Overcoming Microstructural Defects at the Buried Interface of Formamidinium-Based Perovskite Solar Cells.

Since the advent of formamidinium (FA)-based perovskite photovoltaics (PVs), significant performance enhancements have been achieved. However, a critical challenge persists: the propensity for void formation in the perovskite film at the buried perovskite-interlayer interface has a deleterious effect on device performance. With most emerging perovskite PVs adopting the p-i-n architecture, the specific challenge lies at the perovskite-hole transport layer (HTL) interface, with previous strategies to overcome this limitation being limited to specific perovskite-HTL combinations; thus, the lack of universal approaches represents a bottleneck. Here, we present a novel strategy that overcomes the formation of such voids (microstructural defects) through a film treatment with methylammonium chloride (MACl). Specifically, our work introduces MACl via a sequential deposition method, having a profound impact on the microstructural defect density at the critical buried interface. Our technique is independent of both the HTL and the perovskite film thickness, highlighting the universal nature of this approach. By employing device photoluminescence measurements and conductive atomic force microscopy, we reveal that when present, such voids impede charge extraction, thereby diminishing device short-circuit current. Through comprehensive steady-state and transient photoluminescence spectroscopy analysis, we demonstrate that by implementing our MACl treatment to remedy these voids, devices with reduced defect states, suppressed nonradiative recombination, and extended carrier lifetimes of up to 2.3 µs can be prepared. Furthermore, our novel treatment reduces the stringent constraints around antisolvent choice and dripping time, significantly extending the processing window for the perovskite absorber layer and offering significantly greater flexibility for device fabrication.

Optimization of different intensities of exercise preconditioning in protecting exhausted exercise induced heart injury in rats.

This study was to optimize the exercise preconditioning (EP) intensity in protecting from exhaustive exercise-induced cardiac injury (EECI). A total of 98 male Sprague-Dawley rats were divided into 7 groups (n â€‹= â€‹14): the control group (C), the exhaustive exercise group (EE) and the EP â€‹+ â€‹EE groups, which include the V10 (53.0%˙O2max), V15 (58.4%˙O2max), V20 (67.0%˙O2max), V26 (74.0%˙O2max) and V30 (80.0%˙O2max) groups. Except the C group, the other groups were subjected to treadmill running. The serum contents of N terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTn-I) were detected by the enzyme-linked immunosorbent assay method, ECG was recorded, heart function was detected by pressure volume catheter and the activities of mitochondrial electron transfer pathway (ET pathway) complexes I, Ⅱ and IV were measured by high-resolution respiration instrument. Compared to the EE group, the EP groups have shown decrease of NT-proBNP and cTn-I, improvement of mitochondrial respiratory function and cardiac function. Compared to other EP groups, the V26 group has shown significant decrease of myocardial enzymes and improvement of mitochondrial function. The correlation analysis showed the EP effect was proportional to EP intensity in the range of 53.0%˙O2max-74.0%˙O2max. High intensity and long duration of exhaustive exercise caused cardiac injury and EP could decrease serum level of NT-proBNP and cTn-I, improve electrical derangement and the left ventricular function, and raise the activities of ET pathway complexes I, Ⅱ and IV. The protection of EP on EECI was improved as the EP intensity was increased from 53.0%˙O2max to 74.0%˙O2max and when EP intensity was 74.0%˙O2max, the effect was the most obvious among all the setting EP groups.

Comparison of 10- and 20-min hepatobiliary phase images on Gd-EOB-DTPA-enhanced MRI T1 mapping for liver function assessment in clinic.

PURPOSE: To compare hepatobiliary phase (HBP) images obtained 10 and 20 min after Gd-EOB-DTPA-enhanced MRI for liver function assessment in clinic on 3.0 T MR imaging. METHODS: 103 patients were separated into four groups: 38 patients for the normal liver function (NLF) group, 33 patients for the liver cirrhosis with Child-Pugh A (LCA) group, 21 patients for the liver cirrhosis with Child-Pugh B group, and 11 patients for a liver cirrhosis with Child-Pugh C group. T1 relaxation times (T1rt) were measured on T1 mapping and reduction rates of T1rt (rrT1rt) were calculated. HBP images were obtained at the 10- and 20-min mark after Gd-EOB-DTPA enhancement. RESULTS: T1rt on pre-enhancement imaging showed no significant difference (p > 0.05) among all four groups. T1rt for both the 10-min HBP and the 20-min HBP showed a significant difference (p < 0.05) among all groups, but showed no significant difference (p > 0.05) between the NLF group and the LCA group. T1rt and rrT1rt showed no significant difference (p > 0.05) between 10-min HBP and 20-min HBP among all groups. The ROC analysis on 10-min HBP and 20-min HBP showed a lower diagnostic performance between NLF group and LCA group (AUC from 0.532 to 0.582), but high diagnostic performance (AUC from 0.788 to 1.000) among others group. CONCLUSIONS: In comparing 10-min HBP and 20-min HBP T1 mapping after Gd-EOB-DTPA enhancement, our results suggest that 10-min HBP T1 mapping is a feasible option for quantitatively assessing liver function.

Evaluating segmental liver function using T1 mapping on Gd-EOB-DTPA-enhanced MRI with a 3.0 Tesla.

BACKGROUND: Assessing the liver function provides valuable information to evaluate surgical risk and plan accordingly. Current studies focus on whole liver function evaluation. However, assessment of segmental liver function is equally important in the clinical practice. The purpose of this study was to investigate whether Gd-EOB-DTPA-enhanced MRI can evaluate the liver function of each segment by using T1 mapping at 3 Tesla MRI. METHODS: One hundred three patients were classified into one of 4 groups: a normal liver function (NLF) group (n = 38), a liver cirrhosis with Child-Pugh A (LCA) group (n = 33), a liver cirrhosis with Child-Pugh B (LCB) group (n = 21), and a liver cirrhosis with Child-Pugh C (LCC) group (n = 11). All patients underwent Gd-EOB-DTPA-enhanced MRI scans. T1 relaxation times were measured on the liver superimposing T1 mapping images. Reduction rate (△%) of T1 relaxation time of the liver parenchyma were calculated. RESULTS: After 20 min of Gd-EOB-DTPA enhancement, the T1 relaxation time of all liver segments in the LCC group were different from those in all the other groups, and more liver segments from the LCB and LCA groups different from the NLF group (p < 0.05). For the LCB group, the areas under the receiver operating characteristic curves (AUCs) of different liver segments for hepatobiliary phase (HBP) were 0.654-0.904 on T1 relaxation time, and 0.709-0.905 on △%. For the LCC group, the AUCs of different liver segments for HBP were 0.842-0.997 on T1 relaxation time, and 0.887-0.990 on △%. CONCLUSIONS: For LCB patients, segmental liver function evaluation is possible using Gd-EOB-DTPA-enhanced MRI T1 mapping. For LCC patients, all liver segments can be used to evaluate liver function and both T1 relaxation time and the △% of T1 relaxation time have good diagnostic performance.

[CT perfusion study of acute local cerebral infarction in rhesus monkeys].

OBJECTIVE: To explore the value of CT perfusion in early diagnosis and management of superacute local cerebral infarction in rhesus monkeys. METHOD: Acute local cerebral infarction was induced in the rhesus monkeys during digital subtraction angiography (DSA) by introduction of pale thrombus prepared from autologous blood into the M1 branch of the middle cerebral artery (MCA). Plain CT scan and CT perfusion scanning were performed at different time points before and after DSA operation, and the results were analyzed in conjunction with the pathologic changes. RESULTS: Ischemic lesions were displayed on CT perfusion images, which showed local hypoperfusion, reduced cerebral blood flow and volume, and mean transit time delay in the compromised area. Local hypointense infarct area was identified in plain CT scan 24 h after the DSA operation, and the results were in good agreement with pathological examination during autopsy. CONCLUSION: CT perfusion imaging of the brain can accurately capture the cerebral perfusion deficits in acute ischemic stroke before morphologic changes take place, and therefore provides good means for thrombolytic treatment evaluation of stroke.