[Twin girls infected with SARS-CoV-2].

This article reports the diagnosis and treatment of twin girls who were diagnosed with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in Hunan Province, China. The twin girls, aged 1 year and 2 months, were admitted on January 29, 2020 due to fever for one day and cough and sneezing for two days respectively. Both recovered after symptomatic treatment. The two girls had mild symptoms and rapid recovery, suggesting that children with SARS-CoV-2 infection may be mild and have a good prognosis. There were differences in the clinical symptoms and imaging findings between the twin girls, suggesting that SARS-CoV-2 infection has diverse clinical features in children.

Effects of amitraz on cytochrome P450-dependent monooxygenases and estrogenic activity in MCF-7 human breast cancer cells and immature female rats.

This study investigated the ability of amitraz, a formamidine insecticide, to induce cytochrome P450-dependent monooxygenases and to disrupt estrogenic activity in human breast cancer MCF-7 cells and immature female rats. In MCF-7 cells, treatment with 10 microM amitraz for 24 h increased 7-ethoxyresorufin O-deethylase activity in cell homogenate. Treatment of MCF-7 cells with 1 and 10 microM amitraz for 3 h replaced previously bound [(3)H]17beta-estradiol (E(2)) from estrogen receptors. Treatment with 0.1 and 1 microM amitraz for 2 days inhibited [(3)H]thymidine incorporation into the DNA of MCF-7 cells while the inhibition was blocked in cells co-treated with 1 nM E(2) and amitraz. In immature female rats, treatment with 50 mg/kg amitraz intraperitoneally for 3 days increased cytochrome P450 content, 7-ethoxyresorufin, methoxyresorufin and pentoxyresorufin O-dealkylases, and benzo[a]pyrene hydroxylase activities in liver microsomes. The results of immunoblot analysis revealed that amitraz induced liver microsomal CYP1A1/2, 2B1/2B2, and 3A proteins. Treatment with 10 and 25 mg/kg amitraz for 3 days dose-dependently decreased uterine weight and peroxidase activity in immature female rats while the decreases were blocked in rats co-treated with 10 microg/kg E(2) and 10 or 25 mg/kg amitraz. These in vitro and in vivo findings suggest that amitraz induces multiple forms of P450 and exerts weak antiestrogenic activity.

Induction of cytochromes P-450 1A1 and 1B1 by motorcycle exhaust particulate in human breast cancer MCF-7 cells.

The effects of motorcycle exhaust particulate (MEP) on cytochrome P-450-dependent monooxygenases were determined using MCF-7 human breast cancer cells treated with organic extracts of MEP. Treatment with MEP extract produced concentration- and time-dependent increases of monooxygenase activity in S9 fractions. Treatment with 50 microg/ml MEP extract for 24 h increased benzo[a]pyrene hydroxylase and 7-ethoxycoumarin, 7-ethoxyresorufin, and methoxyresorufin O-dealkylases activities in S9. Treatments with 1 and 10 microg/ml MEP extract for 24 h markedly enhanced catabolism of 17beta-estradiol in MCF-7 cells. Cotreatment of the cells with 2 microM alpha-naphthoflavone, a cytochrome P-450 inhibitor and arylhydrocarbon receptor antagonist, blocked the increase of benzo[a]pyrene hydroxylase activity induced by treatment with MEP extract alone. Immunoblot analyses of S9 proteins using a mouse monoclonal antibody 1-12-3 against rat cytochrome P-450 1A1 and a rabbit polyclonal antibody against human cytochrome P-450 1B1 revealed that MEP extract induced proteins immunorelated to cytochromes P-450 1A1 and 1B1. RNA blot analysis of total RNA using human cytochrome P-450 (CYP)1A1 3'-end and human CYP1B1 RT-PCR product cDNA probes showed that MEP extract increased the levels of cytochromes P-450 1A1 and 1B1 mRNA hybridizable to the respective cDNA probes. Treatment with 10 micro M benzo[a]pyrene, a component of MEP extract, for 24 h induced catalytic activity, protein, and mRNA of cytochromes P-450 1A1 and 1B1 in MCF-7 cells. Treatment with MEP extract increased cytochromes P-450 1A1 and 1B1 proteins and mRNA levels in NCI-H322 human lung carcinoma and CL5 human lung adenocarcinoma cells. The extract also increased cytochrome P-450 1A1, but not cytochrome P-450 1B1, protein, and mRNA, in HepG2 human hepatoma cells. The present findings demonstrate that MEP extract has the ability to induce cytochromes P-450 1A1 and 1B1 in the estrogen-responsive MCF-7 cells. Induction of the carcinogen- and estrogen-metabolizing cytochromes P-450 1A1 and 1B1 may be an important factor to consider in assessing the potential health effects associated with human exposure to MEP.

Effect of frying-meat emission particulate on 17beta-estradiol 2- and 4-hydroxylation in human lung adenocarcinoma CL5 cells.

The effect of airborne frying-meat emission particulate (FMEP) on metabolism of 17beta-estradiol (E(2)) to potentially toxic catechol estrogens 2- and 4-hydroxyestradiol (2- and 4-OH-E(2)) was determined using human lung adenocarcinoma CL5 cells treated with organic extracts of beef FMEP. E(2) was incubated with microsomes prepared from untreated CL5 cells or cells treated with 200 microg/ml FMEP extract for 6 h. E(2) metabolites formed were analyzed by high-performance liquid chromatography (HPLC). The results revealed that treatment with FMEP produced three-and twofold increases of 2- and 4-hydroxylation of E(2), respectively. Monooxygenase activity and immunoblot analyses showed that FMEP markedly induced microsomal 7-ethoxyresorufin O-deethylase (EROD) activity and cytochrome P-450 (CYP) IAI and CYPIBI protein levels. Similar increases in E(2) hydroxylation, EROD activity, and CYP protein levels were observed with HepG2 human hepatoma and MCF-7 human breast cancer cells treated with FMEP or 1 microM dibenz[a,h]anthracene. Cotreatment of CL5 cells with FMEP extract and 2 microM alpha-naphthoflavone, an arylhydrocarbon receptor antagonist, blocked the inductive effects of FMEP on E(2) hydroxylation and EROD activity. Additions of 0.01, 0.1, or 1 microM alpha-naphthoflavone, a CYP inhibitor, to microsomes produced concentration-dependent decreases in E(2) 2-hydroxylation and EROD activity of CL5 cells induced by dibenz[a,h]anthracene. The present finding demonstrates that FMEP can increase formation of 2-OH-E(2) and 4-OH-E(2) by human lung cells, and induction of CYP1A1 and CYP1B1 is a potential mechanism underlying increased E(2) metabolism. The toxicological significance of FMEP and estrogen interaction warrants further investigation.

Effects of motorcycle exhaust inhalation exposure on cytochrome P-450 2B1, antioxidant enzymes, and lipid peroxidation in rat liver and lung.

The effects of motorcycle exhaust (ME) on metabolic and antioxidant enzymes and lipid peroxidation were determined using male rats exposed to 1:10 diluted ME by inhalation 2 h daily for 4 wk. For microsomal cytochrome P-450 enzymes, ME resulted in threefold increases of 7-ethoxyresorufin and pentoxyresorufin O-deethylase activities in liver and a sixfold increase of 7-ethoxyresorufin O-deethylase activity and an 80% decrease of pentoxyresorufin O-dealkylase activity in lung. The results of immunoblot analysis of microsomal proteins revealed that ME increased liver and lung cytochrome P-450 1A1 with minimal effects on cytochrome P-450 2E1. ME increased cytochrome P-450 2B1/2 proteins in liver but decreased cytochrome P-450 2B1 in lung. ME did not change microsomal cytochrome P-450 enzyme activity or protein level in kidney. For phase II enzymes, ME resulted in 53% and twofold increases of cytosolic NAD(P)H:quinone oxidoreductase activities in liver and lung, respectively, and no effect on microsomal UDP-glucuronosyltransferase activities. For antioxidant enzymes, ME produced 23% and 35% decreases of superoxide dismutase, 9% and 27% decreases of catalase, and no changes of glutathione peroxidase activities in liver and lung cytosols, respectively. For lipid peroxidation, the results of thiobarbituric acid assay showed that ME resulted in a twofold increase of formation of malondialdehyde by liver microsomes incubated with FeCl(3) -ADP. ME produced a threefold increase of malondialdehyde formation by lung microsomes. The present study demonstrates that ME inhalation exposure differentially modulates cytochrome P-450 2B1 and antioxidant enzymes and increases susceptibility to lipid peroxidation in rat liver and lung.

[Treatment of allergic rhinitis with asthma by different ways of inhaling corticosteroids].

OBJECTIVE: To observe the therapeutical effect on allergic rhinitis with asthma by different ways of inhaling corticosteroids. METHODS: Ninety patients suffering from allergic rhinitis with asthma were classified into three groups in random and treated with budesonide (BUD) by nasal spray, inhaling and nasal spray-inhaling combined administration for 12 weeks, respectively. The concentration of serum total IgE, eosinophil cationic protein (ECP) and IL-5, pulmonary functions were examined before and after treatment. RESULTS: The improvement of symptom scores of rhinitis and asthma in three groups were significant (P < 0.05). The concentration of serum total IgE, ECP and IL-5 in three groups decreased greatly after treatment (P < 0.05). There were significant improvement in FEV1, FEV1/FVC and FEF25%-75% in inhaling group before and after treatment (P < 0.05): FEV1 from (2.04 +/- 0.45) L to (2.47 +/- 0.54) L, FEV1/FVC from (72.73 +/- 5.59)% to (75.42 +/- 5.94)% and FEF25%-75% from 1.69 +/- 0.52 to 2.06 +/- 0.77. There was also significant improvement in nasal spray-inhaling combined groups before and after treatment (P < 0.05): FEV1 from (2.32 +/- 0.56) L to (2.76 +/- 0.58) L, FEV1/FVC from (73.80 +/- 4.17)% to (76.04 +/- 4.49)% and FEF25%-75% from 2.09 +/- 0.45 to 2.34 +/- 0.64. The significant difference of FEV1 among the three treatment groups was observed (P = 0.041). CONCLUSIONS: The symptoms of rhinitis and asthma in three groups by three ways of inhaling BUD were greatly improved, no significant difference in symptom scores and serum parameters was found.

Antiestrogenic effects of motorcycle exhaust particulate in MCF-7 human breast cancer cells and immature female rats.

The emissions from 2- and 4-stroke motorcycles pollute the air of urban areas where motorcycle is a popular means of transportation. This study aimed to determine the endocrine-disrupting activity of motorcycle exhaust particulate (MEP) using MCF-7 human breast cancer cells and immature female Wistar rats treated with organic extracts of MEP. Treatments with 1, 10, and 50 microg/ml MEP extract for 2 and 4 days produced dose-dependent inhibition of thymidine incorporation and cell growth, respectively, in untreated and 1 nM 17beta-estradiol (E2)-treated cells. Treatments of MCF-7 cells with MEP extract replaced [3H]E2 from the estrogen receptor in a time- and concentration-dependent manner. These antiestrogenic and receptor binding properties of MEP extract were blocked by cotreatment of the cells with 2 microM alpha-naphthoflavone, a cytochrome P450 inhibitor and aryl hydrocarbon receptor antagonist. E2 metabolism and HPLC analysis showed that treatment of MCF-7 cells with 50 microg/ml MEP extract for 24 h increased E2 2- and 4-hydroxylation in microsomes. The MEP-mediated increase in E2 2-hydroxylation was inhibited by the addition of 1 microM alpha-naphthoflavone to MCF-7 microsomes. Cotreatment of immature female rats with 10 microg/kg E2 and 10 mg/kg MEP extract intraperitoneally for 3 days decreased the E2-induced uterine weights. MEP extract alone showed no effect on rat uterine weight. The endocrine-disrupting activity of MEP extract was further confirmed in parallel experiments using MCF-7 cells and immature female rats treated with benzo(a)pyrene, an MEP constituent compound. The present findings demonstrate that MEP extract is antiestrogenic in vitro and in vivo and cytochrome P450 induction is an underlying mechanism.