Light intensity differentially mediates the life cycle of lepidopteran leaf feeders and stem borers.

BACKGROUND: Leaf feeders, such as Spodoptera frugiperda and Spodoptera litura, and stem borers Ostrinia furnacalis and Chilo suppressalis, occupy two different niches and are well adapted to their particular environments. Borer larvae burrow and inhabit the interior of stems, which are relatively dark. By contrast, the larvae of leaf feeders are exposed to sunlight during feeding. We therefore designed series of experiments to evaluate the effect of light intensity (0, 2000, and 10 000 lx) on these pests with different feeding modes. RESULTS: The development of all four pests was significantly delayed at 0 lx. Importantly, light intensity affected the development of both male and female larvae of borers, but only significantly affected male larvae of leaf feeders. Furthermore, the proportion of female offspring of leaf feeders increased with increasing light intensity (S. frugiperda: 33.89%, 42.26%, 57.41%; S. litura: 38.90%, 51.75%, 65.08%), but no significant differences were found in stem borers. This research also revealed that the survival rate of female leaf feeders did not vary across light intensities, but that of males decreased with increasing light intensity (S. frugiperda: 97.78%, 85.86%, 61.21%; S. litura: 95.83%, 73.54%, 58.99%). CONCLUSION: These results improve our understanding of how light intensity affects sex differences in important lepidopteran pests occupying different feeding niches and their ecological interactions with abiotic factors in agroecosystems. © 2024 Society of Chemical Industry.

Correlation between crowdedness in emergency departments and anxiety in Chinese patients.

BACKGROUND: Emergency department (ED) overcrowding is a severe health care concern, while anxiety and depression rates among ED patients have been reported to be substantially higher compared to the general population. We hypothesized that anxiety due to over crowdedness may lead to adverse events in EDs. AIM: To investigate correlations between crowdedness in EDs and anxiety of patients and nurses, and to identify factors affecting their anxiety. METHODS: In this prospective observational study, a total 43 nurses and 389 emergency patients from two tier III hospitals located in Beijing were included from January 2016 to August 2017. Patients were grouped into inpatients when they were hospitalized after diagnoses, or into outpatients when they were discharged after treatments. The State Trait Anxiety Inventory (STAI Form Y) questionnaire was used to investigate patient and nurse anxieties, while crowdedness of EDs was evaluated with the National Emergency Department Over Crowding Score. RESULTS: The present results revealed that state anxiety scores (49.50 ± 6.00 vs 50.80 ± 2.80, P = 0.005) and trait anxiety scores (45.40 ± 5.70 vs 46.80 ± 2.70, P = 0.002) between inpatients (n = 173) and outpatients (n = 216) were significantly different, while the state anxiety of nurses (44.70 ± 5.80) was different from those of both patient groups. Generalized linear regression analysis demonstrated that multiple factors, including crowdedness in the ED, were associated with state and trait anxieties for both inpatients and outpatients. In addition, there was an interaction between state anxiety and trait anxieties. However, multivariable regression analysis showed that while overcrowding in the ED did not directly correlate with patients' and nurses' anxiety levels, the factors that did correlate with state and trait anxieties of inpatients were related to crowdedness. These factors included waiting time in the ED, the number of patients treated, and the number of nurses in the ED, whereas for nurses, only state and trait anxieties correlated significantly with each other. CONCLUSION: Waiting time, the number of patients treated, and the number of nurses present in the ED correlate with patient anxiety in EDs, but crowdedness has no effect on nurse or patient anxiety.

Targeted inhibition of the phosphoinositide 3-kinase impairs cell proliferation, survival, and invasion in colon cancer.

BACKGROUND: Colon cancer is the third most common cancer in the world, and its metastasis and drug resistance are challenging for its effective treatment. The PI3K/Akt/mTOR pathway plays a crucial role in the pathogenesis of colon cancer. The aim of this study was to investigate the targeting of PI3K in colon cancer cells HT-29 and HCT-116 in vitro. METHODS: In HT-29 and HCT-116 cells, BEZ235, a dual inhibitor of PI3K/mTOR, and shRNAtarget to PI3KCA were used to inhibit PI3K/Akt/mTOR pathway. The inhibition efficiency of PI3K/Akt/mTOR pathway was detected by RT-PCR and Western blot. Cell proliferation, migration, invasion, and apoptosis were evaluated by Cell Counting Kit-8, Transwell, and flow cytometry assays. The expression of apoptosis-related proteins (cleavage caspase 3, Bcl-2, Bax, and Bim) were also detected. RESULTS: We found that in HT-29 and HCT-116 cells, the treatment of BEZ235 (1 µM) and PI3KCA knockdown inhibited the activation of PI3K/Akt/mTOR pathway and significantly suppressed cell proliferation, migration, and invasion of HT-29 and HCT-116 cells. In addition, we confirmed that knockdown of BEZ235 and PI3KCA induced cell apoptosis through the upregulated levels of cleavage caspase 3 and Bax and downregulated expression of Bcl-2 and Bim. CONCLUSION: Our results indicated that targeted inhibition of the PI3K/Akt/mTOR pathway impaired cell proliferation, survival, and invasion in human colon cancer.

Long-term treatment with nifedipine suppresses coronary hyperconstricting responses and inflammatory changes induced by paclitaxel-eluting stent in pigs in vivo: possible involvement of Rho-kinase pathway.

AIMS: Accumulating evidence indicates that coronary vasoconstricting responses are enhanced at the edges of coronary segment implanted with a drug-eluting stent (DES) compared with a bare-metal stent (BMS) in humans. We have recently demonstrated that Rho-kinase pathway plays an important role in DES-induced coronary hyperconstricting responses associated with inflammatory changes in pigs in vivo. This study examined whether long-term treatment with calcium channel blocker suppresses DES-induced coronary hyperconstricting responses in pigs in vivo. METHODS AND RESULTS: Paclitaxel-eluting stent (PES) and a BMS were randomly implanted in the left coronary arteries in male domestic pigs with and without long-acting nifedipine (NIF, 4 mg/kg/day) for 4 weeks (n = 7 each). Coronary vasomotion was evaluated by quantitative coronary angiography at least 24 h after withdrawal of NIF to avoid its direct effects on coronary vasomotion. In the control group (without NIF), coronary vasoconstricting responses to serotonin (10 and 100 µg/kg, i.c.) were significantly enhanced at the PES site compared with the BMS site (P = 0.009), which were abolished by hydroxyfasudil (90 and 300 µg/kg, i.c.), a selective Rho-kinase inhibitor. The PES-induced vasoconstricting responses were significantly inhibited in the NIF group (P = 0.019). Histological examination showed that inflammatory cell accumulation and microthrombus formation were enhanced at the PES site compared with the BMS site (P < 0.05), both of which were significantly suppressed by NIF associated with reduced Rho-kinase expression and activity (P < 0.05). CONCLUSION: These results indicate that long-term treatment with NIF suppresses PES-induced coronary abnormalities partly through Rho-kinase pathway inhibition in vivo.

Long-term treatment with eicosapentaenoic acid ameliorates myocardial ischemia-reperfusion injury in pigs in vivo. -Involvement of Rho-kinase pathway inhibition-.

BACKGROUND: Eicosapentaenoic acid (EPA), the major n-3 fatty acid in fish oil, exerts cardioprotective effects against ischemic heart disease; however, the detailed mechanisms remain to be elucidated. Rho-kinase plays an important role in the pathogenesis of cardiovascular diseases including ischemia-reperfusion (I/R) injury. Thus, the hypothesis that long-term EPA treatment ameliorates myocardial I/R injury through Rho-kinase pathway inhibition in pigs in vivo was investigated. METHODS AND RESULTS: Male pigs were treated with either a control chow or EPA (600·mg·kg⁻¹·day⁻¹) for 3 weeks (n=8 each) and were subjected to myocardial ischemia by 90-min occlusion of the left circumflex coronary artery and subsequent 60-min reperfusion. The EPA group had an increased EPA level in red blood cells (4.4 ± 0.3mol%). The EPA treatment significantly ameliorated myocardial I/R injury, including regional wall motion abnormality (EPA 5.3 ± 3.6 vs. control 35.1 ± 3.8 unit, P<0.0001), left ventricular ejection fraction (EPA 43 ± 9% vs. control 32 ± 7%, P<0.05), occurrence of ventricular arrhythmias (EPA 181 ± 73 vs. control 389 ± 51 events, P<0.0001) and histological accumulation of inflammatory cells (P<0.01). Importantly, the EPA treatment significantly inhibited myocardial Rho-kinase activity (assessed by the extent of the myosin-binding subunit phosphorylation) (EPA 0.47 ± 0.11 vs. control 0.77 ± 0.14, P<0.05) and preserved myocardial eNOS activity (EPA 0.56 ± 0.13 vs. control 0.23 ± 0.07, P<0.01) with a significant correlation noted between them. CONCLUSIONS: Long-term treatment with EPA ameliorates I/R injury partly through Rho-kinase pathway inhibition in vivo.

Eicosapentaenoic acid reduces ischemic ventricular fibrillation via altering monophasic action potential in pigs.

Although high intake of n-3 fatty acids is associated with reduced mortality of patients with ischemic heart disease, especially reduction in sudden cardiac death (SCD), the detailed mechanisms remain to be elucidated. Thus, the present study was designed to examine whether long-term treatment with eicosapentaenoic acid (EPA), a major component of n-3 fatty acids, reduces ischemia-induced ventricular fibrillation (VF) in pigs in vivo, and if so, what molecular mechanisms are involved. Male pigs were treated with either a control chow (control group) or a control chow plus EPA (600 mg/kg/day, PO, EPA group) for 3 weeks and were subjected to myocardial ischemia for 90 min (n=8 each) with measurement of the monophasic action potential (MAP), as a marker of ventricular electrophysiological activities. The EPA treatment significantly attenuated the occurrence of VF (control 5.1±1.7 vs. EPA 1.5±0.8 times/animal, P<0.05) and markedly reduced the mortality (control 50% vs. EPA 0%, P<0.05), with the attenuation of MAP duration shortening during ischemia (control -28.1±3.0% vs. EPA -18.2±1.4%, P<0.05). These beneficial effects of EPA were abolished by pre-treatment with cromakalim, a K(ATP) channel opener (0.3 µg/kg/min, IC). Furthermore, EPA significantly inhibited the mRNA and protein expression of Kir6.2, a major component of sarcolemmal K(ATP) channels, in both the ischemic region and non-ischemic regions. These results indicate that long-term treatment with EPA reduces ischemia-induced VF and SCD in pigs in vivo, for which attenuation of MAP duration shortening may be involved.