Could sudden sensorineural hearing loss be the sole manifestation of COVID-19? An investigation into SARS-COV-2 in the etiology of sudden sensorineural hearing loss.

OBJECTIVE: This study aimed to investigate the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in patients presenting with only sudden sensorineural hearing loss (SSHNL) during the COVID-19 pandemic. METHODS: The study included five male patients who presented with the sole complaint of unilateral SSNHL to the otolaryngology outpatient clinic between 03-12 April 2020. The patients were referred to the infectious diseases clinic to be evaluated for SARS-CoV-2 by real time polymerase chain reaction (RT-PCR) testing. RESULTS: RT-PCR testing for SARS-CoV-2 was positive in one of the patients and negative in the other four patients. A positive response to COVID-19-specific treatment in the SARS-CoV-2 positive SSNHL patient was noted. CONCLUSION: It should be remembered that non-specific symptoms such as SSNHL could be the only sign with which to recognize a COVID-19 case. Awareness of such a non-specific presentation of COVID-19 patients is crucial during this pandemic period for preventing infectious spread through isolation and early initiation of COVID-19 targeted treatment.

The effects of oxytocin on cognitive defect caused by chronic restraint stress applied to adolescent rats and on hippocampal VEGF and BDNF levels.

BACKGROUND: Because brain development continues during adolescence, the effects of chronic stress on hippocampal changes that occur during that period are permanent. Oxytocin, which is synthesized in the hypothalamus and has many receptors in brain regions, including the hippocampus, may affect learning-memory. This study aimed to investigate chronic restraint stress on hippocampal functions, and hippocampal vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF) levels in adolescent male and female rats and the role of oxytocin in these effects. MATERIAL/METHODS: Experimental groups included control, stress+oxytocin, and stress+saline groups. Restraint stress was applied to all the stress groups for 1 h/day, for 7 days. Learning-memory tests were performed after the 7th day. RESULTS: In the stress+oxytocin groups, the process of finding the platform was shorter than in others groups. The stress+saline groups spent less time, whereas the stress+oxytocin groups spent more time, on the target quadrant in the probe trial. In the stress+oxytocin groups thigmotaxis time (indicating anxiety) decreased, but VEGF and BDNF levels increased. A positive correlation was found between VEGF and BDNF levels and the time spent within the target quadrant. CONCLUSIONS: The results indicate that impaired hippocampal learning and memory loss due to chronic restraint stress can be positively affected by intranasal oxytocin.

Transcutaneous electrical nerve stimulation (TENS) accelerates cutaneous wound healing and inhibits pro-inflammatory cytokines.

The purpose of this study was to evaluate transcutaneous electrical nerve stimulation (TENS) and other common treatment methods used in the process of wound healing in terms of the expression levels of pro-inflammatory cytokines. In the study, 24 female and 24 male adult Wistar-Albino rats were divided into five groups: (1) the non-wounded group having no incision wounds, (2) the control group having incision wounds, (3) the TENS (2 Hz, 15 min) group, (4) the physiological saline (PS) group and (5) the povidone iodine (PI) group. In the skin sections, interleukin-1 beta (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were assessed with enzyme-linked immunosorbent assay and immunohistochemical methods. In the non-wounded group, the expression of IL-1ß, IL-6, and TNF-α signaling molecules was weaker in the whole tissue; however, in the control group, significant inflammatory response occurred, and strong cytokine expression was observed in the dermis, granulation tissue, hair follicles, and sebaceous glands (P < 0.05). In the TENS group, the decrease in TNF-α, IL-1ß, and IL-6 immunoreaction in the skin was significant compared to the other forms of treatment (P < 0.05). Distinctive decreases of pro-inflammatory cytokines observed in the dermis in the TENS group suggest that TENS shortened the healing process by inhibating the inflammation phase.

A Comparison Study of Growth Factor Expression following Treatment with Transcutaneous Electrical Nerve Stimulation, Saline Solution, Povidone-Iodine, and Lavender Oil in Wounds Healing.

This study compared the effects of transcutaneous electrical nerve stimulation (TENS), saline solution (SS), povidone-iodine (PI), and lavender oil (Lavandula angustifolia) through expression of growth factors in a rat model of wound healing. Six experimental groups were established, each containing 8 rats: a healthy group with no incision wounds, an incision-control group, an incision and TENS group, an incision and SS group, an incision and PI group, and an incision and lavender oil group. Experiments continued for 5 days, after which the skin in the excision area was removed. Tissue concentrations of epidermal growth factor (EGF) and platelet-derived growth factor (PDGF)-A were measured using enzyme-linked immunosorbent assay (ELISA). Tissue expressions of EGF, PDGF-A, and fibroblast growth factor (FGF)-2 were determined using immunohistochemistry. Wound closure progressed more rapidly in the TENS and lavender oil groups than in the control and other study groups. In particular, PDGF-A expressions in the dermis and EGF expression in the epidermis were significantly intense in the TENS group (P < 0.05). In addition, ELISA levels of growth factors such as PDGF-A and EGF were significantly higher in TENS group compared to the control group (P < 0.05). These immunohistochemical and ELISA results suggest that TENS may improve wound healing through increasing growth factors in the dermis and epidermis more than other topical applications.

Combined treatment with progesterone and magnesium sulfate positively affects traumatic brain injury in immature rats.

AIM: It is well known that head trauma results in damage in hippocampal and cortical areas of the brain and impairs cognitive functions. The aim of this study is to explore the neuroprotective effect of combination therapy with magnesium sulphate (MgSO4) and progesterone in the 7-days-old rat pups subjected to contusion injury. MATERIAL AND METHODS: Progesterone (8 mg/kg) and MgSO4 (150 mg/kg) were injected intraperitoneally immediately after induction of traumatic brain injury. Half of groups were evaluated 24 hours later, the remaining animals 3 weeks after trauma or sham surgery. Anxiety levels were assessed with open field activity and elevated plus maze; learning and memory performance were evaluated with Morris Water maze in postnatal 27 days. RESULTS: Combined therapy with progesterone and magnesium sulfate significantly attenuated trauma-induced neuronal death, increased brain VEGF levels and improved spatial memory deficits that appear later in life. Brain VEGF levels were higher in rats that received combined therapy compared to rats that received either medication alone. Moreover, rats that received combined therapy had reduced hipocampus and prefrontal cortex apoptosis in the acute period. CONCLUSION: These results demonstrate that combination of drugs with different mechanisms of action may be preferred in the treatment of head trauma.

The effect of intracerebroventricular injection of beta amyloid peptide (1-42) on caspase-3 activity, lipid peroxidation, nitric oxide and NOS expression in young adult and aged rat brain.

AIM: Intracerebroventricular (icv) administration of beta amyloid peptide (Aß) in rats can be used to model certain aspects of Alzheimer disease (AD).The purpose of this study was to examine the effects of intracerebroventricular Aß (1-42) peptide injection on caspase-3 activity and expression of nNOS and iNOS, malondialdehyde (MDA), glutathione (GSH) and NOx in the hippocampus, temporal cortex and parietal cortex. MATERIAL AND METHODS: Groups were defined as 1) young adult control, 2) Aß (1-42) injected young adult, 3) aged control and 4) Aß (1-42) injected aged group. Stereotaxic surgery was performed. Aß (1-42) peptide (5µg/1µl, in each icv) was administered bilateral intracerebroventricularly as a single injection. RESULTS: Caspase-3 activity significantly increased in Aß (1-42) injected aged rats when compared with young adult rats. Aß (1-42) significantly increased lipid peroxidation in both young adult and aged rats. There was an increase in nNOS expression in the temporal cortex of Aß (1-42) injected aged rats. CONCLUSION: The most significant increase was seen in hippocampus in caspase-3 levels of the Aged- Aß 1-42 group. nNOS expression in the hippocampus of aged rats was increased compared to young adult rats. However, nNOX expression in the hippocampus of Aß (1-42) injected aged rats decreased significantly.

Maternal aerobic exercise during pregnancy can increase spatial learning by affecting leptin expression on offspring's early and late period in life depending on gender.

Maternal exercise during pregnancy has been suggested to exert beneficial effects on brain functions of the offspring. Leptin is an adipocytokine which is secreted from adipose tissues and has positive effects on learning, memory, and synaptic plasticity. In this study, pregnant rats were moderately exercised and we observed the effects of this aerobic exercise on their prepubertal and adult offsprings' spatial learning, hippocampal neurogenesis, and expression of leptin. All the pups whose mothers exercised during pregnancy learned the platform earlier and spent longer time in the target quadrant. Their thigmotaxis times were shorter than those measured in the control group. It is shown that hippocampal CA1, CA3 neuron numbers increased in both prepubertal and adult pups, in addition that GD neuron numbers increased in adult pups. Leptin receptor expression significantly increased in the prepubertal male, adult male, and adult female pups. In our study, maternal running during pregnancy resulted in significant increase in the expression of leptin receptor but not in prepubertal female pups, enhanced hippocampal cell survival, and improved learning memory capability in prepubertal and adult rat pups, as compared to the control group. In conclusion, maternal exercise during pregnancy may regulate spatial plasticity in the hippocampus of the offspring by increasing the expression of leptin.

Anxiety caused by traumatic brain injury correlates to decreased prefrontal cortex VEGF immunoreactivity and neuron density in immature rats.

AIM: Traumatic brain injury (TBI) may cause neuropsychiatric disorders such as anxiety disorder which has negative effects on cognitive functions and behavior. The aim of this study is to investigate the effects of TBI on anxiety and vascular endothelial growth factor (VEGF) immunoreactivity on the prefrontal cortex of immature rats, which is one of the anxiety-related regions of the brain in 7-day-old immature rats subjected to contusion injury. MATERIAL and METHODS: Rats were divided into three groups: Control (n=7), Sham (n=7) and TBI (n=7). Anxiety levels were assessed with open field activity and elevated plus maze in postnatal 27 days. Prefrontal cortex damage related to TBI was examined by cresyl violet staining and VEGF immunostaining. Prefrontal cortex neuronal density was calculated. Serum corticosterone levels were determined. RESULTS: The anxiety level in the TBI group was significantly greater than the control and sham groups. The prefrontal cortex VEGF immunostaining score and neuron density were decreased in the TBI group compared to control and sham group. Serum corticosterone levels were significantly increased in the TBI group. CONCLUSION: These results indicate that TBI decreases VEGF immunoreactivity in prefrontal cortex neurons and increases the anxiety levels of immature rats.

Maternal treadmill exercise during pregnancy decreases anxiety and increases prefrontal cortex VEGF and BDNF levels of rat pups in early and late periods of life.

In a previous study we demonstrated that, regular aerobic exercise during pregnancy decreased maternal deprivation induced anxiety. The purpose of this study is to investigate whether the positive effects of maternal exercise on the male and female offspring's early and late period of life. Half of the test subjects in each group were evaluated when they were 26 days old, and the other half were evaluated when they were 4 months old. The anxiety levels of maternally exercised groups were less than the control groups in both sexes and in both prepubertal and adult periods. The locomotor activity more increased in females. The prefrontal VEGF and BDNF levels were greater for both age groups and sexes in the maternally exercised group compared to control group. Moreover, there was a strong positive correlations between prefrontal cortex BDNF levels and results of open field tests; and VEGF levels and results of elevated plus maze tests. There was no difference in serum corticosterone levels between groups. These results indicate that maternal exercise during pregnancy may protect the pups from anxiety in early and late periods of life, and affects the prefrontal cortex positively.

Acute footshock-stress increases spatial learning-memory and correlates to increased hippocampal BDNF and VEGF and cell numbers in adolescent male and female rats.

It is well known that the acute-stress enhances cognitive functions in adults, but is not known in adolescents. The purpose of this study is to investigate the effects of low and high intensities of acute-stress on hippocampus and spatial memory in the adolescent male and female rats. Thirty-eight days aged rats were subjected to 0.2 and 1.6 mA intensity of footshock-stress for 20 min. Spatial memory performance was assessed in the Morris water maze. Learning had been positively affected in stress groups. Neuron density in the CA1 hippocampal region and the gyrus dentatus as well as VEGF and BDNF levels of hippocampus increased in all stress groups. In females, learning process and BDNF levels increased in low-intensity-stress group than high-intensity-stress group. There was no difference in hippocampal apoptosis among groups. We conclude that adolescent hippocampus is affected positively from acute-stress; however, while there is no difference in male response with respect to intensity of stress, females are affected more positively from low-intensity of stress.

Relationship between circulating IGF-1 levels and traumatic brain injury-induced hippocampal damage and cognitive dysfunction in immature rats.

It is well known that traumatic brain injury (TBI) induces the cognitive dysfunction resulting from hippocampal damage. In the present study, we aimed to assess whether the circulating IGF-I levels are associated with cognition and hippocampal damage in 7-day-old rat pups subjected to contusion injury. Hippocampal damage was examined by cresyl violet staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Spatial memory performance was assessed in the Morris water maze. Serum IGF-1 levels decreased in both early and late period of TBI. Decreased levels of serum IGF-1 were correlated with hippocampal neuron loss and spatial memory deficits. Circulating IGF-1 levels may be predictive of cognitive dysfunction resulted from hippocampal damage following traumatic injury in developing brain. Therapy strategies that increase circulating IGF-1 may be highly promising for preventing the unfavorable outcomes of traumatic damage in young children.

Maternal exercise decreases maternal deprivation induced anxiety of pups and correlates to increased prefrontal cortex BDNF and VEGF.

Maternal deprivation (MD) may cause neuropsychiatric disorders such as anxiety disorder by negatively affecting the cognitive functions and behavior in pups. The aim of this study is to investigate whether maternal exercise during pregnancy has beneficial effects on anxiety that increases with MD, and on the levels of VEGF and BDNF which have anxiolytic effects on the prefrontal cortex, the anxiety-related region of the brain. The anxiety level in the deprivation group was greater than the control group and found more in male than female pups. The prefrontal cortex VEGF and BDNF levels were decreased in the deprivation group compared to control group while serum corticosterone levels were increased in the deprivation group. Anxiety and serum corticosterone levels were decreased in maternally exercised female and male pups, while the prefrontal cortex VEGF and BDNF levels were increased, compared to sedentary mother's pups. These results indicate that maternal exercise may attenuate the negative effect of stresses such as maternal deprivation that can be encountered early in life.

The effects of vitamin C administration, acute food deprivation, and acute food intake on vitamin C levels in different brain areas of guinea pigs.

Vitamin C is crucial for the brain. We aimed to investigate the effects of vitamin C administration following 24 hours of acute food deprivation and 24 hours of acute food intake on changes in vitamin C levels in different brain areas of guinea pigs. Vitamin C was administered as a single intraperitoneal dose (500 mg kg(-1) body weight) both before acute food deprivation and before acute food intake. At the end of our study, we measured the vitamin C levels in cerebral cortex lobes, brain stem structures, hypophysis, hypothalamus, cerebellum, hippocampus, and amygdala. Vitamin C levels in the frontal and parietal lobes were found to be significantly higher in animals pretreated with vitamin C prior to 24 hours of food deprivation (p < 0.05). Temporal lobe vitamin C level was significantly lower in animals that were subjected to 24 hours of acute food intake following 24 hours of food deprivation (p < 0.05). Increased vitamin C levels were observed in the occipital lobe of all animals that received vitamin C administration (p < 0.05). Vitamin C levels in the brain stem structures such as mesencephalon and pons were significantly decreased in animals pretreated with vitamin C before normal feeding (p < 0.05). Vitamin C level in the hypothalamus was significantly increased after 24 hours of food deprivation (p < 0.05). In conclusion, different areas of the brain may differ in terms of vitamin C content during nutritional changes with or without vitamin C pretreatment, such as 24 hours of food deprivation or 24 hours of food intake following 24 hours of food deprivation. These differences may be attributed to several functions of vitamin C which may occur under these circumstances.

The effect of intrahippocampal beta amyloid (1-42) peptide injection on oxidant and antioxidant status in rat brain.

In some animal models, cognitive impairment and neurodegenerative disorders that mimic Alzheimer's disease (AD) can be reproduced by intracerebral or intracerebroventricular administration of peptide (Abeta) beta amyloid. Evidence suggests that oxidative stresses are involved in the mechanism of Abeta-induced neurotoxicity and AD pathogenesis. Exposure to Abeta increases lipid peroxidation, protein oxidation, and the formation of hydrogen peroxide in cultured cells. Nitric oxide (NO) has significant physiological roles in the central nervous system and also it can be implicated in neurodegenerative diseases because of its free radical properties. The purpose of this study is to search the effects of intrahippocampal Abeta (1-42) injection on malondialdehyde (MDA), glutathione (GSH), and nitrite plus nitrate (NOx) levels in temporal cortex and basal forebrain in rats. In this study, male adult Wistar albino rats were divided into two groups. Abeta (1-42) peptide (10 mug/2 muL) was administered bilaterally as a single injection into the hippocampal fissure by a Hamilton microsyringe. Distilled water was administered to the control group by using the same procedure. Ten days after the Abeta (1-42) injection, the rats were decapitated and brains were rapidly removed. MDA, GSH, and NOx levels were analyzed spectrophotometrically in temporal cortex and basal forebrain. MDA levels and NOx were increased 10 days after the injection of Abeta (1-42) in temporal cortex and basal forebrain, but no statistical significance was found compared to control group. However, GSH levels were significantly higher in temporal cortex and basal forebrain in the Abeta (1-42)-injected group than the control group (P < 0.05). In conclusion, increased levels of GSH in temporal cortex and basal forebrain after the intrahippocampal Abeta (1-42) injection show that a protective mechanism might develop due to oxidative stress.