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Introduction: Telehealth increases care accessibility to patients with type-2 diabetes mellitus but the duration of its implementation to sustain optimal glycaemic control remains unclear. This study aimed to assess the health outcomes of these patients using the Optimizing care of Patients via Telemedicine In Monitoring and aUgmenting their control of diabetes Mellitus (OPTIMUM) home tele-monitoring (HTM) system 6 months post-intervention, compared to standard care., Methods: An open-labelled randomized controlled trial involving 330 participants with type-2 diabetes mellitus, aged 26-65 years, and suboptimal glycaemic control (HbA1c = 7.5%-10%) was conducted. Intervention group received OPTIMUM HTM for 6 months followed by usual care for another 6 months, while control group received usual care for 12 months. OPTIMUM HTM includes in-app video-based tele-education, tele-monitoring of the blood pressure, capillary glucose and weight via Bluetooth devices and mobile applications, followed by algorithm-based tele-management by the OPTIMUM HTM team. Assessments using self-care inventory scale and medication adherence were administered for both groups at baseline, 6-month, and 12-month timepoints., Results: Complete data from 156 (intervention) and 159 (control) participants, with comparable demographic profiles, were analysed. Both groups showed a significant reduction in HbA1c from baseline ( p  < 0.001). From 6-month to 12-month time-points, the intervention group was twice as likely to maintain their HbA1c ≤ 8% (adjusted odds ratio = 2.02, 95%CI = 1.18-3.49; p  < 0.011). The intervention group demonstrated higher scores for self-care behaviours (adjusted odds ratio = 3.83 [95%CI = 1.68-5.97], p  = 0.001) and not skipping medications (adjusted odds ratio = 2.32 [95%CI = 1.09-4.97], p  = 0.030) at 12 months., Discussion: The OPTIMUM HTM system enabled patients to maintain their glycaemic control beyond the intervention period. The favourable outcomes could be the effect of telehealth in sustaining self-care behaviour and medication adherence., Competing Interests: Declaration of conflicting interestsThe authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Neonicotinoid insecticides, which target insect nicotinic acetylcholine receptors (nAChRs), have been widely and intensively used to control the whitefly, Bemisia tabaci, a highly damaging, globally distributed, crop pest. This has inevitably led to the emergence of populations with resistance to neonicotinoids. However, to date, there have been no reports of target-site resistance involving mutation of B. tabaci nAChR genes. Here we characterize the nAChR subunit gene family of B. tabaci and identify dual mutations (A58T&R79E) in one of these genes (BTβ1) that confer resistance to multiple neonicotinoids. Transgenic D. melanogaster, where the native nAChR Dβ1 was replaced with BTβ1A58T&R79E, were significantly more resistant to neonicotinoids than flies where Dβ1 were replaced with the wildtype BTβ1 sequence, demonstrating the causal role of the mutations in resistance. The two mutations identified in this study replace two amino acids that are highly conserved in >200 insect species. Three-dimensional modelling suggests a molecular mechanism for this resistance, whereby A58T forms a hydrogen bond with the R79E side chain, which positions its negatively-charged carboxylate group to electrostatically repulse a neonicotinoid at the orthosteric site. Together these findings describe the first case of target-site resistance to neonicotinoids in B. tabaci and provide insight into the molecular determinants of neonicotinoid binding and selectivity., Competing Interests: The authors have declared that no conflict of interest exists., (Copyright: © 2024 Yin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

The whitefly, Bemisia tabaci, comes up high metabolic resistance to most neonicotinoids in long-term evolution, which is the key problem of pest control. UGT glycosyltransferase, as a secondary detoxification enzyme, plays an indispensable role in detoxification metabolism. In this study, UGT inhibitors, 5-nitrouracil and sulfinpyrazone, dramatically augmented the toxic damage of neonicotinoids to B. tabaci. A UGT named UGT353G2 was identified in whitefly, which was notably up-regulated in resistant strain (3.92 folds), and could be induced by most neonicotinoids. Additionally, the using of RNA interference (RNAi) suppresses UGT353G2 substantially increased sensitivity to neonicotinoids in resistant strain. Our results support that UGT353G2 may be involved in the neonicotinoids resistance of whitefly. These findings will help further verify the functional role of UGTs in neonicotinoid resistance., Competing Interests: Declaration of Competing Interest The authors declare no conflicts of interest., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Aim: Healthcare professionals are leveraging on telehealth to manage patients with type-2 diabetes mellitus (T2DM). This study aimed to determine the clinical outcomes of patients using a novel tele-monitoring system (OPTIMUM) as compared to the standard of care., Methods: An open-labelled randomised controlled trial involving 330 Asian patients with T2DM, aged 26-65 years, and suboptimal glycaemic control (HbA1c = 7.5-10%) was conducted in a Singapore public primary care clinic. The patients were assigned in a 1:1 ratio by block randomization to the intervention group to receive: in-app video-based tele-education, tele-monitoring of the blood pressure (BP), capillary glucose and weight via Bluetooth devices and mobile application, followed by algorithm-based tele-management by the OPTIMUM telehealth care team for abnormal parameters. Patients received usual care in the control group. Clinical assessments and self-care-related questionnaires were administered for both groups at baseline and 6 months., Results: Complete data of 159 (intervention) and 160 (control) patients with comparable demographic profiles were analysed. Those in the intervention group showed significantly lower HbA1c by 0.34% (95%CI = -0.57 to -0.11; p  = 0.004); first measurement of systolic BP decreased by 2.98 mmHg (95%CI:-5.8 to -0.08; p  = 0.044) and diastolic BP by 4.24 mmHg (95%CI = -6.0 to -2.47; p  = 0.001); and total cholesterol by 0.18 mmol/L (95%CI:  -0.34 to -0.01; p  = 0.040) compared to the control group, after adjusting for baseline variables. Questionnaire scores showed significant improvements in medication adherence and self-care behaviour in the intervention group. No significant weight change was noted between groups., Conclusion: The OPTIMUM tele-monitoring system improved the glycaemic, BP and total cholesterol control in patients with suboptimal T2DM control by enhancing their medication adherence and self-care over 6 months.

Bemisia tabaci (Hemiptera: Gennadius) is a notorious pest that is capable of feeding on >600 kinds of agricultural crops. Imidacloprid is critical in managing pest with sucking mouthparts, such as B. tabaci. However, the field population of B. tabaci has evolved resistance because of insecticide overuse. The overexpression of the detoxification enzyme cytochrome P450 monooxygenase is considered the main mechanism of imidacloprid resistance, but the mechanism underlying gene regulation remains unclear. MicroRNAs are a type of endogenous small molecule compounds that is fundamental in regulating gene expression at the post-transcriptional level. Whether miRNAs are related to the imidacloprid resistance of B. tabaci remains unknown. To gain deep insight into imidacloprid resistance, we conducted on miRNAs expression profiling of two B. tabaci Mediterranean (MED) strains with 19-fold resistance through deep sequencing of small RNAs. A total of 8 known and 1591 novel miRNAs were identified. In addition, 16 miRNAs showed significant difference in expression levels between the two strains, as verified by quantitative reverse transcription PCR. Among these, novel&#95;miR-376, 1517, and 1136 significantly expressed at low levels in resistant samples, decreasing by 36.9%, 60.2%, and 15.6%, respectively. Moreover, modulating novel&#95;miR-1517 expression by feeding with 1517 inhibitor and 1517 mimic significantly affected B. tabaci imidacloprid susceptibility by regulating CYP6CM1 expression. In this article, miRNAs related to imidacloprid resistance of B. tabaci were systematically screened and identified, providing important information for the miRNA-based technological innovation for this pest management., Competing Interests: Declaration of Competing Interest The authors have declared that no competing interests exist., (Copyright © 2023 Elsevier Inc. All rights reserved.)

The sweet potato whitefly, Bemisia tabaci , (Gennadius) (Hemiptera:Aleyrodidae) is a global pest of crops. Neonicotinoids are efficient insecticides used for control of this pest. Insecticidal targets of neonicotinoids are insect nicotinic acetylcholine receptors (nAChRs). Here, we characterized and cloned the full length of the nAChR β1 subunit ( BTβ1 ) in B. tabaci and confirmed the consistency of BTβ1 in B. tabaci MEAM1 and MED. Expression levels of BTβ1 in different developmental stages and body parts of adults were investigated and compared in B. tabaci MED. dsRNA was prepared to knock down BTβ1 in adult B. tabaci and significantly decreases the susceptibility to five neonicotinoid insecticides, including imidacloprid, clothianidin, thiacloprid, nitenpyram, and dinotefuran. This study indicated BTβ1 as a notable site influencing the susceptibility of B. tabaci to neonicotinoids.

The brown planthopper is a notorious rice pest in many areas of Asia. The evolution of insecticide resistance in Nilaparvata lugens has become a serious problem in the effective control of this pest in the paddy field. In this article, the current susceptibility of N. lugens field populations to novel mesoionic insecticide triflumezopyrim and major classes of chemical insecticides was determined and compared. The monitoring results indicated that field populations of N. lugens had developed low resistance to triflumezopyrim (resistance ratio, RR: 1.3-7.3-fold) during 2015-2018 in China, and the median lethal concentration values varied from 0.05 to 0.29 mg/L. Additionally, during 2017 to 2018, field populations of N. lugens showed high resistance levels to thiamethoxam (RR: 456.1-1025.6-fold), imidacloprid (RR: 2195.3-6899.0-fold) and buprofezin (RR: 1241.5-4521.7-fold), moderate to high resistance levels to dinotefuran (RR: 97.6-320.1-fold), clothianidin (RR: 69.4-230.1-fold) and isoprocarb (RR: 44.1-108.0-fold), and low to moderate levels of resistance to chlorpyrifos (RR: 12.0-29.7-fold) and nitenpyram (RR: 6.9-24.1-fold). In contrast, N. lugens just showed low resistance to sulfoxaflor (RR: 3.3-8.5-fold) and etofenprox (RR: 5.0-9.1-fold) in the field. Additionally, the P450 gene CYP6ER1 was found to be significantly overexpressed in all five field populations of N. lugens collected in 2018 when compared with a laboratory susceptible strain. Our findings will provide useful information to delay the evolution of insecticide resistance in N. lugens., (© 2020 Institute of Zoology, Chinese Academy of Sciences.)

Background: After cerebral injury, the proliferation and differentiation of neural stem cells are important for neural regeneration., Methods: We used the SD rat to establish the traumatic brain injury model. Then, we verified molecular expression, interaction through Western blot, immunoprecipitation (IP), immunofluorescence, and other methods. All data were analyzed with Stata 8.0 statistical software., Results: We showed for the first time that the interaction of TRIAD1 and DISC1 plays an important role in neural stem cell proliferation and differentiation after traumatic brain injury. In a rat model of traumatic brain injury, we found that the expression of TRIAD1 increased progressively, reached a peak at 3 to 5 days, and then decreased gradually. While the expression level of DISC1 was correlated with TRIAD1, its expression level at 3 days was significantly lower than at other time points. Immunofluorescence on frozen brain sections showed that TRIAD1 and DISC1 are co-localized in neural stem cells. Immunoprecipitation data suggested that TRIAD1 may interact with DISC1. We transfected 293T tool cells with plasmids containing truncated fragments of TRIAD1 and DISC1 and used additional IPs to reveal that these two proteins interact via specific fragments. Finally, we found that overexpressing TRIAD1 and DISC1 in primary neural stem cells, via lentiviral transfection, significantly affected the proliferation and differentiation of those neural stem cells., Conclusions: Taken together, these data show that the expression of TRIAD1 and DISC1 change after traumatic brain injury and that their interaction may affect the proliferation and differentiation of neural stem cells. Our research may provide a sufficient experimental basis for finding molecular targets for neural stem cell proliferation and differentiation., Trial Registration: We did not report the results of a health care intervention on human participants.