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This study investigates the injection dependence of carrier lifetimes of p‐ and n‐type samples passivated by doped‐polycrystalline silicon (poly‐Si) (p+ and n+ poly‐Si) contacts. A strong apparent injection dependence of the carrier lifetimes is observed in p‐n junction samples (p+ poly‐Si on n‐type or n+ poly‐Si on p‐type) but no injection dependence is observed in high‐low junction samples (p+ poly‐Si on p‐type or n+ poly‐Si on n‐type). Further, photoluminescence images captured at two illumination intensities of 0.05 and 0.87 suns reveal that edge recombination contributed the strong apparent injection dependence in p‐n junction samples. Furthermore, this apparent injection dependence increases as the sample size is reduced, and as the sheet resistance of the doped poly‐Si contacts is decreased, allowing more effective transport of minority carriers to the recombination‐active edge regions. [ABSTRACT FROM AUTHOR]

Aim: We investigated the effects and target of gastrodin (GAS) for treating depression through network pharmacology combined with experimentation. Methods: The therapeutic target and signal of GAS for depression were analyzed by network pharmacology. Depression in mice was mimicked with a chronic unpredictable mouse stress (CUMS) model. Through open field, elevated plus maze, forced swimming, and tail suspension tests, the effects of GAS on the CUMS mice behaviors were examined, and the levels of neurotransmitters were detected. The histopathological changes were assayed by H&E and IHC staining, and the protein expressions were detected by Western blotting. Small molecule‐protein docking and molecular dynamics experiments were conducted to simulate the binding mode between GAS and Caspase‐3. Results: Network pharmacological analysis revealed that Caspase‐3 was the action target of GAS. GAS could improve depression‐like behaviors in CUMS mice, elevate their neurotransmitter levels, ameliorate their nerve cell injury, and inhibit their Caspase‐3 expression. After knocking out Caspase‐3, the effects of GAS were inhibited. Molecular dynamics simulation and small molecule‐protein docking found that GAS bound to Caspase‐3 at SER25, inhibiting the maturation and activation of Caspase‐3. Conclusion: We find that GAS can act as a Caspase‐3 inhibitor, which improves depression‐like behaviors and nerve cell injury in CUMS mice by inhibiting Caspase‐3‐mediated apoptosis. [ABSTRACT FROM AUTHOR]

Doped polysilicon (poly-Si) passivating contacts have emerged as a key technology for the next generation of silicon solar cells in mass production, owing to their excellent performance and high compatibility with the existing passivated emitter and rear cell technology. However, the current solar cell architecture based on a rear-side electron-selective (n+) poly-Si contact is also approaching its practical limit (∼26%) in mass production. The full potential of doped poly-Si passivating contacts can only be realized through incorporation of both electron-selective and hole-selective (p+) poly-Si contacts. While studies of both p+ and n+ poly-Si contacts commenced simultaneously, significant performance differences have arisen. Phosphorus-doped poly-Si contacts consistently outperform boron-doped counterparts, displaying typically lower recombination current density (J0) values (1 – 5 fA/cm2 vs 7 – 15 fA/cm2). This discrepancy can be attributed to inadequate optimization of p+ poly-Si contacts and fundamental limitations related to boron doping. The poorer passivation of p+ poly-Si contacts can be at least partly attributed to boron segregation into the interfacial oxide layers, compromising the interfacial oxide integrity and reducing the chemical passivation effectiveness. This review critically examines the progress of p+ poly-Si contacts characterized by cell efficiency and J0 values, delves into existing challenges, identifies potential solutions, and explores some potential solar cell architectures to enhance efficiency by incorporating p+ poly-Si contacts. [ABSTRACT FROM AUTHOR]

To explore the antidepressant effects and targets of atractylenolide I (ATR) through a network pharmacological approach. Relevant targets of ATR and depression analyzed by network pharmacology were scored (identifying 5‐HT2A targets). Through elevated plus maze, open field, tail suspension, and forced swimming tests, the behavioral changes of mice with depression (chronic unpredictable mild stress [CUMS]) were examined, and the levels of neurotransmitters including serotonin, dopamine, and norepinephrine (5‐HT, DA, and NE) were determined. The binding of ATR to 5‐HT2A was verified by small molecular‐protein docking. ATR improved the behaviors of CUMS mice, elevated their levels of neurotransmitters 5‐HT, DA, and NE, and exerted a protective effect on their nerve cell injury. After 5‐HT2A knockout, ATR failed to further improve the CUMS behaviors. According to the results of small molecular‐protein docking and network pharmacological analysis, ATR acted as an inhibitor by binding to 5‐HT2A. ATR can improve the behaviors and modulate the neurotransmitters of CUMS mice by targeting 5‐HT2A. [ABSTRACT FROM AUTHOR]

Sphenoid sinus inverted papilloma (IP) is a very infrequent tumor, and the combination of sphenoidal IP with pituitary tumor is extremely rare. In this report, the authors describe the case of a 63-year-old male with oculomotor nerve palsy in the left eye due to sellar region tumor. After endoscopic transsphenoidal surgery, the postoperative pathological examination confirmed the co-occurrence of an sphenoidal IP and pituitary adenoma. To our knowledge, the present case is the second reported case of an IP with a pituitary adenoma. [ABSTRACT FROM AUTHOR]

We report two cases of Intracranial inflammatory myofibroblastic tumor (IMT) with recurrent, cystic, and venous sinus occlusion. The cases show imaging progression from a small lesion (case 1) or absence of lesions (case 2). One of cases recurred 2 years after surgery and was treated with corticosteroids but the tumor was still growing and was resected again. We think the best treatment for IMT is surgical resection. [ABSTRACT FROM AUTHOR]

Aim of this research was to examine the impact of paeoniflorin (Pae) in suppressing the occurrence of ferroptosis in individuals with Alzheimer's disease (AD). The study utilized APP/PS1 mice with AD as the experimental subjects. Following the administration of Pae, the cognitive behaviors of mice were evaluated and the key indexes of ferroptosis were measured, as well as levels of oxidative stress (OS). For in‐vitro experiments, Erastin was adopted for inducing the ferroptosis of PC12 cells, and the level of cell ferroptosis was detected after Pae treatment. Pae improved the cognitive ability of AD mice, reduced the level of ferroptosis, decreased the iron ion and MAD levels in brain tissues, and increased SOD expression. In PC12 cells, Pae suppressed the Erastin‐induced ferroptosis, mitigated oxidative damage, and reduced the level of ROS. Based on the findings from our research, it was observed that Pae exhibited a specific binding affinity to P53, leading to the suppression of ferroptosis. This mechanism ultimately resulted in the improvement of nerve injury in mice with AD. [ABSTRACT FROM AUTHOR]