Comparative analysis of anxiety/depression scores in COVID-19 patients with disease severity, sleep patterns, and certain laboratory test results.

Introduction: Coronavirus disease 2019 (COVID-19) is associated with severe emotional changes. This research aims to investigate the prevalence of anxiety and depression in COVID-19 patients and its relationship with disease severity, sleep patterns, lifestyle, and specific laboratory test results. Material and methods: An observational study of 52 Chinese patients with COVID-19 was conducted to assess the relation between anxiety and depression (evaluated with the Hospital Anxiety and Depression Scale) and laboratory findings (lymphocytes, C-reactive proteins, leukocytes, alanine aminotransferase, aspartate aminotransferase). The relationships between the severity of COVID-19 in patients, the Insomnia Severity Index (ISI) score, and the Hospital Anxiety and Depression Scale (HADS) score were also investigated. Results: There were statistically significant associations between disease, smoking, and HADS-A scores (p = 0.011/0.020). The HADS-D score of patients with the disease was higher than in those without a past medical history (p = 0.008). The difference in C-reactive protein (CRP) between different lung infections, the HADS-A and HADS-D scores between different ages and ISI groups, and the correlation between the two scores were statistically significant. Conclusions: Anxiety and depression are associated with poor sleep quality, smoking, and past medical history in patients with COVID-19. Additionally, anxiety and depression were seen to coexist, and there was a positive correlation between them. Further, the inflammatory index CRP was significantly increased in bilateral lung infections.

[Progress in sulfur dioxide biology: from toxicology to physiology].

Based on our studies for more than 20 years, we review the recent advances in sulfur dioxide (SO2) biology. Three sections are involved: (1) The studies on SO2 toxicological effects and its underlying mechanisms; (2) The new investigations on SO2 donor and physiological role of SO2 as a new type-gas transmitter; (3) The observations on pathophysiologic roles of SO2.

[Effects of sulfur dioxide on mRNA expression and activities of hepatic and pulmonary cytochrome P4502B1 and 2E1 in rats].

OBJECTIVE: To study the effects of sulfur dioxide (SO2) on activities and mRNA expression of hepatic and pulmonary cytochrome P4502B1 and 2E1 in rats. METHODS: Male Wistar rats were housed in exposure chambers and treated with 14, 28 and 56 mg/m3 SO2 for 6 h/d for 7 days, while control rats were exposed to filtered air in the same condition. The activities of CYP2E1 of rats were measured by spectrophotometry. Fluorescence spectrophotometry was used to study the activities of CYP2B1. The mRNAs of CYP2B1 and 2E1 were analyzed in livers and lungs by using a reverse transcription-polymerase chain reaction (RT-PCR) assay. RESULTS: In the liver, decreases of CYP2B1 activity and mRNA were observed at higher dose of SO2 (28 and 56 mg/m3). However, the CYP2E1-dependent p-nitrophenol hydroxylases (p-NP) and mRNA were unaltered by SO2 at all detected concentrations. For lungs, CYP2B1 activity was unaltered by SO2 at low concentrations, except for a significant decrease in the rats exposed to SO2 at 56mg/m3, however, SO2 at higher concentrations (28 and 56 mg/m3) significantly decreased CYP2B1 mRNA. Significant inhibition of p-NP was observed in lungs of rats exposed to SO2 at 28 and 56 mg/m3. SO2 at higher concentrations (28 and 56 mg/m3) decreased significantly pulmonary CYP2E1 mRNA relative to control animals. CONCLUSION: It was suggested that SO2 exposure could suppress the activities and mRNA expression of hepatic CYP2B1 and pulmonary CYP2B1 and 2E1 of rats.

[Effects of dust storm fine particles instillation on oxidative damage in hearts, livers, lungs of rats].

OBJECTIVE: In this study, the effects of dust storm PM2.5 on oxidative damage in three organs of rats were investigated. METHODS: After Wistar rats were intratracheally instilled 24h, the activities of SOD, the levels of GSH and LPO in lungs, hearts and livers of rats were measured. RESULTS: (1) Dust storm and normal weather PM2. instillation caused decrease of SOD activities in livers and lungs, but SOD activities in hearts were statistically insignificant. (2) Dust storm and normal weather PM2.5 instillation caused decrease of contents of GSH in lungs, whereas PM2.5, instillation at low concentration caused an increase and at higher PM2.5 instillation caused a significant decrease in livers. And contents of GSH in hearts were statistically insignificant. (3) Dust storm and normal weather PM2.5, instillation caused decrease of levels of LPO in lungs, hearts and livers. (4) Though the effects made by normal weather PM2.5 heavier than dust storm PM2.5 on each examined index, no significant difference was found. However, the dust storm PM2.5 whose airborne concentrations were much higher than that of normal weather PM2.5, so the dust storm PM2.5 should be more harmful. CONCLUSION: Dust storm and normal weather PM2.5 instillation could lead to oxidative damage of different degrees in lungs,hearts and livers of rats. However, the dust storm PM2.5 whose airborne concentrations were much higher should be more harmful.

[Study of toxicity on male reproductive system of mice induced by SO2 inhalation].

OBJECTIVE: In this paper, toxicity of SO2 on male reproductive system of mice was studied. METHODS: 40 mice were divided to 4 groups (10/group): a group for control, the other 3 groups for SO2 inhalation (28, 56, 112mg/m3), 4h/d, 7d. RESULTS: The activities of GST and G-6-PD, as well as the content of GSH decreased significantly with SO2 increased. The content of MDA increased evidently with SO2 increased. CONCLUSION: SO2 can influence GSH oxidation-deoxidation system and cause DNA damage in male reproductive system of mice.

[Effects of sodium metabisulfite on potassium currents in acutely isolated rat hippocampal CA1 neurons].

AIM: To investigate the effects of sodium metabisulfite (SMB), sulfur dioxide (SO2) and its derivatives in vivo, sodium bisulfite and sulfite on K+ channels of the central neurons and its mechanisms. METHODS: By using whole-cell patch-clamp technique, the effects of SMB on transient outward K+ (I(A)) and delayed rectifier K+ currents(IK) were observed. RESULTS: (1) SMB can increase the amplitudes of I(A) and I(K) in a dose-dependent and voltage-dependent manner. Their half-increase doses were 15.8 micromol/L and 11.5 micromol/L respectively. (2) SMB (10 micromol/L) significantly shifted the activation curves of I(A) and I(K) to more positive potentials. Before and after application of 10 micromol/L SMB, the half-activation voltages of I(A) and I(K) were (- 12.6 +/- 1.6) mV and (- 7.0 +/- 1.3) mV, (10.8 +/- 0.9) mV and (21.6 +/- 0.7) mV (P < 0.01, n = 8), respectively, but the slope factors were not changed. (3) The inactivation curve of I(A) was shifted to positive potentials, the half-inactivation voltage of I(A) were (- 97.0 +/- 1.1) mV and (- 84.4 +/- 3.3) mV (P < 0.01, n = 8) before and after application of SMB (10 micromol/L), without changing the slope factors. (4) SOD, CAT and GPx could partly inhibit the incremental effect of SMB on I(A) and I(K). CONCLUSION: SMB, SO2 and its derivatives in vivo, sodium bisulfite and sulfite have the damage effects on the central nervous system, and they can cause extracellular K+ increase and induce the disturbance of the central neuronal functions. Its mechanism may involve oxidation damage in the rat hippocampal CA1 neurons, caused by sulfur- and oxygen-centered free radicals formed in the process of sulfite or bisulfite oxidation.

[Sulfur dioxide-induced liver pathology].

OBJECTIVE: To investigate effects of short-term sulfur dioxide inhalation to the liver. METHODS: Haematoxylin and eosin staining (HE) and transmission electron microscopy (TEM) were used to study the pathologic changes in mice liver after sulfur dioxide (SO(2)) inhalation. RESULTS: Exposure to 56 mg/m(3), 112 mg/m(3) 168 mg/m(3) SO(2) caused increasingly severe liver injuries, as detected by HE staining and TEM. The morphologic changes included spotty necrosis with lymphocyte, monocyte, and neutrophil infiltration, fatty degeneration of hepatocytes with dilatation of rough endoplasmic reticulum and dissociation of ribosomes, as well as degeneration of mitochondria and karyorrhexis. CONCLUSION: SO(2) inhalation can cause marked liver injury in experimental settings.

[Effects of AlCl3 on transient outward K+ current and delayed rectifier K(+) current in acutely isolated rat hippocampal CA1 neurons].

The effects of aluminum chloride (AlCl3) on the transient outward potassium and delayed rectifier K(+) current in hippocampal CA1 neurons of rats were studied by the whole-cell patch clamp technique. It was found that AlCl3 reduced the transient outward potassium current and delayed rectifier K(+) current in a dose-dependent manner. 1000 micromol/L AlCl3 resulted in change in voltage and slope of the half-activation and the half-inactivation of I(A) and I(K). These results imply that AlCl3 may damage potassium channel of the hippocampal CA1 neurons from rats and this may be related to the mechanism of the damage to the central nervous system by aluminum.

[Inhibition of sodium currents in acutely isolated hippocampal CA1 neurons of rats by magnesium sulfate].

The effects of magnesium sulfate (MgSO4) on sodium currents (Na(+) currents) were studied in freshly dissociated hippocampal CA(1) neurons of rat using the whole-cell patch-clamp technique. The results indicated that MgSO4 caused a concentration-dependent and voltage-dependent decrease in Na(+) currents. The half-inhibitory concentration (IC(50)) was 4.05 mmol/L. This action was frequency-independent. The results also showed that 4 mmol/L MgSO4 shifted the steady state activation curve of Na(+) currents towards positive potential (control V(h)=-55.8+/-6.8 mV, MgSO4 V(h)=-34.2+/-6.2 mV, n=8, P<0.01) without changing the slope factor. However, the steady state inactivation curve was not affected. These results suggest that blockade of Na(+) currents by MgSO4 might be an interpretation for its neuroprotection against damages induced by ischemia and oxygen deprivation.

[Effect of SO2 derivatives on sodium currents in acutely isolated rat hippocampal CA1 neurons].

The effect of SO2 derivatives on Na(+) currents was studied in freshly dissociated hippocampal CA1 neurons of rat using the whole-cell patch-clamp technique. The results indicated that SO2 derivatives caused a dose-dependent and voltage-dependent increase in the voltage-activated Na+ currents. The amplitudes of Na(+) currents were increased by 50.59 19.08% and 82.06 18.51% (n=15)by SO2 derivatives at 10 and 100 micromol/L, respectively. The action was frequency-independent. The results also showed that SO2 derivatives did not affect the activation process, but changed the inactivation process significantly. Before and after application of 10 micromol/L SO2 derivatives, the half-inactivation voltage was -69.71+/-4.67 and -53.27+/-4.95 mV (n=10, P<0.01), respectively, but the slope factor was not changed. These results imply that SO2 derivatives have neurotoxic effects and that SO2 pollution is probably related to some diseases of central neuronal system.

[Blockade of magnesium sulfate on transient outward K+ current and delayed rectifier K+ current in acutely isolated rat hippocampal neurons].

AIM: To study the effect of magnesium sulfate on transient outward K+ current (IA) and delayed rectifier K+ current (IK) in freshly dissociated hippocampal neurons of rats. METHODS: The whole-cell patch clamp techniques were used. RESULTS: Magnesium sulfate reversibly reduced the amplitudes of IA and IK in a concentration-dependent and voltage-dependent, but not frequency-dependent manner. Half-blocking concentration (IC50) on IA and IK were 6.30 mmol.L-1 and 7.60 mmol.L-1, respectively. Magnesium sulfate (6 mmol.L-1) affected the activation process of IA and IK. Before and after application of the drug, the half-activation voltages of IA were (7 +/- 6) mV and (-7 +/- 11) mV (n = 10, P < 0.01), and the half-activation voltages of IK were (20 +/- 6) mV and (28 +/- 4) mV (n = 10, P < 0.01), but the slope factors were not changed. In addition, magnesium sulfate (6 mmol.L-1) also affected the inactivation process of IA. Before and after application of the drug, the half-inactivation voltages of IA were (-65 +/- 5) mV and (-89 +/- 6) mV (n = 10, P < 0.01). CONCLUSION: Magnesium sulfate inhibited IA and IK in freshly dissociated hippocampal neurons of rats, which might contribute to protect the central neuronal system (CNS) against damages induced by ischemia and oxygen deprivation.