ISAba1-mediated intrinsic chromosomal oxacillinase amplification confers carbapenem resistance in Acinetobacter baumannii.

Tandem amplification of carbapenemase genes increases gene copy number and enhances carbapenem resistance. These amplifications are often heterogeneous, transient, and located on plasmids, which also contribute to heteroresistance. Amplification of encoding genes is especially important for enzymes with low hydrolysis activity, which are often overlooked. Here, we reported an intrinsic oxacillinase oxaAb amplification flanked by ISAba1. The amplification is in the chromosome and contains up to 25 repeats. We provided genomic, transcriptomic, and proteomic evidence that the amplification resulted in oxacillinase overproduction. Notably, no point mutations of oxaAb were found during the amplification process. Strains of Acinetobacter baumannii with intrinsic amplified or external transformed ISAba1-oxaAb exhibited higher meropenem hydrolysis activity. Furthermore, the number of repeats in the amplification decreased gradually over a period of 21 d cultured with carbapenem withdrawal. However, upon re-exposure to meropenem, the ISAba1 flanked oxaAb responded rapidly, with repeat numbers reaching or exceeding pre-carbapenem withdrawal levels within 24 h. Taken together, these findings suggest that ISAba1-mediated gene amplification and overproduction of intrinsic low-activity oxacillinase oxaAb resulted in carbapenem resistance.

Emergence and ongoing outbreak of ST80 vancomycin-resistant Enterococcus faecium in Guangdong province, China from 2021 to 2023: a multicenter, time-series and genomic epidemiological study.

BACKGROUND: Surveillance systems revealed that the prevalence of vancomycin-resistant Enterococcus faecium (VREfm) has increased. We aim to investigate the epidemiological and genomic characteristics of VREfm in China. METHODS: We collected 20,747 non-redundant E. faecium isolates from inpatients across 19 hospitals in six provinces between January 2018 and June 2023. VREfm was confirmed by antimicrobial susceptibility testing. The prevalence was analyzed using changepoint package in R. Genomic characteristics were explored by whole-genome sequencing. RESULTS: 5.59% (1159/20,747) of E. faecium isolates were resistant to vancomycin. The prevalence of VREfm increased in Guangdong province from 5% before 2021 to 20-50% in 2023 (p < 0.0001), but not in the other five provinces. Two predominant clones before 2021, ST17 and ST78, were substituted by an emerging clone, ST80, from 2021 to 2023 (88.63%, 195/220). All ST80 VREfm from Guangdong formed a single lineage (SC11) and were genetically distant from the ST80 VREfm from other countries, suggesting a regional outbreak. All ST80 VREfm in SC11 carried a new type of plasmid harbouring a vanA cassette, which was embedded in a Tn1546-like structure flanked by IS1678 and ISL3. However, no conjugation-related gene was detected and no transconjugant was obtained in conjugation experiment, indicating that the outbreak of ST80 VREfm could be attributed to clonal transmission. CONCLUSIONS: We revealed an ongoing outbreak of ST80 VREfm with a new vanA-harbouring plasmid in Guangdong, China. This clone has also been identified in other provinces and countries, foreboding a risk of wider spreading shortly. Continuous surveillance is needed to inform public health interventions.

Aldehyde dehydrogenase 2 rs671 a/A Genotype is Associated with an Increased Risk of Early Onset Coronary Artery Stenosis.

Background: The role of aldehyde dehydrogenase 2 (ALDH2) in cardiovascular diseases has been gradually studied. However, it is unclear whether ALDH2 polymorphism is associated with the risk of early onset (onset age ≤55 years old in men and ≤65 years old in women) coronary artery stenosis (CAS). The association between ALDH2 single nucleotide polymorphism (SNP) rs671 and risk in patients with early onset CAS was investigated in this study. Methods: The study included 213 early onset CAS patients and 352 individuals without CAS were set as controls. The ALDH2 rs671 polymorphism was genotyped by polymerase chain reaction (PCR) - microarray. Differences in ALDH2 rs671 genotypes and alleles between patients and controls were compared. Multiple logistic regression analysis was performed after adjusting for gender, body mass index (BMI), smoking history, drinking history, and diabetes mellitus to assess the relationship between ALDH2 rs671 genotypes and early onset CAS risk. Results: The frequency of the ALDH2 rs671 G/G genotype was lower in the early onset CAS patients (43.7% vs 55.3%, p=0.007) than that in the controls. The frequency of the ALDH2 rs671 A allele was higher (32.9% vs 25.0%) than that in the controls (p=0.005). After adjusting for other confounding factors, multivariate logistic regression showed that ALDH2 rs671 A/A genotype (A/A vs G/G: odds ratio (OR) 2.508, 95% confidence interval (CI): 1.130-5.569, p=0.024), overweight (BMI≥24.0 vs 18.5-23.9: OR 5.047, 95% CI: 3.275-7.777, p<0.001), history of smoking (yes vs no: OR 2.813, 95% CI: 1.595-4.961, p<0.001), and diabetes mellitus (yes vs no: OR 2.191, 95% CI: 1.397-3.437, p=0.001) were the independent risk factors of early onset CAS. Conclusion: In men ≤55 years old and women ≤65 years old, individuals with ALDH2 rs671 A/A genotype, overweight (BMI ≥24.0 kg/m2), smoking history, and diabetes mellitus increased risk of developing CAS.

Strategies for Improving Efficiency and Stability of Inverted Perovskite Solar Cells.

Perovskite solar cells (PSCs) have attracted widespread research and commercialization attention because of their high power conversion efficiency (PCE) and low fabrication cost. The long-term stability of PSCs should satisfy industrial requirements for photovoltaic devices. Inverted PSCs with a p-i-n architecture exhibit considerable advantages because of their excellent stability and competitive efficiency. The continuously broken-through PCE of inverted PSCs shows huge application potential. This review summarizes the developments and outlines the characteristics of inverted PSCs including charge transport layers (CTLs), perovskite compositions, and interfacial regulation strategies. The latest effective CTLs, interfacial modification, and stability promotion strategies especially under light, thermal, and bias conditions are emphatically analyzed. Furthermore, the applications of the inverted structure in high-efficiency and stable tandem, flexible photovoltaic devices, and modules and their main obstacles are systematically introduced. Finally, the remaining challenges faced by inverted devices are discussed, and several directions for advancing inverted PSCs are proposed according to their development status and industrialization requirements.

Inhibition of EV71 replication by an interferon-stimulated gene product L3HYPDH.

Enterovirus 71 (EV71) is the common causative agent of hand-foot-mouth disease (HFMD). Despite evidence in mice model suggested that the interferon (IFN) signaling pathways play a role in defending against this virus, knowledge on the IFN-mediated antiviral response is still limited. Here we identified an IFN-stimulated gene (ISG) called L3HYPDH, whose expression inhibits EV71 replication. Mapping assay indicated that amino acids 61-120 and 295-354 are critical for its optimal antiviral activity. Mechanismly, L3HYPDH specifically inhibits protein translation mediated by EV71 internal ribosome entry site (IRES). Our data thus uncovered a new mechanism utilized by the host cell to restrict EV71 replication.

Association of Apolipoprotein E Gene Polymorphism with Type 2 Diabetic Nephropathy in the Southern Chinese Population.

Background: Common polymorphisms within the apolipoprotein E (APOE) gene are rs429358 and rs7412, which result in three major alleles (ɛ2, ɛ3, and ɛ4) and six genotypes (E2/E2, E2/E3, E3/E3, E3/E4, E4/E4, and E2/E4). Although APOE gene polymorphisms have been suggested to be associated with the development of diabetic nephropathy (DN), their potential association remains unclear in different regions. This study aims to unveil the genetic effects of APOE gene polymorphisms on DN susceptibility and serum lipid profiles in southern Chinese population. Methods: A total of 306 DN patients and 483 type 2 diabetic patients as controls were included in the study. The APOE gene polymorphisms were analyzed by polymerase chain reaction (PCR) microarray gene chip. Relevant medical records and information of these participants were collected. Results: There were statistically significant differences (p < 0.05) in gender, SBP, hypertension, hyperuricemia, UTP, TG and HDL-C between DN patients and controls. DN patients exhibited a higher frequency of the ε2 allele and E2/E3 genotype than controls (p < 0.001). Logistic regression analysis indicated that the ε2 allele and E2/E3 genotype were independent risk factors (adjusted OR: 3.237, 95% CI: 1.789-5.854, p < 0.001; adjusted OR: 3.453, 95% CI: 1.873-6.368, p < 0.001), while the ε3 allele or E3/E3 genotype might serve as protective role (adjusted OR: 0.395, 95% CI: 0.255-0.612, p < 0.001) for development of DN. Conclusion: Our study indicates a correlation between APOE polymorphisms and DN in the southern Chinese Hakka population. Specifically, individuals carrying the APOE ε2 allele and E2/E3 genotype are at a higher risk of developing DN. Conversely, those with the APOE ε3 allele and E3/E3 genotype have a lower risk of DN in southern Chinese population.

High-throughput sequencing-based Detection of Japanese encephalitis virus and its effect on micro ribonucleic acid.

it was to explore the mechanism of Japanese encephalitis virus (JEV) and micro ribonucleic acid (miRNA) under high-throughput sequencing. 20 experimental mice, with good growth status and no disease infection, were selected. The cells used in the experiment included mouse microglial cell line (BV2), mouse neuroblastoma cell line (NA), and mouse brain endothelial cell line (bEnd.3). JEV titration was performed with JEV-infected cells, ribonucleic acid (RNA) in the cells was extracted, and finally the miRNA high-throughput sequencing data was analyzed. Agarose gel electrophoresis showed that the 28S and 18S electrophoresis bands were bright. Among the miRNAs detected in mouse brain tissues, 2986 were down-regulated and 1251 were up-regulated. Among miRNAs detected in NA cells, 4238 the decreasing expression and 2356 were expressed increasingly. In reducing miRNA expression, 1 multiplicity of infection (MOI) of P3 strain infection was more significant than 0.1 MOI. 10 miRNAs with significantly decreasing expression were miR-466d-3p, miR-381-3p, miR-540-3p, miR-466a-3p, miR-467a-3p, miR-574-5p, miR-199a-5p, miR-467a-5p, miR-674-5p, and miR-376b-3p. These were all obviously down-regulated in JEV-infected BV2, NA, and bEnd.3 neurons. High-throughput sequencing of JEV-infected mouse brain tissues and mouse neuronal cells found that JEV infection led to down-regulation of overall miRNA expression in host cells.

Component Distribution Regulation in Sn-Pb Perovskite Solar Cells through Selective Molecular Interaction.

Tin-lead (Sn-Pb) perovskite solar cells (PSCs) with near-ideal bandgap still lag behind the pure lead PSCs. Disordered heterojunctions caused by inhomogeneous Sn/Pb ratio in the binary perovskite film induce large recombination loss. Here, an Sn-Pb perovskite film is reported with homogeneous component and energy distribution by introducing hydrazine sulfate (HS) in Sn perovskite precursor. HS can form hydrogen bond network and coordinate with FASnI3 thus no longer bond with Pb2+ , which reduces the crystallization rate of tin perovskite to the level of lead analog. The strong bonding between SO4 2- and Sn2+ can also suppress its oxidation. As a result, the Sn-Pb PSCs with HS exhibit a significantly improved VOC of 0.91 V along with a high efficiency of 23.17%. Meanwhile, the hydrogen bond interaction network, strong bonding between Sn2+ and sulfate ion also improve the thermal, storage, and air stability of resulting devices.

Colorimetry-Based Phosphate Measurement for Polymerase Elongation.

DNA detection, which includes the measurement of variants in sequences or the presence of certain genes, is widely used in research and clinical diagnosis. Both require DNA-dependent DNA polymerase-catalyzed strand extension. Currently, these techniques rely heavily on the instruments used to visualize the results. This study introduced a simple and direct colorimetric method to measure polymerase-directed elongation. First, pyrophosphate (PPi), a by-product of strand extension, is converted into phosphate (Pi). Phosphate levels were measured using either Mo-Sb or BIOMOL Green reagent. This study showed that this colorimetry can distinguish single-base variants and detect PCR products in preset stringent conditions, implicating the potential value of this strategy to detect DNA.

Clinical, epidemiological, and drug resistance insights into HIV-positive patients in Meizhou, China.

The acquired immunodeficiency syndrome (AIDS) epidemic, resulting from human immunodeficiency virus (HIV) infection, exhibits distinct regional characteristics. This study undertakes a retrospective analysis of the epidemiological and clinical features of 195 HIV-positive cases in Meizhou, China, from May 1, 2018 to December 31, 2019. Western blotting (WB) confirmed and assessed these cases. Notably, the majority of cases emanated from socio-economic groups with comparatively lower levels of education, with 80% being male. Strikingly, 90% of the cases were found to be in the middle to late stages of infection based on CD4+ T cell counts. Among the 30 different serum antibody profiles examined, reactivity with seven bands (p24, p31, gp41, p51, p66, gp120, and gp160) emerged as the most commonly observed WB pattern. The absence of specific bands, specifically p55 (17.44%), p39 (32.31%), and p17 (25.64%) were most frequent, with the detection frequency of p17 bands significantly reduced among cases in the AIDS and middle stages. An analysis of drug resistance genotypes indicated that, despite viral mutations conferring resistance to certain reverse transcriptase inhibitors, the first-line treatment regimen remained effective for patients in Meizhou. Notably, mutations resistant to protease inhibitors were infrequent (2.7%), suggesting that incorporating protease inhibitors into the treatment regimen may enhance therapeutic outcomes for local patients. These findings provide essential insights into the specific epidemiological patterns, serum antibody profiles, and drug resistance genotypes of HIV-infected patients in Meizhou. Significantly, this research contributes to the formulation of future treatment strategies tailored to the local context.

IG1, a Mansonone F Analog, Exhibits Antibacterial Activity against Staphylococcus aureus by Potentially Impairing Cell Wall Synthesis and DNA Replication.

Infection caused by Staphylococcus aureus, especially methicillin-resistant S. aureus (MRSA), is very common in communities and hospitals, which poses a great challenge to human health. Therefore, increasing attention has been paid to finding effective antimicrobial agents. Mansonone F is a natural compound which has an oxaphenalene skeleton and anti-S. aureus activity, but its sources are limited and its synthesis is difficult. Thus, IG1, a C9-substituent mansonone F analog, was assessed for its activity against Staphylococcus aureus and its mechanism of action was investigated. Antimicrobial susceptibility assays showed that IG1 has strong antibacterial activity against S. aureus, including MRSA, with minimum inhibitory concentrations (MICs) ranging from 0.5 to 2 µg/mL, which were very close to those of vancomycin, and these changed little, even with an increase in the amount of the inoculum. To further explore the antibacterial properties of IG1, time-kill experiments were conducted. Compared with vancomycin and moxifloxacin, treatment with different concentrations of IG1 reduced the viability of organisms in a very similar manner and the reduction was not significant, which indicated that IG1 is a potentially strong anti-S. aureus agent. Finally, the antibacterial mechanism was analyzed, with flow cytometric analysis revealing that IG1 treatment resulted in a time-dependent decrease in the DNA content of S. aureus. Transmission electron microscopy (TEM) analysis showed that very few dividing cells could be found and the cell wall was damaged in the field of IG1-treated cells. These results indicate that IG1 is a potential new antibacterial agent against S. aureus, including MRSA.

A Novel Multicolor Flow Cytometry Scoring System for the Diagnosis and Prognostic Stratification of Myelodysplastic Syndromes.

BACKGROUND: Myelodysplastic syndromes (MDS) are a class of myeloid neoplasms featuring inefficient maturation and differentiation of hematopoietic cells, blood cytopenia, and a high risk of leukemia onset. The diagnosis of MDS remains a challenging task owing to its complexity, heterogeneity, and the lack of specific characteristics. METHODS: To look for an easy and inexpensive diagnostic method for MDS, we tried to establish an FCM scoring systems (FCSS) with a combination of antibodies for diagnosis and prognostic stratification of MDS. This FCSS adopted four parameters; i.e., the frequency of myeloblasts in nucleated cells, the ratio between pro-B cells and CD117+ cells, the ratio of CD45 mean fluorescence intensity between lymphocytes and myeloblasts, and the ratio of SSC peak values between mature granulocytes and lymphocytes. RESULTS: We tested the correlation between the total FCSS score with conventional IPSS-R. Additionally, the correlation between the score of each FCSS parameter and IPSS-R was also evaluated. We found that total FCSS score had a positive correlation with IPSS-R, while FCSS parameter 1 and 4 were also correlated with IPSS-R. Furthermore, this FCSS had a sound sensitivity and specificity in the diagnosis of MDS. CONCLUSIONS: The FCSS represents a convenient and affordable approach for the diagnosis and prognostic stratification of MDS.

Effects of APOE gene ε4 allele on serum lipid profiles and risk of cardiovascular disease and tumorigenesis in southern Chinese population.

BACKGROUND: Human apolipoprotein E (APOE) polymorphisms are attributable to the presence of three common alleles, namely, ε2, ε3, and ε4, which generate six genotypes, viz, E2/E2, E2/E3, E3/E3, E3/E4, E4/E4, and E2/E4. APOE polymorphisms are associated with all types of tumors and cardiovascular diseases (CVD). However, the relationship between the type of APOE polymorphisms and tumorigenesis remains debatable. Therefore, we aimed to investigate the role of APOE polymorphisms on the tumor with or without CVD in southern China. METHODS: A total of 1438 participants were categorized into 4 groups: 409 patients with tumor, 369 patients with CVD, 338 patients with both tumor and CVD, and 322 controls. APOE polymorphisms were determined by genotyping assay. The factors influencing tumor patients with or without CVD were also analyzed by logistic regression analysis. RESULTS: The present study involved different types of solid tumors. Lung cancer was the most common cancer (20.2%, 151/747), followed by colorectal (17%, 127/747), esophageal (9.8%, 73/747), and liver (8.7%, 65/747) cancers. E3/E3 was the most frequent genotype, and ɛ3 was the greatest allele frequency in our study population. The frequencies of the E3/E3, E3/E4, E2/E3, E2/E4, E4/E4, and E2/E2 genotypes in tumor patients were 76.97% (575/747), 14.19% (106/747), 6.83% (51/747), 1.2% (9/747), 0.4% (3/747), and 0.4% (3/747), respectively. Tumor patients carrying ε3 with or without CVD showed higher levels of TG, TC, and LDL-C and lower levels of HDL-C compared to the controls carrying ε3. On the other hand, the tumor patients carrying ε4 with or without CVD showed higher levels of TG and LDL-C and lower levels of HDL-C (all P < 0.05). The frequency of APOE ε4 allele and the E3/E4 genotype was relatively greater in tumor or CVD patients (P < 0.001). In addition, ε4 allele acted as an independent risk factor for tumor patients group (P = 0.037, adjusted OR = 1.92, 95% CI 1.04-3.55) and tumor + CVD patients group (P = 0.012, adjusted OR = 2.53, 95% CI 1.22-5.23). CONCLUSIONS: Individuals carrying ε4 are at a higher risk of tumor with or without CVD, and APOE polymorphisms affect the serum lipid profiles.

Type I Interferon-Induced TMEM106A Blocks Attachment of EV-A71 Virus by Interacting With the Membrane Protein SCARB2.

Enterovirus A71 (EV-A71) and Coxsackievirus A16 (CV-A16) are the main causative agents of hand, foot and mouth disease (HFMD) worldwide. Studies showed that EV-A71 and CV-A16 antagonize the interferon (IFN) signaling pathway; however, how IFN controls this viral infection is largely unknown. Here, we identified an IFN-stimulated gene, Transmembrane Protein 106A (TMEM106A), encoding a protein that blocks EV-A71 and CV-A16 infection. Combined approaches measuring viral infection, gene expression, and protein interactions uncovered that TMEM106A is required for optimal IFN-mediated viral inhibition and interferes with EV-A71 binding to host cells on the receptor scavenger receptor class B member 2 (SCARB2). Our findings reveal a new mechanism contributing to the IFN-mediated defense against EV-A71 and CV-A16 infection and provide a potential strategy for HFMD treatment by using the antiviral role of TMEM106A against enterovirus.

Inducible co-stimulator inhibits lipid phagocytosis of human aortic smooth muscle cells by down-regulating CD36 expression.

BACKGROUND: To explore the potential mechanism of inducible co-stimulator (ICOS) inhibition of lipid phagocytosis in human aortic smooth muscle cells (HASMCs). METHODS: Excess Dil (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate)-labeled oxidized low-density lipoprotein (ox-LDL) was used to induce HASMCs to form a foam cell model; HASMCs were cultured together with ICOS-overexpressed JurKat (JK-ICOS) cells or recombinant human ICOS protein (rICOS protein) to be stimulated, and a confocal laser microscope was used to observe the lipid phagocytosis of HASMCs. Reverse transcription quantitative polymerase chain reaction (RT-qPCR), western blot, and immunofluorescence staining were used to detect the expression of the lipid phagocytic receptor, cluster of differentiation 36 (CD36) in HASMCs. RESULTS: The uptake of Dil ox-LDL by HASMCs was concentration-dependent, and excessive Dil ox-LDL uptake led to lipid accumulation in HASMCs. Pretreatment with JK-ICOS cells or rICOS protein for HASMCs 48 hours reduced Dil ox-LDL-induced lipid accumulation. Compared with HASMCs co-cultured with empty lentiviral JurKat (JK-EV) cells, the messenger RNA (mRNA) and protein expressions of CD36 in HASMCs co-cultured with JK-ICOS cells were significantly down-regulated. The results of immunofluorescence staining showed that co-culturing with JK-ICOS cells could down-regulate ox-LDL-induced expression of CD36 in HASMCs, but JK-EV cells could not. Similarly, the results of qPCR, western blot, and immunofluorescence staining showed that rICOS protein could down-regulate the ox-LDL-induced expression of CD36 in HASMCs, but this down-regulation was not as significant as that in JK-ICOS cells. CONCLUSIONS: ICOS could inhibit the lipid phagocytosis of HASMCs by down-regulating the expression of CD36, suggesting a potential anti-atherosclerosis (anti-AS) mechanism of ICOS, and preventing ox-LDL-induced formation of myogenic foam cells.

Tanshinone IIA and its derivative activate thermogenesis in adipocytes and induce "beiging" of white adipose tissue.

Tanshinone IIA (TAN2A) is a major active ingredient of Salvia miltiorrhiza used in traditional Chinese medicine and tanshinone 20 (TAN20) is a derivative of TAN2A. In this study, we examined the effects of TAN2A and TAN20 on adipogenesis, lipid metabolism, and thermogenesis. Our experiments showed that both TAN2A and TAN20 increased mitochondria content in adipose tissue, enhanced energy expenditure, reduced body weight, and improved insulin sensitivity and metabolic homeostasis in obese and diabetic mouse models. We demonstrated that TAN20 can facilitate the transformation from white to beige adipose tissue, as well as activate brown adipose tissue. In uncoupling protein 1 (UCP1) knockout mouse model, the effects of TAN2A and TAN20 on body weight and glucose tolerance were not observed, suggesting that such effects were UCP1 dependent. Furthermore, we found that TAN2A and TAN20 increased the expression of UCP1 and other thermogenic genes in adipocytes through AMPK-PGC-1α signaling pathway. Our findings indicate that TAN2A and its derivative TAN20 are potential interesting energy expenditure regulators and may be implicated in treatment of obesity and other metabolic disorders.

Chemical reagents modulate nucleic acid-activated toll-like receptors.

Nucleic acid-mediated interferon signaling plays a pivotal role in defense against microorganisms, especially during viral infection. Receptors sensing exogenous nucleic acid molecules are localized in the cytosol and endosomes. Cytosolic sensors, including cGAS, RIG-I, and MDA5, and endosome-anchored receptors are toll-like receptors (TLR3, TLR7, TLR8, and TLR9). These TLRs share the same domain architecture and have similar structures, facing the interior of endosomes so their binding to nucleic acids of invading pathogens via endocytosis is possible. The correct function of these receptors is crucial for cell homeostasis and effective response against pathogen invasion. A variety of endogenous mechanisms modulates their activities. Nevertheless, naturally occurring mutations lead to aberrant TLR-mediated interferon (IFN) signaling. Furthermore, certain pathogens require a more robust defense against control. Thus, manipulating these TLR activities has a profound impact. High-throughput virtual screening followed by experimental validation led to the discovery of numerous chemicals that can change these TLR-mediated IFN signaling activities. Many of them are unique in selectivity, while others regulate more than one TLR due to commonalities in these receptors. We summarized these nucleic acid-sensing TLR-mediated IFN signaling pathways and the corresponding chemicals activating or deactivating their signaling.

Constructing heterojunctions by surface sulfidation for efficient inverted perovskite solar cells.

A stable perovskite heterojunction was constructed for inverted solar cells through surface sulfidation of lead (Pb)-rich perovskite films. The formed lead-sulfur (Pb-S) bonds upshifted the Fermi level at the perovskite interface and induced an extra back-surface field for electron extraction. The resulting inverted devices exhibited a power conversion efficiency (PCE) >24% with a high open-circuit voltage of 1.19 volts, corresponding to a low voltage loss of 0.36 volts. The strong Pb-S bonds could stabilize perovskite heterojunctions and strengthen underlying perovskite structures that have a similar crystal lattice. Devices with surface sulfidation retained more than 90% of the initial PCE after aging at 85°C for 2200 hours or operating at the maximum power point under continuous illumination for 1000 hours at 55° ± 5°C.

Radical Form of PbI2: A New Defect Passivator for Efficient Perovskite Solar Cells.

PbI2 is a commonly used passivator for defect passivation in perovskite solar cells (PSCs). However, the poor conductivity nature of PbI2 may limit the further improvement of device performance. Here, we report a radical form of PbI2 with high conductivity to passivate defects for efficient PSCs through a combination of N,N,N',N'-tetramethylbenzidine (TMB). When PbI2 is combined with TMB, 4 orders of magnitude higher conductivity will be achieved owing to the formation of a TMB-PbI2 radical. As a result, the device performance is impressively increased from 20.48 to 22.63%. In addition, the device stability is also greatly improved and 95% of the initial efficiency is retained after aging at 85 °C for 600 h.