Neurological manifestation in COVID-19 disease with neuroimaging studies.

OBJECTIVE: Magnetic resonance imaging (MRI) of the brain or spine examines the findings as well as the time interval between the onset of symptoms and other adverse effects in coronavirus disease that first appeared in 2019 (COVID-19) patients. The goal of this study is to look at studies that use neuroimaging to look at neurological and neuroradiological symptoms in COVID-19 patients. METHODS: We try to put together all of the research on how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes neurological symptoms and cognitive-behavioral changes and give a full picture. RESULTS: We have categorized neuroimaging findings into subtitles such as: headache and dizziness; cerebrovascular complications after stroke; Intracerebral Hemorrhage (ICH); Cerebral Microbleeds (CMBs); encephalopathy; meningitis; encephalitis and myelitis; altered mental status (AMS) and delirium; seizure; neuropsychiatric symptoms; Guillain-Barre Syndrome (GBS) and its variants; smell and taste disorders; peripheral neuropathy; Mild Cognitive Impairment (MCI); and myopathy and myositis. CONCLUSION: In this review study, we talked about some MRI findings that show how COVID-19 affects the nervous system based on what we found.

Inhibition of Airway Contraction and Inflammation by Pomalidomide in a Male Wistar Rat Model of Ovalbumin-induced Asthma.

Asthma is a chronic inflammatory disease of the airways of the lungs. Pomalidomide (POM) a therapy for multiple myeloma has been stated to have an anti-inflammatory effect. The main goal of the present study was to assess its possible effect on airway contraction and inflammation in a rat model of ovalbumin-induced asthma. Different groups of rats received saline or pomalidomide (0.4, 0.8 mg/kg) or dexamethasone (0.6 mg/kg). The asthma was induced by ovalbumin (OVA). Trachea contraction was assayed by organ bath system. Airway histology was assessed using hematoxylin and eosin method. Serum Tumor necrosis factor alpha (TNF-α) level was analyzed by Enzyme-Linked Immunosorbent Assay and Platelet-derived growth factor (PDGFα) Gene expressions were evaluated by Real-time PCR. Pomalidomide prevented ovalbumin-induced airway contraction and histopathological damage. In addition serum, TNF-α level was significantly (p<0.05) decreased in POM treated animals compared to control (asthmatic animals that received POM vehicle). Results indicate that POM prevented the PDGF expression induced by ovalbumin. In conclusion, we found that pomalidomide ameliorated the symptoms, histopathological changes and inflammatory markers induced by ovalbumin in asthmatic rats and these effects might be related to its anti-inflammatory properties.

Gap junction blockers: a potential approach to attenuate morphine withdrawal symptoms.

BACKGROUND: The exact mechanisms of morphine-induced dependence and withdrawal symptoms remain unclear. In order to identify an agent that can prevent withdrawal syndrome, many studies have been performed. This study was aimed to evaluate the effect of gap junction blockers; carbenoxolone (CBX) or mefloquine (MFQ); on morphine withdrawal symptoms in male rat. Adult male Wistar rats (225 - 275 g) were selected randomly and divided into 10 groups. All groups underwent stereotaxic surgery and in order to induce dependency, morphine was administered subcutaneously) Sc) at an interval of 12 hours for nine continuous days. On the ninth day of the experiment, animals received vehicle or CBX (100, 400, 600 µg/10 µl/rat, icv) or MFQ (50, 100 and 200 µg/10 µl/rat, icv) after the last saline or morphine (Sc) injection. Morphine withdrawal symptoms were precipitated by naloxone hydrochloride 10 min after the treatments. The withdrawal signs including: jumping, rearing, genital grooming, abdomen writhing, wet dog shake and stool weight, were recorded for 60 minutes. RESULTS: Results showed that CBX and MFQ decreased all withdrawal signs; and the analysis indicated that they could attenuate the total withdrawal scores significantly. CONCLUSION: Taking together it is concluded that gap junction blockers prevented naloxone-precipitated withdrawal symptoms.

Repeated central administration of selegiline attenuated morphine physical dependence in rat.

BACKGROUND: Long-term exposure to opiates induces physical dependence; however, the neurobiological mechanisms of this phenomenon are not completely clear. The purpose of this study was to evaluate the effects of systemic and intracerebroventricular (icv) administration of selegiline (a selective inhibitor of monoamine oxidase B) on the morphine withdrawal syndrome in rats. METHODS: To this aim, adult male Sprague Dawley rats were selected randomly, and then growing doses of morphine were administered subcutaneously at an interval of 12 h for nine days with the intention of inducing dependency. Nine days after, only the morning dose of morphine was administered, followed by systemic or central injection of saline or selegiline. Later, naloxone was injected after 30 min and withdrawal signs recorded for a period of 60 min. RESULTS: Results showed failure of systemic administration of selegiline in changing the withdrawal symptoms; nevertheless, icv injection attenuated the withdrawal signs significantly. CONCLUSION: In conclusion we found that central administration of selegiline attenuated morphine withdrawal symptoms.