Hypothermia has been observed during hypergravity load in mice and rats. This response is beneficial for maintaining blood glucose level, although food intake decreases. However, saving glucose is not enough to maintain blood glucose level during hypergravity load. In this study, we examined the contribution of humoral factors related to glycolysis in maintaining blood glucose level in a 2 G environment. Increased plasma corticosterone levels were observed in mice with intact peripheral vestibular organs, but not in mice with vestibular lesions. Plasma glucagon levels did not change, and decrease in plasma adrenaline levels was observed in mice with intact peripheral vestibular organs. Accordingly, it is possible that increase in plasma corticosterone level and hypothermia contribute to prevent hypoglycemia in a 2 G environment.
ObjectivesNo clinically useful prognostic factors have been identified for idiopathic sudden sensorineural hearing loss (ISSNHL). The current study therefore sought to identify useful prognostic factors for idiopathic sudden sensorineural hearing loss from blood biomarkers while attempting to classify the pathogenic mechanism and formulate treatment strategies based on these results.Study DesignProspective cohort study.SettingTertiary referral center.MethodsA total of 47 patients with acute phase ISSNHL were treated with steroid at an initial dose of 1 mg/kg/day and hyperbaric oxygen therapy and followed up for 6 months. Serum fibrinogen levels, peripheral blood mononu- clear cells (PBMCs), and interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α production levels from PBMCs were measured, after which patient’s pre- and post- treatment hearing was compared.ResultsIn the overall cohort, the mean improvement level, mean recovery rate, and mean fibrinogen level was 20.3 dB, 46.2%, 292.0 mg/mL, respectively. The mean levels of IL-1β, IL-6, and TNF-α produced by peripheral blood mononu- clear cells cultured under lipopolysaccharide stimulation were 318.4, 498.1, and 857.6 pg/mL, respectively. High fibrinogen levels were associated with poor hearing progno- sis. Lipopolysaccharide-stimulated cytokine production by PBMCs did not correlate with hearing changes; however, the prognosis was significantly better in patients with low fibrinogen levels and high IL-1β levels produced by PBMCs than in other patients.ConclusionsOur results suggest that patients with simple inflammatory-type ISSNHL responded well to standard therapy. Therefore, serum fibrinogen levels and PBMCs cytokine production may help determine the management of ISSNHL based on its pathogenic mechanism.
Autonomic nerves, including the sympathetic and parasympathetic nerves, control the immune system along with their physiological functions. On the peripheral side, the interaction between the splenic sympathetic nerves and immune cells is important for the anti-inflammatory effects. However, the central mechanism underlying these anti-inflammatory effects remains unclear. C1 neurons respond to stressors and subsequently determine the outflow of the autonomic nervous system. We have previously shown that C1 neurons protect against acute kidney injury, and found a signaling connection between peripheral vestibular organs and C1 neurons. Thus, we hypothesized that hypergravity load or galvanic vestibular stimulation (GVS) might protect against acute lung injury. We showed that C1 neurons are histologically and functionally activated by stimulating the peripheral vestibular organs. Protection against acute lung injury that was induced by a 2 G load was disappeared due to vestibular lesions or the deletion of C1 neurons. This GVS-induced protective effect was also eliminated by the deletion of the C1 neurons. Furthermore, GVS increased splenic sympathetic nerve activity in conscious mice, and splenic sympathetic denervation abolished the GVS-induced protection against acute lung injury. Therefore, the activated pathway between C1 neurons and splenic sympathetic nerves is indispensable for the GVS-induced protection against acute lung injury.
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