Mild and moderate COVID-19 disease does not affect hearing function permanently: a cross-sectional study involving young and middle-aged healthcare givers.

PURPOSE: To assess the hearing function of patients with mild and moderate COVID-19. METHODS: The hospital staffs recovered from COVID-19 were included. The candidates who had an ear disease or progressive hearing loss prior to COVID-19, or having been hospitalised because of severe and critical COVID-19 were excluded. The age, sex, symptoms during COVID-19, and medications received for the disease were noted. The hearing thresholds (HT) of the participants who had an audiogram before having COVID-19 disease were recorded. A pure tone audiometry was conducted to all. The participants were classified into two groups; Group 1: participants who had an audiogram previously, Group 2: participants who didn't have an audiogram previously. The changes of the HTs of the participants in Group 1 were analyzed. The HTs of the participants in Group 2 were documented without any comparison. The HTs of all participants were also analyzed by classifying them into subgroups according to their symptoms during, and medications received for COVID-19. RESULTS: Fifty-four males and 47 females (18-59 years) were included. The participants' HTs in Group 1 (n = 31) did not change significantly at any of the frequencies after having COVID-19 (p > 0.05). The pure tone averages of the participants in Group 2 (n = 70) were below 25 dB and none of the participants reported worsening of their hearing permanently. The differences between the HTs of none of the subgroups were statistically significant (p > 0.05, p > 0.05). CONCLUSIONS: Mild and moderate COVID-19 and its treatments did not affect the hearing function permanently.

Comparative study of nickel oxide and nickel oxide nanoparticles on oxidative damage, apoptosis and histopathological alterations in rat lung tissues.

BACKGROUND: Nickel oxide nanoparticles (NiONPs) are used as industrial photoelectric and recording materials, catalysts, and sensors. It has been increasingly used in many industrial sectors. Lungs are the important biological barrier that comes into contact with nanomaterials in the inhaled air. This study aimed to compare the effects of nickel oxide (NiO) microparticles and NiONPs on rat lung tissues in different dose administrations, such as oral, intraperitoneal, and intravenous. METHODS: The mature male Wistar rats (n = 42) were divided into seven groups with six animals: Group I (control), Group II NiO gavage (150 mg/kg), Group III NiO intraperitoneally (20 mg/kg), Group IV NiO intravenously (1 mg/kg), Group V NiONP gavage (150 mg/kg), Group VI NiONP intraperitoneal (20 mg/kg), and Group VII NiONP intravenous (1 mg/kg) for 21 days. Oxidative stress (MDA, CAT, SOD, GPx, and GST), apoptotic marker (p53) gene expression, and histopathological changes were determined comparatively. RESULTS: Our data showed that NiO and NiONPs caused an exposure-related increase in the incidence of alveolar/bronchiolar pathological changes, oxidative damage, and p53 gene expression in male rats. Intravenous exposure to NiONPs produces statistically (p < 0.05) more oxidative damage and histopathological changes than exposure to NIO. It also induces higher upregulation of the pro-apoptotic p53 gene. CONCLUSION: NiO and NiONPs induce oxidative damage, histopathological alterations and p53 gene expression in rat lungs. Thus, exposure to NiO and NiONPs, especially intravenously, may indicate more toxicity and carcinogenicity.

The neurovasculature as a target in temporal lobe epilepsy.

The blood-brain barrier (BBB) is a physiological barrier maintaining a specialized brain micromilieu that is necessary for proper neuronal function. Endothelial tight junctions and specific transcellular/efflux transport systems provide a protective barrier against toxins, pathogens, and immune cells. The barrier function is critically supported by other cell types of the neurovascular unit, including pericytes, astrocytes, microglia, and interneurons. The dysfunctionality of the BBB is a hallmark of neurological diseases, such as ischemia, brain tumors, neurodegenerative diseases, infections, and autoimmune neuroinflammatory disorders. Moreover, BBB dysfunction is critically involved in epilepsy, a brain disorder characterized by spontaneously occurring seizures because of abnormally synchronized neuronal activity. While resistance to antiseizure drugs that aim to reduce neuronal hyperexcitability remains a clinical challenge, drugs targeting the neurovasculature in epilepsy patients have not been explored. The use of novel imaging techniques permits early detection of BBB leakage in epilepsy; however, the detailed mechanistic understanding of causes and consequences of BBB compromise remains unknown. Here, we discuss the current knowledge of BBB involvement in temporal lobe epilepsy with the emphasis on the neurovasculature as a therapeutic target.

Dentate gyrus astrocytes exhibit layer-specific molecular, morphological and physiological features.

Neuronal heterogeneity has been established as a pillar of higher central nervous system function, but glial heterogeneity and its implications for neural circuit function are poorly understood. Here we show that the adult mouse dentate gyrus (DG) of the hippocampus is populated by molecularly distinct astrocyte subtypes that are associated with distinct DG layers. Astrocytes localized to different DG compartments also exhibit subtype-specific morphologies. Physiologically, astrocytes in upper DG layers form large syncytia, while those in lower DG compartments form smaller networks. Astrocyte subtypes differentially express glutamate transporters, which is associated with different amplitudes of glutamate transporter-mediated currents. Key molecular and morphological features of astrocyte diversity in the mice DG are conserved in humans. This adds another layer of complexity to our understanding of brain network composition and function, which will be crucial for further studies on astrocytes in health and disease.

Astrocyte-derived Wnt growth factors are required for endothelial blood-brain barrier maintenance.

Maintenance of the endothelial blood-brain-barrier (BBB) through Wnt/ß-catenin signalling is essential for neuronal function. The cells however, providing Wnt growth factors at the adult neurovascular unit (NVU) are poorly explored. Here we show by conditionally knocking out the evenness interrupted (Evi) gene in astrocytes (EviΔAC) that astrocytic Wnt release is crucial for BBB and NVU integrity. EviΔAC mice developed brain oedema and increased vascular tracer leakage. While brain vascularization and endothelial junctions were not altered in 10 and 40 week-old mice, endothelial caveolin(Cav)-1-mediated vesicle formation was increased in vivo and in vitro. Moreover, astrocytic end-feet were swollen, and aquaporin-4 distribution was disturbed, coinciding with decreased astrocytic Wnt activity. Vascular permeability correlated with increased neuronal activation by c-fos staining, indicative of altered neuronal function. Astrocyte-derived Wnts thus serve to maintain Wnt/ß-catenin activity in endothelia and in astrocytes, thereby controlling Cav-1 expression, vesicular abundance, and end-feet integrity at the NVU.

Radiologic Anatomy of the Lumbar Interlaminar Window and Surgical Considerations for Lumbar Interlaminar Endoscopic and Microsurgical Disc Surgery.

OBJECTIVE: The interlaminar window is the most important corridor during both interlaminar approaches to intervertebral discs. The aim of this study was to measure radiologic parameters related to endoscopic and microsurgical interlaminar discectomy. METHODS: Measured parameters included lateral recess line (LRL) width, distance between LRL and endplates of upper intervertebral disc, superior and lateral angles of interlaminar window, interlaminar height, and interpedicular distance via optimized coronal oblique projection computed tomography images. Measurements were performed at L2, L3, L4, and L5 levels. RESULTS: LRL was found to be 16.3 ± 3.4 mm, 17.3 ± 3.3 mm, 21.7 ± 3.4 mm, and 27.7 ± 4.0 mm at L2, L3, L4, and L5. The distances between LRL and both upper endplates decreased from L2 to L5. Distance between LRL and upper endplate of same vertebra and between LRL and lower endplate of upper vertebra was measured. Interlaminar window height decreased from L2 to L5 levels (from 14.0 ± 4.1 mm to 11.1 ± 2.4 mm). CONCLUSIONS: This study showed that width of LRL increases in lower lumbar segments, and height of interlaminar window increases in upper lumbar segments. This study also revealed that intervertebral disc is located cranial to LRL at L2-3, L3-4, and L4-5 levels and is located caudal to LRL at L5-S1 level. The results of this study may help surgical planning in both endoscopic and microscopic interlaminar surgery.