Molecular ecology of plant volatiles in interactions with insect herbivores.

Plant-derived volatile organic compounds (VOCs) play pivotal roles in interactions with insect herbivores. Individual VOCs can be directly toxic or deterrent, serve as signal molecules to attract natural enemies, and/or be perceived by distal plant tissues as a priming signal to prepare for expected herbivory. Environmental conditions, as well as the specific plant-insect interaction being investigated, strongly influence the observed functions of VOC blends. The complexity of plant-insect chemical communication via VOCs is further enriched by the sophisticated molecular perception mechanisms of insects, which can respond to one or more VOCs and thereby influence insect behavior in a manner that has yet to be fully elucidated. Despite numerous gaps in the current understanding of VOC-mediated plant-insect interactions, successful pest management strategies such as push-pull systems, synthetic odorant traps, and crop cultivars with modified VOC profiles have been developed to supplement chemical pesticide applications and enable more sustainable agricultural practices. Future studies in this field would benefit from examining the responses of both plants and insects in the same experiment to gain a more complete view of these interactive systems. Furthermore, a molecular evolutionary study of key genetic elements of the ecological interaction phenotypes could provide new insights into VOC-mediated plant communication with insect herbivores.

More purinergic receptors deserve attention as therapeutic targets for the treatment of cardiovascular disease.

Cardiovascular disease is a major cause of morbidity and mortality worldwide. Innovative new treatment options for this cardiovascular pandemic are urgently needed. Activation of purinergic receptors (PRs) is critically involved in the development and progression of cardiovascular disease including atherosclerosis, ischemic heart disease, hypertension, and diabetes. PRs have been targeted for the treatment of several cardiovascular diseases in a clinical setting. The P2Y12R antagonists such as clopidogrel, ticagrelor, and others are the most successful class of purinergic drugs targeting platelets for the treatment of acute coronary syndrome. In addition to targeting platelets, ticagrelor may exert P2Y12R-independent effect by targeting erythrocyte-mediated purinergic activation. The partial A1R agonist neladenoson and the A2AR agonist regadenoson have been applied in cardiovascular medicine. In experimental studies, many other PRs have been shown to play a significant role in the development and progression of cardiovascular diseases, and targeting these receptors have resulted in promising outcomes. Therefore, many of these PRs including A2BR, A3R, P2X3R, P2X4R, P2X7R, P2Y1R, P2Y4R, P2Y6R, and P2Y11R can be considered as therapeutic targets. However, the multitude of PR subtypes expressed in different cells of the cardiovascular system may constitute a challenge whether single or multiple receptors should be targeted at the same time for the best efficacy. The present review discusses the promising purinergic drugs used in clinical studies for the treatment of cardiovascular disease. We also update experimental evidence for many other PRs that can be considered as therapeutic targets for future drug development.

Intrinsic 4-1BB signals are indispensable for the establishment of an influenza-specific tissue-resident memory CD8 T-cell population in the lung.

The induction of long-lived heterotypic T-cell protection against influenza virus remains elusive, despite the conservation of T-cell epitopes. T-cell protection against influenza is critically dependent on lung-resident memory T cells (Trm). Here we show that intranasal administration of 4-1BBL along with influenza nucleoprotein in a replication-defective adenovirus vector to influenza pre-immune mice induces a remarkably stable circulating effector memory CD8 T-cell population characterized by higher IL-7Rα expression than control-boosted T cells, as well as a substantial lung parenchymal CD69+ CD8 Trm population, including both CD103+ and CD103- cells. These T-cell responses persist to greater than 200 days post-boost and protect against lethal influenza challenge in aged (year old) mice. The expansion of the nucleoprotein-specific CD8 Trm population during boosting involves recruitment of circulating antigen-specific cells and is critically dependent on local rather than systemic administration of 4-1BBL as well as on 4-1BB on the CD8 T cells. Moreover, during primary influenza infection of mixed bone marrow chimeras, 4-1BB-deficient T cells fail to contribute to the lung-resident Trm population. These findings establish both endogenous and supraphysiological 4-1BBL as a critical regulator of lung-resident memory CD8 T cells during influenza infection.

Pulmonary function changes in cirrhosis of the liver.

Pulmonary function tests were performed in 21 cirrhotic patients with ascites, and these were compared with 50 normal controls. The vital capacity in the cirrhotic group was 93.67 +/- 12.5% and in controls was 102.47 +/- 15.22%, p less than 0.05. The maximum voluntary ventilation in cirrhotic patients was 89.33 +/- 25.4% and in controls was 127.48 +/- 28.44%, p less than 0.001. The functional residual capacity in cirrhotic patients was 2362.19 +/- 845.08 ml and in controls was 3085.1 +/- 837.92 ml, p less than 0.01. The total lung capacity in cirrhotic patients was 4675 +/- 1204.09 and in controls was 5791.56 +/- 1033.99, p less than 0.01. The first forced expiratory volume in cirrhotic patients was 70.1 +/- 12.79%, whereas that in controls was 77.74 +/- 9.18%, p less than 0.05. These results imply that in cirrhosis of the liver there are prominent restrictive ventilatory disorders as well as obstructive disorders.