Thyroid transcription factor-1 (TTF-1) expression in patients with non-squamous non-small cell lung cancer (NS-NSCLC) is reportedly useful in selecting treatment regimens and predicting life expectancy. However, only a few studies have reported the association between TTF-1 expression and the efficacy of the current first-line regimens containing immune checkpoint inhibitors. It is unclear whether TTF-1 can be a hematologic toxicity indicator in patients receiving these treatment regimens. Patients who received the three-drug combination regimen of carboplatin, pemetrexed, and pembrolizumab, i.e., KEYNOTE-189, between April 2019 and December 2021 at Tsuyama Chuo Hospital and who had known TTF-1 expression were retrospectively studied using electronic medical records. Among the seven patients included, four patients were TTF-1 positive, while three were TTF-1 negative. TTF-1-positive patients showed a trend toward improved progression-free survival and were more likely to experience thrombocytopenia than the TTF-1-negative patients. These results suggest that TTF-1 expression in patients with NS-NSCLC could play a role in determining both treatment efficiency and hematologic toxicity.

Tranexamic acid exerts various effects on living bodies; however, its effects on asthenopia remain unknown. In this study, an asthenopia-like model was developed and used to investigate the effects of tranexamic acid on asthenopia. Mice were placed in special cages constructed for the test, and continuous irradiation with blue light was applied for 20 days. The tranexamic acid-treated group was orally administered tranexamic acid daily during the test period. Motor activity was measured for 10 days after irradiation, and reactive oxygen species (ROS), plasmin, and transforming growth factor (TGF)-β levels in the ciliary muscle of the mice were measured on the last day. Blue light irradiation induced asthenopia and increased ROS, plasmin, and TGF-β levels. In contrast, tranexamic acid administration improved asthenopia and significantly decreased plasmin and TGF-β levels compared to blue light irradiation alone; however, ROS levels remained unchanged. The study results indicate that blue light irradiation induces asthenopia by activating the ROS/plasmin/TGF-β pathways and that tranexamic acid improves asthenopia by suppressing plasmin production.

The coronavirus disease 2019 is caused by the etiological agent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 is abundant in the saliva of an infected person; therefore, saliva is an important source of infection. The present study evaluated the efficacy of short-term treatment using tea-derived compounds against SARS-CoV-2 infectivity in the saliva. The antiviral efficacy of theaflavin 3,3’-gallate (TF3) and two black tea-derived theaflavin concentrates (TF35 and TF80) against a prototype Wuhan and a recent Omicron strain was evaluated using human saliva. TF3, TF35, and TF80 reduced the infectivity of both strains at high (1 mM or 1 mg/ml) and low (0.25 mM or 0.25 mg/ml) concentrations; however, antiviral efficacy against the Wuhan strain was stronger than that against the Omicron strain. Furthermore, the antiviral agents at high concentrations showed better efficacy against both strains than those at low concentrations. For example, treatment with 1 mM TF3 for 10 min decreased the infectivity of Wuhan and Omicron strains to approximately 0.05% and 3%, respectively; these reduction rates are attributable to the inactivation of large amounts of viruses (9.995 × 10⁵ and 9.7 × 10⁴ TCID₅₀, respectively). Considering these facts, it was expected that the inclusion of the main components of black tea (TF3) and the black tea-derived theaflavin concentrates (TF35 and TF80) in the oral cavity for a short time might inactivate the virus in saliva and, thus, can be considered an effective suppressor of the spread of infection.

Neudesin was identified as a secretory factor expressed in the nervous system. On the other hand, neudesin is expressed in various organs and cells, suggesting that it plays roles in tissues other than neural tissues. We found that neudesin was expressed in dendritic cells (DCs) in the mouse spleen, which play a crucial role in the initiation of adaptive immune responses. Therefore, considering the possibility that neudesin may affect the acquired immune response, we first investigated whether neudesin has an effect on DCs using bone marrow-derived dendritic cells (BMDCs). Neudesin expression levels increased during the differentiation of bone marrow cells to BMDCs, and its expression level in BMDCs was reduced by lipopolysaccharide (LPS) treatment. BMDCs from neudesin knockout mice showed increased production of various cytokines, such as IL-12p70 and TNF-α, under LPS-stimulated conditions, compared with BMDCs from wild-type mice. In addition, treatment with recombinant neudesin suppressed the expression of cytokine genes in LPS-stimulated BMDCs from neudesin knockout mice. T cell proliferation was more strongly induced by co-culture with BMDCs from neudesin knockout mice than by those from wild-type mice. BMDCs from neudesin knockout mice showed increased lactate production, glucose consumption, and expression levels of glycolysis-related factors, suggesting that neudesin inhibits glycolysis, which promotes DC activation. The increased cytokine production in BMDCs from neudesin knockout mice was suppressed by the glycolytic inhibitor, 2-deoxyglucose. These results suggested that neudesin is a novel suppressor of DC function through the inhibition of glycolysis.