reported in Ethiopia, underlines the importance of continued molecular surveillance to monitor the emergence of new strains and to inform vaccine policy decisions. Understanding the local genotype distribution is critical for assessing whether current vaccines provide adequate coverage against the circulating strains and for detecting shifts in genotype prevalence that may occur over time.

The research was funded by the National Institute for Health and Care Research using UK aid from the UK Government to support global health research, with additional support from Addis Ababa University. The laboratory work was facilitated by the Malawi-Liverpool Wellcome Programme, and the study involved collaboration between Ethiopian, Malawian, and British institutions, including Addis Ababa University, Kamuzu University of Health Sciences in Blantyre, and the University of Liverpool.

As rotavirus continues to evolve in the post-vaccine era, studies of this kind provide the molecular evidence base needed to track viral change and to protect the most vulnerable populations. The detection of G8P[4], G10P[8], and G4P[8] in Ethiopia for the first time serves as a reminder that the viral landscape is dynamic, and that sustained genotypic characterization remains indispensable for understanding and ultimately reducing the burden of rotavirus disease among children in Africa and beyond.

Subject of Research: Molecular epidemiology and genotypic characterization of rotavirus among children under five years of age with acute diarrheal illness in Addis Ababa, Ethiopia: cross-sectional hospital-based study

Article Title: Molecular epidemiology and genotypic characterization of rotavirus among children under five years of age with acute diarrheal illness in Addis Ababa, Ethiopia: cross-sectional hospital-based study

Article References: Natei, G. D., Asrat, D., Kalayu, A. A., Msefula, C., Cunliffe, N. A., & Mekasha, A. (2026). Molecular epidemiology and genotypic characterization of rotavirus among children under five years of age with acute diarrheal illness in Addis Ababa, Ethiopia: cross-sectional hospital-based study. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14468-z

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14468-z

Keywords: Molecular, epidemiology, genotypic, characterization, rotavirus, children, under, five, years, acute, diarrheal, illness

The study, led by researchers including Feiyang Gao and Wei Hu, examined data from 340 patients who participated in the ATTENTION trial, a landmark study evaluating endovascular treatment for acute basilar artery occlusion. In this post hoc analysis, patients were categorized into two groups based on the imaging modality used for their baseline evaluation: 277 patients underwent computed tomography, while 63 patients received magnetic resonance imaging. The primary objective was to determine whether the choice of imaging modality influenced the likelihood of achieving a favorable functional outcome, defined as a modified Rankin Scale score of 0 to 3 at 90 days.

The results indicated that baseline imaging modality was not significantly associated with the primary outcome in the overall cohort. The odds ratio for achieving a modified Rankin Scale score of 0 to 3 was 0.99, with a 95% confidence interval ranging from 0.50 to 1.95, and a p-value of 0.976. This statistical finding suggests that patients who underwent MRI were just as likely to achieve good functional recovery as those who underwent CT. The consistency of this finding was further supported by subgroup analyses, which showed similar results among patients who received endovascular treatment and those who were managed with best medical care alone.

A critical concern in acute stroke management is the potential delay in treatment initiation caused by more complex imaging procedures. MRI scans typically require more time to perform and process compared to CT scans, which has historically raised concerns that choosing MRI might delay the critical step of arterial puncture for thrombectomy. However, the study found no significant workflow delays associated with MRI. The mean difference in time from stroke onset to randomization was only 5.23 minutes, with a p-value of 0.843, indicating no statistically significant difference. Similarly, the time from onset to arterial puncture showed a mean difference of 13.16 minutes, with a p-value of 0.701, further confirming that MRI did not hinder the speed of treatment initiation.

The technical implications of these findings are significant for stroke centers aiming to optimize their diagnostic pathways. Computed tomography has long been the standard of care for initial stroke evaluation due to its speed and ability to quickly rule out hemorrhagic stroke. However, MRI, particularly diffusion-weighted imaging, provides more detailed information about the extent of irreversible brain injury, which can be crucial for selecting patients for endovascular therapy. The study’s findings suggest that in the specific context of basilar artery occlusion, the additional diagnostic detail provided by MRI does not translate into a measurable benefit in patient selection or outcome prediction compared to conventional CT.

This conclusion aligns with broader trends in stroke research, where the focus has shifted from identifying the perfect imaging tool to ensuring that the chosen tool integrates seamlessly into the clinical workflow. Previous studies, such as the SWIFT-DIRECT subanalysis, have also explored the comparison between MRI and CT for large artery ischemic stroke, often highlighting the trade-offs between diagnostic accuracy and speed. The current study adds to this body of evidence by specifically addressing the posterior circulation, where the anatomy and clinical presentation of stroke differ significantly from the anterior circulation.

The authors emphasize that conventional imaging appears sufficient as a first-line tool for selecting patients in clinical practice. This recommendation is particularly relevant for hospitals that may not have immediate access to MRI scanners or for those where MRI availability is limited during peak emergency hours. By validating the efficacy of CT, the study supports a streamlined approach to stroke care that prioritizes speed and accessibility without compromising patient outcomes. This is especially important given the high mortality and morbidity rates associated with basilar artery occlusion, where rapid intervention is critical for survival.

Furthermore, the study’s findings have implications for the development of future stroke trials and clinical guidelines. As the field moves toward more personalized medicine, the ability to quickly and accurately assess patients using widely available tools becomes increasingly important. The consistency of the results across different time windows suggests that the choice of imaging modality is robust and not dependent on the specific timing of patient presentation. This robustness enhances the generalizability of the findings and their applicability to diverse clinical settings.

In conclusion, this post hoc analysis of the ATTENTION trial demonstrates that there is no evidence to support the preferential use of MRI over CT as the primary imaging strategy for patient selection in acute basilar artery occlusion. Both modalities provide comparable outcomes in terms of functional recovery and workflow efficiency. These findings reinforce the role of computed tomography as a reliable and efficient first-line imaging tool in the acute management of basilar artery occlusion, allowing clinicians to focus on rapid treatment initiation rather than the complexities of advanced imaging. As stroke care continues to evolve, such studies are essential for refining clinical protocols and ensuring that patients receive the most effective and timely care possible.

Subject of Research: Magnetic resonance imaging vs computed tomography for baseline imaging evaluation in acute basilar artery occlusion

Article Title: Magnetic resonance imaging vs computed tomography for baseline imaging evaluation in acute basilar artery occlusion

Article References: Gao, F., Nguyen, T. N., Wang, A., Li, R., Xu, P., Chen, Y., Nogueira, R. G., Fang, S., & Hu, W. (2026). Magnetic resonance imaging vs computed tomography for baseline imaging evaluation in acute basilar artery occlusion. Journal of Neurology, 273(11), Article 670. https://doi.org/10.1007/s00415-026-14159-4

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14159-4

Keywords: Magnetic, resonance, imaging, computed, tomography, baseline, evaluation, acute, basilar, artery, occlusion, scientific research

The condition in question is acute decompensated heart failure with preserved ejection fraction, abbreviated ADHFpEF. In this disorder, the heart muscle becomes stiff and cannot relax properly between beats, so blood backs up into the lungs and tissues even though the heart’s ejection fraction, the percentage of blood pumped out with each contraction, remains above normal thresholds. Because the pumping numbers look reassuring, emergency physicians and geriatricians frequently miss the diagnosis, especially in elderly patients whose symptoms overlap with common complaints of aging such as fatigue, mild breathlessness, and generalized swelling. Delayed recognition means delayed treatment, and in older adults that delay can be measured in lost function and lost independence.

Researchers at the Third People’s Hospital of Yunnan Province, part of the Second Affiliated Hospital of Dali University in Kunming, turned to bioelectrical impedance analysis, or BIA, as a possible solution. The technique exploits a simple physical principle: lean tissue and water conduct electrical current well, while fat resists it. By passing a weak, harmless alternating current through the body and measuring how it is impeded, multifrequency BIA devices can estimate how much water the body holds and, crucially, where that water sits. The method is already familiar from nutrition clinics and dialysis units, but its value for flagging acute heart failure in elderly hospital populations had not been systematically tested until now.

Two numbers lie at the heart of the new study. The first is the ratio of extracellular water to total body water, written ECW/TBW. In healthy people, most of the body’s water resides inside cells, with only a controlled fraction circulating in the spaces between cells and in blood plasma. When the heart cannot keep up, pressure rises in the capillaries and fluid leaks outward, inflating the extracellular compartment. A rising ECW/TBW ratio therefore acts as a fingerprint of congestion. The second number is the phase angle, a measure derived from the resistance and reactance of body tissues. A healthy cell membrane behaves like a tiny capacitor, storing charge and delaying the electrical signal; intact, hydrated cells with robust membranes produce a larger phase angle, while damaged, depleted cells let current pass more freely, shrinking the number. Low phase angle has long been linked to malnutrition, inflammation, and poor outcomes across many diseases.

To see whether these electrical signatures could distinguish ADHFpEF, the team enrolled 377 older hospitalized patients with an average age of 74.9 years, about 57 percent of them women. Thirty-three of the participants, or 8.8 percent, had been diagnosed with acute decompensated heart failure with preserved ejection fraction. Each patient underwent multifrequency BIA measurements at the whole body, trunk, and leg levels, allowing the researchers to map fluid distribution across different anatomical regions rather than relying on a single global reading. The team then applied a battery of statistical tools, including logistic regression, a restricted cubic spline model, and receiver operating characteristic analysis, to quantify how strongly the BIA parameters tracked with the diagnosis.

The results were strikingly consistent. Higher ECW/TBW ratios at the whole body, trunk, and leg levels all predicted ADHFpEF, with odds ratios ranging from 3.02 to 3.61 and every association reaching statistical significance. In practical terms, patients whose extracellular water fraction was elevated had roughly three times the odds of having the condition for each step up the scale. Phase angle told the opposite story: whole body and leg phase angles were negatively associated with ADHFpEF, with odds ratios of about 0.18 to 0.19, meaning that lower values, reflecting weaker cell membranes and greater cellular distress, strongly marked the disease. Intriguingly, trunk phase angle showed no significant association, suggesting that the trunk, which houses most of the congestion in heart failure, may be better characterized by its water ratio than by its electrical phase.

Perhaps the most thought-provoking finding came from the nonlinear analysis. Using a restricted cubic spline model, the researchers discovered a J-shaped relationship between whole body and trunk ECW/TBW and the likelihood of ADHFpEF, with inflection points at 39.5 percent and 39.7 percent respectively. Below those thresholds, rising extracellular water fractions carried relatively little added risk; above them, the probability of the condition climbed steeply. This kind of tipping-point behavior fits the physiology of decompensation, in which the body compensates for fluid overload until a critical level is crossed and symptoms erupt. If the finding holds in future studies, the roughly 39.5 percent mark could serve as a practical alert threshold for clinicians scanning BIA printouts at the bedside.

The team did not stop at individual markers. They built a basic clinical model from conventional patient information and then tested whether adding BIA parameters improved its diagnostic power. The winning combination incorporated trunk ECW/TBW, pushing the area under the receiver operating characteristic curve, a standard gauge of diagnostic accuracy, to 0.904. An AUC of 0.904 sits well above the 0.5 that represents random guessing and approaches the range where a test becomes genuinely useful for clinical decision-making. In other words, a single trunk measurement of fluid distribution, layered onto routine clinical data, allowed the model to separate patients with ADHFpEF from those without it with impressive reliability.

For a condition that is notoriously difficult to catch early, the implications are considerable. Echocardiography, the current mainstay, requires expensive equipment, trained sonographers, and interpretation by specialists, and it can be inconclusive in the acute setting when volume status is shifting. Natriuretic peptide blood tests help but are influenced by age, kidney function, obesity, and other factors common in the elderly. BIA, by contrast, is non-invasive, radiation-free, and fast enough to repeat daily, making it plausible as a monitoring tool that could track a patient’s fluid trajectory through a hospital stay and flag deterioration before symptoms demand attention. The study’s authors suggest that elevated ECW/TBW and reduced phase angle may help identify older patients with a higher likelihood of ADHFpEF, positioning the measurements as adjunctive bedside markers rather than standalone diagnoses.

Caveats remain, as they do with any cross-sectional study. The research captured a snapshot in time at a single Chinese hospital, and the number of patients with ADHFpEF, 33 in total, was modest, which limits how precisely the thresholds and performance figures can be generalized. The published version is an early-release, citable article carrying a permanent DOI, subject to further editorial refinement before the final version of record appears. Prospective studies following patients over time, and validation in other populations and healthcare systems, will be needed before BIA parameters earn a place in formal diagnostic guidelines. Still, the core message is hard to ignore: the electrical whisper of shifting water in an aging body may carry enough information to reveal one of medicine’s most commonly missed diagnoses, using a device that costs a fraction of an echocardiogram and fits beside a hospital bed.

Subject of Research: Water distribution and phase angle based on bioelectrical impedance analysis: a convenient approach for identifying acute decompensated heart failure with preserved ejection fraction in older adults

Article Title: Water distribution and phase angle based on bioelectrical impedance analysis: a convenient approach for identifying acute decompensated heart failure with preserved ejection fraction in older adults

Article References: Yang, H., Yang, H., Yuan, J., Li, H., Huang, Y., Chen, S., Cao, F., Chen, W., & Duan, Z. (2026). Water distribution and phase angle based on bioelectrical impedance analysis: a convenient approach for identifying acute decompensated heart failure with preserved ejection fraction in older adults. BMC Geriatrics. https://doi.org/10.1186/s12877-026-08337-2

Image Credits: AI Generated

DOI: 10.1186/s12877-026-08337-2

Keywords: Water, distribution, phase, angle, based, bioelectrical, impedance, analysis, convenient, approach, identifying, acute