We disclose a palladium-catalyzed difunctionalization of skipped diene with alkenyl triflates and arylboronic acids to produce 1,3-alkenylarylated products. The reaction proceeded efficiently with Pd(acac) as a catalyst and CsF as a base for a wide range of electron-deficient and electron-rich arylboronic acids as well as oxygen-heterocyclic, sterically hindered, and complex natural product-derived alkenyl triflates bearing various functional groups. The reaction produced 3-aryl-5-alkenylcyclohexene derivatives with 1,3--disubstituted stereochemistry.
View Article and Find Full Text PDFWe disclose a Ni-catalyzed vicinal alkylarylation of unactivated alkenes in γ,δ-alkenylketimines with aryl halides and alkylzinc reagents. The reaction produces γ-C(sp)-branched δ-arylketones with the construction of two new C(sp)-C(sp) and C(sp)-C(sp) bonds. Electron-deficient alkenes play crucial dual roles as ligands to stabilize reaction intermediates and to increase catalytic rates for the formation of C(sp)-C(sp) bonds.
View Article and Find Full Text PDFWe disclose a transmetalation-initiated Ni(I)-catalyzed regioselective -vinylarylation of -alkenyl -cyanocarboxylic esters with vinyl triflates and arylzinc reagents. This reaction proceeds via contraction of six-membered nickellacycles to five-membered nickellacycles to form carbon-carbon bonds at the nonclassical homovicinal sites, and it provides expeditious access to a wide range of complex aliphatic -cyanoesters, -cyanocarboxylic acids, dicarboxylic acids, dicarboxylic acid monoamides, monocarboxylic acids, nitriles, and spirolactones. Control, deuterium labeling, and crossover experiments indicate that (i) the nickellacycle contraction occurs by -H elimination, followed by hydronickellation on transiently formed alkenes, and (ii) the Ni species are stabilized as Ni-enolates.
View Article and Find Full Text PDFJ Oral Maxillofac Surg
May 1989
Am J Obstet Gynecol
August 1988
Several reports suggested using the mean arterial blood pressure during the second trimester to predict the future development of preeclampsia. The value of a second-trimester mean arterial blood pressure greater than or equal to 90 mm Hg was reviewed in 39,876 reported cases of preeclampsia and 207 cases of eclampsia. The sensitivity ranged from 0% to 92% and the specificity varied from 53% to 97%.
View Article and Find Full Text PDFAn analysis has been made of 48 pedigrees selected (ascertained) through an affected mother in the first generation. These pedigrees mainly involve cases of eclampsia which occurred before its recent decline in incidence. The data confirm the genetic determination of susceptibility indicated by published data on eclampsia/preeclampsia.
View Article and Find Full Text PDFThe purpose of this report was to investigate the potential usefulness of average mean arterial pressure, maximal mean arterial pressure, and maximal diastolic pressure during the second trimester in predicting the development of eclampsia in 207 nulliparas and 20 multiparas with eclampsia. In the nulliparas, both the mean arterial pressure and the maximal mean arterial pressure during the second trimester were greater than or equal to 90 mm Hg in 22% and 34% of the patients, respectively. For the multiparas, the percentages with greater than or equal to 90 mm Hg were 30% and 35%, respectively.
View Article and Find Full Text PDFBr Med J (Clin Res Ed)
June 1987
Our report concerns the incidences of pre-eclampsia and eclampsia in 147 sisters, 248 daughters, 74 granddaughters, and 131 daughters-in-law of women who have had eclampsia. The disorder is highly heritable. We have analysed the data in two ways, firstly, as a single gene condition and, secondly, as a multifactorial condition.
View Article and Find Full Text PDFFor the purpose of clinical management, any woman with an acute rise in blood pressure in the latter half of pregnancy must be regarded as having preeclampsia with the possibility of progression to eclampsia. Unfortunately, such diagnoses have been accepted uncritically in the selection of cases for clinical and laboratory studies of preeclampsia, with inevitably erroneous and contradictory conclusions about the disorder. The diagnosis of mild preeclampsia may be correct in roughly one-half of cases, but others may be latent or frank essential hypertension or any of a variety of renal diseases.
View Article and Find Full Text PDFThe relation between bodily build and susceptibility to eclampsia has been controversial for nearly two centuries and the issue has been confused by modern studies of women with nonconvulsive hypertensive disorders in whom the diagnosis of preeclampsia is frequently erroneous. The present study is based upon 193 previously nulliparous and 49 multiparous eclamptic women. Sixty-three of the previously nulliparous women were compared with normal controls matched for age, race, parity, clinic, nonclinic, or private status, and as closely as possible with the time of delivery.
View Article and Find Full Text PDFKidney Int
August 1980
The clinical diagnosis of preeclampsia is often erroneous, for it may be confused with latent hypertension, acute or chronic renal disease, or frank essential hypertension that had abated during much of pregnancy. Eclampsia and "true" preeclampsia run in families with a frequency suggesting that a single recessive gene may be responsible. Eclampsia and "true" preeclampsia do not cause chronic hypertension, whatever their durations.
View Article and Find Full Text PDFAm J Obstet Gynecol
March 1980
All of 134 women classified as having "functionally severe" rheumatic cardiac disease and surviving pregnancies in 1931 through 1943 have been traced to 1975. Ninety-three percent have died at the exponential rate of 6.3% per year.
View Article and Find Full Text PDFClin Exp Hypertens (1978)
January 1981
The diagnosis of preeclampsia is often erroneous in primigravidas and usually so in multiparas. Gestational hypertension, defined as acute hypertension without proteinuria or abnormal edema, is often misdiagnosed as mild preeclampsia. Several follow-up studies are cited as evidence for the conclusions that (1) eclampsia and "true" preeclampsia seldom if ever cause chronic hypertension in women who otherwise never would have developed it; (2) gestational hypertension often is a sign of latent essential hypertension unmasked by pregnancy, and as such it often portends later chronic hypertension; and (3) normotensive pregnancies indicate a low prevalence of later chronic hypertension, and if it does develop, it usually does so at an age later than the average time of onset.
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