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Controlling the perovskite morphology and defects at the buried perovskite-substrate interface is challenging for inverted perovskite solar cells. In this work, we report an amphiphilic molecular hole transporter, (2-(4-(bis(4-methoxyphenyl)amino)phenyl)-1-cyanovinyl)phosphonic acid, that features a multifunctional cyanovinyl phosphonic acid group and forms a superwetting underlayer for perovskite deposition, which enables high-quality perovskite films with minimized defects at the buried interface. The resulting perovskite film has a photoluminescence quantum yield of 17% and a Shockley-Read-Hall lifetime of nearly 7 microseconds and achieved a certified power conversion efficiency (PCE) of 25.4% with an open-circuit voltage of 1.21 volts and a fill factor of 84.7%. In addition, 1–square centimeter cells and 10–square centimeter minimodules show PCEs of 23.4 and 22.0%, respectively. Encapsulated modules exhibited high stability under both operational and damp heat test conditions.

Parkinson’s disease (PD) is a neurodegenerative disorder that severely affects the motor system of patients. Early PD detection will greatly improve the quality of lives. However, existing automatic PD detection systems either rely on customized sensors or require users to perform special activities, using machine learning models whose prediction process is not understandable by medical professionals. In this article, we develop a non-disruptive PD detection system on smartphones based on interpretable prediction models. We design an application named PDGes to passively collect touchscreen and Inertial Measurement Unit data of users’ tapping and swiping actions on smartphones. Meaningful features that reflect finger dexterity , tremor , stiffness , and hand movement are extracted to build the prediction model. To better comprehend the decisions made by the model, we conduct a systematic analysis of feature importance to help validate the conformity of the model with clinical PD diagnosis. We collected data from 108 volunteers to evaluate the performance of PDGes . The experiment results show that PDGes achieves a detection accuracy of more than 94.5% on different smartphones.

Not Applicable.

Voice assistants (VA) have become prevalent on a wide range of personal devices such as smartphones and smart speakers. As companies build voice assistants with extra functionalities, attacks that trick a voice assistant into performing malicious behaviors can pose a significant threat to a user’s security, privacy, and even safety. However, the diverse attacks and stand-alone defenses in the literature often lack a systematic perspective, making it challenging for designers to properly identify, understand, and mitigate the security threats against voice assistants. To overcome this problem, this article provides a thorough survey of the attacks and countermeasures for voice assistants. We systematize a broad category of relevant but seemingly unrelated attacks by the vulnerable system components and attack methods, and categorize existing countermeasures based on the defensive strategies from a system designer’s perspective. To assist designers in planning defense based on their demands, we provide a qualitative comparison of existing countermeasures by the implementation cost, usability, and security and propose practical suggestions. We envision this work can help build more reliability into voice assistants and promote research in this fast-evolving area.

RNA-binding protein (RBP) dysregulation is functionally linked to several human diseases, including neurological disorders, cardiovascular disease, and cancer. Heterogeneous nuclear ribonucleoproteins (hnRNPs) are a diverse family of RBPs involved in nucleic acid metabolism. A growing body of studies has shown that the dysregulated hnRNPs play important roles in tumorigenesis. Here, we found that heterogeneous nuclear ribonucleoprotein C (C1/C2) (HNRNPC) had good performance in distinguishing between hepatocellular carcinoma (HCC) and normal liver tissues through bioinformatics analysis. Further investigation revealed that HNRNPC was significantly correlated with multiple malignant characteristics of HCC, including tumor size, microvascular invasion, tumor differentiation, and TNM stage. Patients with HCC with positive HNRNPC expression exhibited decreased overall survival and increased recurrence rate. HNRNPC downregulation inhibited HCC invasion and metastasis. The decreased expression of hypoxia inducible factor 1 subunit alpha (HIF1A) was identified as the molecular mechanism underlying HNRNPC downregulation-inhibited HCC metastasis by RNA sequencing. Mechanistically, HNRNPC downregulation decreased HIF1A expression by destabilizing HIF1A mRNA. HIF1A overexpression rescued the decrease in invasiveness and metastasis of HCC induced by HNRNPC downregulation. Additionally, interleukin (IL)-6/STAT3 signaling upregulated HNRNPC expression in HCC cells, and knockdown of HNRNPC significantly inhibited IL-6/STAT3-enhanced HCC metastasis. Furthermore, anti-IL-6 antibody siltuximab significantly inhibited IL-6-mediated HCC metastasis. In summary, our research revealed the clinical value, functional role, and molecular mechanism of HNRNPC in HCC and showed the potential of HNRNPC as a biomarker for diagnosis, prognosis, and further therapeutic targets for HCC.

A classification system for endocervical adenocarcinoma (ECA) based on high-risk human papillomavirus (HPV) status has been established; however, the immunohistochemical markers distinguishing HPV-independent and HPV-associated ECAs have not been fully described. Here, we aimed to characterize ECA immunopathological features.We evaluated the immunohistochemical profile of CLDN18, CDX2, PAX8, p16, p53, and CEA in 60 ECAs comprising 10 HPV-independent ECAs and 50 HPV-associated ECAs. Both the membranous and nuclear expression levels of CLDN18 were analyzed.Membranous CLDN18 (CLDN18 [M]) was found to be expressed in the mucinous epithelium of all HPV-independent ECAs, including eight gastric-type ECAs (G-ECAs), one endometrioid ECA, and one clear cell ECA, but no nuclear CLDN18 (CLDN18 [N]) expression was detected in HPV-independent ECAs. Among HPV-associated ECAs, CLDN18 (M) expression levels in intestinal-type (I-ECAs) and usual-type ECAs (U-ECAs) were significantly different from those in invasive stratified mucin-producing (iSMILE) carcinomas (p = 0.036). Positive CLDN18 (M) staining was present in 55.6% (5/9) of intestinal-type and 39.4% (13/33) of usual-type ECAs and was not present in iSMILE ECAs. Silva pattern C cancers expressed higher levels of CLDN18 (M) than Silva pattern A and B cancers (p = 0.004), whereas the CLDN18 (N) expression levels in cancers showing Silva pattern A were significantly higher than those in cancers exhibiting Silva patterns B and C (p 0.001).Membranous CLDN18 is expressed in ECAs and is particularly frequently expressed in HPV-independent ECAs, and membranous CLDN18 expression has potential as a therapeutic target. Nuclear staining of CLDN18 is a new immunohistochemical marker for diagnosing Silva pattern A HPV-associated ECAs and is associated with a good prognosis. Further studies should investigate the therapeutic and prognostic significance of membranous and nuclear CLDN18 expression and develop a related test that can be implemented in the clinical evaluation of ECAs.

Herb-induced liver injury results from the interplay between the herb and host with the herbal components serving as the major origin for hepatotoxicity. Although Polygoni Multiflori Radix (PMR) has been frequently reported to induce liver injury, contributions of its major components such as emodin, emodin-8-O-β-D-glucopyranoside, physcion and 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucopyranoside (TSG) towards its hepatotoxicity have not been clearly identified. Our initial cytotoxicity screenings of the major PMR components using rat hepatocytes identified emodin as the most toxic. Subsequently, the bile acid homeostasis-related mechanisms of emodin and its combination treatment with TSG in PMR-associated liver injury were explored in sandwich-cultured rat hepatocytes (SCRH) and verified in rats. In SCRH, emodin was found to be able to induce total bile acid accumulation in a dose-dependent manner. In both SCRH and rats, the presence of TSG significantly enhanced the hepatotoxicity of emodin via i) increasing its hepatic exposure by inhibiting its glucuronidation mediated metabolism; ii) enhancing its disruption on bile acid homeostasis through amplifying its inhibition on bile acid efflux transporters and its up-regulation on bile acids synthesis enzymes; iii) enhancing its apoptosis. Our study for the first time demonstrated the critical role of the combination treatment with emodin and TSG in PMR-induced liver injury.