The performance of perovskite solar cells (PSCs) strongly depends on the electron transport layer (ETL), perovskite absorber, hole transport layer (HTL), and their interfaces. Herein, the first approach to utilize ultrathin 2D titanium‐carbide MXenes (Ti3C2Tx quantum dots, TQD) by engineering the perovskite/TiO2 ETL interface and perovskite absorber and introducing Cu1.8S nanocrystals to perfect the Spiro‐OMeTAD HTL is represented. A significant hysteresis‐free power conversion efficiency improvement from 18.31% to 21.64% of PSCs is achieved after modifications with the enhanced short‐circuit current density, open‐circuit voltages, and fill factor. Various advanced characterizations, including femtosecond transient absorption spectroscopy, electrochemical impedance spectroscopy, and ultraviolet photoelectron spectroscopy, elucidate that the TQD/Cu1.8S significantly contribute to the improved crystalline quality of the perovskite film with its large grain size and improved electron/holes extraction efficiencies at perovskite/ETL and perovskite/HTL interfaces. Furthermore, the long‐time ambient and light stability of PSCs are largely boosted through the TQD and/or Cu1.8S nanocrystals doping, originating from the better crystallization of perovskite, suppressing the film aggregation and crystallization of HTL, and inhibiting the ultraviolet‐induced photocatalysis of the ETL. The findings highlight the TQD and Cu1.8S can act as a superfast electrons and holes tunnel for the optoelectronic devices.

BackgroundCoronary tortuosity (CT) is a common coronary angiography finding. The exact pathogenesis, clinical implication and long-term prognosis of CT are not fully understood. The purpose of this study is to investigate the clinical characteristics of CT in patients with suspected coronary artery disease(CAD) in a Chinese population.MethodsA total of 1010 consecutive patients underwent coronary angiography with complaints of chest pain or related symptoms were included in the present study (544 male, mean age: 64±11 years). CT was defined by the finding of ≥3 bends (defined as ≥45° change in vessel direction) along main trunk of at least one artery in systole and in diastole. Patients with or without CAD were further divided into CT-positive and CT-negative groups, all patients were followed up for the incidence of major adverse cardiovascular events (MACE) for 2 to 4 years.ResultsThe prevalence of CT was 39.1% in this patient cohort and incidence of CT was significantly higher in female patients than that in male patients (OR = 2.603, 95%CI 1.897, 3.607, P<0.001). CT was positively correlated with essential hypertension (OR = 1.533, 95%CI 1.131, 2.076, P = 0.006) and negatively correlated with CAD (OR = 0.755, 95%CI 0.574, 0.994, P = 0.045). MACE during follow up was similar between CAD patients with or without CT.ConclusionsCT is more often seen in females and positively correlated with hypertension and negatively correlated with coronary atherosclerosis.

Pollution triggered by highly toxic heavy metal ions has become of worldwide critical concern; thus, it is urgent to develop an eco-friendly and nontoxic fluorescence probe for metal ions sensing. The lead-free all-inorganic perovskite quantum dots (PeQDs) could be ideal candidates but are limited by their low photoluminescence quantum yield (PLQY). In this work, we successfully fabricated Eu3+-doped lead-free Cs3Bi2Br9 PeQDs employing a modified ligand-assisted reprecipitation method. The Cs3Bi2Br9:Eu3+ PeQDs demonstrate multicolor emissions including the exciton emission of the PeQDs and the5D0–7F J transition for Eu3+ ion. Compared to the bare Cs3Bi2Br9 PeQDs, the Eu3+-doped PeQDs display highly improved PLQY from 18% to ∼42.4% and excellent water stability. Finally, nontoxic and highly efficient Cs3Bi2Br9:Eu3+ PeQDs were employed as a highly sensitive fluorescent probe for Cu2+ ion detection in water, which demonstrates a good linear range from 5 nM to 3 μM with a correlation coefficient of 0.996 and a low detection limit of 10 nM. Our work not only provides a new strategy to improve the optical performance of lead-free PeQDs but also expands their applications for metal ions sensing.

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Since selective detection of multiple narrow spectral bands in the near-infrared (NIR) region still poses a fundamental challenge, we have, in this work, developed NIR photodetectors (PDs) using photon upconversion nanocrystals (UCNCs) combined with perovskite films. To conquer the relatively high pumping threshold of UCNCs, we designed a novel cascade optical field modulation strategy to boost upconversion luminescence (UCL) by cascading the superlensing effect of dielectric microlens arrays and the plasmonic effect of gold nanorods, which readily leads to a UCL enhancement by more than four orders of magnitude under weak light irradiation. By accommodating multiple optically active lanthanide ions in a core-shell-shell hierarchical architecture, developed PDs on top of this structure can detect three well-separated narrow bands in the NIR region, i.e., those centered at 808, 980, and 1540 nm. Due to the large UCL enhancement, the obtained PDs demonstrate extremely high responsivities of 30.73, 23.15, and 12.20 A W−1 and detectivities of 5.36, 3.45, and 1.91 × 1011 Jones for 808, 980, and 1540 nm light detection, respectively, together with short response times in the range of 80–120 ms. Moreover, we demonstrate for the first time that the response to the excitation modulation frequency of a PD can be employed to discriminate the incident light wavelength. We believe that our work provides novel insight for developing NIR PDs and that it can spur the development of other applications using upconversion nanotechnology.

The chronic inflammatory process including cytomegalovirus (CMV) infection has been hypothesized to induce the progression of atherosclerosis in coronary heart disease (CHD). Numbers studies were conducted to analyze the association between CMV infection and risk of CHD, but no clear consensus had been reached. To assess this relationship more precisely, a meta-analysis was performed. The electronic databases PubMed, Embase, and CNKI were searched; data were extracted and analyzed independently by two investigators. Ultimately, 55 studies, involving 9,000 cases and 8,608 controls from six prospective studies (all with a nested case-control design) and 49 retrospective case-control studies were included. Overall, people exposed to CMV infection had an odds ratio (OR) of 1.67 (95% CI, 1.56-1.79) for CHD risk, relative to those not exposed. CMV infection was clearly identified as a risk factor for CHD in both prospective studies (OR, 1.31; 95% CI, 1.132-1.517) and retrospective studies (OR, 1.79; 95% CI, 1.659-1.939), and in both Asian group (OR, 2.69; 95% CI, 2.304-3.144) and non-Asian group (OR, 1.48; 95% CI, 1.371-1.600). Interestingly, in the subgroup analyses by detection methods of CMV, the increased risk (OR, 8.121) was greater among studies using polymerase chain reaction than the risk (OR, 1.561) among studies using enzyme-linked immunosorbent assay. In conclusion, this meta-analysis suggested that CMV infection is associated with an increased risk for CHD, especially among Asian populations.

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Various diseases can cause skeletal muscle atrophy, usually accompanied by inflammation, mitochondrial dysfunction, apoptosis, decreased protein synthesis, and enhanced proteolysis. The underlying mechanism of inflammation in skeletal muscle atrophy is extremely complex and has not been fully elucidated, thus hindering the development of effective therapeutic drugs and preventive measures for skeletal muscle atrophy. In this review, we elaborate on protein degradation pathways, including the ubiquitin-proteasome system (UPS), the autophagy-lysosome pathway (ALP), the calpain and caspase pathways, the insulin growth factor 1/Akt protein synthesis pathway, myostatin, and muscle satellite cells, in the process of muscle atrophy. Under an inflammatory environment, various pro-inflammatory cytokines directly act on nuclear factor-κB, p38MAPK, and JAK/STAT pathways through the corresponding receptors, and then are involved in muscle atrophy. Inflammation can also indirectly trigger skeletal muscle atrophy by changing the metabolic state of other tissues or cells. This paper explores the changes in the hypothalamic-pituitary-adrenal axis and fat metabolism under inflammatory conditions as well as their effects on skeletal muscle. Moreover, this paper also reviews various signaling pathways related to muscle atrophy under inflammatory conditions, such as cachexia, sepsis, type 2 diabetes mellitus, obesity, chronic obstructive pulmonary disease, chronic kidney disease, and nerve injury. Finally, this paper summarizes anti-amyotrophic drugs and their therapeutic targets for inflammation in recent years. Overall, inflammation is a key factor causing skeletal muscle atrophy, and anti-inflammation might be an effective strategy for the treatment of skeletal muscle atrophy. Various inflammatory factors and their downstream pathways are considered promising targets for the treatment and prevention of skeletal muscle atrophy.