Partial Synthesis of Crassicauline A from Yunaconitine

Both Aconitum hemsleyanum and Aconitum geniculatun have abundant contents of yunaconitine(1).Yunaconitine(1)has similar skeleton to crassicauline A(3);the only difference between them is that 1 contains aα-hydroxyl group at C-3.Our team attempts to convert 1 into 3 because 3 owns pharmacological activity.There are two steps to achieve the transformation above:firstly,use dehydration reaction to transform yunaconitine(1)into dehydroyunaconitine(2);secondly,use hydrogen reduction to acquire crassicauline A(3).Compared with other methods,this one below is more suitable for production application and more concise;moreover,the cost is lower with higher yield.

Serum 25-hydroxyvitamin D deficiency predicts poor outcomes among acute ischemic stroke patients receiving intravenous thrombolysis

To the Editor:Ischemic stroke remains a major cause of death and disability worldwide and contributes to the rising costs of health care.Thrombolytic therapy with tissue plasminogen activator (tPA,alteplase)is beneficial for the treatment of acute ischemic stroke.However,only 40%to 50%of stroke patients show a significant improvement after treatment.In addition,the use of alteplase is restricted because symptomatic intracranial hemorrhase (slCH)occurs in 1.7%to 6.4%of treated patients.[1] 25-hydroxyvitamin D (25(OH)D),which is the major circulating metabolite of vitamin D,has been confirmed to be closely related to cerebrovascular disease (CVD).A series of studies indicated that vitamin D deficiency was associated with an increased risk of ischemic stroke,high stroke severity and poor functional outcomes.

Antiplatelet and myocardial protective effect of Shexiang Tongxin Dropping Pill in patients undergoing percutaneous coronary intervention:A randomized controlled trial

Background:High on-clopidogrel platelet reactivity could be partially explained by loss-of-function alleles of CYP2 C19,the enzyme that converts clopidogrel into its active form.Shexiang Tongxin Dropping Pill(STDP)is a traditional Chinese medicine to treat angina pectoris.STDP has been shown to improve blood flow in patients with slow coronary flow and attenuate atherosclerosis in apolipoprotein E-deficient mice.However,whether STDP can affect platelet function remains unknown.Objective:The purpose of this study is to examine the potential effects of STDP on platelet function in patients undergoing percutaneous coronary intervention(PCI)for unstable angina.The interaction between the effects of STDP with polymorphisms of CYP2 C19 was also investigated.Design,participants and intervention:This was a single-center,randomized controlled trial in patients undergoing elective PCI for unstable angina.Eligible subjects were randomized to receive STDP(210 mg per day)plus dual antiplatelet therapy(DAPT)with clopidogrel and aspirin or DAPT alone.Main outcome measures:The primary outcome was platelet function,reflected by adenosine diphosphate(ADP)-induced platelet aggregation and platelet microparticles(PMPs).The secondary outcomes were major adverse cardiovascular events(MACEs)including recurrent ischemia or myocardial infarction,repeat PCI and cardiac death;blood biomarkers for myocardial injury including creatine kinase-MB isoenzyme(CK-MB)and high-sensitive troponin I(hs Tn I);and biomarkers for inflammation including intercellular cell adhesion molecule-1(ICAM-1),vascular cell adhesion molecule-1(VCAM-1),monocyte chemoattractant protein-1(MCP-1)and galectin-3.Results:A total of 118 subjects(mean age:[66.8±8.9]years;male:59.8%)were included into analysis:58 in the control group and 60 in the STDP group.CYP2 C19 genotype distribution was comparable between the 2 groups.In comparison to the control group,the STDP group had significantly lower CKMB(P<0.05)but similar hs Tn I(P>0.05)at 24 h after PCI,lower ICAM-1,VCAM-1,MCP-1 and galectin-3 at 3 months(all P<0.05)but not at 7 days after PCI(P>0.05).At 3 months,the STDP group had lower PMP number([42.9±37.3]vs.[67.8±53.1]counts/μL in the control group,P=0.05).Subgroup analysis showed that STDP increased percentage inhibition of ADP-induced platelet aggregation only in slow metabolizers(66.0%±20.8%in STDP group vs.36.0%±28.1%in the control group,P<0.05),but not in intermediate or fast metabolizers.The rate of MACEs during the 3-month follow-up did not differ between the two groups.Conclusion:STDP produced antiplatelet,anti-inflammatory and cardioprotective effects.Subgroup analysis indicated that STDP inhibited residual platelet reactivity in slow metabolizers only.