Recent advancements in quantum hardware and classical computing simulations have significantly enhanced the accessibility of quantum system data, leading to an increased demand for precise descriptions and predictions of these systems. Accurate prediction of quantum Hamiltonian dynamics and identification of Hamiltonian parameters are crucial for advancements in quantum simulations, error correction, and control protocols. This Letter introduces a machine learning model with dual capabilities: it can deduce time-dependent Hamiltonian parameters from observed changes in local observables within quantum many-body systems, and it can predict the evolution of these observables based on Hamiltonian parameters. Our model's validity was confirmed through theoretical simulations across various scenarios and further validated by two experiments. Initially, the model was applied to a nuclear magnetic resonance quantum computer, where it accurately predicted the dynamics of local observables. The model was then tested on a superconducting quantum computer with initially unknown Hamiltonian parameters, successfully inferring them. Our approach aims to enhance various quantum computing tasks, including parameter estimation, noise characterization, feedback processes, and quantum control optimization.
In recent years, wavefront shaping technology has made it possible to refocus scattered photons through turbid media. The utilization of photoacoustic signal as feedback for wavefront shaping offers non-invasive and deep-penetrating advantages, making it increasingly attractive in the field of biomedical research. However, due to the short decorrelation time of scattered light in living biological tissues, demonstrating the technique in vivo remains challenging. Digital Micromirror Devices (DMD) with their various modulation modes and high refresh rates hold great potential in addressing this challenge and have been widely employed in Photoacoustic Guided Wavefront Shaping (PAWS) applications. This paper presents the fundamental principles of using photoacoustic signal as feedback to guide wavefront shaping and highlights the advantages of PAWS in biological tissue imaging. Furthermore, a comparative analysis of three commonly used spatial light modulators in PAWS is provided, along with an overview of the three main techniques employed in wavefront shaping. Additionally, methods for improving the signal-to-noise ratio and imaging resolution in PAWS are summarized, followed by a discussion on potential future directions for this field.
Xiao Cheng Qi (XCQ) decoction, an ancient Chinese herbal mixture, has been used in treating slow-transit constipation (STC) for years. The underlying action mechanism in relieving the clinical symptoms is unclear. Several lines of evidence point to a strong link between constipation and gut microbiota. Short-chain fatty acids (SCFAs) and microbial metabolites have been shown to affect 5-HT synthesis by activating the GPR43 receptor localized on intestinal enterochromaffin cells, since 5-HT receptors are known to influence colonic peristalsis. The objective of this study was to evaluate the efficacy of XCQ in alleviating clinical symptoms in a mouse model of STC induced by loperamide. The application of loperamide leads to a decrease in intestinal transport and fecal water, which is used to establish the animal model of STC. In addition, the relationship between constipation and gut microbiota was determined. The herbal materials, composed of Rhei Radix et Rhizoma (Rhizomes of Rheum palmatum L., Polygonaceae) 55.2 g, Magnoliae Officinalis Cortex (Barks of Magnolia officinalis Rehd. et Wils, Magnoliaceae) 27.6 g, and Aurantii Fructus Immaturus (Fruitlet of Citrus aurantium L., Rutaceae) 36.0 g, were extracted with water to prepare the XCQ decoction. The constipated mice were induced with loperamide (10 mg/kg/day), and then treated with an oral dose of XCQ herbal extract (2.0, 4.0, and 8.0 g/kg/day) two times a day. Mosapride was administered as a positive drug. In loperamide-induced STC mice, the therapeutic parameters of XCQ-treated mice were determined, i.e., (i) symptoms of constipation, composition of gut microbiota, and amount of short-chain fatty acids in feces; (ii) plasma level of 5-HT; and (iii) expressions of the GPR43 and 5-HT4 receptor in colon. XCQ ameliorated the constipation symptoms of loperamide-induced STC mice. In gut microbiota, the treatment of XCQ in STC mice increased the relative abundances of Lactobacillus, Prevotellaceae_UCG_001, Prevotellaceae_NK3B31_group, Muribaculaceae, and Roseburia in feces and decreased the relative abundances of Desulfovibrio, Tuzzerella, and Lachnospiraceae_ NK4A136_group. The levels of SCFAs in stools from the STC group were significantly lower than those the control group, and were greatly elevated via treatment with XCQ. Compared with the STC group, XCQ increased the plasma level of 5-HT and the colonic expressions of the GPR43 and 5-HT4 receptor, significantly. The underlying mechanism of XCQ in anti-constipation could be related to the modulation of gut microbiota, the increase in SCFAs, the increase in plasma 5-HT, and the colonic expressions of the GPR43 and 5-HT4 receptor. Our results indicate that XCQ is a potent natural product that could be a therapeutic strategy for constipation.
In skin, melanin is synthesized and stored in melanosomes. In epidermal melanocytes, melanosomes are transported to and internalized by the neighboring keratinocytes, subsequently leading to skin pigmentation. Ultraviolet (UV) radiation induces the release of acetylcholine (ACh) from keratinocytes, which in turn activates ACh receptors (AChRs) on nearby melanocytes, forming a proposed "skin synapse". Here, we illustrated that the UV-induced melanosome release from cultured B16F10 melanoma cells could be mediated by co-actions of ACh. In the cell cultures, UV exposure robustly elicited melanosome release. Applied bethanechol (BeCh), an agonist of muscarinic AChR (mAChR), could significantly enhance the release. In parallel, the intracellular Ca2+ mobilization was regulated. The applied antagonists of M1 and/or M3 mAChRs could block the UV-induced melanosome release and the mobilization of intracellular Ca2+. The phosphorylation of PKC, triggered by UV and BeCh treatments, could be suppressed by the applied mAChR antagonists. The expressions of tethering complex for exocytosis, for example, Sec8, Exo70, and Rab11b, as well as synaptotagmin, were increased under UV exposure together with mAChR agonist: The inductions were fully abolished by M1 or M3 antagonist. Here, we hypothesize that the cholinergic signaling is playing roles in UV-induced exocytosis of melanosomes. Schematic diagram illustrating the role of mAChRs in UVB-mediated melanosome release. Under UVB irradiation, the epidermal keratinocytes and melanocytes release ACh. ACh stimulates M1/M3 mAChRs and leads to activation of PLC, which thereafter increases the levels of IP3 and DAG, as well as the intracellular Ca2+ and PKC. In addition, the expressions of the Ca2+ sensor, synaptotagmin (SYT), and exocyst subunits (Rab11b, Sec8, and Exo70) are induced following mAChR activation. The collaborative events facilitate the UVB-induced release of melanosomes.image
As quantum technology rapidly advances, the need for efficient scalable methods to characterize quantum systems intensifies. Quantum state tomography and Hamiltonian learning are essential for interpreting and optimizing quantum systems, yet a unified approach remains elusive. Such an integration could enhance our understanding of the complex relationship between quantum states and Hamiltonians, contributing to the development of more efficient methodologies. In this paper, we present a method that integrates quantum state tomography and Hamiltonian learning, drawing inspiration from machine translation in the field of natural language processing (NLP). We demonstrate the effectiveness of our approach across a variety of quantum systems, successfully learning the complex relationships between quantum states and Hamiltonians. Furthermore, the scalability and few-shot learning capabilities of our method could potentially minimize the resources required for characterizing and optimizing quantum systems. Our research provides valuable insights into the relationship between quantum states and Hamiltonians, paving the way for further studies on quantum systems and advancing quantum computation and related technologies.
Photoacoustic microscopy(PAM)is a noninvasive imaging technique that has undergone remarkable advancements and applications in the field of life sciences,basic medical research,and medical diagnostics.It operates on the unique principles of detecting photoacoustic signals and reconstructing them to create high-resolution,in-depth structural and functional images.This paper offers a comprehensive overview of the developmental background and unique principles behind photoacoustic microscopy.As we delve deeper,we explored various methods that have been employed to boost imaging performance.These include,but are not limited to,optical enhancement,acoustic enhancement,exploitation of artificial intelligence to augment the entire process.Moreover,there has been a significant focus on the harmonious integration of optics and acoustics in PAM.Ultimately,we discussed the extensive applications of current PAM in modern biomedical research and provided insights into the future developmental trends of this technique.
Acetylcholinesterase (AChE) has functions in neuroinflammation, beyond its classical role in neurotransmission. Understanding the role of AChE in neuroinflammation is of great significance, as it highlights the potential therapeutic targets for the treatment of neurodegenerative diseases. In an in vitro study, the expression of AChE was up-regulated in lipopolysaccharide (LPS)-induced microglia/macrophage and contrarily potentiated the inflammatory responses via disturbing the cholinergic anti-inflammatory pathway (CAP). However, the regulation of AChE in neuroinflammation has not been revealed in vivo yet. Here, we aim to uncover the inflammatory roles of microglial AChE in LPS-induced neuroinflammation by using the conditional AChE over-expression mouse model. AChE was specifically over-expressed in the myeloid cell linkage of mouse by applying CRISPR/cas9 combined with Cre-LoxP system. LPS was intraperitoneally injected into the mice to induce inflammation. The results showed that the inflammation, induced by LPS, was aggravated in the brain of transgenic mice having over-expression of AChE in microglia. The expressions of pro-inflammatory cytokines were robustly up-regulated in the brains of LPS-treated transgenic mice, as compared to the LPS-treated wildtypes. In parallel, the activations of microglia and astrocytes in hippocampus were enhanced significantly in AChE transgenic mice. Transcriptomics analysis further confirmed the severer inflammation in the transgenic mice than the wildtype after LPS administration. These findings shed light on the regulation of microglial AChE in neuroinflammation in vivo for the first time, presenting another angle to understand the role of AChE in neurodegenerative diseases.image
BACKGROUND:In treating depression, the residual anti-depressant in gut interacts with the microbiome, leading to the appearance of multiple drug resistant (MDR) mutants, which poses a challenge for the treatment of infectious complications. Strategy is needed to combat this issue. Acori Tatarinowii Rhizoma (ATR, rhizome of Acorus tatarinowii Schott, Araceae), a traditional Chinese medicine, has been widely used for treatment of neurological disorders and gastrointestinal digestive disease in China. Here, ATR was demonstrated an excellent MDR-preventing effect in fluoxetine-induced Escherichia coli (E. coli). AIM OF THE STUDY:This study aimed to reveal the effective role of ATR and its signaling cascades involved in preventing fluoxetine-induced MDR. MATERIALS AND METHODS:The water extract of ATR was co-applied with sub-minimum inhibitory concentration (100 mg/l) of fluoxetine in E. coli to evaluate its anti-MDR potential. Formation of reactive oxygen species (ROS) and expression of MDR-related genes in bacteria were measured by dichloro-dihydro-fluorescein diacetate assay and real-time PCR, respectively. Two fluorescent dyes, 1-N-phenylnapthylamine and 3,3'-dipropylthiadicarbocyanine were used to analyze the outer membrane permeability and inner membrane depolarization of E. coli. The accumulation of fluoxetine in the treated E. coli was determined via HPLC. The active fraction of ATR was identified. RESULTS:The water extract of ATR significantly decreased the number of MDR mutants induced by fluoxetine and had half effective concentrations (EC50) of 55.5 μg/ml and 16.8 μg/ml for chloramphenicol and tetracycline, respectively. ATR robustly reversed the fluoxetine-induced superoxide response and membrane damage in E. coli. In addition, the inclusion of ATR significantly reduced the accumulation of fluoxetine in E. coli. After further fractionation, the polysaccharide of ATR was demonstrated as the fraction with the most significant anti-MDR activity. CONCLUSIONS:This is the first report to investigate the MDR-preventing effect of ATR. The results of this study proposed ATR as an excellent herbal product to prevent MDR issues, as induced by fluoxetine, with the potential to reduce the side effects during the drug therapy of depression.
目的 制备唾液乳杆菌与蛹虫草或铁皮石斛共培提取物,研究其对慢性皮肤湿疹的抗炎作用.方法 以加入蛹虫草或铁皮石斛的MRS培养基培养唾液乳杆菌,培养后菌体通过发酵、高压破碎、离心制备药液.取小鼠随机分为对照组、模型组、阳性药组、唾液乳杆菌与蛹虫草共培提取物组、唾液乳杆菌与铁皮石斛共培提取物组,建立小鼠湿疹模型,并测量耳部肿胀程度、计算双耳质量差及背部皮肤厚度的变化.以RAW264.7细胞和HaCaT细胞作为炎症细胞模型,采用脂多糖(lipopolysaccharide,LPS)诱导炎症反应,评估唾液乳杆菌与蛹虫草或铁皮石斛共培提取物调节细胞中白细胞介素-1β(interleukin-1β,IL-1β)、一氧化氮(nitric oxide,NO)和白细胞介素-10(interleukin-10,IL-10)及皮肤炎症生物标志物水平的作用.测定RAW264.7细胞在各种提取物处理下的吞噬能力.选择MatTek人体皮肤敏感性测试来研究唾液乳杆菌与蛹虫草/铁皮石斛共培养提取物的过敏反应.结果 唾液乳杆菌与蛹虫草或铁皮石斛共培组小鼠的双耳质量差和背部皮肤厚度均显著低于模型组(P<0.01、0.001).同时,在唾液乳杆菌与蛹虫草或铁皮石斛共培提取物的处理下,LPS诱导的RAW264.7细胞中的炎症介质如IL-1β、NO和抗炎因子IL-10的产生受到显著调节(P<0.05、0.01、0.001),细胞的吞噬率显著降低(P<0.01、0.001).HaCaT细胞在唾液乳杆菌与蛹虫草或铁皮石斛共培提取物处理下,皮肤炎症生物标志物Ⅰ型胶原α1蛋白(alpha-1 type Ⅰ collagen,COL1A1)、Ⅰ 型胶原 α2 蛋白(alpha-2 type Ⅰ collagen,COL1A2)、Ⅲ 型胶原 α1 蛋白(alpha-1 typeⅢ collagen,COL3A1)的mRNA表达水平显著上调(P<0.05、0.01).唾液乳杆菌与蛹虫草或铁皮石斛共培养的提取物对人体皮肤无过敏反应.结论 唾液乳杆菌和蛹虫草或铁皮石斛共培提取物对慢性皮肤湿疹和皮炎具有抗炎和治疗作用,可作为抗炎、抗过敏护肤品的原料,具有较大的应用前景.
BACKGROUND:The medication of synthetic chemical is one of the main treatments for depressive disorders. Different lines of evidence reveal that a long-term exposure to anti-depressants, e.g., fluoxetine, is causing multiple-drug resistance (MDR) of gut microbiomes. The MDR bacterial strains in gut pose a threat to intestinal balance and treatment of future microbial infection. Effective strategies are thus in urgent need to prevent the anti-depressant-mediated MDR of gut microbes.PURPOSE:We aimed to investigate the potential role of Aloe vera (L.) Burm. f. (aloe; Liliaceae family) to prevent MDR of E. coli being co-cultured with fluoxetine.METHODS:The extract of A. vera was co-cultured with E. coli and fluoxetine to analyze the preventive effect of MDR. To figure out the mechanistic action, the formation of reactive oxygen species (ROS) and the expression of key biomarkers, including outer membrane proteins (OmpF and OmpC), superoxidative stress activator (SoxS) and efflux pumps (AcrA/B-TolC), were determined in E. coli being treated with fluoxetine and aloe extract. In addition, the genetic mutation of transcriptional factors of these biomarkers was determined in the fluoxetine-treated E. coli.RESULTS:The water extract of A. vera showed considerable potential to reduce the number of fluoxetine-mediated MDR colonies. The extract robustly suppressed the formation of ROS in E. coli. However, thiourea and N-acetylcysteine, two well-known antioxidants, showed no activity in preventing the formation of bacterial MDR. Additionally, A. vera extract directly affected the fluoxetine-triggered early stress response of E. coli and the expression of downstream genes. Meanwhile, A. vera extract was able to inhibit the genetic mutation of SoxR gene in E. coli, as induced by co-cultured with fluoxetine. By fractionation of the aloe extract, the ethanol precipitate, composing mainly polysaccharides, showed robust activity in preventing the fluoxetine-mediated MDR.CONCLUSION:This study therefore suggested that the extract of A. vera could be an adjuvant agent to combat bacterial MDR during anti-depressant treatment.
Capsaicin, a major ingredient in chili pepper, has broad pharmaceutical applications, including relieving pain, anti-inflammation, and treating psoriasis. In dermatological biology, capsaicin has been shown to prevent the ultraviolet (UV)-induced melanogenesis via TRPV1 receptor. To strengthen the roles of capsaicin in skin function, the damaged skin, triggered by exposure to UV, was reversed by capsaicin in both in vitro and in vivo models. In cultured dermal fibroblasts, the exposure to UV induced a decrease of collagen synthesis and increases expression of matrix metalloproteinases (MMPs), generation of reactive oxygen species (ROS), and phosphorylation of Erk and c-Jun, and these events subsequently led to skin damage. However, the UV-mediated damages could be reversed by pre-treatment with capsaicin in a dose-dependent manner. The effect of capsaicin in blocking the UV-mediated collagen synthesis was mediated by reducing generation of ROS in dermal fibroblasts, instead of the receptor for capsaicin. Hence, capsaicin has high potential value in applying as an agent for anti-skin aging in dermatology.