As heart failure develops, the heart utilizes ketone bodies at increased rates, indicating an adaptive stress response. Thus, increasing ketone body availability exerts protective effects against heart failure. However, although it is the widely used approach for increasing ketone body availability, the ketogenic diet shows limited cardioprotective effects against heart failure. This study was aimed at examining the effects of the ketogenic diet on heart failure and the underlying mechanisms. Pressure overload‐induced heart failure was established by transverse aortic constriction (TAC) in mice. Continuous ketogenic diet feeding for 8 weeks failed to protect the heart against heart failure. It showed no significant effects on cardiac systolic function and fibrosis but aggravated cardiac diastolic function in TAC mice. Specifically, it induced systemic lipid metabolic disorder and hepatic dysfunction in TAC mice. It decreased the content of 3‐hydroxy‐3‐methylglutaryl‐CoA lyase (HMGCL), a key enzyme in ketogenesis, and impaired the capacity of hepatic ketogenesis in TAC mice. It preserved the capacity of hepatic ketogenesis and exerted cardioprotective effects against heart failure, increasing cardiac function and decreasing cardiac fibrosis, in liver‐specific HMGCL‐overexpressed TAC mice. Importantly, we found that alternate‐day ketogenic diet feeding did not impair the capacity of hepatic ketogenesis and exerted potent cardioprotective effects against heart failure. These results suggested that alternate‐day but not continuous ketogenic diet protects against heart failure through preservation of ketogenesis in the liver.

Dyspnea is a subjective sensation often described as a feeling of respiratory effort, tightness, or air hunger. The underlying mechanisms of this symptom are multifaceted and involve factors such as respiratory centers, cardiovascular system, airways, neuromuscular components, and metabolic factors, although not fully elucidated. The classical theory of imbalance between inspiratory neural drive (IND) and the simultaneous dynamic responses of the respiratory system posits that the disruption of a normal and harmonious relationship fundamentally shapes the expression of respiratory discomfort. Assessment and comprehensive treatment of dyspnea are crucial for patient rehabilitation, including subjective self-reporting and objective clinical measurements. Non-pharmacological interventions, such as pulmonary rehabilitation, fan therapy, exercise, chest wall vibration, virtual reality technology, traditional Chinese medicine (acupuncture and acupressure), and yoga, have shown promise in alleviating dyspnea symptoms. Additionally, oxygen therapy, has demonstrated short-term benefits for patients with pre-hospital respiratory distress and hypoxemia. This review provides a comprehensive overview of dyspnea, emphasizing the importance of a multifaceted approach for its assessment and management, with a focus on non-pharmacological interventions that contribute to enhanced patient outcomes and quality of life.

With the development of industrialization in recent years, infrasound has become an important component of public noise. To date, diverse studies have revealed the negative effects of infrasound on the central nervous system (CNS), especially the learning and memory ability. It is widely reported that environmental enrichment (EE) ameliorates the learning and memory deficits in different models of brain injury. Therefore, the present study was designed to determine the possible benefits of pre‐exposure to EE in preventing functional deficits following infrasound exposure and their related mechanism. Adult male rats were given enriched or standard housing for 30 days. Following enrichment, the rats were exposed to 16 Hz, 130 dB infrasound for 14 days, and then their learning and memory ability was assessed. Changes to neuroinflammation, apoptosis, and oxidative stress in the hippocampus were also detected. Our results showed that the infrasound‐induced deficit in learning and memory was attenuated significantly in EE pre‐exposed rats. Pre‐exposure to EE could induce a decrease in proinflammatory cytokines and increased anti‐inflammatory cytokines and antioxidant properties in the hippocampus. Moreover, pre‐exposure to EE also exerted antiapoptosis functions by upregulating the B‐cell lymphoma/leukemia‐2 (Bcl‐2) level and downregulating the P53 level in the hippocampus. In conclusion, the results of the present study suggested that EE is neuroprotective when applied before infrasound exposure, resulting in an improved learning and memory ability by enhancing antioxidant, anti‐inflammatory, and antiapoptosis capacities.

As a kind of environmental noise, infrasonic noise has negative effects on various human organs. To date, research has shown that infrasound impairs cognitive function, especially the ability for learning and memory. Previously, we demonstrated that impaired learning and memory induced by infrasound was closely related with glia activation; however, the underlying mechanisms remain unclear. Connexin 43 hemichannels (Cx43 HCs), which are mainly expressed in hippocampal astrocytes, are activated under pathological conditions, lending support to the hypothesis that Cx43 HCs might function in the impaired learning and memory induced by infrasound. This study revealed that that blocking hippocampal Cx43 HCs or downregulating hippocampal Cx43 expression significantly alleviated impaired learning and memory induced by infrasound. We also observed that infrasound exposure led to the abundant release of glutamate and ATP through Cx43 HCs. In addition, the abundant release of glutamate and ATP depended on proinflammatory cytokines. Our finds suggested that the enhanced release of ATP and glutamate by astroglial Cx43 HCs may be involved in the learning and memory deficits caused by infrasound exposure.

Lung transplantation (LTx) is a well-established option for patients in the end-stage of lung disease that is not responsive to other treatments. Although the survival rate after LTx has seen a significant increase, exercise tolerance is still limited and poses a big obstacle to recovery after LTx. Pulmonary rehabilitation (PR) is a comprehensive intervention that has many benefits for patients with chronic respiratory disease. However, the effectiveness of PR on adult patients with LTx is inconclusive. We performed this meta-analysis to assess the efficacy of PR in adult LTx recipients. Eligible randomized controlled trials (RCTs) and quasi-experimental studies published until March 25, 2024 were searched in MEDLINE, Embase, Web of Science and CINAHL. Additionally, reference lists and published systematic reviews were scanned by manual searching. Studies selection, data extraction, and risk of bias assessment were conducted independently. Stata software (version 17.0) was utilized. There were 21 studies (9 RCTs and 12 quasi-experimental studies) were identified. Pooled analysis showed that PR positive effect in improving 6-minute walking distance (6MWD) [standard mean difference (SMD) =1.28, 95% confidence interval (CI): 1.05–1.50, P<0.001], maximum oxygen consumption (VO₂max) (SMD =0.42, 95% CI: 0.15–0.68, P=0.002), handgrip force (HGF) (SMD =0.49, 95% CI: 0.26–0.73, P<0.001), and quadriceps force (QF) (SMD =0.63, 95% CI: 0.45–0.82, P<0.001). There was no significant publication bias in those outcomes mentioned above. PR shows evidence for being an effective adjunctive strategy for improving exercise capacity after LTx, but multi-center trials on larger populations are required to confirm its clinical benefits in the real-world setting.