Manipulating 2D Membrane Interlayer Channels with Accelerated Mass-Transfer Behavior to Boost Solar Desalination.

The scarcity of fresh water necessitates sustainable and efficient water desalination strategies. Solar-driven steam generation (SSG), which employs solar energy for water evaporation, has emerged as a promising approach. Graphene oxide (GO)-based membranes possess advantages like capillary action and Marangoni effect, but their stacking defects and dead zones of flexible flakes hinders efficient water transportation, thus the evaporation rate lag behind unobstructed-porous 3D evaporators. Therefore, fundamental mass-transfer approach for optimizing SSG evaporators offers new horizons. Herein, a universal multi-force-fields-based method is presented to regularize membrane channels, which can mechanically eliminate inherent interlayer stackings and defects. Both characterization and simulation demonstrate the effectiveness of this approach across different scales and explain the intrinsic mechanism of mass-transfer enhancement. When combined with a structurally optimized substrate, the 4Laponite@GO-1 achieves evaporation rate of 2.782 kg m-2 h-1 with 94.48% evaporation efficiency, which is comparable with most 3D evaporators. Moreover, the optimized membrane exhibits excellent cycling stability (10 days) and tolerance to extreme conditions (pH 1-14, salinity 1%-15%), verifies the robust structural stability of regularized channels. This optimization strategy provides simple but efficient way to enhance the SSG performance of GO-based membranes, facilitating their extensive application in sustainable water purification technologies.

[Analysis on vitamin B_1 and vitamin B_2 proficiency testing assessment in China disease control and prevention system].

OBJECTIVE: To evaluate the detection ability of vitamin B_1 and vitamin B_(2 )in rice flour in the laboratories of disease control and prevention system, by conducting the proficiency testing(PT)activity. METHODS: Before the vitamin B_1 and vitamin B_2 quality control samples were distributed to the laboratories of disease control and prevention system, the uniformity and stability of samples were analyzed by one-way ANOVO respectively. High performance liquid chromatography(HPLC) method was required to determine vitamin B_1(GB 5009.84-2016: determination of vitamin B_1 in food, first method as reference). HPLC method was also required to determine vitamin B_2(GB 5009.85-2016: determination of vitamin B_2 in food, first method as reference). Robust statistics analysis of proficiency testing result was conducted to evaluate laboratory testing ability through Z score. RESULTS: A total of 43 laboratories completed the proficiency testing. In all of the laboratories participated in the determination of vitamin B_(1 )and vitamin B_2, the total satisfactory rate of vitamin B_1 was 88.4%, while vitamin B_2 was 86.0%. CONCLUSION: The ability of vitamin B_1 and vitamin B_2 detection in disease control and prevention system in China is better than expected, and the testing ability of a few laboratory needs to be improved.

Loss of ZIP facilitates JAK2-STAT3 activation in tamoxifen-resistant breast cancer.

Tamoxifen, a widely used modulator of the estrogen receptor (ER), targets ER-positive breast cancer preferentially. We used a powerful validation-based insertion mutagenesis method to find that expression of a dominant-negative, truncated form of the histone deacetylase ZIP led to resistance to tamoxifen. Consistently, increased expression of full-length ZIP gives the opposite phenotype, inhibiting the expression of genes whose products mediate resistance. An important example is JAK2 By binding to two specific sequences in the promoter, ZIP suppresses JAK2 expression. Increased expression and activation of JAK2 when ZIP is inhibited lead to increased STAT3 phosphorylation and increased resistance to tamoxifen, both in cell culture experiments and in a mouse xenograft model. Furthermore, data from human tumors are consistent with the conclusion that decreased expression of ZIP leads to resistance to tamoxifen in ER-positive breast cancer.

CircCRIM1 promotes ovarian cancer progression by working as ceRNAs of CRIM1 and targeting miR-383-5p/ZEB2 axis.

BACKGROUND: Ovarian cancer is the leading cause of death in patients with gynecologic cancer, and circular RNAs (circRNAs) are involved in cancer progression. However, there are limited studies on the roles of circRNAs in ovarian cancer. METHODS: We designed divergent and convergent primers, used sanger sequencing and RNase R digestion to verify the source of circCRIM1. We detected the expression of circCRIM1 and its parental gene cysteine rich transmembrane BMP regulator 1 (CRIM1) in ovarian cancer and normal ovarian samples via qRT-PCR. MTT viability assay, apoptosis assay, wound healing assay and invasion assay were used to investigate the function of circCRIM1 and CRIM1 in ovarian cancer cell lines OVCAR3 and CAOV3. Mice xenografts experiment was performed. Bioinformatics predicted the microRNAs that bond with circCRIM1 and CRIM1, and dual luciferase reporter system confirmed it. Rescue experiments of microRNAs mimics transfection on the basis of circCRIM1 over-expression were carried out to uncover the mechanism by which circCRIM1 played cancer-promoting roles in ovarian cancer. RESULTS: CircCRIM1 was derived from CRIM1 by back-splicing. CircCRIM1 and CRIM1 had higher expression in ovarian cancer than in normal ovarian tissues, and both of them promoted ovarian cancer progression in vitro. In vivo circCRIM1 promoted the growth of tumors. CircCRIM1 and CRIM1 had a positive correlation relationship in the same cohort of ovarian cancer tissues. Bioinformatics predicted and dual luciferase assay confirmed circCRIM1 and CRIM1 bond with miR-145-5p, and circCRIM1 bond with miR-383-5p additionally. CircCRIM1 positively affected the expression of CRIM1. After circCRIM1 was over-expressed, miR-145-5p mimics transfection reversed the expression of CRIM1. Western blot discovered circCRIM1 positively affected the expression of zinc finger E-box binding homeobox 2 (ZEB2). Rescue experiments found miR-383-5p mimics reversed ZEB2 expression and the cancer-promoting effects of circCRIM1. CONCLUSIONS: CircCRIM1 bond with miR-145-5p to work as competing endogenous RNA (ceRNA) of CRIM1, and circCRIM1 bond with miR-383-5p to improve the expression of ZEB2 in ovarian cancer. CircCRIM1 and CRIM1 promoted the ovarian cancer progression and supplied a novel insight into the researches of ovarian cancer.

[Study on determination and quantity transfer of multi index components in Wenjing Decoction].

Based on the textual research on literature, the key information of Wenjing Decoction were tested and identified, and 15 batches of lyophilized powder samples of Wenjing Decoction were prepared. The specific components, including paeoniflorin, glycyrrhizin, ginsenosides(Rg_1, Re and Rb_1), glycyrrhizic acid, and paeonol, were used as indexes to establish the HPLC method for quantitative evaluation, and the content ranges and transfer rates of these components were determined. The results showed that the contents of paeoniflorin, glycyrrhizin, ginsenosides Rg_1 + Re, ginsenoside Rb_1, glycyrrhizic acid, and paeonol in the 15 batches of samples were 0.62%-0.86%, 0.25%-0.76%, 0.14%-0.30%, 0.07%-0.21%, 0.63%-1.16%, and 0.09%-0.25%, respectively, and their transfer rates from the decoction pieces to the reference materials were 14.99%-19.42%, 28.11%-40.93%, 25.92%-61.88%, 25.03%-64.06%, 23.43%-35.53%, and 5.34%-10.44%, respectively. The consistency of the transfer rates between batches indicated that the preparation process was stable. It is suggested that the contents of paeoniflorin, glycyrrhizin, ginsenosides Rg_1 + Re, ginsenoside Rb_1, glycyrrhizic acid, and paeonol in Wenjing Decoction should not be less than 0.52%, 0.35%, 0.15%, 0.10%, 0.63%, and 0.12%, respectively. In this study, we determined the contents and analyzed the quantity transfer process of the index components in Wenjing Decoction, which can provide a basis for the follow-up development of Wenjing Decoction and the quality control of related preparations.

Discovery and evaluation of Atopaxar hydrobromide, a novel JAK1 and JAK2 inhibitor, selectively induces apoptosis of cancer cells with constitutively activated STAT3.

The Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway plays a vital role in immunity, cell division, cell death and tumor formation. Disrupted JAK-STAT signaling may lead to various diseases, especially cancer and immune disorders. Because of its importance, this signaling pathway has received significant attention from the pharmaceutical and biotechnology industries as a therapeutic target for drug design. However, few JAK or STATs inhibitors have been developed for cancer treatment. We used an in vitro STAT3 luciferase reporter assay to find novel inhibitors that could effectively block the JAK-STAT pathway. In our study, we screened 16,081 drug-like chemicals and found that atopaxar hydrobromide (AHB) is a specific inhibitor of JAK-STAT3 signaling. Our results suggest that AHB not only blocks constitutively activated and cytokine-induced STAT3 phosphorylation but also inhibits JAK1 and JAK2 phosphorylation. Moreover, AHB induces G1 phase cell cycle arrest, which stops cancer cell growth and induces apoptosis. AHB also inhibited tumor cell growth in vivo. In conclusion, AHB is a potential inhibitor that could be developed as a JAK-STAT pathway drug.

TGF-ß2 antagonizes IL-6-promoted cell survival.

Transforming growth factor beta is a key cytokine involved in the pathogenesis of fibrosis in many organs, whereas interleukin-6 plays an important role in the regulation of inflammation. They are both potent angiogenesis inducers with opposite effects on cell survival and apoptosis. TGF-ß2 induces apoptosis; in contrast, IL-6 protects cells from apoptosis. The possible interaction between these two cytokines is indicated in various disease states. In this study, we have assessed the effect of TGF-ß2 on IL-6 signaling and found that TGF-ß2 could strongly inhibit IL-6-induced STAT3 activation and synergy with IL-6 resulting in enhanced SOCS3 expression. Interestingly, IL-6 also slows down the decay of TGF-ß2 mRNA. Consistent with this mechanism, we found that TGF-ß2 could antagonize IL-6 effect on cell survival in both γ-irradiation and UV light-induced apoptosis. Taken together, the finding shows that TGF-ß2 serves as a negative regulator of IL-6 signaling and antagonizes the anti-apoptosis effect of IL-6.

E2F is required for STAT3-mediated upregulation of cyclin B1 and Cdc2 expressions and contributes to G2-M phase transition.

Activation of transcription factor STAT3 is involved in cell proliferation, differentiation, and cell survival. Constitutive activation of STAT3 pathway has been associated with the oncogenesis of various types of cancers. It has been reported that STAT3 plays a key role in the G1 to S phase cell cycle transition induced by the cytokine receptor subunit gp130, through the upregulation of cyclins D1, D2, D3, A, and Cdc25A and the concomitant downregulation of p21 and p27. However, its role in mediating G2-M phase transition has not been studied. The cyclin B1/Cdc2 complex is widely accepted as the trigger of mitosis in all organisms and is believed to be necessary for progression through S phase and keep active during the G2-M transition and progression. In the present study, we found that activation of STAT3 stimulates cyclin B1 and Cdc2 expressions. Deletion and site-directed mutations on cyclin B1 and Cdc2 promoters indicated that E2F element mediates the upregulation of these two promoters in a STAT3-dependent manner. The findings reported here demonstrated that STAT3 participates in modulating G2-M phase checkpoint by regulating gene expressions of cyclin B1 and Cdc2 via E2F.

[Comparison and analysis of 5 metal elements in serum between laboratories].

OBJECTIVE: To evaluate the ability for the detection of 5 metal elements in serum in the laboratories of disease prevention and control system. METHODS: The samples for calcium, magnesium, iron, copper and zinc detection were distributed to 48 laboratories of disease prevention and control system. Inductively coupled plasma mass spectrometry( ICP-MS) analysis or self-selected determination method were allowed to use during detection for each laboratory. The results were analyzed by robust statistical analysis and Z value was used to evaluate the detection ability. RESULTS: Of the laboratories involved in the study, 40 reported results of metal elements detection. Among them, 29 laboratories had satisfactory results, and 11 laboratories had unsatisfactory or suspicious results. The laboratory pass rate of this inter-laboratory comparison was60. 4%. CONCLUSION: The detection level of calcium, magnesium, iron, copper and zinc in serum in disease prevention and control system is generally satisfactory, but the detection ability of some laboratories needs to be further improved.

lncRNA DLEU1 contributes to tumorigenesis and development of endometrial carcinoma by targeting mTOR.

lncRNA DLEU1 as a non-coding gene, involves in the occurrence and development of multiple tumors. However, there is no related report in endometrial carcinoma. In order to focus on the role and mechanism of lncRNA DLEU1 in endometrial carcinoma, we used qRT-PCR to detect the expression of lncRNA DLEU1 and found that lncRNA DLEU1 was highly expressed in endometrial carcinoma compared to normal endometrium. Moreover, compared to Ishikawa and KLE, lncRNA DLEU1 was higher in HEC-1B. In addition, up-regulation of lncRNA DLEU1 promoted cell viability, migration, invasion, and reduced the proportion of apoptosis. Otherwise, down-regulation of lncRNA DLEU1 produced opposite results. Xenograft nude mice model assay showed that lncRNA DLEU1 can promote tumorigenesis in vivo. RiP confirmed that lncRNA DLEU1 could bind to mTOR. The rescue experiments revealed that silence of mTOR after up-regulation of lncRNA DLEU1 resulted in decrease of cell viability, migration, and invasion and increase of apoptosis. The expression changes of PI3K, AKT1, p70S6K, rpS6, GSK3ß, STAT3, and Bcl-xl were consistent with lncRNA DLEU1 and mTOR in Western blot. Thus, we suggest that lncRNA DLEU1 combines with mTOR and then increases the expression of PI3K/AKT/mTOR pathway to promote endometrial carcinoma tumorigenesis and progression. The present discovery has probability to provide a biomarker and lay the foundation for targeted therapy of endometrial carcinoma.

[Relationship between Angiotensin Converting Enzyme Gene Polymorphism and Carotid Atherosclerotic Plaque: A Study Based on Vessel Wall Magnetic Resonance Imaging].

Objective To investigate the relationship between angiotensin converting enzyme(ACE) gene polymorphism and carotid plaque composition,vessel wall morphology,and clinical symptoms based on vessel wall magnetic resonance imaging. Methods Totally 75 hypertensive patients(75 internal carotid artery plaques) with maximum plaque thickness≥1.5 mm,according to the ACE insertion(I) or deletion(D) gene polymorphism,were divided into ACE 2 genotype group(n=37) and ACE ID/DD genotype group(n=38). The influences of plaque composition,vessel wall morphology,clinical symptoms,and use of ACE inhibitor or angiotensin receptor blocker(ACEI/ARB) on vessel wall morphology were analyzed. Results Compared with ACE 2 genotype group,the ACE ID/DD genotype group had significantly higher incidence of ischemic stroke(Χ2=3.921,P=0.048). The plaque composition and vessel wall morphology showed no significant difference between these two groups. Inside ACE ID/DD genotype group,the carotid remodeling index was significantly lower in users of ACEI/ARB than non-users of ACEI/ARB(1.85±0.60 vs. 2.48±0.40;t=3.854,P=0.001).Conclusion In primary hypertension,ACE ID/DD genotype may be associated with carotid atherosclerotic plaque.

ZIP restores estrogen receptor expression and response to Tamoxifen in estrogen receptor negative tumors.

As a component of NURD histone deacetylase complex, ZIP serves as a tumor suppressor gene in the development of breast tumors. However, whether it takes part in chemotherapy resistance remains poorly defined. In the present study, we reported that ZIP enhanced the response to SERM chemotherapy in ER-negative cells. Overexpression of ZIP suppressed EGFR expression level and restored ERalpha protein level in cells resistant to Tamoxifen. In vivo data confirmed those in vitro findings.

Dehydrocrenatidine is a novel janus kinase inhibitor.

Janus kinase (JAK) 2 plays a pivotal role in the tumorigenesis of signal transducers and activators of transcription (STAT) 3 constitutively activated solid tumors. JAK2 mutations are involved in the pathogenesis of various types of hematopoietic disorders, such as myeloproliferative disorders, polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Thus, small-molecular inhibitors targeting JAK2 are potent for therapy of these diseases. In this study, we screened 1,062,608 drug-like molecules from the ZINC database and 2080 natural product chemicals. We identified a novel JAK family kinase inhibitor, dehydrocrenatidine, that inhibits JAK-STAT3-dependent DU145 and MDA-MB-468 cell survival and induces cell apoptosis. Dehydrocrenatidine represses constitutively activated JAK2 and STAT3, as well as interleukin-6-, interferon-α-, and interferon-γ-stimulated JAK activity, and STAT phosphorylation, and suppresses STAT3 and STAT1 downstream gene expression. Dehydrocrenatidine inhibits JAKs-JH1 domain overexpression-induced STAT3 and STAT1 phosphorylation. In addition, dehydrocrenatidine inhibits JAK2-JH1 kinase activity in vitro. Importantly, dehydrocrenatidine does not show significant effect on Src overexpression and epidermal growth factor-induced STAT3 activation. Our results indicate that dehydrocrenatidine is a JAK-specific inhibitor.

Understanding visible light and microbe-driven degradation mechanisms of polyurethane plastics: Pathways, property changes, and product analysis.

The accumulation of polyurethane plastics (PU-PS) in the environment is on the rise, posing potential risks to the health and function of ecosystems. However, little is known about the degradation behavior of PU-PS in the environment, especially water environment. To address this knowledge gap, we investigated and isolated a degrading strain of Streptomyces sp. B2 from the surface of polyurethane coatings. Subsequently, a photoreactor was employed to simulate the degradation process of bio-based polyurethane (BPU) and petroleum-based polyurethane (PPU) under three conditions, including single microorganism (SM), single light exposure (SL), and combined light exposure/microorganism action (ML) in aqueous solution. The results indicated that PU-PS mainly relies on biodegradation, with the highest degradation rate observed after 28 d under SM condition (BPU 5.69 %; PPU 5.25 %). SL inhibited microbial growth and degradation, with the least impact on plastic degradation. Microorganisms colonized the plastic surface, secreting relevant hydrolytic enzymes and organic acids into the culture medium, providing a negative charge. The carbon chains were broken and aged through hydrogen peroxide induction or attack by oxygen free radicals. This process promoted the formation of oxidized functional groups such as OH and CO, disrupting the polymer's structure. Consequently, localized fragmentation and erosion of the microstructure occurred, resulting in the generation of secondary microplastic (MPs) particles, weight loss of the original plastic, increased surface roughness, and enhanced hydrophilicity. Additionally, BPU exhibited greater degradability than PPU, as microorganisms could utilize the produced fatty acids, which promoted their reproduction. In contrast, PPU degradation generated a large amount of isocyanate, potentially toxic to cells and inhibiting biodegradation. This study unveils the significant role of microorganisms in plastic degradation and the underlying degradation mechanisms of BPU, providing a novel strategy for polyurethane degradation and valuable information for comprehensive assessment of the behavior and fate of MPs in the environment.

Reversible methylation of promoter-bound STAT3 by histone-modifying enzymes.

Following its tyrosine phosphorylation, STAT3 is methylated on K140 by the histone methyl transferase SET9 and demethylated by LSD1 when it is bound to a subset of the promoters that it activates. Methylation of K140 is a negative regulatory event, because its blockade greatly increases the steady-state amount of activated STAT3 and the expression of many (i.e., SOCS3) but not all (i.e., CD14) STAT3 target genes. Biological relevance is shown by the observation that overexpression of SOCS3 when K140 cannot be methylated blocks the ability of cells to activate STAT3 in response to IL-6. K140 methylation does not occur with mutants of STAT3 that do not enter nuclei or bind to DNA. Following treatment with IL-6, events at the SOCS3 promoter occur in an ordered sequence, as shown by chromatin immunoprecipitations. Y705-phosphoryl-STAT3 binds first and S727 is then phosphorylated, followed by the coincident binding of SET9 and dimethylation of K140, and lastly by the binding of LSD1. We conclude that the lysine methylation of promoter-bound STAT3 leads to biologically important down-regulation of the dependent responses and that SET9, which is known to help provide an activating methylation mark to H3K4, is recruited to the newly activated SOCS3 promoter by STAT3.

Integrated Janus Evaporator with an Enhanced Donnan Effect and Thermal Localization for Salt-Tolerant Solar Desalination and Thermal-to-Electricity Generation.

Solar-driven interfacial evaporation (SIE) technology has great advantages in seawater desalination. However, during the long-term operation of a solar evaporator, salts can be deposited on the solar absorbing surface, which, in turn, hinders the evaporation process. Therefore, there is an urgent need to propose new antisalt strategies to solve this problem. Here, we present a novel cogeneration system leveraging a salt-tolerant, heterogeneous Janus-structured evaporator (FHJE) for simultaneous solar desalination and thermoelectric generation. The top evaporation layer is composed of a graphene-based photothermal membrane pre-embedded with Fe3+ cations, which enhanced solar absorption and energy conversion abilities. Meanwhile, the Fe3+ cations further contribute to the Donnan effect, effectively repelling salt ions in saltwater. The bottom layer comprises a hydrogel composed of hydrophilic phytic acid (PA) and poly(vinyl alcohol) (PVA), fostering facilitation of water transport. The FHJE was demonstrated to exhibit evaporation rate and efficiency as high as 3.655 kg m-2 h-1 and 94.7% in 10 wt% saltwater, respectively, and superior salt resistance ability without salt accumulation after 8 h of continuous evaporation (15 wt%). Furthermore, a hydropower cogeneration evaporator device was constructed, and it possesses an open-circuit voltage (VOC) and a maximum output power density of up to 143 mV and 1.33 W m-2 under 1 sun, respectively. This study is expected to provide new ideas for comprehensive utilization of solar energy.

Rearrangement of GO nanosheets with inner and outer forces under high-speed spin for supercapacitor.

The self-standing graphene membranes are considered as ideal electrode materials for supercapacitors. However, maintaining highly regularized and uniform graphene membranes with satisfied electrochemical performance is still a challenge. Herein, with the chelation of metal cation and the radial shear force introduced by high-speed spinning, the uniform interlayer channels and shrunken cracks between adjacent nanosheets can be achieved in the metal-intercalated graphene oxide (GO) membranes, thus realizing regularization both in normal and radial direction. With the promotion in electron transfer and electrolyte penetration, the iron cross-linked GO membrane with spin coating for 40 cycles exhibits a high specific capacitance (427 F g-1 at 1 A g-1) and rate capability (42.6% capacitance retention from 1 to 40 A g-1), as well as excellent cyclic capability (90.5% capacitance retention after 20,000 cycles). Particularly, a 21% increasement in capacitance can be achieved after high-speed spinning treatment. Moreover, the spin regularization strategy can be extended to GO membranes cross-linked by various multi-valence metal cations, the electrochemical performance of metal-cation cross-linked GO membrane electrodes after high-speed spinning treatment can also be improved obviously. Therefore, this paper provides a novel method to fabricate highly ordered GO membranes with promising electrochemical performance, which presents an immense potential application in membrane materials applied in energy storage, separation and catalysis.

snoRNAs: functions and mechanisms in biological processes, and roles in tumor pathophysiology.

Small nucleolar RNAs (snoRNAs), a type of non-coding RNA, are widely present in the nucleoli of eukaryotic cells and play an important role in rRNA modification. With the recent increase in research on snoRNAs, new evidence has emerged indicating that snoRNAs also participate in tRNA and mRNA modification. Studies suggest that numerous snoRNAs, including tumor-promoting and tumor-suppressing snoRNAs, are not only dysregulated in tumors but also show associations with clinical prognosis. In this review, we summarize the reported functions of snoRNAs and the possible mechanisms underlying their role in tumorigenesis and cancer development to guide the snoRNA-based clinical diagnosis and treatment of cancer in the future.

Insights into roles of METTL14 in tumors.

N6-Methyladenosine (m6A) is considered the most common and endogenous modification of eukaryotic RNAs. Highly conserved in many species, m6A regulates RNA metabolism, cell differentiation, cell circadian rhythm, and cell cycle; it also responds to endogenous and exogenous stimuli and is associated with the development of tumors. The m6A methyltransferase complex (MTC) regulates the m6A modification of transcripts and involves two components, methyltransferase-like enzyme 3 (METTL3) and methyltransferase-like enzyme 14 (METTL14), and other auxiliary regulatory distinct components. Though with no catalytic effect, METTL14 serves as an RNA-binding scaffold in MTC, promotes RNA substrate recognition, activates, and escalates the catalytic capability of METTL3, thus accounting for a pivotal member of the complex. It was reported that METTL14 regulates tumor proliferation, metastasis, and self-renewal, and plays a part in tumorigenesis, tumor progression, and other processes. The present work is a review of the role of METTL14 both as a tumor suppressor and a tumor promoter in the oncogenesis and progression of various tumors, as well as the potential molecular mechanisms.

Developing a Nomogram to Predict the Probability of Subsequent Vascular Events at 6-Month in Chinese Patients with Minor Ischemic Stroke.

PURPOSE: To develop a nomogram to predict the risk of subsequent vascular events (SVE) at 6-month in Chinese patients with minor ischemic stroke (MIS). PATIENTS AND METHODS: We performed a retrospective analysis of 260 MIS patients, which were randomly divided into a derivation set (193 cases) and a verification set (67 cases) at a ratio of 3:1. Multi-factor logistic regression was used to construct a predictive model of SVE from the derivation set and verify it in the verification set. RESULTS: Finally, there were 51 cases (19.6%) of SVE in 260 MIS cases. Age, fasting blood glucose, metabolic syndrome, number of lesions found on MRI, and the infarct size were used to construct the prediction model and nomogram. The AUC in the derivation set was 0.901, with a sensitivity of 0.795, a specificity of 0.877, a positive likelihood ratio of 6.443, and a negative likelihood ratio of 0.234. The AUC in the verification set was 0.897, which was not significantly different from the derivation set (P = 0.937). The predictive model based on clinical parameters has good diagnostic efficiency and robustness. CONCLUSION: The nomogram can provide personalized predictions for the 6-month SVE risk in Chinese MIS patients.