Papaya Ringspot Virus Resistance of Transgenic Rainbow and SunUp is Affected by Gene Dosage, Plant Development, and Coat Protein Homology

R1 plants of the transgenic papaya line 55-1, which expresses a single coat protein (CP) gene of the mild strain of the papaya ringspot virus (PRSV) HA from Hawaii, were previously shown to be resistant only to PRSV isolates from Hawaii. Two transgenic papaya cultivars were subsequently derived from line 55-1. UH SunUp (SunUp) is homozygous for the CP gene insertion and UH Rainbow (Rainbow) is hemizygous for the CP gene because it is a F1 hybrid of a cross between SunUp and the nontransgenic papaya cultivar Kapoho. To determine the various parameters that affect the resistance of SunUp and Rainbow, plants at different developmental stages (younger and older) were inoculated with PRSV isolates from Hawaii, Brazil, Jamaica, and Thailand. Hawaiian isolates shared nucleotide sequence identities of 96.7-99.8% to the CP transgene, and the other isolates shared sequence identities of 89.5-92.5%. Resistance was affected by CP gene dosage, plant developmental stage, and CP sequence identity of the challenge isolate. Young and older hemizygous Rainbow plants were resistant to the homologous PRSV HA (99.8% homology to CP transgene), while only older Rainbow plants were resistant to the other Hawaiian isolates (96.7% homology). However, all inoculated Rainbow plants were susceptible to PRSV isolates collected from Jamaica, Brazil, and Thailand. In contrast, SunUp was resistant to all PRSV isolates, except the one from Thailand, regardless of the plant developmental stage. Resistance to the Thailand isolate, which shares 89.5% homology to the transgene, was observed only with SunUp plants inoculated at an older stage. Steady state RNA analysis and nuclear run-on experiments suggested that resistance of the transgenic papaya is RNA-mediated via post-transcriptional gene silencin

Temperature dependence of single particle excitations in a S=1 chain: exact diagonalization calculations compared to neutron scattering experiments

Exact diagonalization calculations of finite antiferromagnetic spin-1 Heisenberg chains at finite temperatures are presented and compared to a recent inelastic neutron scattering experiment for temperatures T up to 7.5 times the intrachain exchange constant J. The calculations show that the excitations at the antiferromagnetic point q=1 and at q=0.5 remain resonant up to at least T=2J, confirming the recent experimental observation of resonant high-temperature domain wall excitations. The predicted first and second moments are in good agreement with experiment, except at temperatures where three-dimensional spin correlations are most important. The ratio of the structure factors at q=1 and at q=0.5 is well predicted for the paramagnetic infinite-temperature limit. For T=2J, however, we found that the experimentally observed intensity is considerably less than predicted. This suggests that domain wall excitations on different chains interact up to temperatures of the order of the spin band width.Comment: 9 pages revtex, submitted to PR

Haematological and biochemical parameters in Churra-da-Terra-Quente ewes from the northeast of Portugal

Hematological and biochemical parameters, including plasma electrolytes and thyroid hormones, were determined in 73 clinically healthy Churra-da-Terra-Quente ewes, a typical breed from the northeast of Portugal. The hemogram values were: erythrocytes 9.8±1.51012/L; haemoglobin 118.1±19.1g/L; haematocrit 40.8±5.9%; leukocytes 5.7±1.8109/L; and platelets 544.3±177.2109/L. The thrombin time was 17.3±1.7 seconds. The values of biochemical parameters were: total protein 76.4±6.1g/L; glucose 2.87±0.60mmol/L; total cholesterol 1.65±0.33mmol/L; aspartate aminotransferase 155.9±49.2U/L; alanine aminotransferase 23.2±9.6U/L; γ-glutamyl transferase 48.0±18.7U/L; total alkaline phosphatase 121.6±76.1U/L; glutamate dehydrogenase 6.4±3.7U/L; urea 7.32±2.22mmol/L; creatinine 123.0±54.1μmol/L; total calcium 2.53±0.25mmol/L; phosphorus 2.10±0.46mmol/L; magnesium 1.01±0.09mmol/L; sodium 152.04±3.65mmol/L; potassium 4.7±0.4mmol/L; ionized calcium 1.32±0.07mmol/L; total thyroxine 111.75±42.29nmol/L; total triiodothyronine 1.01±0.28nmol/L; free T4 11.93±1.78pmol/L; free T3 4.22±1.33pmol/L; and thyroid-stimulating hormone 0.18±0.19μIU/mL. Although differences among the Churra-da-Terra-Quente breed and other breeds may occur, the hematological and biochemical parameters, plasma electrolytes, and thyroid hormones, for this indigenous breed, were generally situated within the reference intervals previously reported for sheep

On the 3-particle scattering continuum in quasi one dimensional integer spin Heisenberg magnets

We analyse the three-particle scattering continuum in quasi one dimensional integer spin Heisenberg antiferromagnets within a low-energy effective field theory framework. We exactly determine the zero temperature dynamical structure factor in the O(3) nonlinear sigma model and in Tsvelik's Majorana fermion theory. We study the effects of interchain coupling in a Random Phase Approximation. We discuss the application of our results to recent neutron-scattering experiments on the Haldane-gap material ${\rm CsNiCl_3}$.Comment: 8 pages of revtex, 5 figures, small changes, to appear in PR

SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids

Kidney failure is frequently observed during and after COVID-19, but it remains elusive whether this is a direct effect of the virus. Here, we report that SARS-CoV-2 directly infects kidney cells and is associated with increased tubule-interstitial kidney fibrosis in patient autopsy samples. To study direct effects of the virus on the kidney independent of systemic effects of COVID-19, we infected human-induced pluripotent stem-cell-derived kidney organoids with SARS-CoV-2. Single-cell RNA sequencing indicated injury and dedifferentiation of infected cells with activation of profibrotic signaling pathways. Importantly, SARS-CoV-2 infection also led to increased collagen 1 protein expression in organoids. A SARS-CoV-2 protease inhibitor was able to ameliorate the infection of kidney cells by SARS-CoV-2. Our results suggest that SARS-CoV-2 can directly infect kidney cells and induce cell injury with subsequent fibrosis. These data could explain both acute kidney injury in COVID-19 patients and the development of chronic kidney disease in long COVID