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Conservation laws are deeply related to any symmetry present in a physical system1,2. Analogously to electrons in atoms exhibiting spin symmetries3, it is possible to consider neutrons and protons in the atomic nucleus as projections of a single fermion with an isobaric spin (isospin) of t = 1/2 (ref. 4). Every nuclear state is thus characterized by a total isobaric spin T and a projection Tz—two quantities that are largely conserved in nuclear reactions and decays5,6. A mirror symmetry emerges from this isobaric-spin formalism: nuclei with exchanged numbers of neutrons and protons, known as mirror nuclei, should have an identical set of states7, including their ground state, labelled by their total angular momentum J and parity π. Here we report evidence of mirror-symmetry violation in bound nuclear ground states within the mirror partners strontium-73 and bromine-73. We find that a J π = 5/2− spin assignment is needed to explain the proton-emission pattern observed from the T = 3/2 isobaric-analogue state in rubidium-73, which is identical to the ground state of strontium-73. Therefore the ground state of strontium-73 must differ from its J π = 1/2− mirror bromine-73. This observation offers insights into charge-symmetry-breaking forces acting in atomic nuclei. Observations of the decay of 73Sr, when compared to its mirror nucleus 73Br, indicate that the spin assignment of their ground states differ, demonstrating mirror-symmetry violation. [ABSTRACT FROM AUTHOR]

The temperature in the crust of an accreting neutron star, which comprises its outermost kilometre, is set by heating from nuclear reactions at large densities, neutrino cooling and heat transport from the interior. The heated crust has been thought to affect observable phenomena at shallower depths, such as thermonuclear bursts in the accreted envelope. Here we report that cycles of electron capture and its inverse, β− decay, involving neutron-rich nuclei at a typical depth of about 150 metres, cool the outer neutron star crust by emitting neutrinos while also thermally decoupling the surface layers from the deeper crust. This 'Urca' mechanism has been studied in the context of white dwarfs and type Ia supernovae, but hitherto was not considered in neutron stars, because previous models computed the crust reactions using a zero-temperature approximation and assumed that only a single nuclear species was present at any given depth. The thermal decoupling means that X-ray bursts and other surface phenomena are largely independent of the strength of deep crustal heating. The unexpectedly short recurrence times, of the order of years, observed for very energetic thermonuclear superbursts are therefore not an indicator of a hot crust, but may point instead to an unknown local heating mechanism near the neutron star surface. [ABSTRACT FROM AUTHOR]

Excited states in the neutron-rich 121, 123, 125Ag were studied via the fragmentation of a 136Xe beam at 120MeV/nucleon in a thick 9Be target. The levels in 121Ag were populated in the $ \beta$ decay of 121Pd while those assigned to 123, 125Ag were identified via isomer spectroscopy. The transitions identified in 121Ag are consistent with the $ \gamma$ -rays reported in 117, 119Ag . The newly observed transitions were placed in the level schemes of 123, 125Ag based on the analysis of $ \gamma$ - $ \gamma$ coincidences and the systematics. We attribute the onset of isomerism in the 123, 125Ag isotopes to the drop in energy of the negative-parity levels similar to the 5- state in the even-even Cd cores. The proposed level scheme for 125Ag is well described by the NuShellX shell model calculations. [ABSTRACT FROM AUTHOR]

Decay properties of neutron-deficient exotic nuclei close to A=80 have been investigated at the IGISOL facility. The studied nuclei, 81Y, 81Sr, 81mKr, 85Nb, 85Zr, 86Mo and 86Nb, were produced by a 32S beam from the Jyväskylä isochronous cyclotron on 54Fe and natNi targets. The internal conversion coefficient for a 190.5 keV isomeric transition in 81mKr has been measured and the internal transition rate has been determined. The internal transition rate has been used to estimate a neutrino capture rate on 81Br, which yields a log ft of 5.13±0.09 for the reaction 81Br( ν, e-)81mKr. A new isomer with a half-life of 3.3±0.9 s has been observed in 85Nb. The existence of an earlier reported isomer with a half-life of 56 s in 86Nb has not been confirmed. [ABSTRACT FROM AUTHOR]

Despite a lot of experimental and theoretical progress the question of the r-process site and the origin of the heavy elements in nature remains one of the biggest open questions in nuclear astrophysics. We report first results from experiments with rare isotope beams of r-process nuclei at Michigan State University’s National Superconducting Cyclotron Laboratory. This includes a first measurement of the half-life of the doubly-magic waiting point nucleus 78Ni, which serves as a major bottle-neck for the synthesis of heavy elements in many r-process models. [ABSTRACT FROM AUTHOR]

Transforming growth factor β1 (TGFβ1) is a multifunctional growth factor involved in immune function, atherosclerosis, fibrotic disease, diabetic complications and bone turnover. It is synthesized in large quantities by bone cells in response to hormones and mechanical stimuli. Plasma contains inactive "latent" TGFβ1, which consists of the precursor molecule and a TGFβ1-binding protein. Platelets store latent TGFβ1 in their α-granules, and serum therefore contains large amounts of latent TGFβ1. We developed a technique for determining latent plasma TGFβ1 and investigated whether circulating TGFβ1 is affected by the stimulation of bone formation in response to strength training. Ten healthy students with low training activity participated in a heavy exercise programme over 4 weeks. Blood was drawn into citrate-filled syringes containing prostaglandin E1 (PGE1) and immediately centrifuged at 4°C. TGFβ1 was determined with a sandwich ELISA standardized with National Institute for Biological Standards and Controls (NIBSC) materials. Six of the ten students completed the training. Highly reproducible values (500–600 pg/ml) of latent TGFβ1 in plasma were determined. Baseline levels of TGFβ1 were 525 (50) pg/ml [mean (SE)], which is in the range observed for young adults. TGFβ1 concentrations rose significantly to 710 (65) pg/ml after 2 weeks of training and thereafter slowly declined to 650 (62) pg/ml after 2 weeks and 440 (33) pg/ml after 4 weeks, respectively. No active TGFβ1 was detectable in citrate PGE1 plasma samples. Serum levels were between 6000 and 10,000 pg/ml and contained 200–400 pg/ml active TGFβ1. In contrast to previous reports, plasma did not contain measurable amounts of circulating active TGFβ1. We demonstrate that heavy exercise transiently elevates latent TGFβ1 concentrations in plasma. TGFβ1 is produced by osteoblasts in considerable amounts; therefore, we assume that the observed changes are partly due to enhanced TGFβ1 production or release in bone, since the quantities of TGFβ1 produced by other cells are comparably small. [ABSTRACT FROM AUTHOR]

A careful investigation of the isomeric transition of the long-lived state at 228.5 keV excitation energy in 80Y has been done. The HIGISOL facility at the Jyväskylä isochronous cyclotron has been used. We used the electron magnetic transporter to prepare an appropriate source and to measure the electron spectra in clean background conditions. The measured internal conversion coefficient αK = 0.50±0.07 allows unambiguous 1- identification for the 228.5 keV first excited isomeric state in 80Y. With a “bare" half-life of 6.8±0.5 s found in this work, this state is strongly populated in the rp-process during X-ray bursts and has therefore to be taken into account in X-ray burst model calculations. However, because of the similarity of the β-decay half-lives of isomeric and ground states, we find a maximum reduction in the effective β-decay lifetime of 80Y of only 17±2%. Our results pave the way for a future investigation of the impact of the isomeric state on the “effective" 80Y proton capture rate. [ABSTRACT FROM AUTHOR]

Aims/hypothesis. Postprandial hyperglycaemia carries an increased risk of macrovascular disease even without Type II (non-insulin-dependent) diabetes mellitus. Chronic hyperglycaemia activates protein kinase C (PKC) in vitro and in vivo but it is not known whether PKC is regulated by short-term postprandial hyperglycaemia in vivo in humans. We investigated whether PKC is regulated in vivo in hyperglycaemic and hyperinsulinaemic infusion tests and correlated the results to stimulations in vitro. Methods. Protein kinase C regulation was measured in platelets obtained from 8 healthy subjects who were infused with glucose and insulin for 2 h attaining peak concentrations of 16 mmol/l glucose and in platelets from 8 healthy young subjects, 8 older subjects without diabetes, and 10 older subjects with Type II diabetes after incubation in vitro with 16 mmol/l glucose or glucose and insulin. For precise quantification, a shortened PKC β1 standard protein was generated by bacterial expression and PKC α, β1, β2 and δ isoenzyme values were measured by immunoblot analyses. Results. Hyperglycaemic and hyperinsulinaemic in vivo tests increased the amounts of PKC α, β1 and β2 in the membrane fraction of platelets to 225 ± 87 %, 164 ± 22 % and 302 ± 135 %, respectively, when compared with the baseline values in young healthy volunteers (n = 8, p < 0.05). The expression of PKC δ did not change. In comparison to the recombinant PKC β1 standard protein, 5 ng PKC β1/μg protein was measured before the test and 2 ng/μg were translocated to the membrane fraction after the infusion. No change in the absolute amount of PKC β1 was detected. In contrast, after incubation in vitro PKC was not regulated by glucose or glucose and insulin in 8 young healthy subjects (age 26 ± 0.7 years) and in 8 older, healthy subjects (age 64,8 ± 4 years) although 100 nmol/l 12-O-tetradecanoylphorbol 13-acetate caused maximal activation. In marked contrast, PKC β1 and PKC β2, but not PKC α or PKC δ, were increased in vitro in the membrane fraction by 292 ± 61 % and 432 ± 88 % (p < 0.05) in 10 subjects with Type II diabetes mellitus matched for age, sex and BMI. Conclusion/interpretation. We found that short-term hyperglycaemia activates PKC α, β1 and β2 in platelets of healthy persons making them potential candidates for mediating the increased cardiovascular risk of postprandial hyperglycaemia. Hyperglycaemia and hyperinsulinaemia did not cause short-term activation of PKC in platelets in vitro suggesting the existence of additional stimuli. Subjects with Type II diabetes showed a markedly altered reactivity of platelet PKC β in vitro indicating some diabetes-related regulation. [Diabetologia (2001) 44: 188–195] [ABSTRACT FROM AUTHOR]

We report on a 69-year-old woman who presented with myalgia, hearing impairment, fever, night sweats, weight loss, muscular weakness, paresthesia, hypesthesia, and hypalgesia. Sural nerve biopsy showed demyelinative and axonal polyneuropathy due to necrotizing vasculitis with fibrinoid necrosis. A positive test for antineutrophil cytoplasmic antibodies (ANCA) with a perinuclear immunofluorescence pattern directed against myeloperoxidase was more suggestive of microscopic polyangiitis (MPA) than of polyarteritis nodosa (PAN), the possible differential diagnoses. In addition, positive tests for cytomegalovirus (CMV) antibodies (immunoglobulin (Ig)M and IgG) and the detection of CMV-DNA in sputum specimens by polymerase chain reaction (PCR) were indicative of active CMV infection. Treatment with ganciclovir and anti-CMV immunoglobulin in addition to prednisolone medication for 6 months resulted in rapid improvement of the clinical symptoms without relapse. CMV infection has been described to be related to ANCA-associated vasculitis in non-immunocompromized patients and may be either a causative agent or an opportunistic infection. Identification of a viral etiology in patients with atypical ANCA-associated vasculitides may lead to different, less aggressive treatment approaches, including antiviral therapy. [ABSTRACT FROM AUTHOR]

Aims/hypothesis. Proliferative diabetic retinopathy is a major debilitating disease causing most cases of blindness in humans in the Western world. Photocoagulation is the established therapy of proliferative diabetic retinopathy, although the molecular mechanisms of its effects are still not known. Recently angiostatin has been characterized as a potent inhibitor of neovascularization. Apart from a possible down-regulation of angiogenic cytokines, release of angiostatin could initiate the anti-angiogenic effects of retinal photocoagulation.¶Methods. We investigated the regulation of angiostatin and the angiogenic cytokines vascular endothelial growth factor and basic fibroblast growth factor in vivo by comparing vitreal concentrations of 18 control patients and 34 patients with proliferative diabetic retinopathy with and without previous photocoagulation. Concentrations of basic fibroblast growth factor and angiostatin were additionally measured in serum, while vascular endothelial growth factor is known to be regulated locally in the eye. Cytokines were measured by immunological methods.¶Results. Angiostatin could be detected in 2 out of 18 control patients and in 25 out of 34 diabetic patients (p < 0.00 001). Most importantly, production of angiostatin in human vitreous correlated significantly with previous retinal photocoagulation (p < 0.0001) in patients with proliferative diabetic retinopathy. Only two patients (one control and one diabetic) had detectable serum concentrations of angiostatin. Additionally patients with proliferative diabetic retinopathy and with previous photocoagulation had significantly lower concentrations of vascular endothelial growth factor (0.9 ± 0.1 ng/ml; p < 0.0001) than diabetic patients without previous photocoagulation (4.0 ± 0.8 ng/ml). The investigation of vitreal and serum basic fibroblast growth factor concentrations yielded no significant differences between the groups.¶Conclusion/interpretation. Angiostatin is not a regularly expressed angiogenesis inhibitor in human vitreous. The alterations we observed suggest that local release of angiostatin and down-regulation of vascular endothelial growth factor mediate the therapeutic effects of retinal photocoagulation in proliferative diabetic retinopathy. [Diabetologia (2000) 43: 1404–1407] [ABSTRACT FROM AUTHOR]

Aims/hypothesis. The Ca2+/calmodulin-dependent protein kinase II (CaMK II) is highly expressed in pancreatic islets and associated with insulin secretion vesicles. The suppression of CaMK II disturbs insulin secretion and insulin gene expression. There are four isoforms of CaMK II, α to δ, that are expressed from different genes in mammals. Our aim was to identify the isoforms of CaMK II expressed in human beta cells by molecular cloning from a human insulinoma cDNA library and to assess its distribution in humans.¶Methods. The previously unknown complete coding sequences of human CaMK IIβ and the kinase domain of CaMK IIδ were cloned from a human insulinoma cDNA library. Quantitative determination of CaMK II isoform mRNA was carried out in several tissues and beta cells purified by fluorescence activated cell sorting and compared to the housekeeping enzyme pyruvate dehydrogenase.¶Results. We found CaMK IIβ occurred in three splice variants and was highly expressed in endocrine tissues such as adrenals, pituitary and beta cells. Liver showed moderate expression but adipose tissue or lymphocytes had very low levels of CaMK IIβ-mRNA. In human beta cells CaMK IIβ and δ were expressed equally with pyruvate dehydrogenase whereas tenfold lower expression of CaMK IIγ and no expression of CaMK IIα were found.¶Conclusion/interpretation. Although CaMK IIδ is ubiquitously expressed, CaMK IIβ shows preferential expression in neuroendocrine tissues. In comparison with the expression of a key regulatory enzyme in glucose oxidation, pyruvate dehydrogenase, two of the four CaM kinases investigated are expressed at equally high levels, which supports an important role in beta-cell physiology. These results provide the basis for exploring the pathophysiological relevance of CaMK IIβ in human diabetes. [Diabetologia (2000) 43: 465–473] [ABSTRACT FROM AUTHOR]

Focuses on the oribatid mites of the Galápagos Islands. Occurrence of mites from the littoral zones of the Island; Ecological conditions required by oribatid mites for survival; Description of speciation in mites.

Genetic susceptibility contributes significantly to the risk of developing nephropathy in insulin-dependent diabetes mellitus (IDDM). The cellular substrate for this has remained enigmatic. We investigated whether afflicted IDDM patients display an enhanced activation of pertussis toxin (PTX)-sensitive G proteins, a phenomenon which has been demonstrated in patients with essential hypertension. We established immortalised B lymphoblast cell lines from 10 IDDM patients without nephropathy (DC) and 15 IDDM patients with nephropathy (DN). Nephropathy was defined as a persistent albumin excretion rate of more than 20 μg/min (DC 3.9 ± 5.8, DN 562.3 ± 539.0 μg/min, respectively). Subjects were matched with regard to age (DC 28.9 ± 6.5, DN 35.9 ± 9.9 years), diabetes duration (DC 19.3 ± 6.9, DN 22.7 ± 5.8 years) and HbA1 c values (DC 8.5 ± 1.4, DN 8.8 ± 1.6 %). Reactivity of PTX-sensitive G proteins was quantified by measuring platelet-activating factor (PAF)-induced Ca2 + mobilisation (fura 2 method) and by mastoparan-stimulated [35S]GTP γS binding. Expression of Gαi proteins was quantified by Western blot analysis. PAF-evoked Ca2 + increases above baseline averaged 77.0 ± 52.5 nmol/l in DC and 150.7 ± 61.5 nmol/l in DN ( p = 0.005). PAF-evoked Ca2 + increases correlated with stimulated [35S]GTP γS binding ( r 2 = 0.42, p = 0.012). From Western blot analysis an overexpression of Gαi proteins could be excluded in DN. A consequence of the altered metabolic milieu in diabetes is the increased release of vasoactive and proliferative agonists which promote glomerular hyperfiltration, hypertrophy, enhanced matrix deposition, and, finally, glomerulosclerosis. Many of these auto- and paracrine agonists bind to G protein-coupled receptors. Therefore, their cellular effects are reinforced by the enhanced G protein reactivity and increase the propensity to nephropathy in IDDM. [Diabetologia (1998) 41: 94–100] [ABSTRACT FROM AUTHOR]

Long term feeding of a sucrose rich diet to rats is accompanied by a decreased glucose assimilation rate, despite high plasma insulin levels. Hyperinsulinism is at least partially based on a relative obesity, with increased amounts of abdominal- and retroperitoneal fat tissue, but unchanged total body weight compared to starch fed controls. The secretory pattern of insulin release was studied following glucose, arginine, fructose and sulfonylurea administration in the isolated perfused pancreas of sucrose and isocaloric starch fed rats. In addition, isolated islets of Langerhans were used to demonstrate the effects of glucose on insulin secretion and the incorporation of H-3 leucine into the proinsulin and insulin fraction of islet proteins. Following 11 mM glucose, the dynamics of insulin release in the isolated perfused pancreas of sucrose fed rats is characterized by a markedly elevated, late plateau-like response, usually seen only at higher glucose concentrations. Hyperinsulinism, as compared to starch fed controls, can also be demonstrated following arginine and the sulfonylurea HB-419, whereas fructose has no effect in the presence of low glucose concentrations. During incubation of the pancreatic islets, the hyperinsulinism in sucrose-, compared to starch fed rats, is more pronounced at 11 mM glucose than at 5.5 mM glucose. The incorporation of H-3 leucine into the proinsulin-insulin fraction of islet proteins in sucrose compared to starch fed rats, however, is significantly greater with glucose 5.5 mM than at high glucose level. In sucrose fed rats, secretion and biosynthesis of insulin thus appear to be elevated but closely linked only at physiological glucose concentration. [ABSTRACT FROM AUTHOR]

In this paper, we discuss the astrophysically relevant nuclear-physics input for a selected set of explosive nucleosynthesis scenarios leading to rapid protonand neutron-capture processes. Observables (like, e.g., luminosity curves or abundance distributions) witness the interplay between nuclear-structure aspects far from β-stability and the appropriate astrophysical environments, and can give guidance to and constraints on stellar conditions and/or key features of reaction and decay data for radioactive isotopes. [ABSTRACT FROM AUTHOR]

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

We report on the occurrence of CSF rhinorrhea in a group of 17 patients harbouring macroprolactinomas who were treated with a dopamine agonist (DA, bromocriptine) alone or the combination of DA and transcranial operation. In 2 out of 17 cases shrinkage of tumour remnants during therapy with the oral or injectable form of bromocriptine was responsible for delayed occurrence of rhinorrhea. Operative procedures for successfull closure of the fistulae were mandatory in both cases. [ABSTRACT FROM AUTHOR]

Osteocalcin serum levels reflect bone turnover. In renal insufficiency secondary hyperparathyroidism and reduced renal clearance might be responsible for elevated serum levels of osteocalcin. Renal transplantation might improve renal osteodystrophy and therefore could influence osteocalcin serum levels. We determined the influence of renal transplantation on osteocalcin levels in 37 consecutive patients (25m/12f) by RIA. Blood samples were collected prior to, 3 days, 28 days, 6 months and 12 months after renal transplantation. Prior to renal transplantation osteocalcin levels were significantly elevated ( x± s: 23.4±12.8 ng/ml) compared to healthy volunteers (4.1±1.4 ng/ml). Following renal transplantation osteocalcin decreased significantly (9.4±8.9 ng/ml) 3 days and (7.1±7.8 ng/ml) 28 days. However, 6 and 12 months following renal transplantation the mean osteocalcin level increased again (8.3±5.7 ng/ml, 12.1±15.4 ng/ml). At 6 months 11 and at 12 months only 6 of 37 patients had osteocalcin levels in the normal range. 12 months following renal transplantation 21 out of 37 patients with elevated osteocalcin levels had parathyroid hormone levels above the normal range. Additionally to increased osteocalcin levels patients prior to renal transplantation had elevated alkaline phosphatase. Alkaline phosphatase had following renal transplantation a similar pattern as osteocalcin with initial decrease and secondary increase 6 and 12 months after renal transplantation. Parathyroid hormone was elevated in all patients before renal transplantation. Following renal transplantation mean parathyroid hormone levels fell significantly, however remained above normal range in 57% of these 37 patients. Osteocalcin serum levels correlated positively with alkaline phosphatase ( rs=0.43−0.62; p<0.011) and parathyroid hormone (0.3−0.66 p<0.07). This correlation of osteocalcin with alkaline phosphatase and parathyroid hormone prior to and after renal transplantation suggests that osteocalcin may be a confirmative parameter in renal osteodystrophy in patients on chronic intermittent hemodialysis and following renal transplantation. [ABSTRACT FROM AUTHOR]

The decoupling of bone formation and bone resorption causes an insidious bone loss that is responsible for the negative skeletal balance in the frequent form of low turnover osteoporosis. The reduction of bone formation can hardly be verified by clinical methods. Osteocalcin, a non-collagenous bone protein, has proved to be a useful new indicator of bone formation. To establish its predictable value, plasma levels of osteocalcin were compared to conventional serological data of bone turnover and to histomorphometric parameters of iliac crest trabecular bone. In cases of osteoporosis with normal bone turnover activity (as confirmed by histomorphometry) no differences were observed in any of our laboratory data including osteocalcin. However, there was a significant lower mean serum level of osteocalcin in a group of patients with histomorphometrically proven low turnover osteoporosis in comparison to those with normal bone turnover. Serum levels of osteocalcin below 2.0 ng/ml seem to indicate a low turnover in the individual case of osteoporosis while this is unlikely when serum levels above 6.0 ng/ml are measured (according to our RIA). [ABSTRACT FROM AUTHOR]

Insulin secretion and biosynthesis of proinsulin and insulin were determined in isolated pancreatic islets of hypophysectomized rats. Control rats were of both same age and weight. Hypophysectomy was performed either 13 or 5 weeks prior to the investigation, the weight of the animals being either 80 or 170 g. Biosynthesis of insulin was estimated from the amounts of radioactivity incorporated into proinsulin and insulin after incubation of isolated islets at 50 or 300 mg% glucose in the presence ofH-leucine for 3 h. Islet proteins were separated on Sephadex G 50 fine. - Hypophysectomy resulted in a significant decrease of both glucose stimulated secretion and biosynthesis of insulin. It was found that this reduction was 1) more significant when compared with controls of same age 2) more marked in rats which had been hypophysectomized 13 weeks before than in rats after an interval of 5 weeks and 3) less in rats which had been hypophysectomized at a weight of 170 g than in rats in whom pituitary ablation was performed at a weight of 80 g. At basal glucose concentrations, no significant changes of both secretion and biosynthesis of insulin were apparent. The relation of radioactivity incorporated into proinsulin and insulin was unchanged under all conditions. Insulin content of the isolated islets used was found within about the same range in all rats, apart from the animals which had been hypophysectomized 13 weeks before. In islets of these rats, a reduction to 84% was observed. - Our findings may be explained by reduced sensitivity of the pancreatic B-cell to glucose and a slower rate of insulin biosynthesis after hypophysectomy. [ABSTRACT FROM AUTHOR]

Copyright of Diabetologia is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Diabetologia is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Humangenetik (00187348) is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

With the aim of improving nucleosynthesis calculations, we performed for the first time, a direct high-precision mass measurement on the waiting point in the astrophysical rp-process 72Kr. We used the ISOLTRAP Penning trap mass spectrometer located at ISOLDE/CERN. The measurement yielded a relative mass uncertainty of δ m/ m = 1.2×10-7. In addition, the masses of 73Kr and 74Kr were measured directly with relative mass uncertainties of 1.0×10-7 and 3×10-8, respectively. We analyzed the role of 72Kr in the rp-process during X-ray bursts using the ISOLTRAP and previous mass values of 72-74Kr. [ABSTRACT FROM AUTHOR]

: Although infectious agents such as Staphylococcus aureus have been implicated in the pathogenesis of Wegener’s granulomatosis, the role of bacterial infections in the pathogenesis of other types of small-vessel vasculitides associated with antineutrophil cytoplasmic antibodies (ANCA) is less clear. We describe a patient who developed a non-granulomatous necrotising small vessel vasculitis and perinuclear ANCA (p-ANCA) directed against myeloperoxidase (MPO) after recurrent episodes of bacterial endocarditis due to Staph. aureus. Although cytoplasmic ANCA (c-ANCA) directed against proteinase 3 have been reported in single patients with bacterial endocarditis, to our knowledge this patient is the first reported case of an anti-MPO-ANCA positive systemic vasculitis following bacterial endocarditis. [ABSTRACT FROM AUTHOR]

A series of beta decay experiments on nuclei near the Z = N line has been performed using the ISOL technique at the IGISOL facility in Jyväskylä and at ISOLDE, CERN. The decay properties of these neutron-deficient nuclei are important in astrophysics as well as in the studies of isospin symmetry. [ABSTRACT FROM AUTHOR]