To systematically analyzed the reporting status of core elements in publicly available clinical practice guideline(hereafter referred to as "guideline") protocols published domestically and internationally over the past decade, identified existing problems, and provided evidence to inform the standardized writing and publication of future guideline protocols.

Aging has emerged as a cutting edge and hotspot in global life science field， with anti-aging and geriatric disease prevention and treatment becoming critical issues urgently demanding solutions in international medical communities. In the face of the challenge of accelerating global population aging， in-depth exploration of aging mechanisms and the development of effective intervention strategies hold significant scientific and clinical value. This study supported by the national key research and development program of China， employed the essence-Qi-spirit theory of Qiluo doctrine as its guiding framework， focusing on the key scientific issue of the core traditional Chinese pathogenesis of aging， namely "depletion of kidney essence， deficiency of primordial Qi， and impairment of body and spirit". The treatment principle of "tonifying the kidney to replenish essence， harmonizing Yin and Yang， warming and invigorating primordial Qi， and nourishing the body and spirit" was established. Centered on holistic aging， systemic aging， and aging-related diseases， the research integrated multidisciplinary research approaches to construct multi-modal aging models and a multi-dimensional evaluation system， and it utilized multi-omics technologies to deeply analyze aging mechanisms. By systematically reviewing historical kidney-tonifying and anti-aging formulas and combining big data with artificial intelligence technologies， an information database of anti-aging traditional Chinese medicine substance was developed to reveal the differences and synergistic effects of various treatment methods and formulas on anti-aging. Based on this treatment method， the research integrated two millennia of kidney-tonifying medicinal experience to develop the innovative anti-aging traditional Chinese medicine， namely Bazhi Bushen capsules. It was validated that this capsule can delay holistic and systemic aging through multiple targets and mechanisms， thereby elucidating the scientific connotation of the essence-Qi-spirit theory of Qiluo doctrine in guiding anti-aging research from multiple dimensions and providing robust support for leveraging the advantages of traditional Chinese medicine to occupy the commanding heights of international anti-aging research.

Myocardial infarction （MI） and osteoporosis （OP）， as two prevalent metabolic diseases with high morbidity and mortality rates， are respectively characterized by cardiovascular system dysfunction and bone homeostasis imbalance， collectively posing significant global public health challenges. While clinically often considered as independent diseases， recent studies have revealed shared pathological mechanisms between the two. This study initiated its exploration from the traditional Chinese medicine concept of the "heart-bone" axis， systematically analyzing the correlation between MI and OP from perspectives including hemodynamics， neuroendocrinology， calcium homeostasis， inflammation and vascular injury， as well as hormone levels. By discussing the pathological mechanisms of "heart disease affecting the bones and bone disease affecting the heart"， the study also elucidated advancements in both Western and traditional Chinese medicine treatments. The goal is to provide novel insights and methodologies for the prevention and treatment of "heart-bone comorbidities"， thereby facilitating comprehensive management of cardiovascular and skeletal diseases.

Myocardial infarction （MI） and osteoporosis （OP）， as two prevalent metabolic diseases with high morbidity and mortality rates， are respectively characterized by cardiovascular system dysfunction and bone homeostasis imbalance， collectively posing significant global public health challenges. While clinically often considered as independent diseases， recent studies have revealed shared pathological mechanisms between the two. This study initiated its exploration from the traditional Chinese medicine concept of the "heart-bone" axis， systematically analyzing the correlation between MI and OP from perspectives including hemodynamics， neuroendocrinology， calcium homeostasis， inflammation and vascular injury， as well as hormone levels. By discussing the pathological mechanisms of "heart disease affecting the bones and bone disease affecting the heart"， the study also elucidated advancements in both Western and traditional Chinese medicine treatments. The goal is to provide novel insights and methodologies for the prevention and treatment of "heart-bone comorbidities"， thereby facilitating comprehensive management of cardiovascular and skeletal diseases.

BACKGROUND:Hippocampal injury caused by aortic coarctation has been poorly studied,and combined detection of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 expression in aortic dissection has not been reported.OBJECTIVE:To observe histomorphologic changes in the hippocampus of a mouse model of aortic dissection and investigate the expression and significance of tumor necrosis factor alpha,nuclear factor kappaB and ionized calcium binding adaptor molecule-1 in the hippocampus of aortic dissection mice.METHODS:Sixteen healthy 3-week-old male C57BL/6 mice were randomly divided into two groups:control group and aortic dissection group,with eight mice in each group.In the aortic dissection group,mice were given β-aminopropionitrile monofumarate as drinking water for 4 weeks,and the angiotensin Ⅱ microinfiltration pump was then implanted to establish an animal model of aortic dissection.Mice in the control group were given normal diet and water.After the model was established,the maximum diameter of the ascending aorta was measured,hematoxylin-eosin staining and EVG staining were performed to evaluate the model formation rate,and the levels of inflammatory factors tumor necrosis factor α and interleukin 6 in serum were detected by enzyme-linked immunosorbent assay.The hippocampus was dissected and stained with hematoxylin-eosin to observe the pathological changes of the hippocampus in brain sections.The protein expression of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 was detected by western blot analysis.RESULTS AND CONCLUSION:(1)Compared with the control group,the maximum diameter of the ascending aorta in the aortic dissection group was significantly enlarged.(2)Hematoxylin-eosin staining of the aorta showed obvious thickening of the middle aorta and destruction and disorder of the aortic wall structure in mice.Neurons in the CA1 and CA3 regions of mice were sparsely arranged,reduced in size,and showed pyknosis with deeply stained nuclei.(3)Serum levels of inflammatory factors tumor necrosis factor α and interleukin 6 were increased in the aortic dissection group compared with the control group(P＜0.01).(4)The expression levels of tumor necrosis factor α,nuclear factor κB,phosphorylated nuclear factor κB,and ionized calcium binding adaptor molecule-1 in the hippocampus were increased in the aortic dissection group compared with the control group(P＜0.05).To conclude,microglial activation and increased expression of tumor necrosis factor α and nuclear factor κB may be involved in hippocampal neuron injury in aortic dissection mice.

BACKGROUND:Hippocampal injury caused by aortic coarctation has been poorly studied,and combined detection of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 expression in aortic dissection has not been reported.OBJECTIVE:To observe histomorphologic changes in the hippocampus of a mouse model of aortic dissection and investigate the expression and significance of tumor necrosis factor alpha,nuclear factor kappaB and ionized calcium binding adaptor molecule-1 in the hippocampus of aortic dissection mice.METHODS:Sixteen healthy 3-week-old male C57BL/6 mice were randomly divided into two groups:control group and aortic dissection group,with eight mice in each group.In the aortic dissection group,mice were given β-aminopropionitrile monofumarate as drinking water for 4 weeks,and the angiotensin Ⅱ microinfiltration pump was then implanted to establish an animal model of aortic dissection.Mice in the control group were given normal diet and water.After the model was established,the maximum diameter of the ascending aorta was measured,hematoxylin-eosin staining and EVG staining were performed to evaluate the model formation rate,and the levels of inflammatory factors tumor necrosis factor α and interleukin 6 in serum were detected by enzyme-linked immunosorbent assay.The hippocampus was dissected and stained with hematoxylin-eosin to observe the pathological changes of the hippocampus in brain sections.The protein expression of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 was detected by western blot analysis.RESULTS AND CONCLUSION:(1)Compared with the control group,the maximum diameter of the ascending aorta in the aortic dissection group was significantly enlarged.(2)Hematoxylin-eosin staining of the aorta showed obvious thickening of the middle aorta and destruction and disorder of the aortic wall structure in mice.Neurons in the CA1 and CA3 regions of mice were sparsely arranged,reduced in size,and showed pyknosis with deeply stained nuclei.(3)Serum levels of inflammatory factors tumor necrosis factor α and interleukin 6 were increased in the aortic dissection group compared with the control group(P＜0.01).(4)The expression levels of tumor necrosis factor α,nuclear factor κB,phosphorylated nuclear factor κB,and ionized calcium binding adaptor molecule-1 in the hippocampus were increased in the aortic dissection group compared with the control group(P＜0.05).To conclude,microglial activation and increased expression of tumor necrosis factor α and nuclear factor κB may be involved in hippocampal neuron injury in aortic dissection mice.

Membrane proteins are integral components of cellular membranes, accounting for approximately 30% of the mammalian proteome and serving as targets for 60% of FDA-approved drugs. They are critical to both physiological functions and disease mechanisms. Their functional protein-protein interactions form the basis for many physiological processes, such as signal transduction, material transport, and cell communication. Membrane protein interactions are characterized by membrane environment dependence, spatial asymmetry, weak interaction strength, high dynamics, and a variety of interaction sites. Therefore, in situ analysis is essential for revealing the structural basis and kinetics of these proteins. This paper introduces currently available in situ analytical techniques for studying membrane protein interactions and evaluates the characteristics of each. These techniques are divided into two categories: label-based techniques (e.g., co-immunoprecipitation, proximity ligation assay, bimolecular fluorescence complementation, resonance energy transfer, and proximity labeling) and label-free techniques (e.g., cryo-electron tomography, in situ cross-linking mass spectrometry, Raman spectroscopy, electron paramagnetic resonance, nuclear magnetic resonance, and structure prediction tools). Each technique is critically assessed in terms of its historical development, strengths, and limitations. Based on the authors’ relevant research, the paper further discusses the key issues and trends in the application of these techniques, providing valuable references for the field of membrane protein research. Label-based techniques rely on molecular tags or antibodies to detect proximity or interactions, offering high specificity and adaptability for dynamic studies. For instance, proximity ligation assay combines the specificity of antibodies with the sensitivity of PCR amplification, while proximity labeling enables spatial mapping of interactomes. Conversely, label-free techniques, such as cryo-electron tomography, provide near-native structural insights, and Raman spectroscopy directly probes molecular interactions without perturbing the membrane environment. Despite advancements, these methods face several universal challenges: (1) indirect detection, relying on proximity or tagged proxies rather than direct interaction measurement; (2) limited capacity for continuous dynamic monitoring in live cells; and (3) potential artificial influences introduced by labeling or sample preparation, which may alter native conformations. Emerging trends emphasize the multimodal integration of complementary techniques to overcome individual limitations. For example, combining in situ cross-linking mass spectrometry with proximity labeling enhances both spatial resolution and interaction coverage, enabling high-throughput subcellular interactome mapping. Similarly, coupling fluorescence resonance energy transfer with nuclear magnetic resonance and artificial intelligence (AI) simulations integrates dynamic structural data, atomic-level details, and predictive modeling for holistic insights. Advances in AI, exemplified by AlphaFold’s ability to predict interaction interfaces, further augment experimental data, accelerating structure-function analyses. Future developments in cryo-electron microscopy, super-resolution imaging, and machine learning are poised to refine spatiotemporal resolution and scalability. In conclusion, in situ analysis of membrane protein interactions remains indispensable for deciphering their roles in health and disease. While current technologies have significantly advanced our understanding, persistent gaps highlight the need for innovative, integrative approaches. By synergizing experimental and computational tools, researchers can achieve multiscale, real-time, and perturbation-free analyses, ultimately unraveling the dynamic complexity of membrane protein networks and driving therapeutic discovery.

ObjectiveTo explore the regulation of Shaoyaotang on glucose metabolism reprogramming of macrophages and the mechanism of this decoction in inhibiting macrophage polarization toward the M1 phenotype. MethodsHuman monocytic leukemia-1 （THP-1） cells were treated with 100 ng·L^-1 phorbol myristate acetate for induction of macrophages as the normal control group. The cells treated with 100 ng·L^-1 lipopolysaccharide combined with 20 ng·L^-1 interferon （IFN）-γ for induction of M1-type macrophages were taken as the M1 model group. M1-type macrophages were treated with the blank serum， Shaoyaotang-containing serum， 0.5 mol·L^-1 2-deoxy-D-glucose （2-DG）， and Shaoyaotang-containing serum + 2-DG， respectively. After intervention， the expression of CD86 and CD206 was examined by flow cytometry. The levels of interleukin （IL）-6， tumor necrosis factor （TNF）-α， IL-10， and transforming growth factor （TGF）-β were assessed by ELISA. Real-time PCR and Western blot were employed to determine the mRNA and protein levels， respectively， of hypoxia-inducible factor-1 alpha （HIF-1α）， glucose transporter 1 （GLUT1）， hexokinase 2 （HK2）， glyceraldehyde-3-phosphate dehydrogenase （GAPDH）， and 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）. ResultsCompared with that in the normal control group， the expression of CD86， the marker of M1-type macrophages， increased in the M1 model group and blank serum group （P<0.01）， which indicated that the M1 inflammatory model was established successfully. In addition， the M1 model group was observed with up-regulated mRNA and protein levels of proinflammatory cytokines IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 （P<0.01）. Compared with the M1 model group， the Shaoyaotang-containing serum， 2-DG， and combined intervention groups showed decreased expression of CD86 （P<0.01）， down-regulated mRNA and protein levels of proinflammatory factors IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 produced by M1-type macrophages （P<0.01）， increased expression of CD206 （marker of M2-type macrophages） （P<0.01）， and elevated levels of IL-10 and TGF-β produced by M2-type macrophages （P<0.01）. ConclusionShaoyaotang inhibits macrophage differentiation toward pro-inflammatory M1-type macrophages and promotes the differentiation toward anti-inflammatory M2-type macrophages by regulating glucose metabolism reprogramming. The evidence gives insights into new molecular mechanisms and targets for the treatment of ulcerative colitis with Shaoyaotang.

Tangye Jingfa Tu is an important content in the ancient book Fuxingjue from Dunhuang， implying the fundamental principles of formula compatibility in traditional Chinese medicine （TCM）. Our research group has delved into nearly 200 formulas （both classical and contemporary formulas） recorded in the Fangjixue under the theoretical framework of the deficiency or excess syndrome of five Zang-organs together with the reinforcing and reducing effects of Chinese medicinal materials of five flavors. We have initially elucidated the essential principles of the correspondence between formulas and syndromes， revealing the deep-level logic of medicinal material selection and compatibility， thus enriching the understanding about the core characteristics and essence of the diseases and syndromes targeted by formulas. The lunar year of 2024 is Jia Chen year. The formula recorded in Sanyin Jiyi Bingzheng Fanglun for treating the epidemic diseases characterized by excessive earth， prevalent dampness and wetness， and invasion of pathogenic factors into the kidney water in Jia Chen year is Fuzi Shanzhuyutang. Therefore， elucidating the compatibility principle of Fuzi Shanzhuyutang is of great significance for clinical prescription and medication modification in Jia Chen year. According to the Tangye Jingfa Tu theory on the deficiency or excess of syndrome of five Zang-organs and the reinforcing and reducing effects of Chinese medicinal materials of five flavors， this article dissects Fuzi Shanzhuyutang regarding the etiology and pathogenesis of the main indications， as well as the five-element properties and efficacy characteristics of Chinese medicinal materials constituting this formula. It explains the compatibility principles of Fuzi Shanzhuyutang and puts forward suggestions for modifying the formula to address different indications， providing a reference for guiding clinical syndrome differentiation and treatment.

ObjectiveTo explore the regulation of Shaoyaotang on glucose metabolism reprogramming of macrophages and the mechanism of this decoction in inhibiting macrophage polarization toward the M1 phenotype. MethodsHuman monocytic leukemia-1 （THP-1） cells were treated with 100 ng·L^-1 phorbol myristate acetate for induction of macrophages as the normal control group. The cells treated with 100 ng·L^-1 lipopolysaccharide combined with 20 ng·L^-1 interferon （IFN）-γ for induction of M1-type macrophages were taken as the M1 model group. M1-type macrophages were treated with the blank serum， Shaoyaotang-containing serum， 0.5 mol·L^-1 2-deoxy-D-glucose （2-DG）， and Shaoyaotang-containing serum + 2-DG， respectively. After intervention， the expression of CD86 and CD206 was examined by flow cytometry. The levels of interleukin （IL）-6， tumor necrosis factor （TNF）-α， IL-10， and transforming growth factor （TGF）-β were assessed by ELISA. Real-time PCR and Western blot were employed to determine the mRNA and protein levels， respectively， of hypoxia-inducible factor-1 alpha （HIF-1α）， glucose transporter 1 （GLUT1）， hexokinase 2 （HK2）， glyceraldehyde-3-phosphate dehydrogenase （GAPDH）， and 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）. ResultsCompared with that in the normal control group， the expression of CD86， the marker of M1-type macrophages， increased in the M1 model group and blank serum group （P<0.01）， which indicated that the M1 inflammatory model was established successfully. In addition， the M1 model group was observed with up-regulated mRNA and protein levels of proinflammatory cytokines IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 （P<0.01）. Compared with the M1 model group， the Shaoyaotang-containing serum， 2-DG， and combined intervention groups showed decreased expression of CD86 （P<0.01）， down-regulated mRNA and protein levels of proinflammatory factors IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 produced by M1-type macrophages （P<0.01）， increased expression of CD206 （marker of M2-type macrophages） （P<0.01）， and elevated levels of IL-10 and TGF-β produced by M2-type macrophages （P<0.01）. ConclusionShaoyaotang inhibits macrophage differentiation toward pro-inflammatory M1-type macrophages and promotes the differentiation toward anti-inflammatory M2-type macrophages by regulating glucose metabolism reprogramming. The evidence gives insights into new molecular mechanisms and targets for the treatment of ulcerative colitis with Shaoyaotang.