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Cerebral small vessel disease (CSVD) is a group of pathological processes affecting small arteries, arterioles, capillaries, and small veins of the brain. It is one of the most common subtypes of cerebrovascular diseases, especially highly prevalent in elderly populations, and is associated with stroke occurrence and recurrence, cognitive impairment, gait disorders, psychological disturbance, and dysuria. Its diagnosis mainly depends on MRI, characterized by recent small subcortical infarcts, lacunes, white matter hyperintensities (WMHs), enlarged perivascular spaces (EPVS), cerebral microbleeds (CMBs), and brain atrophy. While the pathophysiological processes of CSVD are not fully understood at present, inflammation is noticed as playing an important role. Herein, we aimed to review the relationship between plasma inflammatory biomarkers and the MRI features of CSVD, to provide background for further research.

This article fills the gaps in teaching about the Nernst equation, which is important in medical physiology. Six logical steps are presented that connect the introduction of the equation to its clinical applications to hyperkalemia and hypokalemia, two conditions that can be life-threatening if left untreated. Only when students know how to apply the equation will their learning transition from surface to mastery.

Background Current methods to evaluate the severity of cerebral venous sinus thrombosis (CVST) lack patient-specific indexes. Herein, a novel scoring method was investigated to estimate the thrombus burden and the intracranial pressure (ICP) of CVST. Methods In this retrospective study from January 2019 through December 2021, we consecutively enrolled patients with a first-time confirmed diagnosis of CVST by contrast-enhanced magnetic resonance venography (CE-MRV) or computed tomography venography (CTV). In these patients, a comprehensive CVST-Score was established using magnetic resonance black-blood thrombus imaging (MRBTI) to estimate the thrombus burden semi-quantitatively. The relationship between CVST-Score and ICP was explored to assess the potential of using the CVST-score to evaluate ICP noninvasively and dynamically. Results A total of 87 patients were included in the final analysis. The CVST-Scores in different ICP subgroups were as follows: 4.29±2.87 in ICP2O subgroup, 11.36±3.86 in ICP =250-330mmH2O subgroup and 14.99±3.15 in ICP>330mmH2O subgroup, respectively (p2O, the CVST-Score was linearly and positively correlated with ICP (R2=0.53). The receiver operating characteristic (ROC) curves showed the optimal CVST-Score cut-off values to predict ICP ≥250mmH2O and >330mmH2O were 7.15 and 11.62, respectively (P2O (odds ratio, 2.15; 95% confidence interval, 1.49-3.10; p Conclusions A simple and noninvasive CVST-Score can rapidly estimate the thrombus burden and predict the severity of intracranial hypertension in patients with CVST. The CVST-Score can aid in evaluating therapeutic responses and avoiding unnecessary invasive procedures at long-term follow-up. Graphical Abstract

Background: Existing methods on correcting patent foramen ovale (PFO)-mediated migraine (PFO-migraine) are not satisfactory. Herein, the effect of normobaric oxygenation (NBO) on inhibiting PFO-migraine was analyzed. Methods: Patients with PFO confirmed by Transesophageal Ultrasound were enrolled in this real-world self-control study consecutively. Baseline data of arterial oxygen partial pressure (PaO2) from their blood gas was compared to PaO2 values from 20 volunteers without a PFO. Patients with PFO-migraine underwent NBO (8L/min. for 1h/q8h) treatment through a mask. The clinical symptoms, results of blood gas, and electroencephalograph (EEG) pre-and post-NBO were compared. Results: A total of 67 eligible patients entered final analysis, of whom 39 had PFO-migraines. Of those 39 patients with PFO-migraines, a small-aperture PFO accounted for 36%. The PaO2 in patients with PFO-migraine at baseline were lower than that in non-PFO volunteers. After one round of NBO treatment, 74.4% of all PFO-migraine patients demonstrated dramatic headache attenuation, and their arterial PaO2 increased remarkably (p2 was maintained for 4 hours and then gradually declined. EEG data in 12 patients prior to and post-NBO treatment were compared. EEG maps prior to NBO treatment demonstrated significant abnormal slow waves. After NBO treatment, the abnormal slow waves disappeared on EEG maps. Conclusions: PFO-mediated right-to-left shunts induce arterial hypoxemia resulting in brain hypoxia, which may be the pathological link between PFO and migraines. Patients with PFO–migraine may benefit from NBO treatment.

Objectives. Normobaric oxygen (NBO) therapy has great clinical potential in the treatment of ischemic stroke, but its underlying mechanism is unknown. Our study aimed to investigate the role of autophagy during the application of NBO on cerebral ischemia/reperfusion injury. Methods. Male Sprague Dawley rats received 2 hours of middle cerebral artery occlusion (MCAO), followed by 2, 6, or 24 hours of reperfusion. At the beginning of reperfusion, rats were randomly given NBO (95% O2) or room air (21% O2) for 2 hours. In some animals, 3-methyladenine (3-MA, autophagy inhibitor) was administered 10 minutes before reperfusion. The severity of the ischemic injury was determined by infarct volume, neurological deficit, and apoptotic cell death. Western blotting was used to determine the protein expression of autophagy and apoptosis, while mRNA expression of apoptotic molecules was detected by real-time PCR. Results. NBO treatment after ischemia/reperfusion significantly decreased infarct volume and neurobehavioral defects. The increased expression of the autophagy markers, including microtubule-associated protein 1A light chain 3 (LC3) and Beclin 1, after ischemia/reperfusion was reversed by NBO, while promoting Sequestosome 1 (p62/SQSTM1) expression. In addition, NBO reduced cerebral apoptosis in association with alleviated BAX expression and increased BCL-2 expression. 3-MA reduced autophagy and apoptotic death but did not further improve NBO-attenuated ischemic damage. Conclusion. NBO induced remarkable neuroprotection from ischemic injury, which was correlated with blocked autophagy activity.

Ischemia–reperfusion injury (IRI) is a series of multifactorial cellular events that lead to increased cellular dysfunction after the restoration of oxygen delivery to hypoxic tissue, which can result in acute heart failure and cerebral dysfunction. This injury is severe and would lead to significant morbidity and mortality and poses an important therapeutic challenge for physicians. Nitric oxide (NO) minimizes the deleterious effects of IRI on cells. NO donors, such as organic nitrates and sodium nitroprusside, are used systematically to treat heart failure, angina, and pulmonary hypertension. Inhaled NO gas was approved by the FDA in 1999 to treat hypoxic newborns, and its beneficial ameliorations reach outside the realm of lung disease. This review will summarize the clinical application of NO in IRI.

Underlying Coronary Artery Disease (CAD) complicated by Mental Stress-Induced Myocardial Ischemia (MSIMI) has been linked with an increased risk for adverse cardiovascular events and even sudden death. However, the underlying mechanisms of MSIMI remain unknown. In this study, we investigated cytokine levels at baseline inflammation status and during acute inflammatory responses to mental stress in patients with known CAD who presented with MSIMI.77 patients with known CAD were recruited and all underwent echocardiography before and during arithmetic stress task. MSIMI was diagnosed by new or worsening wall motion abnormalities greater than or equal to a 5% reduction of left ventricle ejection fraction. Inflammatory markers were measured both before and immediately after the Mental Stress (MS) by ELISA kits. Repeated measures models were used to report the responses and mixed linear regression models were used to report the differences between MSIMI negative and positive patients.MS induced a significant increase in Stromal Cell-Derived Factor-1α (SDF-1α) and Monocyte Chemoattractant Protein-1 (MCP-1) in all subjects; 20.78% of the patients with known CAD developed MSIMI during the arithmetic task. MSIMI positive patients had significantly lower baseline levels of Interleukin-1β (IL-1β) and Tumor Necrosis Factor-α (TNF-α), but a higher response in levels of SDF-1α than MSIMI negative patients.MS can induce acute inflammatory responses. MSIMI is associated with lower levels of IL-1β and TNF-α at baseline and higher levels of SDF-1α in response to MS.

Stroke is one of the most prevalent causes of death around the world. When a stroke occurs, many cellular signaling cascades and regulators are activated, which results in severe cellular dysfunction and debilitating long-term disability. One crucial regulator of cell fate and function is mammalian Forkhead box protein O1 (FoxO1). Many studies have found FoxO1 to be implicated in many cellular processes, including regulating gluconeogenesis and glycogenolysis. During a stroke, modifications of FoxO1 have been linked to a variety of functions, such as inducing cell death and inflammation, inhibiting oxidative injury, affecting the blood brain barrier (BBB), and regulating hepatic gluconeogenesis. For these functions of FoxO1, different measures and treatments were applied to FoxO1 after ischemia. However, the subtle mechanisms of post-transcriptional modification and the role of FoxO1 are still elusive and even contradictory in the development of stroke. The determination of these mechanisms will lead to further enlightenment for FoxO1 signal transduction and the identification of targeted drugs. The regulation and function of FoxO1 may provide an important way for the prevention and treatment of diseases. Overall, the functions of FoxO1 are multifactorial, and this paper will summarize all of the significant pathways in which FoxO1 plays an important role during stroke damage and recovery.