Category: 3. Business

  • Geely Automobile Net Profit Rises Sharply on Robust Sales

    Geely Automobile Net Profit Rises Sharply on Robust Sales

    By Jiahui Huang

    Geely Automobile reported stronger earnings in the third quarter, thanks to the Chinese auto giant's robust performance despite stiff competition in its home market.

    Net profit rose to 3.82 billion yuan, equivalent to $538.1 million, from 2.40 billion yuan a year earlier, on revenue that increased 27% to 89.19 billion yuan, the Hangzhou-based automaker said Monday. Geely sold a total of 76,100 vehicles in the third quarter, up 43% from the previous year.

    Geely, China's second-largest electric-vehicle maker, has been growing its market share with strong product offerings. The automaker has experienced rapid growth in sales volume this year, driven by its range of products and competitive pricing. In July, it raised its annual sales target to 3 million units from 2.17 million units.

    Geely's subsidiary Zeekr also posted strong sales in the third quarter, with its total delivery volume rising 12.5% to 140,195 units. The company's revenue climbed 9.1% to 31.56 billion yuan, and its gross profit margin improved to 19.2%.

    Write to Jiahui Huang at jiahui.huang@wsj.com

    (END) Dow Jones Newswires

    November 17, 2025 00:11 ET (05:11 GMT)

    Copyright (c) 2025 Dow Jones & Company, Inc.

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  • Efficacy analysis of a 12-cytokine panel for the diagnosis of Kawasaki

    Efficacy analysis of a 12-cytokine panel for the diagnosis of Kawasaki

    Introduction

    Kawasaki disease (KD) is an acute systemic vasculitis predominantly affecting children and represents one of the leading causes of acquired heart disease in pediatric populations.1 Although standard treatment with intravenous immunoglobulin (IVIG) combined with aspirin has significantly reduced the incidence of coronary artery lesions (CALs), approximately 10–20% of patients remain unresponsive to IVIG therapy. These non-responders are at markedly increased risk of developing CALs.2,3 Early prediction could facilitate timely adjustments to the treatment strategy-such as the early combination of glucocorticoids-which may play a crucial role in improving patient outcomes and shortening the disease course.4 Therefore, early identification of KD and prediction of IVIG resistance are critical for optimizing clinical management and improving outcomes.

    Immune dysregulation plays a central role in the pathogenesis of KD. Previous studies have demonstrated that dynamic changes in the Th1/Th2 cytokine profile are closely associated with disease progression.5 Our prior research5 revealed that a low pretreatment level of tumor necrosis factor-alpha (TNF-α < 2 pg/mL) was predictive of IVIG resistance, with a specificity of 74.2% and a sensitivity of 66.7%. Additionally, an elevated pretreatment interleukin-10 (IL-10 > 8 pg/mL) level was associated with CALs (sensitivity 75.0%, specificity 64.4%), while post-treatment IL-6 > 10 pg/mL showed even greater predictive value (specificity 81.7%). Furthermore, non-responders exhibited delayed clearance of IL-6 and IL-10, along with a paradoxical increase in TNF-α levels following IVIG administration.

    However, the immunological network underlying KD extends beyond the traditional Th1/Th2 paradigm. Recent evidence suggests that Th17-mediated inflammatory responses and monocyte-derived cytokines (eg, IL-1β and IL-8) play pivotal roles in endothelial injury and vascular inflammation.6–9 Moreover, most previous studies have focused on a limited panel of 6–8 cytokines, and a comprehensive analysis of the broader immune landscape is lacking.

    In this study, we aimed to evaluate a panel of 12 key cytokines to establish a multifactor predictive model for KD diagnosis and IVIG responsiveness. By integrating multidimensional immunological indicators, we sought to explore the potential of cytokines as biomarkers for therapeutic response and to provide a novel basis for risk stratification and individualized treatment in KD patients.

    Materials and Methods

    Study Population and Diagnostic Criteria

    We conducted a retrospective case-control study involving pediatric patients admitted to Children’s Hospital, Zhejiang University School of Medicine, between December 1, 2023, and March 30, 2025. Patients diagnosed with KD and febrile controls were enrolled for comparative analysis on the basis of clinical records, laboratory findings, and echocardiographic data. This study was approved by the Medical Ethics Committee of the Children’s Hospital of Zhejiang University School of Medicine (2025-IRB-0318-P-01).

    A KD diagnosis was established according to the following criteria: complete KD: presence of fever lasting ≥5 days and at least four of the following five principal clinical features: (1) bilateral bulbar conjunctival injection; (2) oral and lip changes, including erythema, cracking, strawberry tongue, or diffuse oral mucosal injection; (3) polymorphous rash, including isolated BCG scar erythema; (4) peripheral extremity changes, such as erythema or edema of the hands and feet in the acute phase, or periungual desquamation in the convalescent phase; and (5) cervical lymphadenopathy (≥1.5 cm in diameter), typically unilateral and nonsuppurative. Incomplete KD: Fever persisting ≥5 days with fewer than four principal clinical features, diagnosed according to the 2017 American Heart Association scientific statement guidelines.2

    The febrile controls were defined as children with (1) a body temperature >38.5°C and (2) available results for the 12-cytokine panel.

    Treatment Protocol

    Upon confirmation of KD diagnosis, patients received IVIG at a single dose of 2 g/kg, along with moderate-dose aspirin (30–50 mg/kg/day). In cases where aspirin was contraindicated, clopidogrel (0.2–1 mg/kg/day) was used as an alternative.

    Definitions of IVIG Resistance and CALs

    IVIG resistance was defined as persistent or recurrent fever ≥38°C at least 36 hours after completion of the initial IVIG infusion or recurrence of fever within two weeks (typically between days 2–7) accompanied by at least one principal clinical feature of KD after excluding other potential causes of fever.2 CALs were assessed by echocardiography and defined as a coronary artery z score ≥2.5 on the basis of the internal diameter adjusted for body surface area.2

    Exclusion Criteria

    Patients with incomplete clinical data, those who received IVIG or corticosteroids prior to admission, or those with delayed treatment (IVIG administration >10 days after onset) were excluded from the study.

    Methodology

    Cytokine Analysis: Venous blood samples were collected from patients with KD during the acute phase before IVIG treatment. For febrile controls, blood samples were obtained at the time of admission. A total of 1 mL of venous blood was transferred into a serum separation tube without anticoagulant and allowed to clot at room temperature for 30 minutes. Approximately 0.5 mL of serum was then separated and sent for analysis. All the samples were processed and analyzed within 4 hours of collection. If immediate analysis was not feasible, the serum samples were stored at 2–8°C for no more than 24 hours. Repeated freeze-thaw cycles were strictly avoided.

    Serum levels of 12 cytokines (IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17, IFN-α, IFN-γ, and TNF-α) were quantified using a multiplex immunofluorescence assay (cytometric bead array-based flow fluorescence technology) with a commercial kit (Jiangxi Saiji Biotechnology Co., Ltd). The assay is based on a sandwich immunoassay principle in which polystyrene microspheres, each with a distinct fluorescence intensity, are coated with monoclonal antibodies specific to individual cytokines. After incubation with serum samples, cytokines were captured by the corresponding microspheres, followed by the addition of phycoerythrin (PE)-labeled detection antibodies to form sandwich complexes. The fluorescence intensity was measured using a flow cytometer (BD FACS Calibur), and the cytokine concentrations were calculated based on standard curves.

    Prior to analysis, all the samples were thawed at room temperature and processed strictly according to the manufacturer’s instructions. The linear detection range was 2.5–2500 pg/mL for most cytokines (10–2500 pg/mL for IL-17), with a lower limit of detection of 2.5 pg/mL (10 pg/mL for IL-17). Each batch included negative controls and serially diluted standards to ensure accuracy and reproducibility.

    Clinical characteristics, including sex, age in months, inflammatory markers, echocardiographic findings, treatment regimens, and outcomes, were retrospectively collected from electronic medical records.

    Statistical Analysis

    The normality of continuous variables was assessed using the one-sample Kolmogorov–Smirnov test. Normally distributed data were expressed as the means ± standard deviations and were compared via independent-sample t tests. Nonnormally distributed data were presented as medians (interquartile ranges, P25–P75) and were analyzed via the Mann–Whitney U-test. Categorical variables were expressed as counts and percentages (%) and were compared via the chi-square test. This study employed a binary logistic regression model to identify independent risk factors influencing (1) the diagnosis of KD (yes/no) and (2) IVIG resistance (yes/no).

    Receiver operating characteristic (ROC) curves were constructed using clinical features and cytokine levels from all KD patients and febrile controls. The sensitivity and specificity for predicting KD and IVIG resistance were calculated on the basis of optimal cutoff values derived from ROC analysis. All the statistical analyses were performed via SPSS version 23.0. A two-tailed P value <0.05 was considered statistically significant.

    Results

    Comparison Between Kawasaki Disease Patients and Febrile Controls

    Between December 2023 and March 2025, a total of 864 children diagnosed with KD were hospitalized at our institution. After cases with incomplete data, prior use of IVIG or corticosteroids, or delayed treatment (IVIG administration >10 days after onset) were excluded, 686 KD patients were ultimately enrolled, including 409 males and 277 females, with a mean age of 70.0 (38.0, 109.0) months. Additionally, 101 febrile children without KD admitted during the same period were included as controls (Figure 1). All children have been followed up for more than six months.

    Figure 1 Flow of participants through the study.

    Comparative analysis revealed that KD patients were significantly younger than control patients were, while no significant difference in sex distribution was detected. Compared with those in the controls, the serum levels of IFN-α, IL-10, IL-1β, IL-2, IL-4, IL-5, IL-6, and IL-8 were significantly elevated in the KD group. In addition, the absolute neutrophil count and white blood cell count were significantly greater in KD patients. However, no significant differences in C-reactive protein (CRP) or the erythrocyte sedimentation rate (ESR) were detected between the two groups (Table 1).

    Table 1 Comparison of Clinical Characteristics Between Kawasaki Disease Patients and Febrile Controls

    A logistic regression model was subsequently constructed to identify independent predictors of KD compared with febrile controls. The analysis revealed that age in months (OR=0.974, CI [0.966, 0.982], P<0.001), IL-10 level (OR=1.068, CI [1.020, 1.117], P=0.005), IL-5 level (OR=1.935, CI [1.385, 2.703], P<0.001), absolute neutrophil count (OR=1.170, CI [1.024, 1.337], P=0.021), and white blood cell count (OR=0.878, CI [0.777, 0.992], P=0.037) were independent predictive factors associated with KD (Table 2).

    Table 2 Logistic Regression Model of Variables Independently Associated with Kawasaki Disease Compared with Febrile Controls

    Further analysis revealed the diagnostic performance of individual and combined markers for KD patients compared with febrile controls. The area under the curve (AUC) of the ROC curve for single indicators was as follows: 0.734 for age in months, 0.741 for IL-10, 0.774 for IL-5, 0.613 for white blood cell count, and 0.589 for absolute neutrophil count. The AUC for the combined diagnostic model was 0.853, with a sensitivity of 0.758 and specificity of 0.812 (Figure 2).

    Figure 2 Receiver operating characteristic (ROC) curves for the diagnosis of Kawasaki disease.

    Abbreviations: PRE, predicted probability; N, absolute neutrophil count; WBC, white blood cell count; IL, interleukin; AGE, age in months.

    When the IL-10 concentration was greater than 7.25 pg/mL, the sensitivity and specificity for diagnosing KD were 0.517 and 0.832, respectively. When the concentration of IL-5 exceeded 1.950 pg/mL, the sensitivity and specificity were 0.678 and 0.772, respectively. Similarly, at a cutoff of 2.050 pg/mL for IL-5, the sensitivity and specificity were 0.638 and 0.812, respectively.

    Efficacy of the 12-Cytokine Panel in Predicting IVIG Resistance

    Among the 686 KD patients included in the analysis, there were no significant differences in age or sex between the IVIG-responsive and IVIG-resistant groups. A total of 606 patients were classified as IVIG-responsive, while 80 were identified as IVIG-resistant. Univariate analysis revealed that the levels of IFN-γ (5.20 (3.43, 7.75) vs 3.80 (2.80, 5.50), P<0.001), IL-10 (22.05 (8.90, 71.60) vs 6.85 (3.80, 14.83), P<0.001), IL-17 (6.55 (4.20, 12.45) vs 5.60 (3.50, 9.40), P=0.043), IL-2 (4.80 (3.70, 5.60) vs 4.00 (3.10, 4.80), P<0.001), IL-5 (3.15 (1.90, 6.30) vs 2.50 (1.70, 4.20), P=0.013), IL-6 (124.50 (57.95, 233.18) vs 48.50 (24.73, 94.83), P<0.001), and IL-8 (44.90 (21.05, 108.33) vs 16.95 (9.80, 30.50), P<0.001) were significantly higher in the IVIG-resistant group compared to the IVIG-responsive group. In contrast, IFN-α levels (1.80 (1.50, 2.40) vs 2.10 (1.70, 2.70), P=0.001) were significantly lower in the IVIG-resistant group (Figure 3).

    Figure 3 Comparison of 12-cytokine profiles between the IVIG-responsive and IVIG-resistant groups. *P < 0.05, ***P < 0.001, ****P < 0.0001.

    Abbreviations: IFN, interferon; IL, interleukin; TNF, tumor necrosis factor.

    A logistic regression model was subsequently constructed to identify independent predictors of IVIG resistance in KD patients. The analysis revealed that IL-10 (OR=1.006, CI [1.000, 1.013], P=0.047) and IL-8 (OR=1.016, CI [1.009, 1.024], P<0.001) were independent predictive factors associated with IVIG unresponsiveness (Table 3).

    Table 3 Logistic Regression Model of Variables Independently Associated with IVIG Resistance Compared with IVIG Responsiveness

    To evaluate the predictive value of individual and combined cytokines for IVIG resistance in KD patients, ROC curve analysis was performed. The AUC for individual markers was 0.752 for IL-10 and 0.738 for IL-8. The AUC for the combined diagnostic model was 0.749, with a sensitivity of 0.713 and a specificity of 0.670 (Figure 4).

    Figure 4 ROC curves of cytokines for predicting IVIG resistance in Kawasaki disease.

    Abbreviations: IL, interleukin; PRE, predicted probability.

    When the IL-10 concentration was greater than 14.70 pg/mL, the sensitivity and specificity for predicting IVIG resistance were 0.675 and 0.748, respectively. Similarly, when the concentration of IL-8 was greater than 23.55 pg/mL, the sensitivity and specificity were 0.725 and 0.658, respectively.

    Discussion

    Cytokines, secreted by immune and selected non-immune cells, are pivotal mediators and modulators of immune responses and inflammatory processes.10 The pathogenesis of KD is considered multifactorial, integrating genetic susceptibility with infectious, environmental, or other antigenic triggers that precipitate an exaggerated inflammatory cascade in predisposed individuals, in which cytokines play a central role.11 In the present study, we evaluated the diagnostic and predictive utility of a 12-cytokine panel in KD. Elevated IL-10 and IL-5 have emerged as independent predictors of KD diagnosis, whereas elevated IL-10 and IL-8 independently predict IVIG resistance.

    Cytokines are centrally implicated in the pathogenesis of KD. During the acute phase, multiple pro-inflammatory cytokines—such as TNF-α, IL-6, IL-10, and IFN-γ—along with chemokines (eg, CCL2) and growth factors (eg, VEGF) are markedly elevated, orchestrating endothelial injury and systemic inflammation.5,12–14 These mediators activate immune cells (monocytes and neutrophils) and the vascular endothelium, amplifying the release of inflammatory molecules and upregulating the expression of endothelial adhesion molecules, thereby precipitating vasculitis.15 In the present study, we evaluated the diagnostic utility of a 12-cytokine panel in KD and identified younger age, high IL-10, high IL-5, elevated white blood cell count, and increased absolute neutrophil count as independent predictors. The combined model yielded an AUC of 0.853, with a sensitivity of 0.758 and a specificity of 0.812.

    Approximately 10–20% of children with KD exhibit resistance to IVIG, and IVIG nonresponse constitutes an independent risk factor for coronary artery lesions.2 Consequently, several studies have recommended that patients at high predicted risk of IVIG resistance receive initial combination therapy with IVIG plus corticosteroids such as methylprednisolone or even biologics such as infliximab.4,16 Accumulating evidence indicates that elevated cytokine levels correlate with IVIG refractoriness, underscoring the pivotal role of these mediators in KD pathogenesis and treatment response.17 In the present work, we evaluated a 12-cytokine panel for its ability to predict IVIG resistance and identified high IL-10 and high IL-8 levels as independent predictors of non-response. At a cut-off of 14.70 pg/mL for IL-10, the sensitivity and specificity for predicting IVIG resistance were 0.675 and 0.748, respectively, whereas an IL-8 threshold of 23.55 pg/mL yielded a sensitivity of 0.725 and a specificity of 0.658. Previously published models for predicting IVIG resistance, both domestically and internationally, have consistently included CRP.18,19 Cytokines act as upstream signals, whereas CRP functions as a downstream effector; the two are closely correlated, especially for IL-6.20 Therefore, CRP was not included in our IVIG-resistance prediction model.

    We observed a dual predictive role for IL-10 in both the diagnosis of KD and the identification of IVIG resistance, echoing our 2013 finding that pretreatment with IL-10 > 8 pg/mL is associated with CALs. Functionally, IL-10 suppresses the production of key inflammatory mediators—including TNF-α, IL-6, and IL-1—thereby attenuating excessive inflammation.21 Consistent with a compensatory counter-regulatory response, the serum IL-10 concentration increases markedly during the acute phase of KD and decreases after therapy.22,23 This temporal pattern has been corroborated in patients with KD shock syndrome (KDSS), in whom IL-10 concentrations are significantly higher than those in uncomplicated KD patients and correlate with disease severity, supporting its potential as a biomarker for KDSS.24 At the genetic level, polymorphisms within the IL-10 promoter (eg, −627 A/C and −592 A>C) have been linked to an increased risk of coronary aneurysms, implying that heritable variation in IL-10 expression modulates individual susceptibility and clinical progression.25,26 Collectively, the pleiotropic effects of IL-10 in KD include both anti-inflammatory modulation and, under certain conditions, the promotion of vascular pathology, underscoring the value of serial IL-10 measurements for disease monitoring and prognostic assessment.

    IL-5, a cytokine secreted by Th2 lymphocytes, mast cells, and eosinophils, exerts its biological effects via the IL-5 receptor.27 It drives B-cell differentiation and antibody production, governs eosinophil development and function, and participates in immune regulation.28–30 Consequently, IL-5 is implicated in allergic disorders (eg, asthma and allergic rhinitis), parasitic infections, autoimmune diseases, and selected malignancies.29,30 In the present study, serum IL-5 levels were significantly elevated in KD patients relative to febrile controls and were further increased in those exhibiting IVIG resistance. These findings suggest that IL-5 may contribute to KD pathogenesis and modulate therapeutic responsiveness and suggest that IL-5–targeted therapy could constitute a novel treatment paradigm for KD.

    IL-8 (CXCL8), a prototypical CXC chemokine, serves as a central mediator of inflammation, orchestrating chemotaxis and cellular activation, endothelial regulation, pro-inflammatory cascades, tissue injury, and angiogenesis in chronic inflammation.31 During the acute phase of KD, plasma IL-8 concentrations are markedly elevated and form a synergistic pro-inflammatory network with IL-6, IL-10, and TNF-α. This axis may drive neutrophil-mediated vascular injury, activate the NF-κB signaling pathway, and modulate endothelial dysfunction, thereby contributing to the vasculitic process in KD.32–34 In the present cohort, IL-8 levels were significantly higher in IVIG-resistant patients; at a cutoff of 23.55 pg/mL, IL-8 predicted IVIG unresponsiveness with a sensitivity of 0.725 and a specificity of 0.658.

    Compared with prior investigations, the present study extends the breadth and integrates the depth of existing knowledge. By incorporating IL-5, IL-8, and IL-17 into the panel, we revealed the independent predictive value of Th2-related IL-5 and the chemokine IL-8 and constructed a multidimensional model integrating “cytokine–immune cell–clinical parameter” information (eg, the IL-5 + IL-10 + younger age diagnostic score).

    Nevertheless, several limitations must be acknowledged. First, as a retrospective single-center study with a modest sample size, potential geographic and ethnic biases may limit generalizability to other populations. Second, post-treatment 12-cytokine measurements were not performed, precluding longitudinal kinetic analyses. Third, the use of contemporaneous febrile patients as controls may introduce selection bias. Prospective validation with larger cohorts and, if warranted, multicenter randomized controlled trials are needed to confirm these findings.

    Conclusion

    The 12-cytokine panel effectively supports both the diagnosis of KD and the prediction of IVIG resistance. Elevated IL-10 and IL-5 are independent predictors of KD diagnosis, whereas elevated IL-10 and IL-8 independently predict IVIG unresponsiveness.

    Abbreviations

    KD, Kawasaki disease; IVIG, intravenous immunoglobulin; CALs, coronary artery lesions; AUC, area under the curve.

    Data Sharing Statement

    Anonymized research data are available from the corresponding author upon reasonable request.

    Ethics Declarations

    This retrospective study involving human participants was in accordance with the ethical standards of the institutional and national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards. The medical ethics committee of the Children’s Hospital of Zhejiang University School of Medicine approved this study (NO.: 2025-IRB-0318-P-01). Since the information was anonymized and the submission did not include images that may identify the person, The medical ethics committee of the Children’s Hospital of Zhejiang University School of Medicine waived the need of obtaining individual informed consent forms.

    This study was conducted and reported in accordance with the REporting of studies Conducted using Observational Routinely-collected Data (RECORD) guidelines.

    Author Contributions

    Weixing Kong: Conceptualization, Data curation, Investigation, Methodology and Writing – original draft; Lichao Gao: Conceptualization, Data curation, Formal analysis, Methodology and Writing – original draft; Jian Hu: Investigation, Supervision and Writing – review and editing; Zhufei Xu: Investigation, Supervision and Writing – review and editing; Qing Zhang: Investigation, Supervision and Writing – review and editing; Yujia Wang: Investigation, Supervision and Writing – review and editing; Songling Fu: Investigation, Supervision and Writing – review and editing; Chunhong Xie: Investigation, Supervision and Writing – review and editing; Fangqi Gong: Conceptualization, Funding acquisition, Methodology, Project administration, Supervision and Writing – review and editing. All authors took part in drafting, revising or critically reviewing the article; gave final approval of the version to be published; have agreed on the journal to which the article has been submitted; and agree to be accountable for all aspects of the work.

    Funding

    This work was supported, in part, by grants from Key R&D Program of Zhejiang (2024C03179).

    Disclosure

    The authors report no conflicts of interest in this work.

    References

    1. Jone PN, Tremoulet A, Choueiter N, et al. Update on diagnosis and management of kawasaki disease: a scientific statement from the American heart association. Circulation. 2024;150(23):e481–e500. doi:10.1161/CIR.0000000000001295

    2. McCrindle BW, Rowley AH, Newburger JW, et al. Diagnosis, treatment, and long-term management of kawasaki disease: a scientific statement for health professionals from the American Heart Association. Circulation. 2017;135(17):e927–e999. doi:10.1161/CIR.0000000000000484

    3. Tong T, Gong FQ. Navigating the 2024 AHA guidelines for Kawasaki disease: practical insights for clinicians. World J Pediatr. 2025;21(4):323–327. doi:10.1007/s12519-025-00892-9

    4. Center for Diagnosis and Treatment of Kawasaki Disease/Children’s Hospital of Shaanxi Provincial People’s Hospital. National Children’s Medical Center/Beijing Children’s Hospital, Capital Medical University, Children’s Hospital, Shanghai Jiao Tong University School of Medicine, et al. [Evidence-based guidelines for the diagnosis and treatment of Kawasaki disease in children in China (2023)]. Zhongguo Dang Dai Er Ke Za Zhi. 2023;25(12):1198–1210. Chinese. doi:10.7499/j.issn.1008-8830.2309038

    5. Wang Y, Wang W, Gong F, et al. Evaluation of intravenous immunoglobulin resistance and coronary artery lesions in relation to Th1/Th2 cytokine profiles in patients with Kawasaki disease. Arthritis Rheum. 2013;65(3):805–814. doi:10.1002/art.37815

    6. Zhang Z, Zhao L, Zhou X, Meng X, Zhou X. Role of inflammation, immunity, and oxidative stress in hypertension: new insights and potential therapeutic targets. Front Immunol. 2022;13:1098725. doi:10.3389/fimmu.2022.1098725

    7. Lin IC, Suen JL, Huang SK, et al. Involvement of IL-17 A/IL-17 receptor A with neutrophil recruitment and the severity of coronary arteritis in Kawasaki disease. J Clin Immunol. 2024;44(3):77. doi:10.1007/s10875-024-01673-1

    8. Huang J, Li Y, Jiang Z, et al. IL-1β promotes hypoxic vascular endothelial cell proliferation through the miR-24-3p/NKAP/NF-κB axis. Biosci Rep. 2022;42(1):BSR20212062. doi:10.1042/BSR20212062

    9. Shkundin A, Halaris A. IL-8 (CXCL8) correlations with psychoneuroimmunological processes and neuropsychiatric conditions. J Pers Med. 2024;14(5):488. doi:10.3390/jpm14050488

    10. Liu C, Chu D, Kalantar-Zadeh K, George J, Young HA, Liu G. Cytokines: from clinical significance to quantification. Adv Sci. 2021;8(15):e2004433. doi:10.1002/advs.202004433

    11. Goel AR, Yalcindag A. An update on Kawasaki disease. Curr Rheumatol Rep. 2024;27(1):4. doi:10.1007/s11926-024-01167-4

    12. Chen CY, Huang SH, Chien KJ, et al. Reappraisal of VEGF in the pathogenesis of Kawasaki disease. Children. 2022;9(9):1343. doi:10.3390/children9091343

    13. Shikishima Y, Saeki T, Matsuura N. Chemokines in Kawasaki disease: measurement of CCL2, CCL22 and CXCL10. Asian Pac J Allergy Immunol. 2003;21(3):139–143.

    14. Bordea M, Costache C, Grama A, et al. Cytokine cascade in Kawasaki disease versus kawasaki-like syndrome. Physiol Res. 2022;71(1):17–27. doi:10.33549/physiolres.934672

    15. Noval Rivas M, Arditi M. Kawasaki disease: pathophysiology and insights from mouse models. Nat Rev Rheumatol. 2020;16(7):391–405. doi:10.1038/s41584-020-0426-0

    16. Jone PN, Anderson MS, Mulvahill MJ, Heizer H, Glodé MP, Dominguez SR. Infliximab plus Intravenous Immunoglobulin (IVIG) versus IVIG alone as initial therapy in children with Kawasaki disease presenting with coronary artery lesions: is dual therapy more effective? Pediatr Infect Dis J. 2018;37(10):976–980. doi:10.1097/INF.0000000000001951

    17. Wang Y, Qian SY, Yuan Y, et al. Do cytokines correlate with refractory Kawasaki disease in children? Clin Chim Acta. 2020;506:222–227. doi:10.1016/j.cca.2020.03.014

    18. Kobayashi T, Inoue Y, Takeuchi K, et al. Prediction of intravenous immunoglobulin unresponsiveness in patients with Kawasaki disease. Circulation. 2006;113(22):2606–2612. doi:10.1161/CIRCULATIONAHA.105.592865

    19. Egami K, Muta H, Ishii M, et al. Prediction of resistance to intravenous immunoglobulin treatment in patients with Kawasaki disease. J Pediatr. 2006;149(2):237–240. doi:10.1016/j.jpeds.2006.03.050

    20. Ridker PM. From C-reactive protein to interleukin-6 to interleukin-1: moving upstream to identify novel targets for atheroprotection. Circ Res. 2016;118(1):145–156. doi:10.1161/CIRCRESAHA.115.306656

    21. Williams LM, Ricchetti G, Sarma U, Smallie T, Foxwell BMJ. Interleukin-10 suppression of myeloid cell activation–a continuing puzzle. Immunology. 2004;113(3):281–292. doi:10.1111/j.1365-2567.2004.01988.x

    22. Chang L, Yang HW, Lin TY, Yang KD. Perspective of immunopathogenesis and immunotherapies for Kawasaki disease. Front Pediatr. 2021;9:697632. doi:10.3389/fped.2021.697632

    23. Guo MM, Huang YH, Kuo HC. Corticosteroid effects on IL-10 and IL-1β in U937-derived macrophages: a model for Kawasaki disease-associated inflammation. Cytokine. 2025;185:156809. doi:10.1016/j.cyto.2024.156809

    24. Li Y, Zheng Q, Zou L, et al. Kawasaki disease shock syndrome: clinical characteristics and possible use of IL-6, IL-10 and IFN-γ as biomarkers for early recognition. Pediatr Rheumatol Online J. 2019;17(1):1. doi:10.1186/s12969-018-0303-4

    25. Jin HS, Kim HB, Kim BS, et al. The IL-10 (−627 A/C) promoter polymorphism may be associated with coronary aneurysms and low serum albumin in Korean children with Kawasaki disease. Pediatr Res. 2007;61(5 Pt 1):584–587. doi:10.1203/pdr.0b013e3180459fb5

    26. Ferdosian F, Dastgheib SA, Morovati-Sharifabad M, et al. Cumulative evidence for association between IL-10 polymorphisms and kawasaki disease susceptibility: a systematic review and meta-analysis. Fetal Pediatr Pathol. 2021;40(2):153–165. doi:10.1080/15513815.2019.1686789

    27. Takatsu K. Interleukin-5 and IL-5 receptor in health and diseases. Proc Jpn Acad Ser B Phys Biol Sci. 2011;87(8):463–485. doi:10.2183/pjab.87.463

    28. Antosz K, Batko J, Błażejewska M, Gawor A, Sleziak J, Gomułka K. Insight into IL-5 as a potential target for the treatment of allergic diseases. Biomedicines. 2024;12(7):1531. doi:10.3390/biomedicines12071531

    29. Farne HA, Wilson A, Milan S, Banchoff E, Yang F, Powell CV. Anti-IL-5 therapies for asthma. Cochrane Database Syst Rev. 2022;7(7):CD010834. doi:10.1002/14651858.CD010834.pub4

    30. Buchheit KM, Shaw D, Chupp G, et al. Interleukin-5 as a pleiotropic cytokine orchestrating airway type 2 inflammation: effects on and beyond eosinophils. Allergy. 2024;79(10):2662–2679. doi:10.1111/all.16303

    31. Russo RC, Garcia CC, Teixeira MM, Amaral FA. The CXCL8/IL-8 chemokine family and its receptors in inflammatory diseases. Expert Rev Clin Immunol. 2014;10(5):593–619. doi:10.1586/1744666X.2014.894886

    32. Asano T, Ogawa S. Expression of IL-8 in Kawasaki disease. Clin Exp Immunol. 2000;122(3):514–519. doi:10.1046/j.1365-2249.2000.01395.x

    33. Barron KS. Kawasaki disease: etiology, pathogenesis, and treatment. Cleve Clin J Med. 2002;69(Suppl 2):SII69–78. doi:10.3949/ccjm.69.Suppl_2.SII69

    34. Rife E, Gedalia A. Kawasaki disease: an update. Curr Rheumatol Rep. 2020;22(10):75. doi:10.1007/s11926-020-00941-4

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  • Inside TikTok Shop’s incentives for the 2025 holiday period

    Inside TikTok Shop’s incentives for the 2025 holiday period

    In recent weeks, the short-form video app has shared a plethora of incentives and challenges with its TikTok Shop Partners (TSP) which Digiday has seen — almost gamifying the process, in a bid to encourage more spending. The result: if they qualify, TSPs could receive ad credits or cash bonuses.

    And here’s what those incentives are:

    Daily GMV Incentive Program
    TSPs can earn cash incentives between $5,000 and $20,000 between Oct. 1 to Dec. 31, based on their Q4 incremental daily GMV growth — or how much they sell.

    Partner onboard and upgrade incentive
    TSPs can earn up to $10,000 in cash for upgrading through TikTok Shop’s partner rankings for the first time, provided they stay at their new ranking for the duration of the incentive period (Oct. 1 to Dec. 31).

    Vertical creator incubation incentive
    TSPs can earn between $1,000 and $10,000 per creator between Oct. 1 to Dec. 31 for successfully incubating TikTok’s target list creators.

    Affiliate service incentive — milestone program

    • Incentive 1: Between Oct. 1 and Dec. 31, TikTok will rank its TSPs in descending order from 15 to one, based on their target plan short video GMV increment. Each month, those which also meet the minimum incremental GMV requirement can earn between $1,000 and $5,000 in ad credits. There’s even the option to earn a bonus $2,000 in ad credits for ranking in the top 15 for all three months.
    • Incentive 2: Between Oct. 1 and Dec. 31, TSPs that provide creator services can earn up to $1,000 in ad credits per seller (up to 70 sellers), provided they meet all eligibility requirements and incentive conditions.

    Black Friday/Cyber Monday offerings

    BFCM partner challenge
    Between Nov. 12 and Dec. 1, TikTok created the following challenges depending on TSPs ranking level (according to the number of new short video posts):

    • Challenge 1: TSPs that provide creator matchmaking services can earn up to $25,000 in cash.
    • Challenge 2: TSPs with a daily GMV either greater than or equal to $20,000 in October can earn up to $12,000.
    • Challenge 3: TSPs with a daily GMV of less than $20,000 in October can earn up to $2,000.

    There’s even three content challenges specifically for BFCM around short video, a livestream championship and key livestream (by invitation only).

    TikTok covers the costs
    And for those sellers who aren’t in the mood for free cash or ad credits, for Black Friday and Cyber Monday, TikTok is still offering brands fully-funded and partially-funded coupons and discounts, where TikTok will cover all or part of their marketing costs, as well as the invitation-only flash sales.

    The big picture

    For the most part, TikTok Shop has been one of the short-form video app’s huge success stories since it launched in the U.S. in September 2023. Since then, it appears to have gone from strength to strength in terms of revenues generated, so much so it’s been reportedly likened and compared to its 30-year-old competitor, eBay. 

    Between September 2023 to August 2024, TikTok Shop recorded $1.1 billion in gross merchandise value (GMV), and shifted around 67 million units of stock, according to data from Charm.io. This increased to $2.5 billion GMV and around 139 million units of stock between September 2024 and August 2025.

    And BFCM has been a big part of that story. According to TikTok’s internal data, which was presented on its 2025 TikTok Shop Black Friday & Cyber Monday seller deck that Digiday has seen, BFCM raked in more than 100 million sales, while sellers saw a three times uplift in GMV (compared to the previous year). Added to that, TikTok Shop saw more than four billion views on #TikTokShopBlackFriday and a third of TikTok Shop purchases went to small- to medium-sized businesses.

    When it comes to ad spend, from January 2025 through to Nov. 10 this year, TikTok Shop has raked in $498.8 million in ad spend, per Charm.io.

    “As a bet, TikTok Shop has already hit, but the payoff is only just beginning to roll in,” said Max Willens, principal analyst, social media and the creator economy at eMarketer. “It will be interesting to see how TikTok’s AI-powered ad solution, GMV Max, influences TikTok Shop’s growth, now that merchants are required to use it. If GMV Max can continue to deliver efficient results as its use keeps scaling, it could push TikTok Shop into another gear of growth.”

    But that’s only been part of its focus. Motivating marketers to push harder on its e-commerce arm comes at a time when TikTok has already been aggressively on the hunt for ad dollars in recent weeks. It’s been reported that the platform has been encouraging brands and agencies to boost their ad spend — despite there still being no clarity around its U.S. deal.

    “It makes perfect sense for TikTok to try to boost its business ahead of the deal, especially given the underwhelming valuation of $14 billion,” said Jasmine Enberg, co-founder and co-CEO of Scalable. “TikTok will want to make its business as attractive as possible to buyers and give itself as much negotiating power as possible. It wants to get as many advertisers on board and spending ahead of the sale to try to mitigate the inevitable disruption to its business.” 

    If all goes well, the short-form video app will be on track to meet WARC’s global social media ad spend forecast.

    Social media ad spend is projected to rise 14.9% to $306.4 billion, according to WARC’s updated global ad spend forecasts. Within that, TikTok is expected to take 10.3% of all social media spend this year, increasing to 11.7% by 2027.

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  • O’Melveny Represents Joint Sponsors and Underwriters in the Approximate US$450 Million A+H Listing of CNGR Advanced Material

    O’Melveny Represents Joint Sponsors and Underwriters in the Approximate US$450 Million A+H Listing of CNGR Advanced Material

    FOR IMMEDIATE RELEASE

    HONG KONG—November 17, 2025—O’Melveny represented the joint sponsors and underwriters in connection with CNGR Advanced Material Co., Ltd.’s (“CNGR Advanced Material”, 2579.HK) A+H listing on the Main Board of the Hong Kong Stock Exchange. The total offering size was approximately US$450 million (HK$3.5 billion).

    CNGR Advanced Material is a new energy materials company engaged in the research and development, production and sales of new energy battery materials, with a focus on cathode active material precursors (pCAM), and new energy metal products. It is a global leader of nickel-based and cobalt-based cathode active material precursors (pCAM) for lithium-ion batteries. CAGR Advanced Material has been listed on the Shenzhen Stock Exchange since 2020.

    The Global Offering was led by joint sponsors Morgan Stanley Asia Limited and Huatai Financial Holdings (Hong Kong) Limited. Overall Coordinators included Morgan Stanley Asia Limited, Huatai Financial Holdings (Hong Kong) Limited, China International Capital Corporation Hong Kong Securities Limited, BNP Paribas Securities (Asia) Limited, and ABCI CAPITAL LIMITED. Additional underwriters include other reputable financial institutions as outlined in the prospectus.

    The O’Melveny team was led by partners Ke Zhu and Ke Geng. The core team included counsels Vincent Wang, Mengying Li, and Jerry Gao, associate Estella Zhang, China associate Baixi Wu, legal managers Lauren Huang and Karen Sun, legal consultant Zhenfang Ma, and trainee solicitor Priscilla Yeung. Counsel Edward Poon, associate Jingwei Huang, legal consultant Audrey Zhan, legal manager Belinda Zhu, and trainee solicitor Wilson Tang also provided valuable support.

    About O’Melveny

    It’s more than what you do: it’s how you do it. Across sectors and borders, in board rooms and courtrooms, we measure our success by yours. And in our interactions, we commit to making your O’Melveny experience as satisfying as the outcomes we help you achieve. Our greatest accomplishment is ensuring that you never have to choose between premier lawyering and exceptional service. So, tell us. What do you want to achieve? Visit us at www.omm.com; learn more in our firm at-a-glance; and find us on LinkedIn, Facebook, Instagram, and YouTube.

    Contact:

    Brandon Jacobsen
    O’Melveny & Myers LLP
    +1 213 430 8024
    bjacobsen@omm.com

    Chris Schob
    O’Melveny & Myers LLP
    +86 21 2307 7000
    cschob@omm.com

    # # #


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  • Rupee falls 6 paise to 88.72 against U.S. dollar in early trade

    Rupee falls 6 paise to 88.72 against U.S. dollar in early trade

    Image used for representative purpose only.
    | Photo Credit: Reuters

    The rupee declined 6 paise to 88.72 against the U.S. dollar in early trade on Monday (November 17, 2025) amid a firm American currency and relentless outflow of foreign capital.

    Positive sentiment in domestic equity markets and lower crude oil prices overseas, however, prevented a sharp fall in the Indian currency, forex analysts said.

    They said investors are also watching the progress on the proposed India-U.S. trade deal as well as the domestic PMI data to be released later this week.

    At the interbank foreign exchange market, the rupee opened at 88.70 and slipped further to trade at 88.72 against the greenback in initial deals, registering a loss of 6 paise from its previous closing level.

    On Friday, the rupee settled 4 paise higher at 88.66 against the U.S. dollar.

    Meanwhile, the dollar index, which gauges the greenback’s strength against a basket of six currencies, was trading 0.15% higher at 99.35.

    Brent crude, the global oil benchmark, was trading 0.85% lower at $63.84 per barrel in futures trade.

    On the domestic equity market front, Sensex climbed 212.98 points or 0.25% to 84,775.76 in early trade, while the Nifty advanced 50.90 points or 0.20% to 25,960.95.

    Foreign institutional investors sold equities worth ₹4,968.22 crore on Friday, according to exchange data.

    The government data released on Friday showed the country’s wholesale price inflation fell to a 27-month low of (-) 1.21% in October, led by a sharp deflation in food items like pulses and vegetables, and lower prices of fuel and manufactured items.

    Wholesale Price Index (WPI)-based inflation was 0.13% in September and 2.75% in October last year, the data showed.

    Also, foreign exchange reserves dropped by another $2.699 billion to $687.034 billion during the week ended November 7, the RBI said on Friday.

    The forex kitty has been on a declining trend for the past few weeks, and had decreased by $5.623 billion to $689.733 billion in the previous reporting week.

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  • Dow Jones Top Company Headlines at 11 PM ET: Tesla Wants Its American Cars to Be Built Without Any Chinese Parts | Layoff …

    Dow Jones Top Company Headlines at 11 PM ET: Tesla Wants Its American Cars to Be Built Without Any Chinese Parts | Layoff …

    Tesla Wants Its American Cars to Be Built Without Any Chinese Parts

    This year’s U.S. tariffs on Chinese imports pushed the EV maker to accelerate its strategy of cutting China-made components out of its U.S. production.

    —-

    Layoff Tactics Keep Changing, and the Blunders Keep Coming

    Amazon informed staffers via a text-email combo. Target asked them to stay home. Does any of it make job cuts less painful?

    —-

    Nvidia Helped Spark the AI Rally. Its Earnings Could Revive It.

    The chip maker blew the AI trade wide open in the spring of 2023. It might need to do it again.

    —-

    Meta Opens Pop-Up Stores to Build Buzz for Its AI Glasses

    The stores, in New York City, Los Angeles and Las Vegas, have coffee stations and full-length mirrors for customers to take selfies in their Ray-Bans.

    —-

    Disney and YouTube TV Reach Deal, Ending 15-Day Standoff

    ESPN, ABC and other Disney networks return to roughly 10 million YouTube TV customers.

    —-

    AIG Hit by More Executive Churn as Incoming President Will No Longer Join

    Former Lloyd’s executive John Neal was recently hired to fill in as AIG’s No. 2. He was slated to start in two weeks.

    —-

    Walmart Picks Insider to Take Over as Next CEO

    Doug McMillon is handing the top job to John Furner, who spent six years running the U.S. business.

    —-

    China-U.S. Robotaxi Race Kicks off in U.K.

    Waymo, Alphabet’s self-driving car company, has partnered Uber-backed ride-hailing company Moove to enter the U.K. market next year.

    —-

    JBS Boosts Ground Beef, Wagyu Steak Production to Stem Beef Losses

    Meatpackers like JBS and Tyson Foods are being squeezed by the lowest U.S. cattle supply since the 1950s. It is driving their beef costs to record levels, and leading to hundreds of millions of dollars in losses as a result.

    —-

    Purdue Pharma Wins Court Approval for $7.4 Billion Opioid Settlement

    The move clears a path for the OxyContin maker to exit its six-year bankruptcy and resolve mass lawsuits.

    —-

    Charlie Javice Billed Hotels and Cellulite Butter as Legal Fees, JPMorgan Says

    JPMorgan is seeking to get out of paying her and a co-executive’s legal defense, which has cost more than $142 million.

    —-

    Enbridge $1.4 Billion Project Aims to Boost Canadian Oil Flow to U.S. Refineries

    Pipeline operator Enbridge will push ahead with a $1.4 billion expansion of its core network to boost deliveries of Canadian heavy oil and reach key refining markets in the U.S. Midwest and Gulf Coast.

    —-

    BHP Liable for Deadly Brazilian Dam Disaster, Court Rules

    The ruling potentially exposes the mining company to billions of dollars in compensation claims.

    (END) Dow Jones Newswires

    November 16, 2025 23:15 ET (04:15 GMT)

    Copyright (c) 2025 Dow Jones & Company, Inc.

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  • Johann Strydom Buys Handful Of Shares In Old Mutual

    Johann Strydom Buys Handful Of Shares In Old Mutual

    Old Mutual Limited (JSE:OMU) shareholders (or potential shareholders) will be happy to see that the CEO & Director, Johann Strydom, recently bought a whopping R10.0m worth of stock, at a price of R13.27. There’s no denying a buy of that magnitude suggests conviction in a brighter future, although we do note that proportionally it only increased their holding by -100%.

    Trump has pledged to “unleash” American oil and gas and these 15 US stocks have developments that are poised to benefit.

    Notably, that recent purchase by Johann Strydom is the biggest insider purchase of Old Mutual shares that we’ve seen in the last year. So it’s clear an insider wanted to buy, at around the current price, which is R13.46. Of course they may have changed their mind. But this suggests they are optimistic. While we always like to see insider buying, it’s less meaningful if the purchases were made at much lower prices, as the opportunity they saw may have passed. In this case we’re pleased to report that the insider bought shares at close to current prices. The only individual insider to buy over the last year was Johann Strydom.

    You can see a visual depiction of insider transactions (by companies and individuals) over the last 12 months, below. If you click on the chart, you can see all the individual transactions, including the share price, individual, and the date!

    Check out our latest analysis for Old Mutual

    JSE:OMU Insider Trading Volume November 17th 2025

    There are plenty of other companies that have insiders buying up shares. You probably do not want to miss this free list of undervalued small cap companies that insiders are buying.

    Looking at the total insider shareholdings in a company can help to inform your view of whether they are well aligned with common shareholders. We usually like to see fairly high levels of insider ownership. Based on our data, Old Mutual insiders have about 0.07% of the stock, worth approximately R38m. I generally like to see higher levels of ownership.

    The recent insider purchase is heartening. And an analysis of the transactions over the last year also gives us confidence. Given that insiders also own a fair bit of Old Mutual we think they are probably pretty confident of a bright future. So while it’s helpful to know what insiders are doing in terms of buying or selling, it’s also helpful to know the risks that a particular company is facing. You’d be interested to know, that we found 1 warning sign for Old Mutual and we suggest you have a look.

    Of course, you might find a fantastic investment by looking elsewhere. So take a peek at this free list of interesting companies.

    For the purposes of this article, insiders are those individuals who report their transactions to the relevant regulatory body. We currently account for open market transactions and private dispositions of direct interests only, but not derivative transactions or indirect interests.

    Have feedback on this article? Concerned about the content? Get in touch with us directly. Alternatively, email editorial-team (at) simplywallst.com.

    This article by Simply Wall St is general in nature. We provide commentary based on historical data and analyst forecasts only using an unbiased methodology and our articles are not intended to be financial advice. It does not constitute a recommendation to buy or sell any stock, and does not take account of your objectives, or your financial situation. We aim to bring you long-term focused analysis driven by fundamental data. Note that our analysis may not factor in the latest price-sensitive company announcements or qualitative material. Simply Wall St has no position in any stocks mentioned.

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  • Nabta Health closes $2 million pre-Series A to expand hybrid women’s health model

    Nabta Health closes $2 million pre-Series A to expand hybrid women’s health model

    Nabta Health closes $2 million pre-Series A to expand hybrid women’s health model

    News

    • UAE-based Nabta Health has closed a $2 million Pre-Series A round, bringing its total funding to $4.5 million. The company uses an AI-powered hybrid model combining digital, at-home and in-clinic care.
    • Founded in 2017 by Sophie Smith, NABTA is a healthcare company dedicated to transforming women’s health in the Middle East through a hybrid model that combines digital, at-home and in-clinic care.
    • Nabta will use the new capital to expand across MEA, build new diagnostic and at-home testing pathways, and strengthen clinical infrastructure through hospital partnerships.

    Press release:

    Nabta Health (“NABTA”) is pleased to announce the closing of a $2 million Pre-Series A funding round, bringing its total funding to date to US $4.5 million.

    The Pre-Series A funding will enable NABTA to accelerate its mission to deliver accessible, evidence-based women’s healthcare and to expand its AI-powered hybrid model across the Middle East and Africa. 

    The investment will be used to deepen partnerships with employers, insurers, and healthcare providers; introduce new diagnostic and at-home testing pathways; and strengthen NABTA’s clinical infrastructure in collaboration with leading hospitals. 

    This year, NABTA was named to TIME Magazine’s Top HealthTech Companies 2025 list, announced the launch of a Women’s Health Centre of Excellence in partnership with Clemenceau Medical Center Hospital Dubai, and expanded its corporate health solutions across the region. 

    Together, these milestones reflect NABTA’s growing role as the MEA region’s hub for innovation in women’s health – a model that blends virtual, in-clinic, and community care to improve health outcomes across every stage of a woman’s life.

    Sophie Smith, Founder and CEO, Nabta Health, said: 

    “We are delighted to have closed this Pre-Series A round and to bring our total funding to date to US$4.5 million. This investment validates our vision – that women’s health in the region can be reimagined through an AI-powered, hybrid care model that meets women where they are, respects cultural context and delivers measurable outcomes. We are now looking to accelerate our growth so that more women and employers benefit from what we believe is the future of women-centred health: affordable, mobile-first, and engineered for sovereignty.”

    “For employers and insurers in the region, addressing the women’s health gap is not just a moral imperative; it is a business and productivity one,” added Smith. “With this funding, we will drive scale, deepen impact and prepare for the next chapter of growth.”

    Iain McMillan, Chair, Nabta Health, said:

    “The closing of this Pre-Series A round is confirmation that Nabta Health is being increasingly recognised in the region as a key enabler of measurably better women’s health. The business has steadily gained traction and grown its customer base throughout 2025 and I am looking forward to seeing further acceleration in our success as we move forward into 2026 and beyond.

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  • Visa leans into AI-enabled payments and stablecoins to stay ahead of the game, says Asia-Pacific president Stephen Karpin

    Visa leans into AI-enabled payments and stablecoins to stay ahead of the game, says Asia-Pacific president Stephen Karpin

    Societies are shifting away from cash, and embracing new ways to make payments and transfer money. In Asia, many have turned to e-wallets, QR codes, and super apps—skipping physical credit cards entirely. 

    Traditional card companies are reinventing themselves to stay ahead of the game. “These days, when people talk about ‘cards’, it’s not just a piece of plastic. It’s a digital network proposition where you can pay or be paid,” Stephen Karpin, Visa’s Asia-Pacific president, told Fortune on Tuesday.

    On Wednesday, on the sidelines of the Singapore FinTech Festival, Visa revealed two new features for its regional clientele: AI-enabled payments and stablecoin settlements.

    The first marks the company’s expansion into agentic commerce, where consumers across Asia can tap on AI-powered agents to shop and pay on their behalf. 

    OpenAI’s release of ChatGPT catalyzed a fundamental shift in commerce, Karpin said. “The breadth with which it’s transforming how one understands and finds things in the world is quite profound. Yet one of the things missing from the current state of a LLM-powered chatbot is the ability to make payment via an agent,” he said.

    This means that online shoppers can use AI chatbots to discover, browse and select items—but can’t yet use them to complete payments. 

    Customers can load their Visa cards on an agent system—just as they might with Apple or Google Pay. They are then given the option to opt in for ‘personalization’, to receive recommendations of “intelligent shopping decisions” based on their past preferences.

    Users are then prompted to make payment within the AI platform—securely, with tokenization and authentication—completing an end-to-end online shopping process. 

    Stablecoins

    The second initiative is Visa’s stable settlement pilot, which enables select partners to pay using stablecoins across supported blockchains. Stablecoins are digital currencies designed to have a stable value, by pegging them to less volatile assets such as fiat currencies, most commonly the U.S. dollar).

    Karpin said that Visa had recognized the value of blockchain technology for payments since the time first emerged a decade ago. Today, more cross-border transactions than ever are taking place via stablecoins.

    “​​We want to make [stablecoins] one of the options to make and receive payments all around the world, when the regulatory environment is ready,” Karpin added. “We’ve got some assets in the form of technology and capability, and want to help businesses large and small start conducting commerce in Web3.”

    Asia’s shifting payments space

    Karpin has worked at Visa for over a decade, cutting his teeth in the South Pacific, Southeast Asian, and Japanese markets—before becoming the firm’s Asia-Pacific president in 2023.

    Things are shifting in Asia’s payments space, he said, noting that more change has happened in the last five years as compared to the previous fifty.

    Super apps—single apps consolidating multiple services like ride-hailing, food delivery and digital payments—is one such disruptor, he said. 

    They first took off in mainland China, with the founding of Alipay in 2004 and WeChat Pay in 2013. Southeast Asian tech giant Grab followed suit, launching GrabPay in 2016.

    But instead of regarding super apps and e-wallets as competition, Visa is looking for ways to work with them.

    “You can live your life on a super app now, so we’re partnering with them to digitalize the Visa credential,” Karpin said.

    He cited Visa’s partnership with Taiwan’s Line Pay as an example, which allows Taiwanese users to travel abroad and pay by scanning any QR codes connected to the Visa network.

    Visa is also widely accepted in global destinations beyond Asia, making it easier for long-distance travelers to make seamless payments overseas.

    “[When traveling further abroad], you can’t use a super app with a QR. We’re partnering with e-wallets so you can use your phone to tap to get onto the New York subway, or buy lunch in London,” Karpin said.

    Visa is the world’s second-largest card payment organization based on the annual value of card payments transacted and the number of issued cards, after being surpassed by China’s UnionPay in 2015. Yet Visa, No. 127 on the Fortune 500, leads in global transaction volume.

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  • Microsoft AI CEO Calls Superintelligence an ‘Anti-Goal’

    Microsoft AI CEO Calls Superintelligence an ‘Anti-Goal’

    While much of Silicon Valley races to build godlike AI, Microsoft’s AI chief is trying to pump the brakes.

    Mustafa Suleyman said on an episode of the “Silicon Valley Girl Podcast” published Saturday that the idea of artificial superintelligence shouldn’t just be avoided. It should be considered an “anti-goal.”

    Artificial superintelligence — AI that can reason far beyond human capability — “doesn’t feel like a positive vision of the future,” said Suleyman.

    “It would be very hard to contain something like that or align it to our values,” he added.

    Suleyman, who cofounded DeepMind before moving to Microsoft, said his team is “trying to build a humanist superintelligence” — one that supports human interest.

    Suleyman also said that granting AI anything resembling consciousness or moral status is a mistake.

    “These things don’t suffer. They don’t feel pain,” Suleyman said. “They’re just simulating high-quality conversation.”

    The debate on superintelligence

    Suleyman’s comments come as some industry leaders speak about building artificial superintelligence. Some say that it could arrive this decade.

    OpenAI CEO Sam Altman has repeatedly described artificial general intelligence — AI that can reason like a human — as the company’s core mission. Altman said earlier this year that OpenAI is already looking beyond AGI to superintelligence.

    “Superintelligent tools could massively accelerate scientific discovery and innovation well beyond what we are capable of doing on our own, and in turn massively increase abundance and prosperity,” Altman said in January.

    Altman also said in an interview in September that he’d be very surprised if superintelligence doesn’t emerge by 2030.

    Google DeepMind’s cofounder, Demis Hassabis, offered a similar timeline. He said in April that AGI could be achieved “in the next five to 10 years.”

    “We’ll have a system that really understands everything around you in very nuanced and deep ways and kind of embedded in your everyday life,” he said.

    Other leaders have urged skepticism. Meta’s chief AI scientist, Yann LeCun, said we may still be “decades” away from achieving AGI.

    “Most interesting problems scale extremely badly,” LeCun said at the National University of Singapore in April. “You cannot just assume that more data and more compute means smarter AI.”


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