Search

Measurements of the semileptonic branching ratios of charmed D/sup +/ and D/sup 0/ mesons are presented, from data collected at the psi(3770) in the Mark III detector at SPEAR. From a sample of events kinematically selected as charmed D/sup +/D/sup -/ or D/sup 0/D /sup 0/ pairs, the branching ratios R(D/sup +/..-->..e/sup +/+X) = (17.0 +- 1.9 +- 0.7)% and R(D/sup 0/..-->..e/sup +/+X) = (7.5 +- 1.1 +- 0.4 )% are obtained. The ratio of these measurements can be interpreted as the ratio of D/sup +/ and D/sup 0/ lifetimes tau/sup +//tau/sup 0/ = 2.3/sub -0.4-0.1/ /sub +0.5+0.1/ by neglect of the contribution of Cabibbo-suppressed decays to the total decay width.

The conformational changes induced by the binding of Ca(II) to rabbit skeletal muscle troponin-C (TNC) have been followed by proton magnetic resonance spectroscopy. Ca(II)-free TNC (apo-TNC) contains definite ordered regions. Ca(II) titration of the high affinity sites (cf. Potter , Gergely, 1975) causes a large folding of the backbone, some of which involves refolding of an ordered region(s) and changes in several side-chains e.g. Glu, Asp and Phe. Titration of the low affinity sites does not alter the backbone but leads to changes among hydrophobic side-chains (one or more Val, Leu, Ile; two or more Phe, Glu and Asp) that define an ordered region(s) of apo-TNC. The rate constants for the conformation changes of the low and high affinity sites are approximately 10 s−1 and < 20 s−1, respectively. Final stages of the titration include a downfield shifted methyl group (likely Ile) and a Phe residue. The thermal stabilities of apo-TNC, TNC · Ca2(II) and native TNC were compared. It was concluded that Ca(II) binding by the two high affinity sites both directs and stabilizes much of the structure. The role of the changes of the low affinity sites, which are thought to activate contraction, are briefly discussed.

An insulin hexamer containing one B10-bound Co(III) ion and one unoccupied B10 site has been synthesized. The properties of the monosubstituted hexamer show that occupancy of only one B10 site by Co3+ is sufficient to stabilize the hexameric form under the conditions of pH and concentration used in these studies. The experimentally determined, second-order rate constants for the binding of Zn2+ and Co2+ to the unoccupied B10 site are consistent with literature rate constants for the rate of association of these divalent metal ions with similar small molecule ligands. These findings indicate that the rate-limiting steps for Zn2+ and Co2+ binding involve the removal of the first aqua ligand. The rate constant for the binding of Cd2+ is significantly lower than the literature values for small molecule chelators, which suggests that some other protein-related process is rate-limiting for Cd2+ binding to the unoccupied, preformed B10 site. The kinetics of the assembly of insulin in the presence of limiting metal ion provides strong evidence indicating that the B13 site of the tetramer species can bind Zn2+, Cd2+, or Ca2+ prior to hexamer formation and that such binding assists hexamer formation. Both the tetramer and the hexamer B13 sites were found to exhibit similar affinities for Zn2+ and Cd2+ (Kd congruent to 9 microM), whereas the tetramer B13 sites bind Ca2+ much more weakly (Kd congruent to 1 mM for tetramer vs 83 microM for hexamer). The second-order rate constants estimated for the association of Zn2+ and Cd2+ to the tetrameric site indicate that the loss of the first inner-sphere aqua ligand is the rate-limiting step for binding.

The use of vasodilator drugs in peripheral vascular disease is reviewed. Discussed are actions and efficacy of direct-acting drugs such as isoxsuprine, papaverinek niacin and cyclandelate; the beta-receptor stimulating drug, nylidrin; and drugs which affect the sympathetic nervous system, such as tolazoline, reserpine, guanethidine, methyldopa, ergot alkaloids and alcohol. Both animal and clinical studies reveal little evidence of the effectiveness of vasodilator drugs in the treatment of obstructive arterial disease. In some patients with vasospastic diseases, vasodilators which act upon the sympathetic nervous system (reserpine and guanethidine) may have an ameliorating effect by increasing cutaneous capillary blood flow.

We present an analysis of the decay J/psi..--> gamma..4..pi.. in the final states ..gamma pi../sup +/..pi../sup -/..pi../sup +/..pi../sup -/ and ..gamma pi../sup +/..pi../sup 0/..pi../sup -/..pi../sup 0/. The branching fractions obtained are B(J/psi..--> gamma pi../sup +/..pi../sup -/..pi../sup +/..pi../sup -/) = (3.05 +- 0.08 +- 0.45) x 10/sup -3/ and B(J/psi..--> gamma pi../sup +/..pi../sup 0/..pi../sup -/..pi../sup o/) = ( 8.3 +- 0.2 +- 3.1) x 10/sup -3/ for m/sub 4pi/ less than 2 GeV/c/sup 2/. The 4..pi.. invariant-mass distributions extend from 1.0 to 3.0 GeV/c/sup 2/, showing peaks at approximately 1.55 and 1.8 GeV/c/sup 2/. In an analysis of the 4..pi.. final state we find that roughly-equal50% of the events below 2 GeV/c/sup 2/ are pseudoscalar rhorho, the product branching fraction of which is determined to be B(psi..--> gamma..X/sub 0/-)B(X/sub 0/-..-->..rhorho) = (4.7 +- 0.3 +- 0.9) x 10/sup -3/. No other significant rhorho component is found, and upper limits on the product branching fraction B(J/psi..--> gamma..X)B(X..-->..rhorho) are presented for the theta(1690) and the g/sub T/ states near 2.2 GeV/c/sup 2/.

We report a new measurement of the D∗ branching ratios, using data obtained with the Mark III detector at the e^+e^− storage ring SPEAR at s=4.14GeV. A fit to the recoil mass squared spectrum of D mesons reconstructed through the decay modes K^−π^+π^+ and K^−π^+ is used to extract the D^(∗+) → γD^+, π^0D^+, π^+D^0 and D^(∗0) → γD^0, π^0D^0 branching ratios.

We present evidence for the radiative decay J/\ensuremath{\psi}\ensuremath{\rightarrow}\ensuremath{\gamma}\ensuremath{\omega}\ensuremath{\omega} with a branching fraction of (1.76\ifmmode\pm\else\textpm\fi{}0.09\ifmmode\pm\else\textpm\fi{}0.45)\ifmmode\times\else\texttimes\fi{}${10}^{\mathrm{\ensuremath{-}}3}$. The \ensuremath{\omega}\ensuremath{\omega} invariant-mass distribution peaks at 1.8 GeV/${c}^{2}$, just above threshold. Analysis of angular correlations indicates that \ensuremath{\omega}\ensuremath{\omega} system below 2 GeV/${c}^{2}$ is predominantly pseudoscalar. Upper limits are presented for the branching fractions of \ensuremath{\omega}\ensuremath{\omega} decays of the \ensuremath{\theta}(1690), the ${g}_{T}$ states near 2.2 GeV/${c}^{2}$, and the ${\ensuremath{\eta}}_{c}$.

Dalitz plot analyses of four Kππ decays of the D 0 and D + mesons are presented. The relative amounts of K ∗ π, Kϱ and non-resonant Kππ in each decay mode are determined, and isospin amplitudes and phases are derived. These results are compared with predictions from QCD. The K − π + π + mode has a non-uniform, non-resonant contribution; attempts to fit this distribution are described.

In a study of 2.7 million J/psi decays with the Mark III, a new magnetic detector at SPEAR, we have observed the sequential decay J/psi..--> gamma..eta/sub c/, eta/sub c/..-->..phiphi. The product branching fraction is (1.02 +- 0.25 +- 0.14) x 10/sup -4/, where the quoted errors are statistical and systematic, respectively. Analysis of the final-state angular distributions provides the first experimental determination that the spin and parity of the eta/sub c/ are 0/sup -/.

The decays J/\ensuremath{\psi}\ensuremath{\rightarrow}\ensuremath{\gamma}${\ensuremath{\pi}}^{+}$${\ensuremath{\pi}}^{\mathrm{\ensuremath{-}}}$ and J/\ensuremath{\psi}\ensuremath{\rightarrow}\ensuremath{\gamma}${K}^{+}$${K}^{\mathrm{\ensuremath{-}}}$, 2.0 GeV/${c}^{2}$, have been studied. Measurements are presented for B(\ensuremath{\psi}\ensuremath{\rightarrow}\ensuremath{\gamma}f(1270))B(f(1270)\ensuremath{\rightarrow}${\mathrm{\ensuremath{\pi}}}^{+}$${\mathrm{\ensuremath{\pi}}}^{\mathrm{\ensuremath{-}}}$), B(\ensuremath{\psi}\ensuremath{\rightarrow}\ensuremath{\gamma}f(1270))B(f(1270)\ensuremath{\rightarrow}${\mathrm{\ensuremath{\pi}}}^{+}$${\mathrm{\ensuremath{\pi}}}^{\mathrm{\ensuremath{-}}}$), B(\ensuremath{\psi}\ensuremath{\rightarrow}\ensuremath{\gamma}f'(1525))B(f'(1525)\ensuremath{\rightarrow}${\mathrm{K}}^{+}$${\mathrm{K}}^{\mathrm{\ensuremath{-}}}$), and B(\ensuremath{\psi}\ensuremath{\rightarrow}\ensuremath{\gamma}theta)B(theta(1270)\ensuremath{\rightarrow}${\mathrm{K}}^{+}$${\mathrm{K}}^{\mathrm{\ensuremath{-}}}$). A higher-mass structure is observed in the ${\ensuremath{\pi}}^{+}$${\ensuremath{\pi}}^{\mathrm{\ensuremath{-}}}$ channel. The spin of the theta(1720) is established with high confidence. The polarization structure of the f(1270), f'(1525), and theta(1720) have been determined.

The effects of intra-arterial administration of alpha 1- and alpha 2-adrenoceptor and S2-serotonergic agonists and antagonists on human digital blood flow were studied before and during reflex sympathetic vasoconstriction caused by body cooling in normal subjects. Total finger blood flow (FBF) was measured by venous occlusion plethysmography and capillary blood flow (FCF) by the disappearance rate of a radioisotope from a local injection in a fingerpad. Intra-arterial phenylephrine and clonidine produced dose-related decreases in FBF and increases in finger vascular resistance (FVR); clonidine was the more potent vasoconstrictor. Prazosin effectively blocked the vasoconstrictor effect of phenylephrine but not clonidine and yet caused no significant change in FBF and FVR during reflex sympathetic vasoconstriction. Yohimbine blocked the effect of clonidine but not phenylephrine and caused a significant increase in FBF and decrease in FVR during vasoconstriction. No significant changes occurred in FCF with prazosin or yohimbine. 5-Hydroxytryptamine decreased FBF and increased FVR. The S2-serotonergic antagonist, ketanserin, blocked the effects of 5-hydroxytryptamine. Ketanserin, in the presence of prazosin, significantly increased FBF and decreased FVR in the reflex vasoconstricted subjects. These studies suggest that both alpha 1- and alpha 2-adrenoceptors are present in the digital vascular bed and that sympathetic nerves control the flow through arteriovenous anastomoses primarily by alpha 2-adrenoceptors. S2-serotonergic receptors are also present in the digital vasculature and may be another important mechanism mediating digital vasoconstriction.

The digital vasospastic phenomena, which are induced by beta-adrenergic-blocking agents, suggest a beta-adrenergic finger vasodilator mechanism. We measured fingertip total blood flow with venous occlusion plethysmography and studied nutritional blood flow with Na131I clearance. During fingertip vasoconstriction caused by branchial artery infusion of norepinephrine or angiotensin, intra-arterial isoproterenol caused a sustained increase in fingertip total blood flow. Furthermore, propranolol significantly potentiated the vasoconstriction caused by intra-arterial norepinephrine and attenuated the vasodilator action of isoproterenol. No change in branchial artery blood pressure occurred to explain the changes in fingertip blood flow. Isoproterenol did not change nutritional flow, implying beta-adrenergic vasodilation solely of the fingertip arteriovenous shunts. When fingertip vasoconstriction was induced by reflex sympathetic nerve action during environmental cooling and mental stress, or by norepinephrine release from sympathetic nerves caused by intra-arterial tyramine infusion, isoproterenol and propranolol had no effect on fingertip total blood flow. This effect is probably specific for the beta-receptor agonist, since intra-arterial histamine caused a large increase in finger blood flow during environmental cooling. We conclude that there is a beta-adrenergic vasodilator mechanism in human digital arteriovenous shunts that may be humorally activated, but which has no apparent functional role in modulating sympathetic vasoconstriction. Our results suggest a spatial dissociation of the effector sites for vasoactive humoral agents and sympathetic vasoconstrictor nerves.

A new technique is applied to data collected at the $\ensuremath{\psi}(3770)$ resonance to derive charmed-$D$-meson branching fractions without relying on the measurement of $D$-production cross sections. Measurements are presented for three decay modes of the ${D}^{0} ({K}^{\ensuremath{-}}{\ensuremath{\pi}}^{+}, {D}^{\ensuremath{-}}{\ensuremath{\pi}}^{\ensuremath{-}}{\ensuremath{\pi}}^{+}{\ensuremath{\pi}}^{+}, \mathrm{and} {K}^{\ensuremath{-}}{\ensuremath{\pi}}^{+}{\ensuremath{\pi}}^{0}$ and four decay modes of the ${D}^{+} ({K}^{\ensuremath{-}}{\ensuremath{\pi}}^{+}{\ensuremath{\pi}}^{+},{K}^{\ensuremath{-}}{\ensuremath{\pi}}^{+}{\ensuremath{\pi}}^{+}{\ensuremath{\pi}}^{0},{K}_{S}^{0}{\ensuremath{\pi}}^{+}, \mathrm{and} {K}_{S}^{0}{\ensuremath{\pi}}^{+}{\ensuremath{\pi}}^{0})$. The resulting branching fractions are significantly larger than previous measurements.

The weak hadronic decay D/sup 0/..-->..K/sup 0/K/sup +/K/sup -/ is observed in a data sample of 9.3 pb/sup -1/ collected with the Mark III detector at the psi(3770) resonance. An analysis of the K/sup +/K/sup -/ subsystem suggests that while the decay proceeds in part through the K-bar/sup 0/phi channel, providing evidence for the presence of nonspectator amplitudes in D/sup 0/ decays, a significant fraction of the decays occur through both higher- and lower-mass K/sup +/K/sup -/ systems. A limit is set on the decay D/sup 0/..-->..K/sup 0/K/sup 0/, also thought to proceed by nonspectator processes.

We present evidence for the exclusive reaction e+e−→Ds±Ds*∓, observed with the Mark III detector at the SLAC storage ring SPEAR. The Ds± is reconstructed in the φπ± decay mode, while the Ds*∓ is detected as a narrow peak in the recoil-mass distribution. The mass of the Ds* is found to be 2109.3±2.1±3.1 MeV/c2, yielding a Ds*−Ds mass difference of 137.9±2.1±4.3 MeV/c2. The width of the Ds* is

1. In patients with congestive heart failure, both the sympathetic nervous system and renin-angiotensin system are often stimulated. In order to assess the contribution of the renin-angiotensin system to limb vascular resistance, the forearm haemodynamic response to captopril was studied in 13 patients with heart failure. 2. Seven subjects were studied while supine and during 60° head-up tilt. To eliminate α-adrenergic effects, six additional patients with heart failure were pretreated with intra-arterial phentolamine and then given captopril. Venous occlusion plethysmography was used to determine forearm blood flew and forearm vascular resistance. 3. Tilt did not significantly increase pretreatment plasma renin activity or plasma noradrenaline concentration, nor did it decrease forearm blood flow. Furthermore, captopril did not alter forearm vascular resistance during supine or upright posture. During the phentolamine infusion, however, captopril reduced forearm vascular resistance by 19% (P < 0.05). 4. Despite increased plasma renin activity, captopril did not cause forearm vasodilatation during supine or upright posture in these patients with heart failure. When the contribution of the sympathetic nervous system was eliminated, captopril decreased forearm vascular resistance. Therefore, in patients with congestive heart failure, the sympathetic nervous system is important in limb vasoregulation, and the contribution of the renin-angiotensin system is apparent only after α-adrenergic blockade.

The stability of reserpine injections and tablets that had been stored in hospital pharmacies across the United States was studied. Through a voluntary FDA drug stability program, all hospital pharmacies in the United States were asked to complete a response card indicating information about the reserpine injections and tablets they had in stock. Based on the responses, FDA selected 93 samples of reserpine injections and 51 samples of reserpine tablets. The samples of injections were subjected to tests for identification, pH, presence of other alkaloids, presence of 3,4-dehydroreserpine, and strength. All samples of reserpine injections met USP requirements. Two samples of reserpine tablets representing one lot each from two manufacturers failed to meet USP requirements for content uniformity. Reserpine injections and tablets appear to be stable under actual marketplace conditions.

It is not known whether the renin-angiotensin-aldosterone (RAA) system contributes to the regulation of the limb circulation in normal human beings. Accordingly, the effect of the angiotensin converting-enzyme inhibitor, captopril, on forearm vascular resistance (FVR) and forearm venous volume (FVV) was studied in nine normal subjects during states of both sodium loading and sodium depletion. All subjects were studied in the supine position and during 60 degrees head-up tilt. By analysis of variance, the combined intervention of sodium depletion and converting-enzyme inhibition was responsible for a decrease in both FVR and mean blood pressure (BP). In sodium-depleted subjects, converting-enzyme inhibition decreased supine mean BP 7.0% and supine FVR 22.8% but did not change FVV. Neither the fall in BP nor the fall in FVR, however, was significantly augmented by tilting from a supine to upright posture. In sodium-loaded subjects, captopril did not alter BP, FVR, or FVV in recumbent or upright positions. Therefore, the RAA system contributes to the maintenance of blood pressure and limb vascular resistance only in sodium-depleted subjects. Limb venous capacitance in normal subjects is not regulated by the RAA system.

We report a revised determination of charmed--D-meson absolute branching fractions based on complete reconstruction of DD-bar events at the psi(3770). Two backgrounds, Cabibbo-suppressed and multi-..pi../sup 0/D decays, are addressed in detail. The first measurement of the decay D/sup 0/..-->..K/sup -/..pi../sup +/..pi../sup 0/..pi../sup 0/ establishes the sensitivity to hitherto unobserved multi-..pi../sup 0/ modes. Removal of both backgrounds reduces the values of our previously reported branching fractions by (21--24)% leaving their ratios largely unchanged. The new values are unable to account fully for a reported deficit in charm production in B-meson decay.

A search for the lepton family number violating decay D 0 → μ e is reported. No signal is observed in a data sample of 9.3 pb −1 collected at the ζ (3770) resonance with the MARK III detector, where 0.18±0.06±0.05 background events are expected. A 90% confidence level upper limit on the branching fraction B (D 0 → μ e) of 1.5 × 10 −4 is obtained.

DRUGS that increase blood flow by direct or indirect action on the peripheral blood vessels are termed "vasodilators." These agents are widely advertised in medical journals and consume a substantial percentage of the drug dollar in this country.1 Although most vasodilator drugs have been shown to increase blood flow to the limbs and various organs in animal experiments and sometimes in normal human subjects, their use in peripheral vascular diseases remains questionable. For therapeutic purposes, peripheral vascular diseases can be generally classified into obstructive or vasospastic; the most common examples of each category are arteriosclerosis obliterans and Raynaud's disease, respectively. . . .

The relationship of arterial blood flow and venous volume to venous flow velocity was studied in normal subjects. The effects of current modes of treatment in venous thrombosis and of a vasodilator drug on venous flow velocity were also investigated. Total calf flow and venous volume were measured by venous occlusion plethysmography while venous flow axial velocity was determined by the transit time of 131-I albumin from calf to inguinal region. Local intravenous epinephrine administration induced venoconstriction and increased venous flow velocity. Intra-arterial isoproterenol and angiotensin increased and decreased arterial flow, respectively, with no change in venous flow velocity of volume, but local heat increased arterial flow and venous flow velocity with no change in venous volume. Local cold, despite venoconstriction, decreased venous flow velocity accompanied by a decreased arterial flow. Intravenous heparin did not affect venous flow velocity. Intravenous but not oral nylidrin increased venous flow velocity. Therefore venous flow velocity can be significantly increased by venocontriction, by large increases in arterial flow (local heat), and by a parenteral vasodilator drug. These experiements indicate that there is a basis for applying heat but not cold in the prevention and treatment of venous thrombosis.

We present measurements of the two-body decays of the J/psi into a vector and a pseudoscalar meson. The data, taken with the Mark III detector at the SLAC e/sup +/e/sup -/ storage ring SPEAR, consist of 5.8 x 10/sup 6/ produced J/psi's. The branching ratios for the J/psi decays into rho..pi.., rhoeta, rhoeta', ..omega pi../sup 0/, ..omega..eta, ..omega..eta', phieta, phieta', and K/sup */K are measured; an upper limit on J/psi..-->..phi..pi../sup 0/ is obtained. Using the measured branching ratios we obtain parameters of a phenomenological model of J/psi decays, indicating that the eta and eta' are consistent with being composed only of light and strange quarks. The model is used to obtain the mixing angle in the pseudoscalar nonet. The ..omega pi../sup 0/ electromagnetic form factor is determined. The upper limit on J/psi..-->..phi..pi../sup 0/ is used to study the contributions from electromagnetic doubly--Okubo-Zweig-Iizuka--suppressed decays of the J/psi. .AE

Evidence is presented for a narrow state, called xi, in the decay modes J/psi elxi, xi K K , and xi K/sub S/K/sub S/. In the K K mode, the xi has a mass of 2.230 +- 0.006 +- 0.014 GeV/cS, a width of GAMMA = 0.026/sub -0.016//sup +0.020/ +- 0.017 GeV/cS, a product branching ratio of (4.2/sub -1.4//sup +1.7/ +- 0.8) x 10 V, and a statistical significance of approx.4.5 standard deviations. In the K/sub S/K/sub S/ mode, it has a mass of 2.232 +- 0.007 +- 0.007 GeV/cS, a width of GAMMA = 0.018/sub -0.015//sup +0.023/ +- 0.010 GeV/cS, a product branching ratio of (3.1/sub -1.3//sup +1.6/ +- 0.7) x 10 V, and a statistical significance of approx.3.6 standard deviations. Limits on xi decay to other final states are presented.

Pairs of $\ensuremath{\tau}$ leptons produced at $\sqrt{s}=3.77$ GeV have been studied in $e\ensuremath{\mu}$, $\mathrm{ee}$, and $\ensuremath{\mu}\ensuremath{\mu}$ final states. The leptonic branching ratios have been measured to be $B(\ensuremath{\tau}\ensuremath{\rightarrow}e\ensuremath{\nu}\ensuremath{\nu})=(18.2\ifmmode\pm\else\textpm\fi{}0.7\ifmmode\pm\else\textpm\fi{}0.5)%$ and $B(\ensuremath{\tau}\ensuremath{\rightarrow}\ensuremath{\mu}\ensuremath{\nu}\ensuremath{\nu})=(18.0\ifmmode\pm\else\textpm\fi{}1.0\ifmmode\pm\else\textpm\fi{}0.6)%$. Limits have been set for the two-body decays $\ensuremath{\tau}\ensuremath{\rightarrow}\mathrm{eG}$ and $\ensuremath{\tau}\ensuremath{\rightarrow}\ensuremath{\mu}G$, where $G$ is a light Goldstone boson.

Idiopathic Raynaud's phenomenon (Raynaud's disease) is very common among young women. A thorough history and physical examination are the keys to determining the extent of a diagnostic workup. In an otherwise normal and asymptomatic young woman with vasospastic attacks involving symmetric aspects of the digits, a CBC, urinalysis, chest film, and ESR are recommended as a cost-effective workup. If these studies are negative, the disease is probably benign. A history or physical findings consistent with collagen vascular disease, obstructive arterial disease, or carpal tunnel or thoracic outlet syndrome should lead to selected diagnostic tests. Men, persons with onset of vasospastic attacks after age 40, and those with severe disease or trophic changes of the digits deserve a more comprehensive workup to screen for underlying causes.

The proliferative capacity of thymocytes from C3H/HeJ mice decreases as the animals attain maturity. The proliferative response of thymocytes from 24- to 28-week-old mice to stimulation with concanavalin A (Con A) is only 20% of that observed at 4 weeks of age. The decreased proliferative capacity of thymocytes in response to Con A stimulation observed between 4 and 24 weeks of age closely correlates to the drop in thymic weight and cellularity observed during this period. In contrast, the spontaneous proliferative capacity of thymocytes, as well as proliferation of thymocytes in response to stimulation with phorbol myristate acetate (PMA) and ionomycin, drops only slightly during this period, as proliferation under these conditions in thymocytes from 24- to 28-week-old mice is approximately 65–70% of that observed in 4-week-old animals. We have previously shown that cytoplasmic extracts from proliferating lymphoid cells contain a factor, termed the activator of DNA replication (ADR), which is capable of inducing DNA synthesis in isolated, quiescent nuclei. We show in this study that the decreased proliferative capacity of thymocytes during whole organism maturation and thymic involution is associated with decreased endogenous levels of ADR, while nuclear sensitivity of thymocytes to ADR was retained during these processes. The diminution of ADR activity during thymic involution was quantitatively greater than the loss in proliferative capacity.

The effect on finger blood flow (FBF) of 5-hydroxytryptamine (5-HT) in a 25 degrees C room and the S2-serotonergic receptor antagonist, ketanserin, during reflex sympathetic vasoconstriction was studied in normal subjects. Total FBF was measured by venous occlusion, air plethysmography, and capillary blood flow (FCF) by the disappearance rate of a radioisotope from a fingertip injection. 5-HT in doses of 4 and 8 micrograms/min, given by constant infusion via a brachial artery catheter, significantly decreased FBF [32 +/- (SE) 10.4 to 12.8 +/- 6.6 for 4 micrograms/min and to 5.4 +/- 2.6 ml.min-1.100 ml-1 for 8 micrograms/min, P less than 0.05]. Ketanserin (50 micrograms/min) blocked the vasoconstriction caused by 5-HT. During reflex sympathetic vasoconstriction produced by body cooling, ketanserin increased FBF from 4.1 +/- 1.1 to 39.9 +/- 12.9 ml.min-1.100 ml-1 (P less than 0.025). The vasodilation caused by ketanserin was specific for serotonergic receptors, since it occurred during alpha 1-adrenoceptor blockade with prazosin. Furthermore, the decreases in FBF induced by clonidine and angiotensin II were not significantly different before and during ketanserin infusion. Also, ketanserin further increased FBF after vasodilation of reflexly vasoconstricted fingers by the alpha 2-adrenoceptor antagonist, yohimbine, and phentolamine increased FBF during ketanserin infusions. FCF decreased during 5-HT and increased during ketanserin infusions, demonstrating that both capillary and arteriovenous shunt flow were affected.(ABSTRACT TRUNCATED AT 250 WORDS)

The stability of sterile dexamethasone acetate suspensions and dexamethasone sodium phosphate injections that had been stored in hospital pharmacies across the United States was studied. Through a voluntary FDA drug stability program, all hospital pharmacies in the United States were asked in October 1981 to complete a response card indicating information about the sterile dexamethasone acetate suspensions and dexamethasone sodium phosphate injections they had in stock. Based on the responses, FDA selected 21 samples of sterile dexamethasone acetate suspensions (representing two manufacturers) and 114 samples of dexamethasone sodium phosphate injection (representing 11 manufacturers). These samples were analyzed for identification, pH, and strength. All samples of sterile dexamethasone acetate suspension met USP requirements. Eleven samples of dexamethasone sodium phosphate injection representing 10 lots from three manufacturers failed USP assay requirements for strength. All samples that failed to meet strength requirements showed evidence of degradation by oxidation. Sterile dexamethasone acetate suspensions appear to be stable when stored under actual marketplace conditions, but there is a problem with the shelf-life stability of dexamethasone sodium phosphate injections made by some manufacturers.

Measurements of the branching ratios of ten Cabibbo-suppressed hadronic weak decays of the D/sup +/ and D/sup 0/ are presented from data collected with the Mark III detector SPEAR. In addition to the previously observed channels D/sup 0/..-->..K/sup -/K/sup +/ and ..pi../sup -/..pi../sup +/, we report new measurements of D/sup 0/..--> pi../sup -/..pi../sup +/..pi../sup 0/ and ..pi../sup -/..pi../sup +/..pi../sup -/..pi../sup +/, and D/sup +/..-->..K/sup 0/K/sup +/, ..pi../sup 0/..pi../sup +/, K-bar/sup asterisk0/(892)K/sup +/, phi..pi../sup +/, K/sup -/K/sup +/..pi../sup +/, and ..pi../sup -/..pi../sup +/..pi../sup +/.

PROBLEMS of the foot in patients with diabetes mellitus are often ascribed to "small-vessel disease." In particular, there is a widespread misconception that patients with diabetes mellitus have arteriolar occlusive disease, which can cause ischemic lesions even in the presence of normal pedal pulses. This view often leads to inappropriate care of the patient and a hopeless attitude on the part of the physician. The prevailing view regarding the presence of microvascular occlusive disease probably originated in an early study by Goldenberg et al.1 Specimens obtained by amputation from patients with and without diabetes were studied retrospectively with light microscopy. . . .

The stability of digitoxin tablets that had been stored in hospital pharmacies across the United States was studied. Through a voluntary FDA drug stability program, all hospital pharmacies in the United States were asked in October 1981 to complete a response card indicating information about the digitoxin products they had in stock. Based on the responses, FDA selected 25 samples (representing seven manufacturers) from pharmacies that represented an adequate cross section of the country. These samples were analyzed for content uniformity, strength, dissolution, identification, and other digitoxosides. Of the 25 samples, 19 lots were represented, including 11, 6, 1, and 1 lots of 0.1-mg, 0.2-mg, 0.15-mg and 0.05-mg tablets, respectively. Samples from two lots failed to meet USP requirements for strength, content uniformity, and dissolution; samples from four lots failed to meet the requirements for dissolution only. All six defective lots did not show an expiration date, indicating that they were manufactured before 1975. Digitoxin tablet products still within the expiration date showed no evidence of degradation after storage under actual marketplace conditions.

New drug therapy for peripheral vascular disease includes the use of nifedipine or sympathetic blocking agents for Raynaud's phenomenon and the use of lower doses of warfarin to prevent recurrence of thromboembolic disease. In prophylaxis of deep venous thrombosis, minidose heparin with or without dihydroergotamine and pneumatic boots are effective. Exercise regimens and the cessation of smoking remain the best therapy for intermittent claudication.

Fingertip blood flow was measured by venous occlusion plethysmography before and during a stressful mental task consisting of rapid serial arithmetic calculations in a 25 degrees C room. Significant rises in heart rate and blood pressure indicated that stress was actually induced in all individuals. During mental stress in normal subjects, blood flow decreased (46.4 +/- 6.2 to 22.4 +/- 4.9 ml X min-1 per 100 ml tissue; P less than 0.01) and vascular resistance increased (2.1 +/- 0.4 to 7.6 +/- 2.2 units; P less than 0.01). Patients with Raynaud's disease unexpectedly increased blood flow (15.4 +/- 4.2 to 21.6 +/- 5.7; P = 0.05) and decreased vascular resistance (9.7 +/- 2.3 to 7.1 +/- 1.4; P = 0.05). Ten additional normal subjects were studied in a cool room (20 degrees C). Their digits remained vasoconstricted during stress, as blood flow (7.4 +/- 2.9 to 5.1 +/- 1.3) and vascular resistance (31.5 +/- 11.1 to 34.4 +/- 8.2) varied insignificantly (P greater than 0.10). The digital vasodilatation which occurs during mental stress in patients with Raynaud's disease was not altered by pretreatment with oral indomethacin, with intra-arterial propranolol or atropine, or by digital nerve block. These findings suggest the existence of an active digital vasodilatory mechanism in patients with Raynaud's disease.

The mechanism of tumor necrosis factor (TNF)-induced cytotoxicity has been investigated using two clonal variants of the ME-180 human cervical carcinoma cell line. The clonal lines were characterized with respect to their expression of TNF receptors, kinetics of cell death, and their ability to communicate intercellularly through gap junctions. The ME-180.4 and ME-180.8 clones were identified by their relative sensitivity to TNF induced lysis in a 24-h assay. The dose of TNF required to kill 50% of the target cells was 60 pM for the sensitive ME-180.4 and 2.5 nM for the ME-180.8. However, when assay times were extended, the dose response for both clones was the same, indicating that a difference in the kinetics of cell death and not absolute TNF sensitivity existed between the ME-180.4 and ME-180.8 clones. Both clones were gap junction deficient as judged by their inability to transfer Lucifer yellow or 6-carboxyfluorescein, a characteristic phenotype of cells sensitive to cytotoxicity by TNF. The level of surface receptor expressed on these clones was nearly identical with a Kd = 0.3 nM and 5,000 binding sites per cell. Measurement of the kinetics of cell death revealed that the time between the addition of TNF and the onset of observed cell death (induction phase) was much shorter for the ME-180.4 (32-55 h) than for the resistant ME-180.8 (55-80 h). Mitomycin C, a DNA alkylating agent, significantly reduced the length of the induction phase for both clones, although the kinetic difference between the clones remained unchanged. Two epipodophyllotoxins, VP-16 and VM-26, which specifically inhibit the rejoining activity of DNA topoisomerase II, showed a 10-100-fold synergistic effect when combined with TNF as shown by isobologram analysis. VM-26 when added to the resistant ME-180.8 clones decreased the length of induction phase and abolished the kinetic difference observed with the ME-180.4 clone. These results indicate that the variance in the TNF response of these two clones was closely associated with DNA topoisomerase II, and suggest that this enzyme may play an important role in TNF mediated cytotoxicity.

We describe the algorithm that is used to find and fit charged particle trajectories in the Mark III detector at SPEAR. The computer program uses a novel non-numerical pattern recognition technique analogous to that used by the digital hardware in the experiment's track finding trigger processor. The technique is both fast and efficient. The complete reconstruction of events is performed at a rate of 37 ms per track on an IBM 3081K, compared with 91 ms per track with a more conventional technique. A preliminary fit of all tracks, suitable for online monitoring, is available after 15 ms per track. Similar techniques are also applicable to future experiments operating in high multiplicity environments. The organization of the algorithms is such as to lead to simple implementation on vector processors.

One hundred years ago, public school vocal music was taught primarily by regular classroom teachers and not by music specialists. What was the quality of the preparation of these teachers and the extent of their music teaching? What can today's music educators learn from a time when music could have been called a “basic” in the classroom? This study reviewed educational philosophies of the period from 1885 to 1905, teacher preparation at normal institutes, certification examinations in vocal music, techniques of classroom teacher supervision by music specialists, and methods of teaching vocal music. Four contemporary national surveys regarding the status of public school music were also examined. The study found that teachers trained at normal schools received between ten and fifty hours of music instruction, primarily in music theory. Supervision of grade teachers (instuctors of the period who were primarily responsible for grades one through eight) by music supervisors produced some striking successes and some failures. The study's findings suggest that music educators pursue joint efforts between music specialists and classroom teachers.

Measurements of the exclusive branching fractions B(D^0→π^-e^+ν_e) and B(D^0→K^-e^+ν_e), using data collected at the ψ(3770) with the Mark III detector at the SLAC e^+e^- storage ring SPEAR, are used to determine the ratio of the Kobayashi-Maskawa matrix elements │V_(cd)/V_(cs)│^2 =0.057_(-0.015)^(+0.038)±0.005.

Methods for the preparation of fiber-forming polymeric amides from ω-amino acids and The variation in melting points of the polymeric their amide-forming derivatives are described. The variation in melting points of the polymeric amides with increasing chain length of the recurring unit is discussed.

As the first member of the haloprene or halogen-substituted butadiene series, fluoroprene (2-fluoro-1,3-butadiene) occupies a position between butadiene and chloroprene in most of its properties and characteristics. For example, it polymerizes at a rate approximately twenty-five times that of butadiene under comparable conditions, but it is somewhat slower than chloroprene in its rate of polymerization. However, fluoroprene resembles butadiene in that it copolymerizes readily in wide proportions with most 1,3-dienes and many monovinyl compounds, whereas chloroprene copolymerizes only incompletely with many monomers. In sharp contrast to the other haloprenes, fluoroprene polymers, like those of butadiene, have an amorphous rather than crystalline structure in the stretched state, and they require reinforcement with fillers to develop high tensile properties in their vulcanizates. Polyfluoroprene rubbers obtained in 85 to 90 per cent conversions using selected emulsion systems have exhibited tensile strengths of 2800 to 3200 pounds per square inch at 400 to 500 per cent elongation in tread type of vulcanizates. These vulcanizates are highly freeze resistant and have the good oil resistance of corresponding chloroprene polymers. The resilience of the vulcanizates is excellent and their resistance to ozone and sunlight is good although not so outstanding as that of corresponding polychloroprene products. Polyfluoroprene vulcanizates, unlike those of polychloroprene, propagate a flame when ignited, but they burn at a much slower rate than GR-S or natural rubber. In electrical properties they are superior to polychloroprene vulcanizates, and approach natural rubber in resistivity and power factor.