The number of patients with reduced blood volume due to haemorrhage, fractures, severe infections, extensive burns and tumours is increasing, and traditional blood products are no longer able to meet the increasing clinical demand. Therefore, plasma substitutes have become particularly important in fluid resuscitation, especially artificial colloidal solutions, which have a sustained volume expansion time and a good volume expansion effect, and can significantly improve the circulatory status of patients. This article aims to review the classification of artificial colloidal plasma substitutes and their research progress in clinical practice, in order provide a more rigorous, professional and standardized reference for medicine.

ObjectiveTo observe the clinical efficacy and safety of Modified Guomin Decoction （加味过敏煎， MGD） in patients with mild to moderate atopic dermatitis （AD） of the traditional Chinese medicine （TCM） pattern of heart fire and spleen deficiency， and to explore its possible mechanisms. MethodsIn this randomized， double-blind， placebo-controlled study， 72 patients with mild to moderate AD and the TCM pattern of heart fire and spleen deficiency were randomly divided into a treatment group and a control group， with 36 cases in each group. The treatment group received oral MGD granules combined with topical vitamin E emulsion， while the control group received oral placebo granules combined with topical vitamin E treatment. Both groups were treated twice daily for 4 weeks. Clinical efficacy， TCM syndrome scores， Visual Analogue Scale （VAS） for pruritus， Dermatology Life Quality Index （DLQI） scores， Scoring Atopic Dermatitis （SCORAD） and serum biomarkers， including interleukin-33 （IL-33）， interleukin-1β （IL-1β）， immunoglobulin E （IgE）， and tumor necrosis factor-α （TNF-α） were compared before and after treatment. Safety indexes was also assessed. ResultsThe total clinical effective rates were 77.78% （28/36） in the treatment group and 38.89% （14/36） in the control group， with cure rates of 19.44% （7/36） and 2.78% （1/36）， respectively. The treatment group showed significantly better clinical outcomes compared to the control group （P＜0.05）. The treatment group exhibited significant reductions in total TCM syndrome scores， including erythema， edema， papules， scaling， lichenification， pruritus， irritability， insomnia， abdominal distension， and fatigue scores， as well as reductions in VAS， DLQI， SCORAD， and serum IgE and IL-33 levels （P＜0.05 or P＜0.01）. Compared to the control group， the treatment group had significantly better improvements in all indicators except for insomnia （P＜0.05）. No adverse events occurred in either group. ConclusionMGD is effective and safe in treating mild to moderate AD patients with heart fire and spleen deficiency pattern. It significantly alleviates pruritus， improves TCM syndromes and quality of life， and enhances clinical efficacy， possibly through modulation of immune responses.

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.

The pathogenesis of cardiovascular diseases (CVD) is complex, and dynamic imbalances in protein acylation modification are significantly associated with the development of CVD. In recent years, most studies on exercise-regulated protein acylation modifications to improve cardiovascular function have focused on acetylation and lactylation. Protein acylation modifications are usually affected by exercise intensity. High-intensity exercise directly affects oxidative stress and cellular energy supply, such as changes in ATP and NAD⁺ levels; moderate-intensity exercise is often accompanied by improvements in aerobic metabolism, such as fatty acid β-oxidation and TCA cycle, which modulate mitochondrial biogenesis. The above processes may affect the acylation status of relevant regulatory enzymes and functional proteins, thereby altering their function and activity and triggering signaling cascades to adapt to exercise’s metabolic demands and stresses. Exercise regulates the levels of acylation modifications of H3K9, H3K14, H3K18, and H3K23, which are involved in regulating the transcriptional expression of genes involved in oxidative stress, glycolysis, inflammation, and hypertrophic response by altering chromatin structure and function. Exercise can regulate the acylation modification of non-histone-specific sites in the cardiovascular system involved in mitochondrial function, glycolipid metabolism, fibrosis, protein synthesis, and other biological processes, and participates in the regulation of protein activity and function by altering the stability, localization, and interaction of proteins, and ultimately works together to achieve the improvement of cardiovascular phenotypes and biological functions. Exercise affects acyl donor concentration, acyltransferase, and deacetylase expression and activity by influencing acyl donor concentration, acyltransferase, and deacetylase. Exercise regulates the abundance of acyl donors such as acetyl coenzyme A, propionyl coenzyme A, butyryl coenzyme A, succinyl coenzyme A, and lactoyl coenzyme A by promoting glucose and lipid metabolism and improving intestinal bacterial flora, which in turn affects protein acylation modification, accelerates oxidative decarboxylation of pyruvic acid in the body, and activates the energy-sensing molecule, adenosine monophosphate-activated protein kinase (AMPK), to improve cardiovascular function. Exercise may affect protein acylation modifications in the cardiovascular system by regulating the activity and expression of adenoviral E1A binding protein of 300 kDa (p300)/cyclic adenosine monophosphate response element-binding protein (CBP), general control nonderepressible 5-related N-acetyltransferases (GNAT), and alanyl-transfer t-RNA synthetase (AARS), which in turn improves cardiovascular function. The relationship between exercise and cardiovascular deacetylases has attracted much attention, with SIRT1 and SIRT3 of the silence information regulator (SIRT) family of proteins being the most studied. Exercise may exert transient or long-term stable cardiovascular protective benefits by promoting the enzymatic activity and expression of SIRT1, SIRT3, and HDAC2, inhibiting the enzymatic activity and expression of HDAC4, and mediating the deacylation of metabolic regulation-related enzymes, cytokines, and molecules of signaling pathways. This review introduces the role of protein acylation modification on CVD and the effect of exercise-mediated protein acylation modification on CVD. Based on the existing studies, it analyzes the possible mechanisms of exercise-regulated protein acylation modification to improve CVD from the perspectives of acylation modification donors, acyltransferases, and deacetylases. Deciphering the regulation of cardiovascular protein acylation and modification by exercise and exploring the essential clues to improve cardiovascular disease can enrich the theoretical basis for exercise to promote cardiovascular health. However, it is also significant for developing new cardiovascular disease prevention and treatment targets.

Hydrogen peroxide (H₂O₂) and nitric oxide (NO) has a short half-life, low bioavailability, poor tumor targeting and systemic adverse reactions in the physiological environment. In this study, phacoemulsification and nano-precipitation were used to synthesize didecyl dimethyl ammonium bromide (DDAB)/polylactic acid nanoparticles (PLA), then L-arginine (L-Arg) and glucose oxidase (GOx)-loaded nanoparticles (GADP) were prepared, and the in vitro antitumor activity was investigated．The particle size, potential, embedding rate and the ability to produce H₂O₂/NO of the nanoparticles were investigated. Meanwhile, in vitro cell cytotoxicity against human hepatoma cells (HepG2) was evaluated．The results showed that the prepared L-Arg-DDAB/PLA (ADP) nanoparticles were spherical particles. And the particle size and zeta potential were (225.7 ± 6.33) nm and (+23.5 ± 0.12) mV, respectively. The adsorption rate of GOx was 87.23% ± 0.02%. The drug loading of L-Arg was 15.6% ± 0.22%. The pH value of glucose solution and the amount of H₂O₂ showed that GADP had good catalytic activity. In vitro cytotoxicity experiments showed that blank nanoparticles were nontoxic, while the drug-loaded nanoparticles presented enhanced antitumor effect on HepG2 cells. And can inhibit tumor cell migration. The low dose nano-scale NO delivery system GADP can effectively inhibit the migration of tumor cells and kill tumor cells, thus producing therapeutic benefits.

Humans ; Adolescent ; Acne Vulgaris/therapy* ; Skin Care ; Surveys and Questionnaires ; Cognition ; China ; Skin

Objective To investigate the effects of raddeanin A(RA)on the proliferation and apoptosis of HCT116 cells and on the β-catenin/c-Myc pathway.Methods Human colon cancer HCT116 cells were divided into four groups:Control group,experimental-L group,experimental-M group and experimental-H group.Experimental-L,experimental-M,experimental-H groups were treated with 5,10 and 20 μmol·L-1raddeanin A,and the control group was given the same amount of normal saline,respectively.The inhibitory effect of RA on the proliferation of HCT116 cells of colon cancer was detected by cell counting kit-8(CCK-8)method.Cell nucleus morphology change was observed with the fluorescence;the apoptosis rate was detected by flow cytometry;and the expression of related proteins of β-catenin/c-Myc signaling pathway was detected by western blot.Results After 48 h,the cell inhibitory rates of the control group,experimental-L,experimental-M,experimental-H groups were 0,(19.15±0.65)％,(35.11±0.40)％and(49.93±1.13)％,respectively;the cell apoptosis rates were(0.16±0.18)％,(9.26±0.42)％,(17.87±2.54)％and(38.10±2.70)％,respectively;the protein expression levels of β-catenin were 0.74±0.03,0.69±0.01,0.33±0.02 and 0.16±0.04,respectively;the protein expression levels of c-Myc were 0.89±0.01,0.54±0.03,0.29±0.03 and 0.13±0.04,respectively;the protein expression levels of Cyclin D1 were 0.84±0.04,0.66±0.01,0.48±0.06 and 0.21±0.03,respectively;the expression levels of Cleaved-Caspase3 protein were 0.19±0.03,0.26±0.04,0.45±0.04 and 0.78±0.01,respectively.The above indicators in the experimental-L,experimental-M,experimental-H groups showed statistically significant differences compared to those of control group(all P＜0.05).Conclusion RA can inhibit the proliferation of HCT116 cells and induce apoptosis,which may be related to the inhibition of β-catenin/c-Myc signaling pathway.

Objective To investigate the impact of emodin(EM)on vascular endothelial cell injury in rats with diabetes macroangiopathy by regulating hypoxia inducible factor-1α(HIF-1α)/vascular endothelial growth factor(VEGF)signaling pathway.Methods SD rats were divided into blank group and modeling group,the rats in the modeling group were fed with high fat and high sugar combined with N-nitro-L-arginine methyl ester to build the diabetes macroangiopathy model,and the blank group was fed with ordinary diet.The vascular endothelial cells successfully isolated from the thoracic aorta of rats in blank group and modeling group were named control group and model group,respectively.The vascular endothelial cells in the modeling group were divided into model group,dimethyloxallyl glycine(DMOG)group(10 μmol·L-1DMOG),combined group(80 mg·L-1EM+10 μmol·L-1 DMOG)and experimental-L,-M,-H groups(20,40,80 mg·L-1 EM).The apoptosis of rat vascular endothelial cells was detected by flow cytometry;Western blot was applied to detect the expression of HIF-1αand VEGF proteins in rat vascular endothelial cells.Results The apoptosis rates of vascular endothelial cells in experimental-M,-H groups,DMOG group,combined group,model group and control group were(10.18±0.36)％,(6.28±0.20)％,(24.96±1.18)％,(12.36±0.49)％,(18.76±0.68)％and(4.59±0.26)％;HIF-1α protein levels were 0.96±0.07,0.78±0.06,2.03±0.12,1.05±0.13,1.58±0.12 and 0.69±0.05;VEGF protein levels were 0.59±0.05,0.23±0.02,0.98±0.06,0.63±0.04,0.86±0.07 and 0.11±0.01.The above indexes in the model group were compared with the control,DMOG,experimental-M and experimental-H groups,and the above indexes in the combined group were compared with the experimental-H group,and the differences were statistically significant(all P＜0.05).Conclusion EM may inhibit HIF-1α/VEGF pathway to improve vascular endothelial cell injury in rats with diabetes macroangiopathy.

Objective To explore the effect of Wenyang Huazhuo Tongluo recipe on pulmonary microvascular injury in mice with scleroderma based on mitophagy.Methods Fifty mice were randomly divided into blank control group(0.9％NaCl,by gavage),control group(0.9％NaCl,by gavage),model group,Wenyang Huazhuo Tongluo recipe group(47mg·kg-1·d-1 Wenyang Huazhuo Tongluo recipe by gavage),positive control group(10 mg·kg-1·d-1 KC7F2 dissolved in phosphate buffer solution intraperitoneal injection),continuous administration for 4 weeks.The expression levels of in vitro membrane translocation enzyme 20(TOMM20),hypoxia inducible factor-1α(HIF-1α),B cell lymphoma-2/adenovirus E1B-19 kDa interacting protein 3(BNIP3),PTEN inducible muscle enzyme protein 1(PINK1)and E3 ubiquitin ligase(Parkin)in lung tissue were detected by immunohistochemistry(IHC).Western blot(WB)was used to detect the expression levels of mitophagy-related proteins(TOMM20,LC3B)and HIF-1α/BNIP3/PINK1/Parkin pathway proteins in pulmonary microvascular endothelial cells.Results The relative content of HIF-1α in microvascular endothelial cells of lung tissue in the control group,model group,Wenyang Huazhuo Tongluo recipe group and positive control group were 0.17±0.02,0.98±0.01,0.66±0.03 and 0.48±0.01;the relative content of BNIP3 were 0.40±0.02,0.74±0.01,0.56±0.01 and 0.60±0.02;the relative content of PINK1 were 0.26±0.04,0.88±0.01,0.65±0.02 and 0.67±0.02;the relative contents of Parkin were 0.33±0.02,0.89±0.01,0.65±0.02 and 0.77±0.02;the relative contents of TOMM20 were 1.10±0.02,0.58±0.01,1.02±0.01 and 0.98±0.03;the relative contents of LC3B-Ⅰ/LC3B-Ⅱ were 0.24±0.01,0.80±0.01,0.53±0.02 and 0.70±0.02,respectively.The content of HIF-1α,BNIP3,PINK1,Parkin and LC3B-Ⅰ/LC3B-Ⅱ in model group was higher than those in control group.Wenyang Huazhuo Tongluo recipe can effectively reduce its content.The content of TOMM20 in the model group was lower than that in control group,and Wenyang Huazhuo Tongluo recipe can effectively increase its content.Conclusion Wenyang Huazhuo Tongluo recipe may inhibit mitophagy and improve SSc pulmonary microvascular injury by increasing TOMM20 and inhibiting the protein expression of LC3B and HIF-1α/BNIP3/PINK1/Parkin signaling pathway.

Objective To establish a method for the determination of lorlatinib in human plasma by two-dimensional high performance liquid chromatography.Methods In the two-dimensional high performance liquid chromatography method,one-dimensional column SX1E-1A(50 mm × 3.5 mm,5 μm)and two-dimensional column SCB-C18(125 mm × 4.6 mm,5 μm)were used with flow rates of 0.8 mL·min-1 and 1.0 mL·min-1,respectively.The column temperature was 40 ℃,The UV detection wavelength was 317 nm,and the sample size was 500 μL.This study investigated the specificity,standard curve and minimum quantification limit,precision and recovery rate,as well as stability of the method.Results The concentration of lolatinib in human plasma showed a good linear relationship in the range of 11.72-1 018.98 ng·mL-1,and the regression equation was y=944.50x-588.90(R2=0.999 7).The minimum limit of quantification was 11.72 ng·mL-1.The extraction recovery rates of the three quality control samples were 97.61％-99.86％,and the intra-day and inter-day precisions were less than 5.29％,indicating that the detection performance of the method was good.Conclusion The method has the characteristics of good stability,high sensitivity and strong anti-interference ability,and is suitable for the determination of loratinib in human plasma.