RbPbI3 Seed Embedding in PbI2 Substrate Tailors the Facet Orientation and Crystallization Kinetics of Perovskites.

High power conversion efficiencies (PCEs) in perovskite solar cells (PSCs) have always been awe-inspiring, but perovskite films scalability is an exacting precondition for PSCs commercial deployment, generally unachievable through the antisolvent technique. On the contrary, in the two-step sequential method, the perovskite's uncontrolled crystallization and unnecessary PbI2 residue impede the device's performance. These two issues motivated to empower the PbI2 substrate with orthorhombic RbPbI3 crystal seeds, which act as grown nuclei and develop orientated perovskites lattice stacks, improving the perovskite films morphologically and reducing the PbI2 content in eventual perovskite films. Thence, achieving a PCE of 24.17% with suppressed voltage losses and an impressive life span of 1140 h in the open air.

A Functional Biological Molecule Restores the PbI2 Residue-Induced Defects in Two-Step Fabricated Perovskites.

Coating the perovskite layer via a two-step method is an adaptable solution for industries compared to the anti-solvent process. But what about the impact of unreacted PbI2? Usually, it is generated during perovskite conversion in a two-step method and considered beneficial within the grain boundaries, while also being accused of enhancing the interface defects and nonradiative recombination. Several additives are mixed in PbI2 precursors for the purpose of improving the perovskite crystallinity and hindering the Pb2+ defects. Herein, in lieu of adding additives to the PbI2, the effects of the PbI2 residue via the electron transport layer/perovskite interface modification are explored. Consequently, by introducing artemisinin decorated with hydrophobic alkyl units and a ketone group, it reduces the residual PbI2 and improves the perovskites' crystallinity by coordinating with Pb2+. In addition, artemisinin-deposited perovskite enhances both the stability and efficiency of perovskite solar cells by suppressing nonradiative recombination.

High level of D-dimer predicts ischemic stroke in patients with infective endocarditis.

BACKGROUND: Ischemic stroke is one of the most prominent and serious neurological complications of infective endocarditis (IE). Our study was designed to evaluate the predictive value of higher level of plasma D-dimer on admission for the development of ischemic stroke in patients with IE. METHODS: In this prospective study, a total of 173 consecutive patients with IE were recruited from January 2016 to December 2018. Plasma D-dimer and other clinical indexes of IE patients were measured after admission. The number of patients who developed ischemic stroke during 6-month follow-up was recorded, as well as the occurrence time of ischemic stroke. RESULTS: Ischemic stroke was observed in 38 (22%) patients during 6-month follow-up since definite diagnosis of IE. Patients with ischemic stroke had significantly higher levels of plasma D-dimer than those of patients without stroke (4982 vs 2205 µg/L, P < .001). In addition, Staphylococcus aureus infection (HR: 1.96, 95% CI: 1.51-2.42), mitral valve vegetation (HR: 1.52, 95% CI: 1.32-1.75), and higher levels of on-admission plasma D-dimer (HR: 1.35, 95% CI: 1.27-1.43) were significantly associated with ischemic stroke. Moreover, D-dimer levels ≥3393 µg/L served as a strong predictor for ischemic stroke in patients with IE, and the sensitivity and specificity were 78% and 83%, respectively. CONCLUSION: Our study suggested that higher level of D-dimer on admission was an independent predictor for ischemic stroke in patients with IE. These patients may require special attention, in particular within the first trimester after IE diagnosis.

Effects of eplerenone on cerebral aldosterone levels and brain lesions in spontaneously hypertensive rats.

Evidence indicates that renin-angiotensin-aldosterone system (RAS) inhibitors can protect the brain in Alzheimer's disease and Parkinson's disease. The current study evaluated the relationship between aldosterone and tissue damage in the brains of spontaneously hypertensive rats (SHRs) and whether the RAS inhibitor eplerenone can mitigate the damage seen in these rats. SHRs were randomly divided into eplerenone (n = 10) and SHR (n = 10) groups, and Wistar-Kyoto (WKY) rats (n = 10) were used as controls. Eplerenone 50 mg/kg/day was administered orally to the eplerenone group. Pathological changes to the hippocampal formation, plasma and encephalic aldosterone, and plasma potassium levels were compared among the groups. After 10 weeks, rats in the eplerenone and SHR groups showed higher systolic BP (p = .01) than the control group. Aldosterone levels in the brain were higher in the SHR group (0.20 ± 0.06 pg/ml) than in the eplerenone (0.14 ± 0.05 pg/ml, p = .044) or control (0.12 ± 0.07 pg/ml, p = .007) groups. Plasma aldosterone levels in the SHR group were 1.7 times higher than those in the control group (p = .006). Cerebral cortex was thinner in the SHR group (225.18 ± 15.43 µm) than in the eplerenone (240.38 ± 12.85 µm, p < .01) or control (244.72 ± 18.92 µm, p < .01) groups. Thickness did not differ between the latter two groups. The SHR group exhibited apoptotic cells in the hippocampal formation, which were rare in the eplerenone and control groups. Plasma potassium levels were higher in the eplerenone group than those in the other two groups (p < .05). Our results showed that eplerenone can alleviate brain damage (thinning of cortex and increased apoptosis) caused by aldosterone in a rat model of hypertension.

Mesenchymal stromal cell biotherapy for Parkinson's disease premotor symptoms.

Parkinson's disease (PD) is a neurodegenerative disorder with motor deficits due to nigrostriatal dopamine depletion and with the non-motor/premotor symptoms (NMS) such as anxiety, cognitive dysfunction, depression, hyposmia, and sleep disorders. NMS is presented in at least one-fifth of the patients with PD. With the histological information being investigated, stem cells are shown to provide neurotrophic supports and cellular replacement in the damaging brain areas under PD conditions. Pathological change of progressive PD includes degeneration and loss of dopaminergic neurons in the substantia nigra of the midbrain. The current stem cell beneficial effect addresses dopamine boost for the striatal neurons and gliovascular mechanisms as competing for validated PD drug targets. In addition, there are clinical interventions for improving the patient's NMS and targeting their autonomic dysfunction, dementia, mood disorders, or sleep problems. In our and many others' research using brain injury models, multipotent mesenchymal stromal cells demonstrate an additional and unique ability to alleviate depressive-like behaviors, independent of an accelerated motor recovery. Intranasal delivery of the stem cells is discussed for it is extensively tested in rodent animal models of neurological and psychiatric disorders. In this review, we attempt to discuss the repairing potentials of transplanted cells into parkinsonism pathological regions of motor deficits and focus on preventive and treatment effects. From new approaches in the PD biological therapy, it is believed that it can as well benefit patients against PD-NMS.

Energy effective utilization of circulating fluidized bed fly ash to prepare silicon-aluminum composite aerogel and gypsum.

To reduce the cost of Si-Al aerogels preparation, circulating fluidized bed fly ash (CFA) was developed to be as the alternative to synthetic precursors. High energy consumption of alkali-melting and secondary wastes production were the major challenges. Here, a technique characterized by effective energy consumption and non-secondary waste was developed to convert CFA into Si-Al aerogel. The process consists two stages, preparation of Si-Al sol by sintering of CFA and Na2CO3 followed by sulfuric acid leaching, and synthesis of Si-Al aerogel by so-gel with trimethyl chlorosilane modification and ambient pressure drying. The optimization results of proportion and sintering temperature showed that the optimal temperature of sintering of Na2CO3 and CFA with the mass ratio of 0.7 was 750 °C, 100 °C lower than that of most other waste aluminosilicate materials. CaSO4·0.5H2O which meet building gypsum requirement was obtained by specifying the drying temperature of acid-leached residue at 126 °C for 2 h. The modification procedure was explored to obtain Si-Al aerogel with a large specific surface area of 857 m2/g and hydrophobic angle of 139.3°. Thermal and mechanical properties tests indicated that the Si-Al aerogels and gypsum produced from CFA exhibited promising thermal insulation and the potential application in construction.

Differentiated human alveolar type II cells secrete antiviral IL-29 (IFN-lambda 1) in response to influenza A infection.

Alveolar type II epithelial cells (ATIIs) are one of the primary targets for influenza A pneumonia. The lack of a culture system for maintaining differentiated ATIIs hinders our understanding of pulmonary innate immunity during viral infection. We studied influenza A virus (IAV)-induced innate immune responses in differentiated primary human ATIIs and alveolar macrophages (AMs). Our results indicate that ATIIs, but not AMs, support productive IAV infection. Viral infection elicited strong inflammatory chemokine and cytokine responses in ATIIs, including secretion of IL-8, IL-6, MCP-1, RANTES, and MIP-1beta, but not TNF-alpha, whereas AMs secreted TNF-alpha as well as other cytokines in response to infection. Wild-type virus A/PR/8/34 induced a greater cytokine response than reassortant PR/8 virus, A/Phil/82, despite similar levels of replication. IAV infection increased mRNA expression of IFN genes IFN-beta, IL-29 (IFN-lambda1), and IL-28A (IFN-lambda2). The major IFN protein secreted by type II cells was IL-29 and ATIIs appear to be a major resource for production of IL-29. Administration of IL-29 and IFN-beta before infection significantly reduced the release of infectious viral particles and CXC and CC chemokines. IL-29 treatment of type II cells induced mRNA expression of antiviral genes MX1, OAS, and ISG56 but not IFN-beta. IL-29 induced a dose-dependent decrease of viral nucleoprotein and an increase of antiviral genes but not IFN-beta. These results suggest that IL-29 exerts IFN-beta-independent protection in type II cells through direct activation of antiviral genes during IAV infection.

High Flow Nasal Cannula Decreased Pulmonary Complications in Neurologically Critically Ill Patients.

Objective: Pulmonary complications could badly affect the recovery of neurological function and neurological prognosis of neurological critically ill patients. This study evaluated the effect of high-flow nasal cannula (HFNC) therapy on decreasing pulmonary complications in neurologically critically ill patients. Patients and Methods: The patients admitted to the intensive care unit (ICU) with serious neurological disease and receiving oxygen therapy were retrospectively reviewed (Ethical No. IRB2021-YX-001). Patients were divided into the HFNC group and the conventional oxygen therapy (COT) group. We analyzed the data within these two groups, including patients' baseline data, short-term outcomes of respiratory complications, general outcomes including hospital stay, ICU stay and mortality, and neurological functions. To analyze the relevant factors, we performed multivariable logistic regression analysis. Results: A total of 283 patients met the criteria, including 164 cases in the HFNC group and 119 cases in the COT group. The HFNC group had remarkably less mechanical ventilation requirement with lower phlegm viscosity. Even more, ICU stay and total hospital stay were significantly shortened in the HNFC group. Conclusion: HFNC decreased pulmonary complications in neurologically critically ill patients and improved recovery of neurological function and neurological prognosis.

Glial Cell-Based Vascular Mechanisms and Transplantation Therapies in Brain Vessel and Neurodegenerative Diseases.

Neurodevelopmental and neurodegenerative diseases (NDDs) with severe neurological/psychiatric symptoms, such as cerebrovascular pathology in AD, CAA, and chronic stroke, have brought greater attention with their incidence and prevalence having markedly increased over the past few years. Causes of the significant neuropathologies, especially those observed in neurological diseases in the CNS, are commonly believed to involve multiple factors such as an age, a total environment, genetics, and an immunity contributing to their progression, neuronal, and vascular injuries. We primarily focused on the studies of glial involvement/dysfunction in part with the blood-brain barrier (BBB) and the neurovascular unit (NVU) changes, and the vascular mechanisms, which have been both suggested as critical roles in chronic stroke and many other NDDs. It has been noted that glial cells including astrocytes (which outnumber other cell types in the CNS) essentially contribute more to the BBB integrity, extracellular homeostasis, neurotransmitter release, regulation of neurogenic niches in response to neuroinflammatory stimulus, and synaptic plasticity. In a recent study for NDDs utilizing cellular and molecular biology and genetic and pharmacological tools, the role of reactive astrocytes (RACs) and gliosis was demonstrated, able to trigger pathophysiological/psychopathological detrimental changes during the disease progression. We speculate, in particular, the BBB, the NVU, and changes of the astrocytes (potentially different populations from the RACs) not only interfere with neuronal development and synaptogenesis, but also generate oxidative damages, contribute to beta-amyloid clearances and disrupted vasculature, as well as lead to neuroinflammatory disorders. During the past several decades, stem cell therapy has been investigated with a research focus to target related neuro-/vascular pathologies (cell replacement and repair) and neurological/psychiatric symptoms (paracrine protection and homeostasis). Evidence shows that transplantation of neurogenic or vasculogenic cells could be achieved to pursue differentiation and maturation within the diseased brains as expected. It would be hoped that, via regulating functions of astrocytes, astrocytic involvement, and modulation of the BBB, the NVU and astrocytes should be among major targets for therapeutics against NDDs pathogenesis by drug and cell-based therapies. The non-invasive strategies in combination with stem cell transplantation such as the well-tested intranasal deliveries for drug and stem cells by our and many other groups show great translational potentials in NDDs. Neuroimaging and clinically relevant analyzing tools need to be evaluated in various NDDs brains.

[Study on mechanical ventilation pressure under continuous cuff pressure monitoring in critical patients].

OBJECTIVE: To explore the effective pressure range under continuous cuff pressure monitoring in critical patients with mechanical ventilation, so as to achieve the goal of ensuring ventilation quality and reducing mucosal injury without increasing the incidence of endotracheal catheter displacement and aspiration. METHODS: Ninety critically ill patients with non-pulmonary diseases admitted to the department of intensive care unit (ICU) of Airport Hospital of Tianjin Medical University from June 2017 to June 2019 were enrolled, and divided into three groups according to the random number table, with 30 patients in each group. For all patients in the three groups , the head of the bed was raised by 30 degree angleand the balloon was measured continuously. Cuff pressure in the three groups were maintained at 20, 25 and 30 cmH2O (1 cmH2O = 0.098 kPa) respectively. The patient's air leakage, oxygen saturation, tracheal tube displacement of each group were recorded every hour when the patients were calm. Fiberbronchoscope was used to aspirate sputum during extubation to check for mucosal damage. Chest X-ray examination was used to evaluate pulmonary infection and sputum bacteria culture examination was conducted at the same time. RESULTS: There was no significant difference in gender, age and critical condition among the three groups. The number of patients with airway mucosal injury in the 30 cmH2O group was significantly higher than that in the 20 cmH2O group (cases: 8 vs. 4, P < 0.05). There was no significant difference in airway mucosal injury between Group 20 cmH2O and Group 25, Group 25 cmH2O and Group 30 cmH2O. When the balloon pressure was 20, 25, and 30 cmH2O, there was no significant difference in air bag leakage (cases: 14, 10, 12), trachea catheter displacement (cases: 18, 11, 16), ventilator-associated pneumonia (cases: 3, 4, 3), all P > 0.05, and there was no significant difference in mechanical ventilation time and the hospitalization time [mechanical ventilation time (hours): 77.07±65.34, 80.80±70.20, 77.60±65.23; the length of ICU stay (days): 5.70±3.74, 5.30±4.57, 6.23±3.51, all P > 0.05]. CONCLUSIONS: The cuff pressure of 20 cmH2O will not increase the mechanical ventilation time and hospitalization time of patients, while 20 cmH2O is much safer in airway mucosal injury.

Quantitative structure-property relationships for direct photolysis of polybrominated diphenyl ethers.

Using semiempirical quantum chemical descriptors, by partial least squares (PLS) regression, quantitative structure-property relationships (QSPRs) were established for direct photolysis quantum yields (Phi) and rate constants (k) of polybrominated diphenyl ether congeners dissolved in water/methanol and methanol solutions, respectively, and irradiated by artificial ultraviolet A light. Q(cum)(2), a parameter indicating robustness and predictive abilities of PLS models, for the significant QSPR models is larger than 0.702. The gap of frontier molecular orbital energies (E(LUMO)-E(HOMO)) and the most positive Mulliken atomic charges on a hydrogen atom (q(H+)) are two main molecular structural factors governing the logPhi values. logPhi increases with increasing E(LUMO)-E(HOMO) and q(H+) values. logk is mainly related to bromination degree and pattern which can be characterized by molecular weight (Mw), average molecular polarizability (alpha), and average Mulliken atomic charges on bromine atoms (q(Br)). logk increases with bromination degree (Mw, alpha) and q(Br).

Ozone induces oxidative stress in rat alveolar type II and type I-like cells.

Ozone is a highly reactive gas present in urban air, which penetrates deep into the lung and causes lung injury. The alveolar epithelial cells are among the first cell barriers encountered by ozone. To define the molecular basis of the cellular response to ozone, primary cultures of rat alveolar type II and type I-like cells were exposed to 100 ppb ozone or air for 1 h. The mRNA from both phenotypes was collected at 4 and 24 h after exposure for gene expression profiling. Ozone produced extensive alterations in gene expression involved in stress and inflammatory responses, transcription factors, antioxidant defenses, extracellular matrix, fluid transport, and enzymes of lipid metabolism and cell differentiation. Real-time reverse transcription-polymerase chain reaction and Western blot analysis verified changes in mRNA and protein levels of selected genes. Besides the increased stress response, ozone exposure downregulated genes of cellular differentiation. The changes were more prominent at 4 h in the type I-like phenotype and at 24 h in the type II phenotype. The type I-like cells were more sensitive to ozone than type II cells. The genome-wide changes observed provide insight into signal pathways activated by ozone and how cellular protection mechanisms are initiated.

SARS-CoV replicates in primary human alveolar type II cell cultures but not in type I-like cells.

Severe acute respiratory syndrome (SARS) is a disease characterized by diffuse alveolar damage. We isolated human alveolar type II cells and maintained them in a highly differentiated state. Type II cell cultures supported SARS-CoV replication as evidenced by RT-PCR detection of viral subgenomic RNA and an increase in virus titer. Virus titers were maximal by 24 h and peaked at approximately 10(5) pfu/mL. Two cell types within the cultures were infected. One cell type was type II cells, which were positive for SP-A, SP-C, cytokeratin, a type II cell-specific monoclonal antibody, and Ep-CAM. The other cell type was composed of spindle-shaped cells that were positive for vimentin and collagen III and likely fibroblasts. Viral replication was not detected in type I-like cells or macrophages. Hence, differentiated adult human alveolar type II cells were infectible but alveolar type I-like cells and alveolar macrophages did not support productive infection.

Differentiated human alveolar epithelial cells and reversibility of their phenotype in vitro.

Cultures of differentiating fetal human type II cells have been available for many years. However, studies with differentiated adult human type II cells are limited. We used a published method for type II cell isolation and developed primary culture systems for maintenance of differentiated adult human alveolar epithelial cells for in vitro studies. Human type II cells cultured on Matrigel (basolateral access) or a mixture of Matrigel and rat tail collagen (apical access) in the presence of keratinocyte growth factor, isobutylmethylxanthine, 8-bromo-cyclicAMP, and dexamethasone (KIAD) expressed the differentiated type II cell phenotype as measured by the expression of surfactant protein (SP)-A, SP-B, SP-C, and fatty acid synthase and their morphologic appearance. These cells contain lamellar inclusion bodies and have apical microvilli. In both systems the cells appear well differentiated. In the apical access system, type II cell differentiation markers initially decreased and then recovered over 6 d in culture. Lipid synthesis was also increased by the addition of KIAD. In contrast, type II cells cultured on rat tail collagen (or tissue culture plastic) slowly lose their lamellar inclusions and expression of the surfactant proteins and increase the expression of type I cell markers. The expression of the phenotypes is regulated by the culture conditions and is, in part, reversible in vitro.