Quantitative structure-retention relationship (QSRR) is an important tool in chromatography. QSRR examines the correlation between molecular structures and their retention behaviors during chromatographic separation. This approach involves developing models for predicting the retention time (RT) of analytes, thereby accelerating method development and facilitating compound identification. In addition, QSRR can be used to study compound retention mechanisms and support drug screening efforts. This review provides a comprehensive analysis of QSRR workflows and applications, with a special focus on the role of artificial intelligence-an area not thoroughly explored in previous reviews. Moreover, we discuss current limitations in RT prediction and propose promising solutions. Overall, this review offers a fresh perspective on future QSRR research, encouraging the development of innovative strategies that enable the diverse applications of QSRR models in chromatographic analysis.

Triggering receptor expressed on myeloid cells 2 (TREM2)-mediated microglial phagocytosis is an energy-intensive process that plays a crucial role in amyloid beta (Aβ) clearance in Alzheimer's disease (AD). Energy metabolic reprogramming (EMR) in microglia induced by TREM2 presents therapeutic targets for cognitive impairment in AD. Jiawei Xionggui Decoction (JWXG) has demonstrated effectiveness in enhancing energy supply, protecting microglia, and mitigating cognitive impairment in APP/PS1 mice. However, the mechanism by which JWXG enhances Aβ phagocytosis through TREM2-mediated EMR in microglia remains unclear. This study investigates how JWXG facilitates microglial phagocytosis and alleviates cognitive deficits in AD through TREM2-mediated EMR. Microglial phagocytosis was evaluated through immunofluorescence staining in vitro and in vivo. The EMR level of microglia was assessed using high-performance liquid chromatography (HPLC) and enzyme-linked immunosorbent assay (ELISA) kits. The TREM2/protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway was analyzed using Western blotting in BV₂ cells. TREM2^-/- BV₂ cells were utilized for reverse validation experiments. The Aβ burden, neuropathological features, and cognitive ability in APP/PS1 mice were evaluated using ELISA kits, immunohistochemistry (IHC), and the Morris water maze (MWM) test. JWXG enhanced both the phagocytosis of EMR disorder-BV₂ cells (EMRD-BV₂) and increased EMR levels. Notably, these effects were significantly reversed in TREM2^-/- BV₂ cells. JWXG elevated TREM2 expression, adenosine triphosphate (ATP) levels, and microglial phagocytosis in APP/PS1 mice. Additionally, JWXG reduced Aβ-burden, neuropathological lesions, and cognitive deficits in APP/PS1 mice. In conclusion, JWXG promoted TREM2-induced EMR and enhanced microglial phagocytosis, thereby reducing Aβ deposition, improving neuropathological lesions, and alleviating cognitive deficits.
Drugs, Chinese Herbal/pharmacology* ; Microglia/drug effects* ; Phagocytosis ; Cognitive Dysfunction/drug therapy* ; Metabolic Reprogramming ; Animals ; Mice ; Cell Line ; Receptors, Immunologic/metabolism* ; Membrane Glycoproteins/metabolism* ; Signal Transduction ; Amyloid beta-Peptides/metabolism* ; Energy Metabolism

The high content of sucrose and raffinose reduces the prebiotic value of soybean oligosaccharides. Fructan sucrases can catalyze the conversion of sucrose and raffinose to high-value products such as fructooligosaccharides and melibiose. To obtain a fructan sucrase that can efficiently convert soybean oligosaccharides, we first mined the fructan sucrase gene from microorganisms in the coastal areas of Xisha Islands and Bohai Bay and then characterized the enzymatic and catalytic properties of the enzyme. Finally, recombinant extracellular expression of this gene was carried out in Bacillus subtilis. The results showed that a novel fructan sucrase, BhLS 39, was mined from Bacillus halotolerans. With sucrose and raffinose as substrates, BhLS 39 showed the optimal temperatures of 50 ℃ and 55 ℃, optimal pH 5.5 for both, and K_cat/K_m ratio of 3.4 and 6.6 L/(mmol·s), respectively. When 400 g/L raffinose was used as the substrate, the melibiose conversion rate was 84.6% after 30 min treatment with 5 U BhLS 39. Furthermore, BhLS 39 catalyzed the conversion of sucrose to produce levan-type-fructooligosaccharide and levan. Then, the recombinant extracellular expression of BhLS 39 in B. subtilis was achieved. The co-expression of the intracellular chaperone DnaK and the extracellular chaperone PrsA increased the extracellular activity of the recombinant BhLS 39 by 5.2 folds to 17 U/mL compared with that of the control strain. BhLS 39 obtained in this study is conducive to improving the quality and economic benefits of soybean oligosaccharides. At the same time, the strategy used here to enhance the extracellular expression of BhLS 39 will also promote the efficient recombinant expression of other proteins in B. subtilis.
Oligosaccharides/metabolism* ; Glycine max/metabolism* ; Bacillus subtilis/metabolism* ; Sucrase/biosynthesis* ; Raffinose/metabolism* ; Fructans/metabolism* ; Sucrose/metabolism* ; Bacillus/genetics* ; Recombinant Proteins/biosynthesis* ; Bacterial Proteins/biosynthesis*

Objective:To visualize the relationship between different combinations of mechanical power exposure intensity-duration and death risk in mechanical ventilation patients using a visualization method.Methods:Critically ill patients receiving mechanical ventilation were selected from the Medical Information Mart for Intensive Care-Ⅳ v1.0 (MIMIC-Ⅳ v1.0) database. The patients were divided into four subgroups according to oxygenation index (PaO 2/FiO 2) including > 300 mmHg (1 mmHg≈0.133 kPa) group, 201-300 mmHg group, 101-200 mmHg group and ≤100 mmHg group. The baseline characteristics, ventilator parameters, and prognostic indicators for different patient populations were collected. For each patient, the mechanical power thresholds from low to high (5-30 J/min, increasing at intervals of 1 J/min) were used to evaluate the different exposures of mechanical power (above the set threshold was recorded as one exposure), and the number of events with different exposure intensity-duration combinations was counted based on their corresponding durations. Based on the 28-day survival/non-survival status, the number of exposures for survivors and non-survivors in each exposure intensity-duration combination was calculated, and the survival odds ratio ( OR) for different mechanical power exposure intensity-duration combinations was subsequently computed. Two-dimensional tables were generated with mechanical power exposure duration on the x-axis and exposure intensity on the y-axis, and the heatmap and its corresponding equipotential line view were used to visualize the OR value to assess the risk of death. Results:A total of 5 378 patients receiving mechanical ventilation were enrolled in the study, of whom 2 069 patients in the PaO 2/FiO 2 > 300 mmHg group, 813 patients in the 201-300 mmHg group, 1 493 patients in the 101-200 mmHg group, and 1 003 patients in the ≤100 mmHg group. The severity scores of patients, including sequential organ failure assessment (SOFA) score and simplified acute physiology score Ⅱ (SAPSⅡ), gradually increased following the decrease in PaO 2/FiO 2, and the incidence of co-morbidities also gradually increased. In terms of ventilator parameters, mechanical power was increased gradually with decrease in PaO 2/FiO 2, measuring 10.4 (7.8, 13.9), 11.3 (8.5, 14.7), 13.6 (10.0, 18.2), and 16.7 (12.5, 22.0) J/min ( P < 0.01). In terms of prognosis, 28-day mortality of patients was gradually increased with decrease in PaO 2/FiO 2 [29.1% (601/2 069), 26.9% (219/813), 28.1% (420/1 493), and 33.3% (334/1 003), respectively, P < 0.05]. In the heatmap, it could be observed that the 28-day death risk of mechanical ventilation patients was gradually increased with increase in mechanical power exposure intensity and long duration, showing two distinct areas: a region near the bottom left corner (representing low mechanical power exposure intensity and short duration) was blue, indicating a greater chance of survival. In contrast, another region near the top right corner (representing high mechanical power exposure intensity and long duration) was red, indicating a higher risk of death. According to the fitted lines of death risk, for the same risk of death, a shorter mechanical power exposure duration was required for higher exposure intensity, while lower mechanical power exposure intensity required a longer exposure duration. The above trend of change was similarly reflected in the overall population and different oxygenation populations. Conclusions:Cumulative mechanical power exposure to higher intensity and/or longer duration is associated with worse outcomes in mechanical ventilation patients. Considering both the mechanical power exposure intensity and duration may help to evaluate the effectiveness of lung protection in mechanical ventilation patients and guide adjustments in mechanical ventilation strategy to reduce the risk of ventilator-induced lung injury.

Background The average sleep quality of mariners during ocean voyages is notably worse than that of the general populace, and the incidence of sleep disorders among them is higher. Sleep disorders closely associate with fatigue and cognitive decline, increasing error and accident rates, and are a major safety hazard in marine navigation. At present, research on factors influencing the sleep quality of mariners during ocean voyages in China is limited and needs further investigation. Objective To investigate the sleep quality of mariners during ocean voyages and analyze its influencing factors, in order to provide reference for constructing sleep intervention plans and mitigating their sleep disorders. Methods Using convenience cluster sampling, a questionnaire survey was carried out in 408 crew members of a fleet who returned from a voyage on March 21, 2024. The questionnaires included a general information questionnaire, Pittsburgh Sleep Quality Index (PSQI) , and Self Rating Anxiety Scale (SAS), and the data were analyzed by SPSS 26.0 software. Results A total of 399 valid questionnaires were collected, with an effective recovery rate of 97.8%. The mean score of PSQI for the mariners during ocean voyages was (6.41±2.44), with 33.6% (134/399) of the mariners reporting sleep disorders. The PSQI scores varied by family structures (t=2.235, P=0.031), labor types (F=3.789, P=0.023), noise exposure (F=53.218, P＜0.001), dietary patterns (F=63.311, P＜0.001), exercise habits (F=16.416, P＜0.001), and anxiety states (t=5.963,P＜0.001). The results of linear regression showed that incomplete family structure (β=0.102, P=0.010), noise exposure (β=0.323, P<0.001), and anxiety (β=0.117, P=0.006) positively associated with the total score of PSQI, while dietary patterns (β=-0.331, P<0.001) and exercise habits (β=-0.147, P<0.001) negatively associated with the total PSQI score, and the 5 variables jointly explained 38.9% of the total variation in the PSQI score (F=37.159, P<0.01). Conclusion The sleep quality of mariners during ocean voyages is relatively low and the incidence of sleep disorders is relatively high, which is jointly influenced by factors such as family structure, noise exposure, dietary habits, exercise habits, and anxiety.

In order to realize the diagnosis of slit lamp in cross-regional patients and improve the real-time and convenience of diagnosis,a remote slit lamp diagnosis platform based on Internet of Things(IoT)technology is designed.Firstly,the feasibility of remote slit lamp is analyzed.Secondly,the IoT platform architecture of doctor/server/facility(D/S/F)is proposed and a remote slit lamp is designed.Finally,the performance of the remote slit lamp diagnostic platform is tested.The platform solves the communication problem of distributed slit lamps and realizes respectively numerical control of multi-area slit lamp by multi-eye experts.The test results show that the remote control delay of the platform is less than 20 ms,which supports multiple experts to diagnose multiple patients separately.

Objective To investigate the protective effect of exogenous leptin against focal cerebral ischemia-reperfusion(I/R)injury in mice and explore the underlying mechanism.Methods A total of 100 C57BL/6 mice were randomly divided into 5 groups,including a sham-operated group,cerebral I/R model group,and 3 leptin treatment groups with intraperitoneal injections of 0.5,1.0 or 2.0 leptin immediately after occlusion of the internal carotid artery.At 24 h after reperfusion,neurological function scores of the mice were assessed,and TTC staining was used to determine the area of cerebral infarction.The pathological changes in the cortical brain tissue of the mice were observed using HE staining,and degenerative damage of the cortical neurons were assessed with Fluoro-Jade C staining.The expression of glial fibrillary acidic protein in cortical brain tissues was detected using immunohistochemistry and Western blotting.In another 45 C57BL/6 mice with sham operation,I/R modeling,or leptin(1 mg/kg)treatment,glutamic acid in the cortical brain tissue was detected using glutamate assay,and cortical glutamate-aspartate transporter(GLAST)and glutamate transporter-1(GLT-1)protein expressions were detected using immunohistochemistry.Results Compared with the I/R model mice,the leptin-treated mice had significantly lower neurological deficit scores,smaller cerebral infarct area,milder pathologies in the cortical brain tissue,and lessened cortical neuronal damage with normal morphology and less excessive proliferation of the astrocytes.Leptin treatment significantly up-regulated the expressions of GLT-1 and GLAST and lowered the content of glutamic acid in the brain tissue of the I/R mice.Conclusion Exogenous leptin has obvious neuroprotective effect against cerebral I/R injury in mice,mediated probably by controlling excessive astrocyte proliferation and up-regulating cortical GLT-1 and GLAST expressions to reduce glutamate-mediated excitotoxic injury of the astrocytes.

Objective To develop a deep learning method for volumetric assessment of traumatic intracerebral hemorrhage(TICH)using the Trans-UNet model and to compare its performance with traditional formula-based methods.Methods CT data from 141 TICH patients admitted to Army Medical Center of PLA between May 2018 and May 2023 were collected.A deep learning method based on the Trans-UNet model was established.Manual delineation via picture archiving and communication system(PACS)was served as the gold standard for comparing the accuracy,consistency,and time efficiency of our method against 10 different formula-based methods for measuring the amount of TICH.Results The median volume of TICH,as manual delineation via PACS,was 1.167 mL,with a median measurement time of 135 s per patient.The median percentage error in volume between the deep learning method and manual delineation via PACS was 3.59％.Spearman correlation coefficient was 0.999(P＜0.001),and a median measurement time was only 4.38 s per patient.In contrast,in the formula-based methods,the lowest median percentage error in volume was 16.451％,the highest Spearman correlation coefficient was 0.986(P＜0.001),and the lowest median measurement time was 20 s for a single patient.The statistical differences were observed in percentage error in volume and measurement time between the 2 types of methods(all P＜0.001).Conclusion Our developed deep learning method for volumetric assessment of TICH is superior to the formula-based methods in terms of measurement accuracy and time efficiency.

Objective To investigate the protective effect of exogenous leptin against focal cerebral ischemia-reperfusion(I/R)injury in mice and explore the underlying mechanism.Methods A total of 100 C57BL/6 mice were randomly divided into 5 groups,including a sham-operated group,cerebral I/R model group,and 3 leptin treatment groups with intraperitoneal injections of 0.5,1.0 or 2.0 leptin immediately after occlusion of the internal carotid artery.At 24 h after reperfusion,neurological function scores of the mice were assessed,and TTC staining was used to determine the area of cerebral infarction.The pathological changes in the cortical brain tissue of the mice were observed using HE staining,and degenerative damage of the cortical neurons were assessed with Fluoro-Jade C staining.The expression of glial fibrillary acidic protein in cortical brain tissues was detected using immunohistochemistry and Western blotting.In another 45 C57BL/6 mice with sham operation,I/R modeling,or leptin(1 mg/kg)treatment,glutamic acid in the cortical brain tissue was detected using glutamate assay,and cortical glutamate-aspartate transporter(GLAST)and glutamate transporter-1(GLT-1)protein expressions were detected using immunohistochemistry.Results Compared with the I/R model mice,the leptin-treated mice had significantly lower neurological deficit scores,smaller cerebral infarct area,milder pathologies in the cortical brain tissue,and lessened cortical neuronal damage with normal morphology and less excessive proliferation of the astrocytes.Leptin treatment significantly up-regulated the expressions of GLT-1 and GLAST and lowered the content of glutamic acid in the brain tissue of the I/R mice.Conclusion Exogenous leptin has obvious neuroprotective effect against cerebral I/R injury in mice,mediated probably by controlling excessive astrocyte proliferation and up-regulating cortical GLT-1 and GLAST expressions to reduce glutamate-mediated excitotoxic injury of the astrocytes.

Objective:To analyze the types and functions of CD34 + cells in full-thickness skin defect wounds of normal mice and diabetic mice by single-cell RNA sequencing. Methods:This study was an experimental study. The CD34 + cell lineage tracing mouse was produced, and the visualization of CD34 + cells under the fluorescent condition was realized. Six male CD34 + cell lineage tracing mice aged 7-8 weeks (designated as diabetic group) were intraperitoneally injected with streptozotocin to establish a diabetic model, and full-thickness skin defect wounds were prepared on their backs when they reached 13 weeks old. Another 6 male CD34 + cell lineage tracing mice aged 13 weeks (designated as control group) were also subjected to full-thickness skin defect wounds on their backs. On post-injury day (PID) 4, wound tissue was collected from 3 mice in control group and 2 mice in diabetic group, and digested to prepare single-cell suspensions. CD34 + cells were screened using fluorescence-activated cell sorting, followed by single-cell RNA sequencing. The Seurat 4.0.2 program in the R programming language was utilized for dimensionality reduction, visualization, and cell clustering analysis of CD34 + cell types, and to screen and annotate the marker genes for each CD34 + cell subpopulation. Kyoto encyclopedia of genes and genomes (KEGG) and gene ontology (GO) enrichment analysis was performed to analyze the differentially expressed genes (DEGs) of CD34 + fibroblasts (Fbs), smooth muscle cells (SMCs), keratinocytes (KCs), and chondrocyte-like cells (CLCs) in the wound tissue of two groups of mice for exploring cellular functions. Results:On PID 4, CD34 + cells in the wound tissue of both groups of mice were consisted of 7 cell types, specifically endothelial cells, Fbs, KCs, macrophages, T cells, SMCs, and CLCs. Among these, Fbs were further classified into 5 subpopulations. Compared with those in control group, the proportions of CD34 + endothelial cells, Fbs subpopulation 1, Fbs subpopulation 4, KCs, and CLCs in the wound tissue of mice were increased in diabetic group, while the proportions of CD34 + Fbs subpopulation 2, Fbs subpopulation 3, and SMCs were decreased. The marker genes for annotating CD34 + CLCs, endothelial cells, Fbs subpopulation 1, Fbs subpopulation 2, Fbs subpopulation 3, Fbs subpopulation 4, Fbs subpopulation 5, KCs, macrophages, SMCs, and T cells were respectively metastasis-associated lung adenocarcinoma transcript 1, fatty acid binding protein 4, Gremlin 1, complement component 4B, H19 imprinted maternally expressed transcript, Dickkopf Wnt signaling pathway inhibitor 2, fibromodulin, keratin 5, CD74 molecule, regulator of G protein signaling 5, and inducible T-cell co-stimulator molecule. KEGG and GO enrichment analysis revealed that, compared with those in control group, DEGs with significant differential expression (SDE) in CD34 + Fbs from the wound tissue of mice in diabetic group on PID 4 were significantly enriched in terms related to inflammatory response, extracellular matrix (ECM) organization, regulation of cell proliferation, and aging (with Pvalues all <0.05), DEGs with SDE in CD34 + SMCs were significantly enriched in terms related to cell migration, apoptotic process, positive regulation of transcription, and phagosome (with P values all <0.05), DEGs with SDE in CD34 + KCs were significantly enriched in terms related to mitochondrial function, transcription, and neurodegenerative diseases (with P values all <0.05), and DEGs with SDE in CD34 + CLCs were significantly enriched in terms related to rhythm regulation, ECM, and viral infection (with P values all <0.05). Conclusions:CD34 + cells display high heterogeneity in the healing process of full-thickness skin defect wounds in both normal mice and diabetic mice. The significantly enriched functions of DEGs with SDE in CD34 + cell subpopulations in the wound tissue of the two mouse groups are closely related to the wound healing process.