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C31H48O5, monoclinic, P21 (no. 4), a = 11.0421(3) Å, b = 6.49710(16) Å, c = 20.4687(4) Å, β = 97.922(2)°, V = 1454.45(6) Å3, Z = 2, Rgt(F) = 0.0382, wRref(F2) = 0.1024, T = 293(2) K.

C7H6BrN5, triclinic, P1̄ (no. 2), a = 8.3319(4) Å, b = 10.0666(5) Å, c = 11.4042(6) Å, α = 107.213(5)°, β = 99.394(4)°, γ = 95.540(4)°, V = 890.71(8) Å3, Z = 4, Rgt(F) = 0.0452, wRref(F2) = 0.0972, T = 293(2) K.

C31H48O5, monoclinic, P21 (no. 4), a = 11.0421(3) Å, b = 6.49710(16) Å, c = 20.4687(4) Å, β = 97.922(2)°, V = 1454.45(6) Å3, Z = 2, Rgt(F) = 0.0382, wRref(F2) = 0.1024, T = 293(2) K. [ABSTRACT FROM AUTHOR]

Woad root has been used for the prevention of influenza for hundreds of years in many Asian countries. In this study, the antiviral modes of clemastanin B (CB), epigoitrin, phenylpropanoid portion (PEP), and the mixture of phenylpropanoids, alkaloids, and organic acid portions (PEP + ALK + OA) from wood root extract against influenza virus A FM1 were investigated. The results revealed that CB, epigoitrin, PEP, and PEP + ALK + OA exert their anti-influenza activity via inhibiting the virus multiplication, prophylaxis, and blocking the virus attachment. The primary mode of action of PEP and PEP + ALK + OA is the inhibition of virus replication. The inhibitory effect on virus attachment and multiplication is the main modes for epigoitrin. All the compounds or chemical portions from woad root extract tested in this study do not have direct virucidal activity. Our results provided the comprehensive analysis of the antiviral mechanism of wood root extract. [ABSTRACT FROM AUTHOR]

C7H6BrN5, triclinic, P1̄ (no. 2), a = 8.3319(4) Å, b = 10.0666(5) Å, c = 11.4042(6) Å, α = 107.213(5)°, β = 99.394(4)°, γ = 95.540(4)°, V = 890.71(8) Å3, Z = 4, Rgt(F) = 0.0452, wRref(F2) = 0.0972, T = 293(2) K. [ABSTRACT FROM AUTHOR]

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Background: Weight gain and type 2 diabetes mellitus (DM) are often linked to antipsychotics treatment. The aim of the study is to investigate serum free fatty acids (FFA) levels in schizophrenic patients who received long-term antipsychotics treatment, and to explore the associations between serum FFA and fasting blood glucose, and insulin resistance. Methods: 308 inpatients with schizophrenia who met with the criteria of DSM-IV were recruited into this study, and were divided into four groups: control subjects, single obesity, impaired glucose tolerance (IGT) and type 2 DM according to different body mass index, fasting blood glucose level and 2-hour postprandial blood glucose. Serum FFA was measured with colorimetry. Serum insulin and leptin were measured with radioimmunoassay respectively. Results: There was a significant elevation in serum FFA levels in schizophrenic patients who received long-term antipsychotics treatment, especially in single obesity, IGT, and DM groups. The elevated serum FFA was remarkably positive correlated with fasting blood glucose and insulin resistance. Conclusions: The study suggested the elevated serum FFA in schizophrenic patients with long-term antipsychotics treatment affected the blood glucose metabolism, may have played an important role in insulin resistance and type 2 DM, and was also an important trait of metabolic syndromes. [Copyright &y& Elsevier]