Sleep apnea is traditionally diagnosed with polysomnography (PSG), which, while effective, is costly, time-consuming, and obtrusive. Recent advancements in biosensing technologies have facilitated the development of under-the-mattress devices as potential alternatives for detecting sleep apnea.

We reviewed the literature across PubMed, Embase, Web of Science, and Scopus, focusing on studies that assessed mattress-like or under-the-mattress biosensing devices for sleep apnea. 15 studies were included as illustrative examples of recent progress.

Our review assessed studies on innovative sensor technologies for sleep apnea detection. These studies demonstrated the efficacy of various sensors-such as Load Cells, Emfit, and PVDF-along with advanced radar and machine learning methods, in accurately identifying sleep apnea events. Results indicated that most studies reported good overall performance of mattress-based systems compared to traditional polysomnography, though variability across devices was observed.

Under-the-mattress biosensing devices appear to be promising as cost-effective, user-friendly, and unobtrusive alternatives to PSG for sleep apnea detection. Their high-performance metrics suggest that these devices are viable options for both clinical settings and home use.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a respiratory pathogen that emerged in December 2019 and caused a global pandemic by March 2020, with >7 million deaths due to coronavirus disease 2019 (COVID-19) globally as of September 2025. The clinical syndrome of COVID-19 ranges from asymptomatic infection to severe disease with pneumonia and death. SARS-CoV-2 variant type, inoculum, previous exposure and host factors influence the clinical trajectory. Identification of key structural proteins of SARS-CoV-2 and insights into the pathophysiology of the immune response to infection led to the development of effective preventive (vaccines and monoclonal antibodies) and therapeutic (antivirals and immunomodulatory agents) agents. Antiviral agents, such as remdesivir and nirmatrelvir-ritonavir, inhibit viral replication and immunomodulatory agents, such as tocilizumab and baricitinib, act to reduce a dysregulated immune response to SARS-CoV-2. The pandemic had economic and socio-cultural consequences that affected the quality of life and overall life expectancy of individuals. As the emergency phase of the pandemic concludes, robust monitoring and surveillance systems must be sustained and research to improve vaccines and therapeutics must continue to maintain control of SARS-CoV-2 in the population and be prepared for emerging pathogens with pandemic potential.

Essential hypertension is associated with structural and functional cardiac changes, including left ventricular hypertrophy (LVH), which significantly increases cardiovascular risk. Left anterior fascicular block (LAFB), historically considered benign, has recently been linked to adverse outcomes. Carotid intima-media thickness (CIMT) is a noninvasive marker of subclinical atherosclerosis. The interplay between LAFB, LVH, and CIMT in hypertensive patients remains poorly defined.

We conducted a cross-sectional study of 256 patients with essential hypertension, divided into LAFB (n = 60) and non-LAFB (n = 196) groups. All participants underwent 12-lead electrocardiography, echocardiography, and carotid ultrasonography. CIMT was measured as a surrogate of vascular remodeling. Echocardiographic indices of cardiac remodeling and CIMT were compared between groups. Logistic regression identified independent predictors of LAFB.

Patients with LAFB had significantly higher left atrial diameter (LAD), left atrial volume index (LAVI), interventricular septal thickness (IVST), posterior wall thickness (PWT), left ventricular mass (LVM), left ventricular mass index (LVMI), and prevalence of LVH compared with those without LAFB (all p < 0.001). Mean CIMT values were also greater in the LAFB group (0.82 ± 0.27 vs. 0.72 ± 0.19 mm, p = 0.003). ROC analysis identified LAD >35 mm and LVMI >81 g/m² as useful predictors of LAFB. Multivariate logistic regression showed increased LAD (OR = 7.94, 95% CI: 2.24-28.10, p = 0.001) and LVM (OR = 3.37, 95% CI: 1.49-7.57, p = 0.003) as independent predictors of LAFB.

In essential hypertension, LAFB is associated with more advanced cardiac remodeling and increased CIMT. LAD and LVM were independent predictors of LAFB, suggesting that this ECG finding may serve as a simple marker of higher cardiovascular risk.

Insulin resistance (IR)-related indices are validated prognostic markers in metabolic disorders, but have not been applied to preclinical or clinical obesity. This study aimed to investigate the relationship between IR-related indices and cardiovascular disease (CVD) incidence, considering genetic factors and biomarkers.

This prospective study analyzed 112,866 UK Biobank participants with preclinical or clinical obesity. IR-related indices were evaluated: triglyceride-glucose (TyG) index, TyG-body mass index (TyG-BMI), TyG-waist circumference (TyG-WC), and TyG-waist-to-height ratio (TyG-WHtR). Genetic risk was estimated using the polygenic risk score. Outcomes, including total CVD, coronary artery disease (CAD), and stroke, were ascertained through medical records linkage. Cox proportional hazard models were used to evaluate the associations and modification effects of genetic risk. Incremental predictive value was assessed by net reclassification index (NRI) and integrated discrimination improvement index (IDI). Mediation analyses explored the role of inflammatory, hepatic, and renal biomarkers.

Over a median follow-up period of 13.45 years, 21,601 total CVD, 11,942 CAD, and 3347 stroke cases were documented. Compared with the lowest quartile of IR-related indices, participants in the highest quartile presented increased CVD risk. For total CVD, hazard ratios (HRs) (95% confidence intervals, CIs) for the fourth versus the first quartiles were 1.33 (1.28-1.39) for TyG-BMI, 1.41 (1.34-1.48) for TyG-WC, and 1.25 (1.20-1.31) for TyG-WHtR. All IR-related indices demonstrated significant associations with CAD. Borderline significant associations were observed for stroke. Distinct dose-response association patterns with total CVD were observed: TyG-BMI and TyG-WHtR exhibited nonlinear relationships, while TyG-WC demonstrated a linear association. The CVD risk was highest in individuals with high genetic risk and high IR indices, with an additive interaction between TyG-WC and genetic risk being observed. Significantly higher NRI and IDI were observed for TyG-WC, TyG-BMI, and TyG-WHtR in predicting CVD, with TyG-WC achieving the highest performance. Mediation analyses indicated that inflammation, liver, and renal biomarkers might partially mediate the relationship.

Elevated IR-related indices, particularly TyG-WC, were associated with increased total CVD and CAD risks in preclinical or clinical obesity. Additive effects of TyG-WC and genetic risk on CVD were revealed, with mediating biomarkers suggesting potential targeted interventions for CVD risk reduction.

To analyze the prevalence of hypertension in patients with acromegaly and assess the impact of acromegaly treatment on blood pressure (BP) outcomes.

Retrospective multicenter study of 434 patients with acromegaly surveilled at 25 tertiary hospitals in Spain and Portugal. The cohort was divided into two subgroups: patients with (n = 209) and without (n = 225) hypertension at the time of acromegaly diagnosis.

Of the 434 patients, 209 (48.2%) had hypertension at the time of acromegaly diagnosis. Patients with acromegaly and hypertension were older and had a higher prevalence of cardiovascular disease and risk factors. A significant BP improvement was observed 3 months after pituitary surgery, with a marked reduction of the SBP (ΔSBP - 5.0mmHg, 95%CI -2.37 to -7.61) and DBP (ΔDBP - 2.2mmHg, 95% CI -0.66 to -3.75). Over a median follow-up of 8.4 years [IQR 4.8-12.8], 16% (n = 35/218) of initially normotensive patients developed hypertension, while 14.1% (n = 27/192) of hypertensive patients achieved hypertension remission. Hypertension remission was more likely in patients taking fewer antihypertensive drugs and with higher IGF1 levels at diagnosis, and in those who had a greater decrease in GH and IGF-1 after surgery.

At the time of acromegaly diagnosis up to 50% of patients have hypertension, and around 15% of them experience hypertension remission after pituitary surgery. The probability of remission is higher in patients with milder baseline hypertension and higher IGF-1 levels and in those achieving a greater postoperative decrease of GH and IGF-1.

Tetralogy of Fallot (TOF) is one of the most common cyanotic congenital heart malformations, characterized by four pathological features: right ventricular outflow tract obstruction/pulmonic stenosis, a ventricular septal defect, an overriding aorta, and right ventricular hypertrophy. It was initially partially defined by Nicholas Steno in the 17th century and completely described by Étienne-Louis Arthur Fallot and Maude Abbott in the 19th and 20th centuries. The advances in multimodality imaging and innovative surgical and transcatheter techniques have led to advances in the management of TOF. While initial management in the mid-20th century favored palliative procedures in infancy followed by complete surgical repair, data now support an early complete surgical repair in infancy. The major post-repair complication is the development of significant pulmonary regurgitation, necessitating either surgical or transcatheter valve replacement. Multimodality imaging is essential to the initial identification of TOF, preoperative planning, and post-procedural complication assessment. In this review, we provide a historical perspective of the discovery and clinical management of TOF from the 1600s to the present day, as well as the role of multimodality imaging in TOF management.

Disruption of the blood-brain barrier (BBB) is a critical mechanism of global cerebral ischemic injury and neurological deficits under cardiac arrest (CA). Compared to traditional sinusoidal wave chest compression (SW-CPR), the trapezoidal wave chest compression (TW-CPR) technique has been shown to improve blood flow and increase microcirculation during CPR. However, the effect of TW-CPR on BBB and the underlying molecular mechanism remains to be illustrated. In this study, TW-CPR and SW-CPR were respectively used on rats following CA. After resuscitation, the cerebral cortical perfusion, BBB integrity, and neurological outcomes were assessed. RT-qPCR, immunofluorescence staining, and Western blot analyses were employed to measure the expression of mechanotransducer proteins. The integrin β3 inhibitor (cRGDfk) and adeno-associated virus-ITGB3 shRNA were administered, and protein expression was assessed by Western blot, including the expression of downstream signals of differentially expressed proteins. We found that rats receiving TW-CPR showed significantly higher survival rates (73.3% vs. 53.3%, p = 0.014) and improved neurological function scores compared to SW-CPR (p = 0.020). TW-CPR also reduced BBB disruption, as evidenced by decreased Evans blue dye extravasation and elevated levels of tight junction proteins occludin and claudin-5. Hemodynamic measurements indicated that TW-CPR enhanced peripheral circulation, as shown by increased arterial pressure and left common carotid artery blood flow velocity. Additionally, cerebral cortical microcirculation was better preserved in the TW-CPR group, with higher perfused vessel density (PVD) and microvascular flow index (MFI) compared to SW-CPR. TW-CPR was also associated with reduced integrin β3 expression in BMECs, which may contribute to its protective effects on the BBB. In conclusion, TW-CPR can improve cerebral microcirculation, thus attenuating BBB injury via inhibiting integrin β3 in BMECs after CA/CPR in rats.

The progression of acute kidney injury (AKI) to chronic kidney disease (CKD) represents a unique renal disease scenario, yet its exact mechanisms remain unclear. The transport of renal metabolic byproducts plays a crucial role in maintaining systemic homeostasis and the repair process. The glutathione-based lipid oxidation-reduction system is essential for preserving cellular function. However, the relationship between the disruption of the redox system during the AKI-CKD transition and renal transport proteins remains unclear. We investigated the mechanisms by which the transport protein multidrug resistance-associated protein 1 (MRP1) mediates the destruction of the redox system during renal ischemia-reperfusion injury (IRI) and devised interventions related to renal ferroptosis. Transcriptome analysis and a unilateral kidney IRI model were employed to explore changes in MRP1 expression during the AKI-CKD process. Functional experiments simulating in vivo renal IRI were conducted using Carbonyl Cyanide m-Chlorophenylhydrazine (CCCP)-treated renal tubular epithelial cells. MK571(MRP1 inhibitor) and Fer-1 were used to inhibit MRP1 and ferroptosis, respectively. Kidney tissue damage and fibrosis area were evaluated using staining methods like KIM1 and Masson. In the renal IRI model, upregulation of the transport protein MRP1 expression in renal tissue was observed. MRP1 is responsible for transporting glutathione outside the cell. MK571 significantly inhibited the AKI- CKD transition and immune cell infiltration. Both the deletion or inhibition of MRP1 can also alleviate ferroptosis. However, the combined use of MK571 and Fer-1 did not show additional kidney protective effects. Elevated expression of the renal transport protein MRP1 during renal IRI induces the extracellular leakage of glutathione, leading to ferroptosis. Inhibiting MRP1 can slow down renal ferroptosis and the progression from AKI-CKD.

Approximately 30% of patients with Crohn's disease (CD) experience primary loss of response (PLR) to ustekinumab. However, studies integrating imaging parameters to predict PLR remain limited. This study aimed to quantify endoluminal and intestinal wall parameters using computed tomography enterography (CTE) and assess their predictive value for PLR to ustekinumab.

This multicenter study analyzed 466 intestinal segments from 161 patients with CD between March 2020 and May 2024. A national survey identified 10 CTE parameters for evaluating disease activity and predicting PLR. Logistic regression models were used to assess predictive performance in a validation cohort.

Ten CTE parameters related to lesion characterization-including length, luminal narrowing, and bowel wall thickness-were defined, with newly introduced metrics, including length, area, effective luminal diameter (EffLD), mean bowel wall thickness, and stenosis. A total of 352 baseline and 114 follow-up segments from 161 patients across six centers were analyzed to assess changes following ustekinumab treatment. Paired analysis across all patients showed significant improvements in eight parameters (p < 0.001); in contrast, unpaired comparisons between PLR and non-PLR groups revealed significant differences in six parameters (p < 0.001), with greater improvements in the non-PLR group. EffLD emerged as an independent predictor of ustekinumab response, with an AUC of 0.858 and an accuracy of 0.780 in the validation cohort.

Novel endoluminal parameters, particularly EffLD, provide a detailed characterization of intestinal lesions in inflammatory bowel disease and exhibit strong predictive value for PLR in ustekinumab-treated patients with CD.

This study first applied cardiovascular imaging software to quantify endoluminal CT enterography parameters, establishing effective luminal diameter as a novel, clinically applicable predictor of ustekinumab response in Crohn's disease.

Cardiovascular imaging software can facilitate image analysis in Crohn's disease. Endoluminal CT enterography parameters predict primary loss of response in Crohn's disease. Effective luminal diameter independently predicts ustekinumab response.

People experiencing mental illness smoke tobacco at disproportionately higher rates than the general population. Staff at mental health services are well placed to assist clients with smoking cessation, yet such support is often limited by time or knowledge constraints. Guided by the COM-B model, this study explored barriers and facilitators of smoking cessation among people receiving treatment for mental health disorders as perceived by staff members of community mental health services in Brisbane, Australia. Three focus groups were conducted in August-October 2021 with 29 healthcare professionals and peer support workers employed at three community mental health services. Data were analysed qualitatively using a combined deductive and inductive approach to identify themes grouped by the COM-B domains of capability, opportunity, and motivation. Capability barriers included clients' reliance on smoking to manage anxiety or other mental illness symptoms and difficulties engaging with cessation support, while staff knowledge was a facilitator. Opportunity barriers included smoking being perceived as social currency and clients' limited support networks, whereas facilitators included cessation assistance from peer workers and smokefree environments. Motivation barriers were entrenched behaviours and using smoking as a coping mechanism, with facilitators including staff prioritising cessation and peer-led programs. These findings highlight the need for staff training to address misperceptions about smoking, improve confidence in offering cessation support, and foster trust with clients. Expanding the range of available smoking cessation support options, including peer support programs, and creating supportive service environments may enhance smoking cessation success for individuals experiencing mental illness.