1,628 research outputs found
A First Class Constraint Generates Not a Gauge Transformation, But a Bad Physical Change: The Case of Electromagnetism
No full textIn Dirac-Bergmann constrained dynamics, a first-class constraint typically does not _alone_ generate a gauge transformation. By direct calculation it is found that each first-class constraint in Maxwell's theory generates a change in the electric field E by an arbitrary gradient, spoiling Gauss's law. The secondary first-class constraint p^i,_i=0 still holds, but being a function of derivatives of momenta, it is not directly about E (a function of derivatives of A_mu). Only a special combination of the two first-class constraints, the Anderson-Bergmann (1951)-Castellani gauge generator G, leaves E unchanged. This problem is avoided if one uses a first-class constraint as the generator of a _canonical transformation_; but that partly strips the canonical coordinates of physical meaning as electromagnetic potentials and makes the electric field depend on the smearing function, bad behavior illustrating the wisdom of the Anderson-Bergmann (1951) Lagrangian orientation of interesting canonical transformations.
The need to keep gauge-invariant the relation dot{q}- dH/dp= -E_i -p^i=0 supports using the primary Hamiltonian rather than the extended Hamiltonian. The results extend the Lagrangian-oriented reforms of Castellani, Sugano, Pons, Salisbury, Shepley, _etc._ by showing the inequivalence of the extended Hamiltonian to the primary Hamiltonian (and hence the Lagrangian) even for _observables_, properly construed in the sense implying empirical equivalence.
Dirac and others have noticed the arbitrary velocities multiplying the primary constraints outside the canonical Hamiltonian while apparently overlooking the corresponding arbitrary coordinates multiplying the secondary constraints _inside_ the canonical Hamiltonian, and so wrongly ascribed the gauge quality to the primaries alone, not the primary-secondary team G. Hence the Dirac conjecture about secondary first-class constraints rests upon a false presupposition. The usual concept of Dirac observables should also be modified to employ the gauge generator G, not the first-class constraints separately, so that the Hamiltonian observables become equivalent to the Lagrangian ones such as the electromagnetic field F
Bergmann–Lebowitz model and adaptive resolution simulation
No full textThis article deals with the molecular dynamics simulation of open systems that
can exchange energy and matter with a reservoir; the physics of the reservoir
and its interactions with the system are described by the model introduced by
Bergmann and Lebowitz (P G Bergmann and J L Lebowitz 1955 Phys. Rev. 99 578).
Despite its conceptual appeal, the model did not gain popularity in the field
of molecular simulation and, as a consequence, did not play a role in the
development of open system molecular simulation techniques, even though it can
provide the conceptual legitimation of simulation techniques that mimic open
systems. We shall demonstrate that the model can serve as a tool in devising
both numerical procedures and conceptual definitions of physical quantities
that cannot be defined in a straightforward way by systems with a fixed number
of molecules. In particular, we discuss the utility of the Bergmann–Lebowitz
(BL) model for the calculation of equilibrium time correlation functions
within the grand canonical adaptive resolution method (GC-AdResS) and report
numerical results for the case of liquid water
Molecular dynamics in a grand ensemble: Bergmann-Lebowitz model and adaptive resolution simulation
No full textThis article deals with the molecular dynamics simulation of open systems that can exchange energy and matter with a reservoir; the physics of the reservoir and its interactions with the system are described by the model introduced by Bergmann and Lebowitz (P G Bergmann and J L Lebowitz 1955 Phys. Rev. 99 578). Despite its conceptual appeal, the model did not gain popularity in the field of molecular simulation and, as a consequence, did not play a role in the development of open system molecular simulation techniques, even though it can provide the conceptual legitimation of simulation techniques that mimic open systems. We shall demonstrate that the model can serve as a tool in devising both numerical procedures and conceptual definitions of physical quantities that cannot be defined in a straightforward way by systems with a fixed number of molecules. In particular, we discuss the utility of the Bergmann-Lebowitz (BL) model for the calculation of equilibrium time correlation functions within the grand canonical adaptive resolution method (GC-AdResS) and report numerical results for the case of liquid water.Deutsche Forschungsgemeinschaft (DFG); Heisenberg grant [DE 1140/5-2]; DFG grant [DE 1140/7-1]; National High Technology Research and Development Program of China [2015AA011201]; North German Supercomputing Alliance (HLRN) [bec00100]; Heisenberg grant; [CRC 1114]SCI(E)[email protected]
Tectonic gene mutations in patients with Joubert syndrome
No full textSo far very few patients with sequence variants in the closely related tectonic genes TCTN1-3 have been described. By multi-gene panel next-generation sequencing (NGS) in patients with Joubert syndrome, we identified two more patients and summarize what is currently known about the phenotypes associated with sequence variants in these genes. In a boy aged 12 years with intellectual disability and the classical molar tooth sign on MRI, a homozygous splice-site sequence variant in TCTN3 leading to in-frame skipping of exon 7 was detected. A previously described non-truncating sequence variant in TCTN3 was also associated with Joubert syndrome, whereas four truncating sequence variants were detected in patients with Meckel-Gruber or Mohr-Majewski syndrome. The second patient, a boy aged 7 years with severe psychomotor retardation, was found to carry a homozygous canonic splice-site sequence variant in TCTN2. So far, only three sequence variants associated with Joubert syndrome and two with Meckel-Gruber syndrome have been described in this gene. Reviewing the clinical data on patients with sequence variants in the tectonic genes TCTN1-3 reveals that all of them have a neurological phenotype with vermis hypoplasia or occipital encephalocele associated with severe intellectual disability in the surviving patients. In contrast, other features frequently seen in patients with ciliopathies such as nephronophthisis, liver fibrosis, retinal dystrophy or coloboma have not been reported. Our patients emphasize the usefulness and efficacy of a comprehensive NGS panel approach. A concise genetic diagnosis may help to prevent unnecessary investigations and improve the clinical management of these patients
Gustav Bergmann, New Foundations of Ontology
No full textThe formal ontology here presented is what we might call a typed combinatorial Meinongian mereology. Its author seeks to formulate the laws, here called ‘canons’, regulating how entities can combine together in wholes of different sorts. The method, as in Bergmann’s earlier works, involves the construction of an ideal language of such a sort that the analysis of complex wholes can be achieved by transforming our natural-language representations of reality into what we might think of as artificial characteristic maps or diagrams which allow the relevant ontological structures to be read off immediately from the symbolic representations which results. In former works Bergmann had held that the symbolic language of Principia Mathematica could serve as the appropriate diagrammatic device for the standard first-order functional calculus and develops instead a new sort diagrammatic languag
Testing Mechanisms of Bergmann's Rule: Phenotypic Decline but No Genetic Change in Body Size in Three Testing Mechanisms of Bergmann's Rule: Phenotypic Decline but No Genetic Change in Body Size in Three Passerine Bird Populations
No full textJSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact [email protected]. abstract: Bergmann's rule predicts a decrease in body size with increasing temperature and has much empirical support. Surprisingly, we know very little about whether "Bergmann size clines" are due to a genetic response or are a consequence of phenotypic plasticity. Here, we use data on body size (mass and tarsus length) from three long-term ) study populations of great tits (Parus major) that experienced a temperature increase to examine mechanisms behind Bergmann's rule. We show that adult body mass decreased over the study period in all populations and that tarsus length increased in one population. Both body mass and tarsus length were heritable and under weak positive directional selection, predicting an increase, rather than a decrease, in body mass. There was no support for microevolutionary change, and thus the observed declines in body mass were likely a result of phenotypic plasticity. Interestingly, this plasticity was not in direct response to temperature changes but seemed to be due to changes in prey dynamics. Our results caution against interpreting recent phenotypic body size declines as adaptive evolutionary responses to temperature changes and highlight the importance of considering alternative environmental factors when testing size clines. The University of Chicago Press an
Vier Bausteine. Prävention, Kondition, Torwarttraining, Taktik
No full textBrandwein A, Johanning C, Bsufka M, Kache C, Ludwig J, Bergmann F. Vier Bausteine. Prävention, Kondition, Torwarttraining, Taktik. Fussballtraining. Praxis-Plus. 2017;57(1/2):2-15
Congenital Hyperinsulinism in Humans and Insulin Secretory Dysfunction in Mice Caused by Biallelic DNAJC3 Variants
No full textThe BiP co-chaperone DNAJC3 protects cells during ER stress. In mice, the deficiency of DNAJC3 leads to beta-cell apoptosis and the gradual onset of hyperglycemia. In humans, biallelic DNAJC3 variants cause a multisystem disease, including early-onset diabetes mellitus. Recently, hyperinsulinemic hypoglycemia (HH) has been recognized as part of this syndrome. This report presents a case study of an individual with HH caused by DNAJC3 variants and provides an overview of the metabolic phenotype of individuals with HH and DNAJC3 variants. The study demonstrates that HH may be a primary symptom of DNAJC3 deficiency and can persist until adolescence. Additionally, glycemia and insulin release were analyzed in young DNACJ3 knockout (K.O.) mice, which are equivalent to human infants. In the youngest experimentally accessible age group of 4-week-old mice, the in vivo glycemic phenotype was already dominated by a reduced total insulin secretion capacity. However, on a cellular level, the degree of insulin release of DNAJC3 K.O. islets was higher during periods of increased synthetic activity (high-glucose stimulation). We propose that calcium leakage from the ER into the cytosol, due to disrupted DNAJC3-controlled gating of the Sec61 channel, is the most likely mechanism for HH. This is the first genetic mechanism explaining HH solely by the disruption of intracellular calcium homeostasis. Clinicians should screen for HH in DNAJC3 deficiency and consider DNAJC3 variants in the differential diagnosis of congenital hyperinsulinism
Identifizierung von Interaktionspartnern des Polyductin-Proteins für die autosomal-rezessive polyzystische Nierenerkrankung (ARPKD) mittels Yeast-Two-Hybrid-Verfahren
No full textCharakterisierung der Interaktion zwischen dem Usher-Syndrom-Protein Harmonin und dem ARPKD-Zystennierenprotein Polyductin
No full textCilia are hair-like structures that extend from the surface of epithelial cells. Human diseases referred to as ciliopathies arise from defects in cilia function. Autosomal recessive polycystic kidney disease (ARPKD), the most frequent cause of hereditary cystic kidney disease in infancy and childhood, and Usher syndrome, the most frequent hereditary cause for combined deaf-blindness, are two important ciliopathies. Senior-Løken syndrome as another ciliopathy affects both organs, the kidney and the eye. The characterization of protein-protein-interactions is of particular interest for the understanding of ciliopathies. The intention of this thesis was to characterize the interaction between the ARPKD protein Polyductin and the Usher syndrome protein Harmonin. As indispensable prerequisite for interaction, the proteins show a partly overlapping expression pattern, e.g. in renal primary cilia. Due to its PDZ-domains, Harmonin acts as a scaffold protein. In line, an extended network including Polyductin can be hypothesized. Although Polyductin lacks certain characteristics of a typical binding partner of Harmonin, such as a characteristic PDZ-binding motif, the interaction of both proteins seems well plausible. In a yeast-two-hybrid screen previously performed in our group, the intracellular domain of Polyductin as bait protein, Harmonin was among the proteins detected as potential binding partner of Polyductin. In the following, respective Polyductin- and Harmonin-constructs were cloned, transfected into COS7-cells and finally expressed. Afterwards co-immunoprecipitation and western blot experiments confirmed the result of the yeast-two-hybrid screen. Thus, overall the interaction of these two proteins is likely albeit. Further experiments for validation are reasonable. Characterization of protein networks will help to elucidate the pathogenesis and molecular and cellular mechanisms underlying ciliopathies like ARPKD and Usher syndrome. Hopefully new therapeutic options will evolve from this and other studies
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