The Herbarium And Type Specimens Of Thomas Henry Kearney, Jr. From 1890‐1901

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149754/1/tax02826.pd

Summer 1967

Massachusetts Turf and Lawn Grass CouncilBetter Turf Through Research and Educatio

Big bounce from spin and torsion

The Einstein-Cartan-Sciama-Kibble theory of gravity naturally extends general relativity to account for the intrinsic spin of matter. Spacetime torsion, generated by spin of Dirac fields, induces gravitational repulsion in fermionic matter at extremely high densities and prevents the formation of singularities. Accordingly, the big bang is replaced by a bounce that occurred when the energy density $\epsilon\propto gT^4$ was on the order of $n^2/m_\textrm{Pl}^2$ (in natural units), where $n\propto gT^3$ is the fermion number density and $g$ is the number of thermal degrees of freedom. If the early Universe contained only the known standard-model particles ($g\approx 100$), then the energy density at the big bounce was about 15 times larger than the Planck energy. The minimum scale factor of the Universe (at the bounce) was about $10^{32}$ times smaller than its present value, giving \approx 50 \mum. If more fermions existed in the early Universe, then the spin-torsion coupling causes a bounce at a lower energy and larger scale factor. Recent observations of high-energy photons from gamma-ray bursts indicate that spacetime may behave classically even at scales below the Planck length, supporting the classical spin-torsion mechanism of the big bounce. Such a classical bounce prevents the matter in the contracting Universe from reaching the conditions at which a quantum bounce could possibly occur.Comment: 6 pages; published versio

Sigma-term physics in the perturbative chiral quark model

We apply the perturbative chiral quark model (PCQM) at one loop to analyse meson-baryon sigma-terms. Analytic expressions for these quantities are obtained in terms of fundamental parameters of low-energy pion-nucleon physics (weak pion decay constant, axial nucleon coupling, strong pion-nucleon form factor) and of only one model parameter (radius of the nucleonic three-quark core). Our result for the piN sigma term of about 45 MeV is in good agreement with the value deduced by Gasser, Leutwyler and Sainio using dispersion-relation techniques and exploiting the chiral symmetry constraints.Comment: 19 pages, LaTeX-file, 2 Figure

Chromodomain Ligand Optimization via Target-Class Directed Combinatorial Repurposing

Efforts to develop strategies for small molecule chemical probe discovery against the readers of the methyl-lysine (Kme) post-translational modification have been met with limited success. Targeted disruption of these protein-protein interactions via peptidomimetic inhibitor optimization is a promising alternative to small molecule hit discovery; however, recognition of identical peptide motifs by multiple Kme reader proteins presents a unique challenge in the development of selective Kme reader chemical probes. These selectivity challenges are exemplified by the Polycomb repressive complex 1 (PRC1) chemical probe, UNC3866, which demonstrates sub-micromolar off-target affinity toward the non-PRC1 chromodomains CDYL2 and CDYL. Moreover, since peptidomimetics are challenging subjects for structure-activity relationship (SAR) studies, traditional optimization of UNC3866 would prove costly and time-consuming. Herein, we report a broadly applicable strategy for the affinity-based, target-class screening of chromodomains via the repurposing of UNC3866 in an efficient, combinatorial peptide library. A first-generation library yielded UNC4991, a UNC3866 analog that exhibits a distinct selectivity profile while maintaining sub-micromolar affinity toward the CDYL chromodomains. Additionally, in vitro pull-down experiments from HeLa nuclear lysates further demonstrate the selectivity and utility of this compound for future elucidation of CDYL protein function

Baryon masses in a chiral expansion with meson-baryon form factors

The chiral expansion of the one-loop corrections to baryon masses is examined in a generic meson-cloud model with meson-baryon form factors. For pion loops, the expansion is rapidly convergent and at fourth order in $m_\pi$ accurately reproduces the full integral. In contrast, the expansion is found to converge very slowly for kaon loops, raising questions about the usefulness of chiral expansions for kaon-baryon physics. Despite the importance of high-order terms, relations like that of Gell-Mann and Okubo are well satisfied by the baryon masses calculated with the full integral. The pion cloud cloud makes a significant contribution to the $\pi N$ sigma commutator, while kaon cloud gives a very small strangeness content in the nucleon.Comment: 20 pages (RevTeX), 2 figures (attached

A novel mutation of the calcium sensing receptor gene is associated with chronic pancreatitis in a family with heterozygous SPINK1 mutations

BACKGROUND: The role of mutations in the serine protease inhibitor Kazal type 1 (SPINK1) gene in chronic pancreatitis is still a matter of debate. Active SPINK1 is thought to antagonize activated trypsin. Cases of SPINK1 mutations, especially N34S, have been reported in a subset of patients with idiopathic chronic pancreatitis. However, the inheritance pattern is still unknown. Some cases with N34S heterozygosity have been reported with and without evidence for CP indicating neither an autosomal recessive nor dominant trait. Therefore SPINK1 mutations have been postulated to act as a disease modifier requiring additional mutations in a more complex genetic model. Familial hypocalciuric hypercalcemia (FHH) caused by heterozygous inactivating mutations in the calcium sensing receptor (CASR) gene is considered a benign disorder with elevated plasma calcium levels. Although hypercalcemia represents a risk factor for pancreatitis, increased rates of pancreatitis in patients with FHH have not been reported thus far. METHODS: We studied a family with a FHH-related hypercalcemia and chronic pancreatitis. DNA samples were analysed for mutations within the cationic trypsinogen (N29I, R122H) and SPINK1 (N34S) gene using melting curve analysis. Mutations within CASR gene were identified by DNA sequencing. RESULTS: A N34S SPINK1 mutation was found in all screened family members. However, only two family members developed chronic pancreatitis. These patients also had FHH caused by a novel, sporadic mutation in the CASR gene (518T>C) leading to an amino acid exchange (leucine->proline) in the extracellular domain of the CASR protein. CONCLUSION: Mutations in the calcium sensing receptor gene might represent a novel as yet unidentified predisposing factor which may lead to an increased susceptibility for chronic pancreatitis. Moreover, this family analysis supports the hypothesis that SPINK1 mutations act as disease modifier and suggests an even more complex genetic model in SPINK1 related chronic pancreatitis

In Utero Gene Therapy (IUGT) Using GLOBE Lentiviral Vector Phenotypically Corrects the Heterozygous Humanised Mouse Model and Its Progress Can Be Monitored Using MRI Techniques

Funder: UK Thalassaemia SocietyAbstract: In utero gene therapy (IUGT) to the fetal hematopoietic compartment could be used to treat congenital blood disorders such as β-thalassemia. A humanised mouse model of β-thalassemia was used, in which heterozygous animals are anaemic with splenomegaly and extramedullary hematopoiesis. Intrahepatic in utero injections of a β globin-expressing lentiviral vector (GLOBE), were performed in fetuses at E13.5 of gestation. We analysed animals at 12 and 32 weeks of age, for vector copy number in bone marrow, peripheral blood liver and spleen and we performed integration site analysis. Compared to noninjected heterozygous animals IUGT normalised blood haemoglobin levels and spleen weight. Integration site analysis showed polyclonality. The left ventricular ejection fraction measured using magnetic resonance imaging (MRI) in treated heterozygous animals was similar to that of normal non-β-thalassemic mice but significantly higher than untreated heterozygous thalassemia mice suggesting that IUGT ameliorated poor cardiac function. GLOBE LV-mediated IUGT normalised the haematological and anatomical phenotype in a heterozygous humanised model of β-thalassemia