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In this work, we develop a novel capacitive humidity sensor based on Al–Si acceptor–donor co-doped SnO2 for real-time monitoring of ambient humidity and human respiration. XRD measurements reveal that all samples exhibit a tetragonal rutile phase and the crystallite size of SnO2 decreases with increasing Al–Si content. The high intensity of the Raman peak at 762 cm−1 confirms the presence of bridging mode oxygen vacancies in (Al + Si)0.02Sn0.98O2. The EPR results show that the amount of singly ionized oxygen vacancies increases after the introduction of Al–Si. Both types and amounts of oxygen vacancy defects are particularly sensitive to the adsorption of water molecules. Moreover, according to DFT calculations, the contribution of the Si 3s orbital and Al 3s orbital to the band edge verifies the formation of acceptor–donor complexes in Al–Si co-doped SnO2. The humidity sensing results reveal that the (Al + Si)0.02Sn0.98O2 humidity sensor shows high sensitivity (S = 839), low hysteresis (1.94%) and fast response/recovery times (25 s/5 s). The respiratory intervals during shallow, medium and deep breathing states of (Al + Si)0.02Sn0.98O2 were measured at 2.8 s, 3.8 s and 4.5 s, respectively. The chemical mechanism for the enhancement of humidity sensing performance corresponding to the oxygen vacancy defects induced by Al–Si interplay is proposed. [ABSTRACT FROM AUTHOR]

Vestibular and psychiatric disorders are very closely related. Previous research shows that the discomfort and dysfunction caused by dizziness in patients can affect psychological processes, leading to anxiety and depression, and the irritation of anxiety and depression can aggravate the discomfort of dizziness. But the causal relationship between dizziness in the recovery period of stroke and Post-stroke depression (PSD) / Post-stroke anxiety (PSA) is not clear. Identifying the causal relationship between them can enable us to conduct more targeted treatments. We review the epidemiology and relationship of dizziness, anxiety, and depression, along with the related neuroanatomical basis. We also review the pathophysiology of dizziness after stroke, vestibular function of patients experiencing dizziness, and the causes and mechanisms of PSD and PSA. We attempt to explore the possible relationship between post-stroke dizziness and PSD and PSA. The treatment approach for post-stroke dizziness depends on its underlying cause. If the dizziness is a result of PSD and PSA, addressing these psychological factors may alleviate the dizziness. This can be achieved through targeted treatments for PSD and PSA, such as psychotherapy, antidepressants, or anxiolytics, which could indirectly improve dizziness symptoms. Conversely, if PSA and PSD are secondary to vestibular dysfunction caused by stroke, a thorough vestibular function assessment is crucial. Identifying the extent of vestibular impairment allows for tailored interventions. These could include vestibular rehabilitation therapy and medication aimed at vestibular restoration. By improving vestibular function, secondary symptoms like anxiety and depression may also be mitigated. [ABSTRACT FROM AUTHOR]

The pathophysiology of saccular aneurysm rupture (berry aneurysm) secondary to cocaine and methamphetamine use has been classically attributed to their effects on cerebrovasculature. We conducted a literature review to determine the contribution of cocaine and methamphetamines to aneurysm formation and subarachnoid hemorrhage (SAH). Our literature search revealed the contribution to berry aneurysm by both cocaine and methamphetamines is multifactorial and includes: hemodynamic compromise, hypertensive effects, inflammation, wall stress and hypoperfusion of cerebral vasculature. The pathophysiological mechanisms by which these drugs contribute to saccular aneurysm and SAH is reviewed. We further discuss current grading scales used to measure the severity and extent of SAH in cocaine and methamphetamine users. Additionally, conflicting data regarding the specific role of cocaine and methamphetamines was retrieved. Although questions remain regarding the exact role of cocaine and methamphetamines, the evidence suggests that they do increase the probability of saccular aneurysm formation, rupture and poor patient prognosis.