Alpha-Photon Coincidence Spectroscopy Along Element 115 Decay Chains

Produced in the reaction 48Ca+243Am, thirty correlated α-decay chains were observed in an experiment conducted at the GSI Helmholzzentrum für Schwerionenforschung, Darmstadt, Germany. The decay chains are basically consistent with previous findings and are considered to originate from isotopes of element 115 with mass numbers 287, 288, and 289. A set-up aiming specifically for high-resolution charged particle and photon coincidence spectroscopy was placed behind the gas-filled separator TASCA. For the first time, γ rays as well as X-ray candidates were observed in prompt coincidence with the α-decay chains of element 115

Recoil-α-fission and recoil-α-α-fission events observed in the reaction 48Ca + 243Am

Products of the fusion-evaporation reaction 48Ca + 243Am were studied with the TASISpec set-up at the gas-filled separator TASCA at the GSI Helmholtzzentrum für Schwerionenforschung, Darmstadt, Germany. Amongst the detected thirty correlated α-decay chains associated with the production of element Z=115, two recoil-α-fission and five recoil-α-α-fission events were observed. The latter five chains are similar to four such events reported from experiments performed at the Dubna gas-filled separator, and three such events reported from an experiment at the Berkeley gas-filled separator. The four chains observed at the Dubna gas-filled separator were assigned to start from the 2n-evaporation channel 289115 due to the fact that these recoil-α-α-fission events were observed only at low excitation energies. Contrary to this interpretation, we suggest that some of these recoil-α-α-fission decay chains, as well as some of the recoil-α-α-fission and recoil-α-fission decay chains reported from Berkeley and in this article, start from the 3n-evaporation channel 288115

How to manage refractory intracranial hypertension?

Intracranial hypertension is one of the major causes of secondary injury in traumatic brain injury leading to a significant burden of morbidity and mortality. We here present a review of available therapies for the treatment of refractory intracranial hypertension that is defined as an intracranial hypertension that does not respond to the firstline therapies. Second-line therapies that are available for the treatment of refractory intracranial hypertension include mild induced hypothermia, inotropes, and vasopressors for the control of cerebral perfusion pressure, transient hyperventilation, barbiturates, and decompressive craniectomy. Apart from decompressive craniectomy, these therapies are supported by the last guidelines published by the Brain Trauma Foundation (BTF). However, the level of evidence supporting them is low to moderate. This is probably partly explained by the fact that traumatic brain injury is extremely heterogeneous and requires multimodal and individualised care, which makes randomised clinical trials difficult to set up. On-going studies like those conducted on induced hypothermia (EUROTHERM3235) and on decompressive craniectomy (RESCUEicp) may lead to new perspectives for the management of patients suffering from refractory intracranial hypertension

On the decay properties of

In bombardments of 248Cm with 143.7-146.8 MeV 26Mg ions the nuclides 269Hs and presumably 270Hs were produced. After chemical isolation, Hs atoms were identified by observing genetically linked nuclear-decay chains. Three chains originating from 269Hs confirmed the decay properties observed previously in the decay of 277112. Two chains exhibited the characteristics expected for the new nuclide 270Hs, which was predicted to be a deformed ”doubly magic” nucleus. From the measured $E_\alpha =9.16^{+0.07}_{-0.03}$ MeV an $\alpha$-decay half-life of 3.6+0.8 -1.4 s was estimated

Non-coding region variants upstream of MEF2C cause severe developmental disorder through three distinct loss-of-function mechanisms.

Clinical genetic testing of protein-coding regions identifies a likely causative variant in only around half of developmental disorder (DD) cases. The contribution of regulatory variation in non-coding regions to rare disease, including DD, remains very poorly understood. We screened 9,858 probands from the Deciphering Developmental Disorders (DDD) study for de novo mutations in the 5′ untranslated regions (5′ UTRs) of genes within which variants have previously been shown to cause DD through a dominant haploinsufficient mechanism. We identified four single-nucleotide variants and two copy-number variants upstream of MEF2C in a total of ten individual probands. We developed multiple bespoke and orthogonal experimental approaches to demonstrate that these variants cause DD through three distinct loss-of-function mechanisms, disrupting transcription, translation, and/or protein function. These non-coding region variants represent 23% of likely diagnoses identified in MEF2C in the DDD cohort, but these would all be missed in standard clinical genetics approaches. Nonetheless, these variants are readily detectable in exome sequence data, with 30.7% of 5′ UTR bases across all genes well covered in the DDD dataset. Our analyses show that non-coding variants upstream of genes within which coding variants are known to cause DD are an important cause of severe disease and demonstrate that analyzing 5′ UTRs can increase diagnostic yield. We also show how non-coding variants can help inform both the disease-causing mechanism underlying protein-coding variants and dosage tolerance of the gene