Accidental hepatic artery ligation in humans

Despite the vast amount of information from experimental animals, it has been difficult to obtain a clear-cut picture of the effects of ligation of the hepatic artery in humans with relatively normal livers. The last complete review of this subject in 1933 indicated that a mortality in excess of 50 per cent could be expected in non-cirrhotic patients with injury of the hepatic artery or its principal branches. Five cases of dearterialization of the normal human liver have been observed. These were due to accidental interruption of the right hepatic artery in four and the proper hepatic artery in one. The injured vessel was repaired in one case and ligated in the others. In four of the five patients the vascular disruption was the sole injury. In the other the common bile duct was also lacerated. There was no evidence of hepatic necrosis in any case although one patient died from complications of common duct repair. Transient changes in SGOT and temporary low grade bilirubinemia were commonly noted. In addition, all cases of ligation of the hepatic artery reported since 1933 have been compiled. On the basis of reviewed, as well as the presently reported cases, it is concluded that ligation of the hepatic artery or one of its branches in the patient with relatively normal hepatic function is not ordinarily fatal in the otherwise uncomplicated case. Adequate perfusion of the liver can usually be provided by the remaining portal venous flow and whatever arterial collaterals are present, unless additional factors further reduce the portal venous flow or increase hepatic oxygen need. These factors include fever, shock and anoxia. The key to therapy in unreconstructed injuries to the hepatic artery is avoidance of these secondary influences. © 1964

Astronomical Distance Determination in the Space Age: Secondary Distance Indicators

The formal division of the distance indicators into primary and secondary leads to difficulties in description of methods which can actually be used in two ways: with, and without the support of the other methods for scaling. Thus instead of concentrating on the scaling requirement we concentrate on all methods of distance determination to extragalactic sources which are designated, at least formally, to use for individual sources. Among those, the Supernovae Ia is clearly the leader due to its enormous success in determination of the expansion rate of the Universe. However, new methods are rapidly developing, and there is also a progress in more traditional methods. We give a general overview of the methods but we mostly concentrate on the most recent developments in each field, and future expectations. © 2018, The Author(s)

Photometric and spectroscopic evolution of the interacting transient at 2016jbu(Gaia16cfr)

We present the results from a high-cadence, multiwavelength observation campaign of AT 2016jbu (aka Gaia16cfr), an interacting transient. This data set complements the current literature by adding higher cadence as well as extended coverage of the light-curve evolution and late-time spectroscopic evolution. Photometric coverage reveals that AT 2016jbu underwent significant photometric variability followed by two luminous events, the latter of which reached an absolute magnitude of MV ∼-18.5 mag. This is similar to the transient SN 2009ip whose nature is still debated. Spectra are dominated by narrow emission lines and show a blue continuum during the peak of the second event. AT 2016jbu shows signatures of a complex, non-homogeneous circumstellar material (CSM). We see slowly evolving asymmetric hydrogen line profiles, with velocities of 500 km s-1 seen in narrow emission features from a slow-moving CSM, and up to 10 000 km s-1 seen in broad absorption from some high-velocity material. Late-time spectra (∼+1 yr) show a lack of forbidden emission lines expected from a core-collapse supernova and are dominated by strong emission from H, He i, and Ca ii. Strong asymmetric emission features, a bumpy light curve, and continually evolving spectra suggest an inhibit nebular phase. We compare the evolution of H α among SN 2009ip-like transients and find possible evidence for orientation angle effects. The light-curve evolution of AT 2016jbu suggests similar, but not identical, circumstellar environments to other SN 2009ip-like transients

Progenitor, environment, and modelling of the interacting transient AT 2016jbu (Gaia16cfr)

We present the bolometric light curve, identification and analysis of the progenitor candidate, and preliminary modelling of AT 2016jbu (Gaia16cfr). We find a progenitor consistent with a ∼22-25 M⊙ yellow hypergiant surrounded by a dusty circumstellar shell, in agreement with what has been previously reported. We see evidence for significant photometric variability in the progenitor, as well as strong Hα emission consistent with pre-existing circumstellar material. The age of the environment, as well as the resolved stellar population surrounding AT 2016jbu, supports a progenitor age of >10 Myr, consistent with a progenitor mass of ∼22 M⊙. A joint analysis of the velocity evolution of AT 2016jbu and the photospheric radius inferred from the bolometric light curve shows the transient is consistent with two successive outbursts/explosions. The first outburst ejected material with velocity ∼650 km s-1, while the second, more energetic event ejected material at ∼4500 km s-1. Whether the latter is the core collapse of the progenitor remains uncertain. We place a limit on the ejected 56Ni mass of <0.016 M⊙. Using the Binary Population And Spectral Synthesis (BPASS) code, we explore a wide range of possible progenitor systems and find that the majority of these are in binaries, some of which are undergoing mass transfer or common-envelope evolution immediately prior to explosion. Finally, we use the SuperNova Explosion Code (SNEC) to demonstrate that the low-energy explosions within some of these binary systems, together with sufficient circumstellar material, can reproduce the overall morphology of the light curve of AT 2016jbu

Plasma lipid profiles discriminate bacterial from viral infection in febrile children

Fever is the most common reason that children present to Emergency Departments. Clinical signs and symptoms suggestive of bacterial infection ar

Sphingosine-1-Phosphate–dependent activation of p38 MAPK maintains elevated peripheral resistance in heart failure through increased myogenic vasoconstriction

Rationale: Mechanisms underlying vasomotor abnormalities and increased peripheral resistance exacerbating heart failure (HF) are poorly understood. Objective: To explore the role and molecular basis of myogenic responses in HF. Methods and Results: 10 weeks old C57Bl6 mice underwent experimental myocardial infarction (MI) or sham surgery. At 1 to 12 weeks postoperative, mice underwent hemodynamic studies, mesenteric, cerebral, and cremaster artery perfusion myography and Western blot. Organ weights and hemodynamics confirmed HF and increased peripheral resistance after MI. Myogenic responses, ie, pressure-induced vasoconstriction, were increased as early as 1 week after MI and remained elevated. Vasoconstrictor responses to phenylephrine were decreased 1 week after MI, but not at 2 to 6 weeks after MI, whereas those to endothelin (ET)-1 and sphingosine-1-phosphate (S1P) were increased at all time points after MI. An antagonist (JTE-013) for the most abundant S1P receptor detected in mesenteric arteries (S1P2R) abolished the enhanced myogenic responses of HF, with significantly less effect on controls. Mice with genetic absence of sphingosine-kinases or S1P2R (Sphk1-/-; Sphk1 -/-/Sphk2+/-; S1P2R-/-) did not manifest enhanced myogenic responses after MI. Mesenteric arteries from HF mice exhibited increased phosphorylation of myosin light chain, with deactivation of its phosphatase (MLCP). Among known S1P-responsive regulators of MLCP, GTP-Rho levels were unexpectedly reduced in HF, whereas levels of activated p38 MAPK and ERK1/2 (extracellular signal-regulated kinase 1/2) were increased. Inhibiting p38 MAPK abolished the myogenic responses of animals with HF, with little effect on controls. Conclusions: Rho-independent p38 MAPK-mediated deactivation of MLCP underlies S1P/S1P2R-regulated increases in myogenic vasoconstriction observed in HF. Therapeutic targeting of these findings in HF models deserves study