THE VIBRATIONAL ANALYSIS OF HALOGEN DERIVATIVES OF METHYLSILANES, AND DIMETHYLARSINE AND DIMETHYLPHOSPHINE.

Source: Dissertation Abstracts International, Volume: 40-04, Section: B, page: 1706. Thesis (Ph.D.)--University of Windsor (Canada), 1979

Obstructive pancreatolithiasis in a cat with triaditis and concurrent hypercalcaemia.

CASE SUMMARY: A 7-year-old neutered female domestic longhair cat was presented for further investigation of suspected hepatobiliary disease. Increases in serum 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester lipase and hepatobiliary enzymes, with concurrent hypoalbuminaemia, were documented on blood biochemistry. Abdominal ultrasonography findings were consistent with acute pancreatitis with multiple pancreatoliths visualised within the pancreatic duct. Treatment for suspected triaditis was initiated with a hydrolysed protein diet, amoxicillin-clavulanate, hepatoprotectants and buprenorphine. Fifty-three days later, the patient presented with hypercalcaemia and obstructive pancreatolithiasis, and was euthanased. Post-mortem examination revealed severe chronic active pancreatitis with moderate chronic lymphocytic, plasmacytic cholangiohepatitis and mild chronic lymphocytic-plasmacytic duodenal enteritis (triaditis). Multiple calcium carbonate pancreatoliths present within the pancreatic ducts had resulted in pancreatic duct obstruction. RELEVANCE AND NOVEL INFORMATION: Pancreatolithiasis is a very rare condition in cats, with only five reports to date. In human medicine, pancreatolithiasis is often a sequala to chronic pancreatitis, seen in up to 50-90% of patients. However, in cats the aetiology of pancreatolithiasis, and indeed chronic pancreatitis, is poorly understood. This report describes a case of obstructive pancreatolithiasis in a cat with histopathological confirmation of triaditis and is the first report of hypercalcaemia in a cat with obstructive pancreatolithiasis. This further adds to the evidence base that pancreatolithiasis may have a similar pathogenesis to humans and can develop secondarily to chronic pancreatitis in cats

Obstructive pancreatolithiasis in a cat with triaditis and concurrent hypercalcaemia.

CASE SUMMARY: A 7-year-old neutered female domestic longhair cat was presented for further investigation of suspected hepatobiliary disease. Increases in serum 1,2-o-dilauryl-rac-glycero-3-glutaric acid-(6'-methylresorufin) ester lipase and hepatobiliary enzymes, with concurrent hypoalbuminaemia, were documented on blood biochemistry. Abdominal ultrasonography findings were consistent with acute pancreatitis with multiple pancreatoliths visualised within the pancreatic duct. Treatment for suspected triaditis was initiated with a hydrolysed protein diet, amoxicillin-clavulanate, hepatoprotectants and buprenorphine. Fifty-three days later, the patient presented with hypercalcaemia and obstructive pancreatolithiasis, and was euthanased. Post-mortem examination revealed severe chronic active pancreatitis with moderate chronic lymphocytic, plasmacytic cholangiohepatitis and mild chronic lymphocytic-plasmacytic duodenal enteritis (triaditis). Multiple calcium carbonate pancreatoliths present within the pancreatic ducts had resulted in pancreatic duct obstruction. RELEVANCE AND NOVEL INFORMATION: Pancreatolithiasis is a very rare condition in cats, with only five reports to date. In human medicine, pancreatolithiasis is often a sequala to chronic pancreatitis, seen in up to 50-90% of patients. However, in cats the aetiology of pancreatolithiasis, and indeed chronic pancreatitis, is poorly understood. This report describes a case of obstructive pancreatolithiasis in a cat with histopathological confirmation of triaditis and is the first report of hypercalcaemia in a cat with obstructive pancreatolithiasis. This further adds to the evidence base that pancreatolithiasis may have a similar pathogenesis to humans and can develop secondarily to chronic pancreatitis in cats

Adventures in boron chemistry – the prediction of novel ultra-flexible boron oxide frameworks

We predict a wide range of ultra-flexible low-energy forms of boron oxides in which rigid B–O–B bridges link boron–oxygen heterocycles.</p

Mechanistic basis of the Cu(OAc)2 catalyzed azide-ynamine (3 + 2) cycloaddition reaction

R.P.B. and G.A.B. thank GSK and the Engineering and Physical Sciences Research Council (EPSRC) for an industrial CASE studentship (EP/P51066X/1). G.A.B., F.P., and A.J.B.W. thank the Leverhulme Trust (RP-2020-380). A.T.S. and G.A.B. thank the Biotechnology and Biological Research Council (BBSRC) for its support (BB/V017586/1; BB/T000627/1). A.J.B.W. and M.J.A. thank the EPSRC for its support (EP/R025754/1). A.J.B.W. thanks the Leverhulme Trust for a Research Fellowship (RF-2022-014).The Cu-catalyzed azide–alkyne cycloaddition (CuAAC) reaction is used as a ligation tool throughout chemical and biological sciences. Despite the pervasiveness of CuAAC, there is a need to develop more efficient methods to form 1,4-triazole ligated products with low loadings of Cu. In this paper, we disclose a mechanistic model for the ynamine-azide (3 + 2) cycloadditions catalyzed by copper(II) acetate. Using multinuclear nuclear magnetic resonance spectroscopy, electron paramagnetic resonance spectroscopy, and high-performance liquid chromatography analyses, a dual catalytic cycle is identified. First, the formation of a diyne species via Glaser–Hay coupling of a terminal ynamine forms a Cu(I) species competent to catalyze an ynamine-azide (3 + 2) cycloaddition. Second, the benzimidazole unit of the ynamine structure has multiple roles: assisting C–H activation, Cu coordination, and the formation of a postreaction resting state Cu complex after completion of the (3 + 2) cycloaddition. Finally, reactivation of the Cu resting state complex is shown by the addition of isotopically labeled ynamine and azide substrates to form a labeled 1,4-triazole product. This work provides a mechanistic basis for the use of mixed valency binuclear catalytic Cu species in conjunction with Cu-coordinating alkynes to afford superior reactivity in CuAAC reactions. Additionally, these data show how the CuAAC reaction kinetics can be modulated by changes to the alkyne substrate, which then has a predictable effect on the reaction mechanism.Peer reviewe

Distribution of cholinergic nerve terminals in the aged human brain measured with [18F]FEOBV PET and its correlation with histological data

Introduction: [18F]fluoroetoxybenzovesamicol ([18F]FEOBV) is a positron emission topography (PET) tracer for the vesicular acetylcholine transporter (VAChT), a protein located predominantly in synaptic vesicles in cholinergic nerve terminals. We aimed to use [18F]FEOBV PET to study the cholinergic topography of the healthy human brain. Materials and methods: [18F]FEOBV PET brain data volumes of healthy elderly humans were normalized to standard space and intensity-normalized to the white matter. Stereotactic atlases of regions of interest were superimposed to describe and quantify tracer distribution. The spatial distribution of [18F]FEOBV PET uptake was compared with histological and gene expression data. Results: Twenty participants of both sexes and a mean age of 73.9 ± 6.0 years, age-range [64; 86], were recruited. Highest tracer binding was present in the striatum, some thalamic nuclei, and the basal forebrain. Intermediate binding was found in most nuclei of the brainstem, thalamus, and hypothalamus; the vermis and flocculonodular lobe; and the hippocampus, amygdala, insula, cingulate, olfactory cortex, and Heschl's gyrus. Lowest binding was present in most areas of the cerebral cortex, and in the cerebellar nuclei and hemispheres. The spatial distribution of tracer correlated with immunohistochemical post-mortem data, as well as with regional expression levels of SLC18A3, the VAChT coding gene. Discussion: Our in vivo findings confirm the regional cholinergic distribution in specific brain structures as described post-mortem. A positive spatial correlation between tracer distribution and regional gene expression levels further corroborates [18F]FEOBV PET as a validated tool for in vivo cholinergic imaging. The study represents an advancement in the continued efforts to delineate the spatial topography of the human cholinergic system in vivo

Mechanistic basis of the Cu(OAc)2 catalyzed azide-ynamine (3+2)cycloaddition reaction

The Cu-catalyzed azide-alkyne cycloaddition (CuAAC) reaction is used as a ligation tool throughout the chemical and biological sciences. Despite the pervasiveness of the CuAAC, there is a need to develop more efficient methods to form 1,4-triazole ligated products with low loadings of Cu. In this manuscript, we disclose a mechanistic model for the ynamine-azide (3+2)cycloadditions catalyzed by copper(II) acetate. Using multinuclear NMR spectroscopy, EPR spectroscopy and HPLC analyses, a dual catalytic cycle is identified. First, the formation of a diyne species via Glaser-Hay coupling of a terminal ynamine forms a Cu(I) species competent to catalyze an ynamine-azide (3+2)cycloaddition. Second, the benzimidazole unit of the ynamine structure effects multiple roles: assisting C-H activation, Cu-coordination and the formation of a post-reaction resting state Cu complex after completion of the (3+2)cycloaddition. Finally, reactivation of the Cu resting state complex is shown by addition of isotopically labelled ynamine and azide substrates to form a labelled 1,4-triazole product. This work provides a mechanistic basis for the use of mixed valency binuclear catalytic Cu species in conjunction with Cu-coordinating alkynes to afford superior reactivity in CuAAC reactions. Additionally, these data show how the CuAAC reaction kinetics can be modulated by changes to the alkyne substrate, which then has a predictable impact on the reaction mechanism