Explore the vast range of titles available.

The water submersion test (W-test) has the risk of overlooking air leaks during lung resection. We assessed the relationship between alveolar air leakage and intrathoracic gas concentrations as a novel intraoperative air leak detection method. We compared the W-test results with intrathoracic gas concentrations of desflurane, oxygen (O2), and carbon dioxide (CO2), prospectively measured using a gas analyser built-in into the anaesthesia machine before and after lung resection. Eighty-eight patients were included; 32 patients had a positive W-test, 31 of whom had elevated levels of all three gases. Eight of the 56 W-test negative patients had elevated levels of all three gases and were positive in a reconfirmation W-test. After repair, 27/31 patients demonstrated negative W-tests, but two patients with elevated levels of all three gases concentrations had postoperative air leaks. When intrathoracic O2 concentration increased, all patients showed an air leak. Conversely, no air leak was detected when intrathoracic concentrations without O2 were measured. We found a positive correlation (correlation coefficients: desflurane, r = 0.84; O2, r = 0.80; CO2. r = 0.77) between the number of bubbles observed in the W-test and gas concentrations. Intrathoracic gas concentration measurements could be a useful alternative or complementary method to the W-test for detecting intraoperative alveolar air leaks. Given that high concentration O2 is frequently use for reinflate the collapsed lungs, intrathoracic O2 measurement could be the most effective way to detect alveolar leakage.

The transcription factor IRF5 has been implicated as a therapeutic target for the autoimmune disease systemic lupus erythematosus (SLE). However, IRF5 activation status during the disease course and the effects of IRF5 inhibition after disease onset are unclear. Here, we show that SLE patients in both the active and remission phase have aberrant activation of IRF5 and interferon-stimulated genes. Partial inhibition of IRF5 is superior to full inhibition of type I interferon signaling in suppressing disease in a mouse model of SLE, possibly due to the function of IRF5 in oxidative phosphorylation. We further demonstrate that inhibition of IRF5 via conditional Irf5 deletion and a newly developed small-molecule inhibitor of IRF5 after disease onset suppresses disease progression and is effective for maintenance of remission in mice. These results suggest that IRF5 inhibition might overcome the limitations of current SLE therapies, thus promoting drug discovery research on IRF5 inhibitors. IRF5 is a potential target for therapy in systemic lupus erythematosus (SLE). Here the authors show using mouse SLE-like models that genetic or chemical inhibition of IRF5 after SLE onset could be more effective than, or an add on for, currently utilised type I interferon inhibition.

Tobamovirus resistance in Capsicum plants, which is mediated by L genes (L(1), L(2), L(3) or L(4)), is known to be temperature sensitive. However, the L(1a ) gene, a newly identified tobamovirus resistance gene that is mapped to the L locus, confers temperature-insensitive resistance against the tobamovirus P(0) pathotype. To identify the viral elicitor that activates the L(1a )-gene-mediated resistance, several chimeric viral genomes were constructed between tobacco mosaic virus-L (P(0) pathotype), paprika mild mottle virus-J (P(1 )pathotype) and pepper mild mottle virus-J (P(1,2) pathotype). Infection patterns of these chimeric viruses in L(1a )-harboring plants revealed that the L(1a )-gene-mediated resistance was activated by the CP of a particular pathotype of tobamovirus, like other L-gene-mediated resistances, but the L(1a )-gene-mediated resistance differs from those conferred by other L genes in terms of temperature sensitivity.

Tobamovirus resistance in Capsicum plants, which is mediated by L genes (L ¹ , L ² , L ³ or L ⁴ ), is known to be temperature sensitive. However, the L ¹a gene, a newly identified tobamovirus resistance gene that is mapped to the L locus, confers temperature-insensitive resistance against the tobamovirus P₀ pathotype. To identify the viral elicitor that activates the L ¹a -gene-mediated resistance, several chimeric viral genomes were constructed between tobacco mosaic virus-L (P₀ pathotype), paprika mild mottle virus-J (P₁ pathotype) and pepper mild mottle virus-J (P₁,₂ pathotype). Infection patterns of these chimeric viruses in L ¹a -harboring plants revealed that the L ¹a -gene-mediated resistance was activated by the CP of a particular pathotype of tobamovirus, like other L-gene-mediated resistances, but the L ¹a -gene-mediated resistance differs from those conferred by other L genes in terms of temperature sensitivity.

Tobamovirus resistance in Capsicum plants, which is mediated by L genes ( L 1 , L 2 , L 3 or L 4 ), is known to be temperature sensitive. However, the L 1a gene, a newly identified tobamovirus resistance gene that is mapped to the L locus, confers temperature-insensitive resistance against the tobamovirus P 0 pathotype. To identify the viral elicitor that activates the L 1a -gene-mediated resistance, several chimeric viral genomes were constructed between tobacco mosaic virus-L (P 0 pathotype), paprika mild mottle virus-J (P 1 pathotype) and pepper mild mottle virus-J (P 1,2 pathotype). Infection patterns of these chimeric viruses in L 1a -harboring plants revealed that the L 1a -gene-mediated resistance was activated by the CP of a particular pathotype of tobamovirus, like other L -gene-mediated resistances, but the L 1a -gene-mediated resistance differs from those conferred by other L genes in terms of temperature sensitivity.

Tobamovirus resistance in Capsicum plants, which is mediated by L genes (L super(1), L super(2), L super(3) or L super(4)), is known to be temperature sensitive. However, the L super(1a) gene, a newly identified tobamovirus resistance gene that is mapped to the L locus, confers temperature-insensitive resistance against the tobamovirus P sub(0) pathotype. To identify the viral elicitor that activates the L super(1a)-gene-mediated resistance, several chimeric viral genomes were constructed between tobacco mosaic virus-L (P sub(0) pathotype), paprika mild mottle virus-J (P sub(1 )pathotype) and pepper mild mottle virus-J (P sub(1,2) pathotype). Infection patterns of these chimeric viruses in L super(1a)-harboring plants revealed that the L super(1a)-gene-mediated resistance was activated by the CP of a particular pathotype of tobamovirus, like other L-gene-mediated resistances, but the L super(1a)-gene-mediated resistance differs from those conferred by other L genes in terms of temperature sensitivity.

Tobamovirus resistance in Capsicum plants, which is mediated by L genes (L 1 , L 2 , L 3 or L 4 ), is known to be temperature sensitive. However, the L 1a gene, a newly identified tobamovirus resistance gene that is mapped to the L locus, confers temperature-insensitive resistance against the tobamovirus P0 pathotype. To identify the viral elicitor that activates the L 1a -gene-mediated resistance, several chimeric viral genomes were constructed between tobacco mosaic virus-L (P0 pathotype), paprika mild mottle virus-J (P1 pathotype) and pepper mild mottle virus-J (P1,2 pathotype). Infection patterns of these chimeric viruses in L 1a -harboring plants revealed that the L 1a -gene-mediated resistance was activated by the CP of a particular pathotype of tobamovirus, like other L-gene-mediated resistances, but the L 1a -gene-mediated resistance differs from those conferred by other L genes in terms of temperature sensitivity. [PUBLICATION ABSTRACT]