Weiqiang Zhang

Off-target drift from aerial pesticide applications in croplands can be a major source of pesticide exposure to pollinators. Pesticide adjuvants (PAs) are added to pesticides but can be as toxic as pesticides’ active ingredients. Ongoing experiments have identified sodium alginate (SA) as a drift-reducing PA less toxic to honeybees. Hence, SA and fenugreek polymer (FP) have been tested as drift-reducing PAs for aerial applications using the Remotely Piloted Aerial Application System (RPAAS). Two spray experiments were carried out in the field: (i) water only (W) and (ii) water and adjuvant (WA). Droplet spectrum and on-target coverage were collected using a VisiSize P15 image analyzer and kromekote cards, respectively. The drift reduction potentials (DRPs) of the adjuvants were analyzed based on droplet size (diameters of 10%, 50%, and 90% volume) and the proportion of driftable volume with droplets < 200 µm. Compared to the W only, the W-A treatment produced larger droplets, suggesting the presence of DRP. There were 14.5%, 8.3% to 14.4%, and 2.3% to 7.7% driftable fines in the W, WA (SA), and WA (FP) treatments, respectively. The FP treatment improved the on-target coverage (3.0% to 3.1%) compared to water (2.7%). Our results indicate that SA and FP have the potential to mitigate off-target drift and protect pollinator health.

Many metastatic cancers with poor prognoses correlate to downregulated CD82, but exceptions exist. Understanding the context of this correlation is essential to CD82 as a prognostic biomarker and therapeutic target. Oral squamous cell carcinoma (OSCC) constitutes over 90% of oral cancer. We aimed to uncover the function and mechanism of CD82 in OSCC. We investigated CD82 in human OSCC cell lines, tissues, and healthy controls using the CRISPR-Cas9 gene knockout, transcriptomics, proteomics, etc. CD82 expression is elevated in CAL 27 cells. Knockout CD82 altered over 300 genes and proteins and inhibited cell migration. Furthermore, CD82 expression correlates with S100 proteins in CAL 27, CD82KO, SCC-25, and S-G cells and some OSCC tissues. The 37–50 kDa CD82 protein in CAL 27 cells is upregulated, glycosylated, and truncated. CD82 correlates with S100 proteins and may regulate their expression and cell migration. The truncated CD82 explains the invasive metastasis and poor outcome of the CAL 27 donor. OSCC with upregulated truncated CD82 and S100A7 may represent a distinct subtype with a poor prognosis. Differing alternatives from wild-type CD82 may elucidate the contradictory functions and pave the way for CD82 as a prognostic biomarker and therapeutic target.

Background: To determine the safety of Botox and its potential effect on alleviating radiation therapy (RT)‐induced sialadenitis in head and neck cancer patients.Methods: Twenty patients with stage III/IV head and neck cancer were randomized to receive Botox or saline injections into both submandibular glands (SMG). There were three visits: one before RT (V1); 1 week after RT (V2); and 6 weeks after RT (V3), each of which included saliva collection, a 24‐h dietary recall, and a quality‐of‐life survey.Results: No adverse events were observed. While the control group was much older, the Botox group more commonly underwent induction chemotherapy compared with controls. From V1 to V2, salivary flow decreased in both groups, but only in the control group from V1 to V3. CXCL‐1 (GRO), a neutrophil chemoattractant, was lower in the Botox group compared with the control group at V3.Conclusion: Botox can be safely administered to the salivary glands prior to external beam radiation without observed complications or side‐effects. After an initial reduction in salivary flow following RT, the Botox group showed lack of further flow reduction compared with controls. The inflammatory marker CXCL 1, which was reduced in the in Botox group at V3, may be a candidate for further studies of radiation‐induced sialadenitis.

A design method of electrode-tissue interface equivalent circuit for the voltage injection test of active implantable neurostimulator (INS) is presented and analyzed. In this proposed method, characteristic frequencies of the equivalent circuit are determined, based on the published data of human tissue permittivity and conductivity. The equivalent circuit structure is defined, according to "electrode-tissue" interface model. Appropriate values of electronic components are matched by simulation. In addition, a method of replacing the electrode-tissue interface equivalent circuit with purely resistance is also proposed. According to ISO14708-3, voltage injection tests are carried out with these different equivalent circuits and INS. Results showed that these design methods can meet test requirements with no significant difference. This study explored convenient and universal methods for the voltage injection test of INS, which is useful to improve the guarantee of the electromagnetic compatibility (EMC) safety of the INS.Clinical Relevance— This study is helpful to realize the convenient EMC test of INS, and provide guarantee for the safety of clinical use.

The disruption of the inflammatory microenvironment in the uterus affects pregnancy outcome. However, the exact quantification and distribution of leukocyte subpopulations in the uterus in preeclampsia (PE) have not been clearly characterized. Inflammasomes promote the release of proinflammatory cytokines interleukin (IL)-β and IL-18. A higher expression of NLRP3 inflammasome in placentas contributes to excessive inflammation in PE. However, related studies on the uterus are scarce. We aimed to investigate changes in the infiltration of leukocyte subpopulations in decidual and uterine tissues, and explore the role of activation of uterine NLRP3 inflammasomes in PE. Decidual tissues were collected from normotensive pregnant women and preeclamptic women. A PE-like model was established via administration of lipopolysaccharide to normal pregnant rats. Uterine and decidual tissues were collected from all experimental groups. It was found that the number of leukocytes was significantly elevated in decidual and uterine tissues in PE patients compared to normal controls. The leukocytes (predominantly macrophages and NK cells) particularly infiltrated into the decidua and uterine decidua in PE-like rats, and these were sparse in the myometrium. The NLRP3 immunoreactivity in the uterus was extremely little in control rats, its immunoreactivity and caspase-1 immunoreactivity were significantly elevated in the PE-like rats; the mRNA expression results also indicated an upward trend in the activation of NLRP3 inflammasomes. These results support that leucocyte infiltration in the decidua and uterine deciduas, and the activation of NLRP3 inflammasome in the uterus, which participate in the pathogenesis, are responsible for the excessive inflammation at the maternal-fetal interface during PE. This article is protected by copyright. All rights reserved

Two siblings with CF are homozygous for F508del (referred to as Subject A and Subject B). Despite having the same CFTR genotype and similar environment, these two subjects exhibited different disease phenotypes. We analyzed their medical records and CF Foundation Registry data and measured inflammatory protein mediators in their sputum samples. Then, we examined the longitudinal relationships between inflammatory markers and disease severity for each subject and compared between them. Subject A presented a more severe disease than Subject B. During the study period, Subject A had two pulmonary exacerbations (PEs) whereas Subject B had one mild PE. The forced expiratory volume in 1 s (FEV₁, % predicted) values for Subject A were between 34–45% whereas for Subject B varied between 48–90%. Inflammatory protein mediators associated with neutrophils, Th1, Th2, and Th17 responses were elevated in sputum of Subject A compared with Subject B, and also in samples collected prior to and during PEs for both subjects. Neutrophilic elastase (NE) seemed to be the most informative biomarkers. The infectious burden between these two subjects was different.

(1) Background: many rare cystic fibrosistransmembrane conductance regulator (CFTR) mutations remain poorly characterized with regard to functional consequences of the mutation. We present the clinical features of two pediatric cystic fibrosis (CF) subjects who are heterozygous for F1099L (c.3297C>G), one with G551D (a class III mutation) and one with 3849 + 10kbC->T (a class V mutation). We also identified the molecular defect(s) that are associated with F1099L mutation to correlate with the clinical features that we observed; (2) Methods: clinical findings and history were extracted from the electronic medical record and de-identified. F1099L-CFTR protein expression level and maturation status, channel function, and the effects of CFTR modulation on these characteristics were investigated using western blotting and iodide efflux assay; (3) Results: these two subjects have mild CF phenotypes when F1099L is combined with two known disease-causing mutations. F1099L-CFTR has a moderate defect in processing and maturation, causing fewer CFTR channels at the cell surface and, therefore, impaired channel activities. These defects could be effectively corrected using VX-809 (lumacaftor); and, (4) Conclusions: our biochemical data correlate with the disease manifestations and suggest that F1099L is potentially a CF-causing mutation. The study expands our knowledge of rare CFTR mutations and may help in developing effective therapies for subjects with F1099L mutation.