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  • The Lego Technic NASA Lunar RV set is an incredibly detailed reproduction of the historic Apollo lunar buggy — now with 32% off, its lowest ever price at Walmart

    The Lego Technic NASA Lunar RV set is an incredibly detailed reproduction of the historic Apollo lunar buggy — now with 32% off, its lowest ever price at Walmart

    Walmart is currently offering some of the best Lego deals and exclusive bundles during what it’s calling the “Bricktember Lego Sale”, which will run throughout September. Walmart is dropping Lego deals regularly during the month and will include some of the best Lego space sets, as well as the best Lego Star Wars sets, and some of the most collectable sets from Lego, so it’s well worth checking back regularly if you’re after a specific set.

    One Lego set, discounted at Walmart to its best-ever price, is one of the best space Lego sets – the Lego Technic NASA Lunar Roving Vehicle, which is an incredibly detailed reproduction of the historic NASA buggy that took to the Moon’s surface during the Apollo 15, 16 and 17 lunar missions.

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  • Synergistic impact of glycaemic control and coronary stenosis severity

    Synergistic impact of glycaemic control and coronary stenosis severity

    Introduction

    Type 2 diabetes mellitus (T2DM) affects 537 million adults globally, with projections exceeding 783 million by 2045.1 It has attracted much attention in recent years due to its dominant global prevalence (accounting for 90–95% of diabetes cases) and its strong epidemiological link to coronary artery disease (CAD).2 Cardiovascular disease (CVD) accounts for 50% of mortality in T2DM, and CAD represents its most lethal manifestation.3 Unlike type 1 diabetes, T2DM involves insulin resistance, chronic inflammation and dyslipidaemia, which synergistically accelerate atherosclerosis.4

    Prolonged hyperglycaemia drives CAD pathogenesis through multiple pathways: (1) oxidative stress-induced endothelial dysfunction, (2) advanced glycation end-product (AGE)-mediated vascular inflammation and (3) dyslipidaemia-enhanced plaque instability.5–7 Although intensive glucose control reduced microvascular complications in landmark trials (such as the UK Prospective Diabetes Study), its macrovascular benefits remain contested. The Action to Control Cardiovascular Risk in Diabetes trial reported increased mortality with glycated haemoglobin (HbA1c) <6.5%,8 whereas the Action in Diabetes and Vascular Disease: PreterAx and DiamicroN Controlled Evaluation and the Veterans Affairs Diabetes Trial found neutral effects on major CVD events.9 This paradox underscores the need for personalised glycaemic targets tailored to factors such as diabetes duration, comorbidities and vascular pathology.10,11 Given these unique mechanisms and the rising burden of T2DM in ageing populations, clarifying optimal glycaemic targets for this subgroup remains clinically urgent.

    Current guidelines lack granularity for patients with T2DM with established CAD. The 2023 American Diabetes Association (ADA) standards advocate HbA1c <7–8% for high-risk patients but omit stratification by coronary stenosis severity.12 Similarly, the European Society of Cardiology chronic coronary syndrome (CCS) guidelines prioritise lipid and blood pressure control without specifying glucose targets for advanced atherosclerosis.13

    To bridge this gap, we investigate how glycaemic control, diabetes duration and coronary stenosis severity (quantified by the Gensini score) jointly influence long-term mortality in patients with T2DM–CCS.

    Methods

    Study Design and Population

    This study retrospectively included a total of 390 patients with T2DM and CCS who underwent coronary angiography between 2011 and 2012. The inclusion criteria were as follows: (1) participants aged >18 years; (2) patients clinically diagnosed with T2DM and confirmed to have CAD through coronary angiography. The exclusion criteria were as follows: (1) patients lacking essential laboratory data, such as HbA1c levels; (2) patients with severe liver or kidney dysfunction or malignant tumours; (3) patients with concomitant congenital heart diseases or cardiomyopathies.

    After screening, a total of 150 patients were included for final analysis (Figure 1). Patients were stratified into the intensified control group and the relaxed control group based on their HbA1c levels being ≤7.5% or >7.5%, respectively. The HbA1c threshold of 7.5% was selected based on three considerations: (1) the ADA guidelines recommend individualised targets (HbA1c <7.5%) for patients with advanced CVD;14 (2) this cutoff aligns with studies focusing on high-risk T2DM populations, where stringent control (<6.5%) showed no mortality benefit;15 (3) it reflects real-world clinical practice balancing hypoglycaemia risk and glycaemic management in comorbid patients.16

    Figure 1 Flow chart.

    All reporting adhered to the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) standards.17 All patients were assessed at the Second Affiliated Hospital of Xi’an Medical University through outpatient visits every 6 months or telephone interviews. The clinical information and outcome events were recorded in study-specific databases. The participants were telephoned with their consent and informed of the purpose of the study. In this study, patients or their family members agreed by telephone or verbal consent during outpatient follow-up. They were told that this was a retrospective study and all data were anonymised during the analysis process and did not compromise the privacy of patients; furthermore, the study covered a long period and involved a retrospective analysis of hospitalised patients from up to 10 years ago. Some patients died or were unable to sign informed consent due to complications during the follow-up.

    Ethical approval was obtained from the Institutional Review Board of The Second Affiliated Hospital of Xi’an Medical University (No. X2Y202352). The study adhered to the Declaration of Helsinki and STROBE guidelines. All participants or their legal surrogates provided verbal informed consent via telephone interviews. The process of obtaining consent was meticulously documented through audio recordings, which were stored securely and archived. Participants were informed about the purpose of the study, the nature of the data collection, and how their data would be used. It was explicitly stated that all data would be anonymised during the analysis process to ensure the privacy and confidentiality of the participants. Additionally, participants were assured that their participation was voluntary and that they could withdraw from the study at any time without any repercussions.

    Variables Collection

    The Beckman Coulter Automatic Biochemical Analyzer AU5800 and Beckman Coulter reagents were used to test the baseline data of laboratory measurements, such as low-density lipoprotein cholesterol (LDL-C), triglycerides, total cholesterol, high-density lipoprotein cholesterol (HDL-C), blood glucose, uric acid, total bilirubin (TBIL), direct and indirect bilirubin (DBIL and IBIL, respectively) and serum creatinine. Glycated haemoglobin was measured using the AU5800 analyser with immunoturbidimetric reagents certified by the National Glycohemoglobin Standardization Program. The results of the coronary angiography were interpreted by a cardiologist who had >5 years of working experience. The results of the angiographic CAD were quantified precisely using the Gensini score,18 which quantifies coronary artery stenosis severity by assigning weights to each lesion based on its location and degree of luminal narrowing; higher scores indicate more extensive coronary disease.

    Outcomes

    Patients were divided into two categories based on their HbA1c levels at the index date, and the incidence of all-cause and cardiovascular death was compared between the subgroups. The incidence of each component was evaluated in the same way. Any death recorded in the diagnosis procedure combination data for the whole observable period following the index date was considered an all-cause death. Cardiovascular death was defined as myocardial infarction (MI), angina pectoris, malignant arrhythmia, acute heart failure or ischaemic stroke.

    Statistical Analysis

    All data analyses were performed using the statistical software SPSS 26.0, GraphPad Prism 7 and R version 4.2.2. The median (interquartile, Q1–Q3) was used to express the non-normally distributed data, whereas the mean and standard deviation (SD) were used to portray the variables with a normal distribution. Student’s t-test (data with a normal distribution) and Pearson’s chi-squared test (categorical variables) were run for the comparative analysis between the two groups. The multivariate Cox proportional hazards model was used to compare the risk of endpoints between the HbA1c subgroups. Kaplan–Meier survival analyses with Log rank tests were performed to show differences between groups.

    Results

    Study Population and Patient Characteristics

    Patients were recruited between 1 January 2012 and 31 December 2013, and observation continued until 31 May 2022, for a total of 104.8 ± 35.7 months. In total, 150 patients with T2DM and stable CAD were registered in the cohort. The median diabetic duration was 2.0 years (0.50–10.0 years).

    The mean (standard deviation) of age, Hb A1c, follow-up period, fasting glucose, 2-hour postprandial blood glucose, haemoglobin, serum albumin, serum total protein, total cholesterol, creatinine and urea nitrogen at enrolment was 63.5 years (10.8 years), 7.3% (1.8%), 104.8 months (35.7 months), 8.0 mmol/L (2.9 mmol/L), 13.1 mmol/L (4.8 mmol/L), 133 g/L (18.7 g/L), 42.3 g/L (4.3 g/L), 65.6 g/L (5.7 g/L), 1.6 mmol/L (0.8 mmol/L), 81.6 mmol/L (82.5 mmol/L) and 6.7 mmol/L (5.9 mmol/L), respectively. The number (proportion) of men, smokers, hypertension and history of MI or percutaneous coronary intervention were 83 (55.3%), 44 (29.3%), 102 (68%) and 52 (34.7%), respectively.

    Hypertension, triglycerides, HDL-C, LDL-C, uric acid, TBIL and DBIL had no statistically significant differences between groups (all p > 0.05). During the observation period, a total of 53 patients died (35%); Table 1 displays the characteristics of the study participants divided into the deceased and surviving groups. Clinical outcomes at 10 years are summarised in Table 2.

    Table 1 Characteristics of Study Participants

    Table 2 Clinical Outcomes at 10 Years

    All-Cause Mortality Risk Factors and Survival Analysis

    Multivariate Cox regression analysis showed that all-cause mortality was significantly associated with age, HbA1c, diabetic duration, creatinine and Gensini score (Table 3). Adjusted hazard ratios (HRs) (95% CIs) of all-cause mortality were 1.10 (1.06–1.15) for age, 1.29 (1.12–1.48) for HbA1c, 1.06 (1.02–1.10) for diabetic duration, 1.00 (1.00–1.01) for creatinine and 1.02 (1.01–1.02) for Gensini score. Figure 2 displays the survival curve of different groups according to the level of HbA1c (>7.5% or ≤7.5%). A higher mortality rate was observed in patients with HbA1c of >7.5% among those with diabetic duration >10 years (p = 0.0115, Figure 2a). There was no significant difference between the two groups among those with diabetic duration of <5 years (p = 0.1425, Figure 2b). In the group of Gensini scores of >60 points, no significant differences were detected between patients with HbA1c of >7.5% and ≤7.5% (p = 0.1182, Figure 2c). However, patients with HbA1c of ≤7.5% had less all-cause survival than those with HbA1c of >7.5%, with Gensini scores of ≤60 points (p = 0.0160, Figure 2d). Figure 2d.

    Table 3 Cox Survival Analysis of All-Cause Mortality

    Figure 2 All-cause mortality risk factors and Survival Analysis. (a) The survival curve of DM duration>10 years group according to the level of HbA1c. (b) The survival curve of DM duration< 5 years group according to the level of HbA1c. (c) The survival curve of Gensini score>60 group according to the level of HbA1c. (d) The survival curve of Gensini score≤60 group according to the level of HbA1c.

    Cardiovascular Mortality Risk Factors and Survival Analysis

    As shown in Table 4, six variables were selected by the Cox model: age, HbA1c, diabetic duration, DBIL, serum total protein and Gensini score. The adjusted HRs (95% CIs) of cardiovascular mortality were 1.10 (1.05–1.15) for age, 1.36 (1.16–1.58) for HbA1c, 1.06 (1.00–1.10) for the diabetic duration, 1.12 (1.04–1.23) for DBIL, 0.89 (0.83–0.95) for serum total protein and 1.02 (1.01–1.03) for Gensini score. Kaplan–Meier analysis revealed a higher cardiovascular mortality rate in patients with HbA1c of >7.5% and diabetic duration of >10 years (p = 0.0004, Figure 3a). There was no significant difference between the two groups with a diabetic duration of <5 years (p = 0.1340, Figure 3b). Figures 3c and d show that higher mortality rates were observed in patients with HbA1c of >7.5% and Gensini score of >60 points or ≤60 points (p = 0.0154, p = 0.0104).

    Table 4 Cox Survival Analysis of Cardiovascular Death

    Figure 3 Cardiovascular mortality risk factors and Survival Analysis. (a) The survival curve of DM duration>10 years group according to the level of HbA1c. (b) The survival curve of DM duration< 5 years group according to the level of HbA1c. (c) The survival curve of Gensini score>60 group according to the level of HbA1c. (d) The survival curve of Gensini score≤60 group according to the level of HbA1c.

    Discussion

    In this retrospective analysis with a 10-year follow-up, in the population with a diabetes course of >10 years, the risk of cardiovascular and all-cause death was substantially lower in the intensive group (HbA1c ≤7.5%) than in the relaxed glycaemic group (HbA1c >7.5%). Our finding that intensive glycaemic control reduced cardiovascular mortality across all stenosis levels (Gensini >60 and ≤60) but improved all-cause survival only in milder stenosis aligns with the ’vascular vulnerability’ hypothesis. In advanced atherosclerosis (Gensini >60), plaques exhibit thin fibrous caps, necrotic cores and macrophage infiltration. This observation indicates that in patients with highly narrowed coronary arteries, solely focusing on blood glucose control may not be sufficient to improve prognosis comprehensively; it may be necessary to consider other risk factors, such as blood pressure and lipid levels, and their management. Here, aggressive HbA1c-lowering may fail to reverse structural instability, and hypoglycaemia episodes could trigger catecholamine surges, plaque rupture and fatal arrhythmias.19 Conversely, in early-stage CAD (Gensini ≤60), glucose control mitigates endothelial nitric oxide synthase uncoupling, suppresses AGE-RAGE signalling and stabilises plaque phenotype.20 Furthermore, this observation also indicates that in more advanced stages of the disease process, the potential benefit of blood glucose control on overall survival may be somewhat limited, underscoring the need for a more comprehensive treatment approach in clinical practice.

    In our study, we also found that the Gensini score was independently associated with mortality in patients with T2DM and CCS. More recently, a retrospective cohort study showed that patients with high Gensini scores had higher event rates for all-cause mortality than those with low Gensini scores.18 Severe stenosis (Gensini >60) reflects advanced atherosclerosis, where plaque instability and ischaemia-reperfusion injury amplify systemic inflammation. Reynolds et al21 have reported that the Gensini score was a highly important predictor of all-cause and cardiac mortality in patients with CAD. Our study results reaffirmed that the Gensini score was an important predictor of a worse prognosis for patients with stable CAD.

    Our finding is consistent with previous studies that age is a well-known risk factor for all-cause and CAD mortality; older patients had higher prevalence rates than younger patients.22 Another study has also shown that the rate of mortality significantly increased with diabetes duration.23 For individuals with T2DM, advancing age often complicates the disease course, as prolonged hyperglycaemia leads to cumulative vascular damage, increasing the risk of CVD. Elderly patients are more prone to developing multiple complications such as hypertension, dyslipidaemia and renal insufficiency, all of which further exacerbate the progression of CVD. Consequently, elderly individuals with T2DM face a relatively higher risk of cardiovascular mortality.

    To the best of our knowledge, this is the first study that evaluated the associations of creatinine with total and cardiovascular mortality in the T2DM and CAD population. A retrospective cohort study has shown that a small creatinine increase had a high HR for all-cause mortality (HR 1.577, CI 1.329–1.871) in patients with CVD.24 Previous studies have shown that patients with DM usually have higher serum creatinine and could develop chronic kidney disease.25,26 The results of this study also demonstrate that creatinine levels are independently associated with all-cause mortality in individuals with T2DM and CAD.

    Our study found that in T2DM with CCS, a higher DBIL level, rather than TBIL or IBIL, was positively associated with cardiovascular mortality. Elevated DBIL may indicate impaired hepatic conjugation capacity, linked to oxidative stress and endothelial dysfunction in T2DM. The association between serum bilirubin and T2DM with CAD has been reported in several studies, although the results are inconsistent. Serum bilirubin is a potent endogenous antioxidant and has been identified as a cardiovascular risk in cohort studies,27 although the relation to T2DM and CAD remains unclear. The serum TBIL, which is the sum of the DBIL and IBIL, was the primary focus of previous studies. The meta-analysis reported that TBIL had an inverse association with adverse metabolic outcomes and confirmed a protective role of bilirubin in vascular disease outcomes, such as CAD.28 In contrast, the Dongfeng–Tongji cohort study reported that DBIL concentrations were positively associated with the risk of incident T2DM in middle-aged and elderly adults,29 which was consistent with our results. The controversy in the studies may be due to both genetics and the environment. Additionally, in our study, we found that serum total protein was a protective factor for cardiovascular mortality in T2DM with CCS.

    In our study, we also first proposed the glycaemic control strategy using the duration of diabetes and the degree of coronary stenosis. In the ADA guidelines, glycaemic targets are suggested by the number and severity of comorbidities.30 Previous studies have reported that prolonged exposure to hyperglycaemia coupled with several cardiovascular risk factors raises mortality in patients with long-duration diabetes.31 We found that long diabetes duration (≥10 years) and strict glycaemic control (≤7.5%) were associated with an decreased risk of death (Figures 2a and 3a). However, for individuals with short diabetes duration (<5 years), good glycaemic control did not further decrease the risk of death. In this study, we also found that severe coronary stenosis (Gensini score >60) and strict glycaemic control were associated with decreased risk of cardiovascular mortality but not all-cause mortality (Figures 2c and 3c), whereas tight glycaemic control further reduced the risk of death among patients with milder coronary stenoses (Gensini score ≤60). According to prior research, targets for glycaemic control should be tailored to each person’s fragility or functional dependency and life expectancy.32,33 The present study extends prior research by demonstrating that glycaemic control should consider not only the diabetic duration but also the severity of CAD.

    This study has several strengths and limitations. It is the first retrospective study that focuses on mortality and glycaemic control based on coronary stenosis and diabetes duration among Chinese people with long-term follow-up (10 years). The following are some of the current study’s flaws: (1) This is a single-centre retrospective study, and the sample size is relatively small. Further large clinical studies are required to validate our findings; (2) the fluctuating relationship over time between HbA1c levels and all-cause mortality was not examined – HbA1c values at various time points would more accurately reflect the risk of mortality because HbA1c fluctuates throughout time. Also, we were unable to obtain complete baseline HbA1c data, glycemic variability or trajectories (for example, patients improving from high to low HbA1c or vice versa) or perform a correlation analysis between baseline HbA1c and the Gensini score due to incomplete longitudinal data in this retrospective cohort. These limitations highlight the need for future prospective, multi-centre studies with more comprehensive data collection to further explore these relationships; (3) the major goal of this experiment was to determine whether there was a link between a single baseline measurement of exposures and variables and mortality. We did not examine how risk factors or therapies changed over time; thus, we were unable to draw any inferences about the association between longitudinal risk factor control and clinical outcomes; (4) limitations are imposed by the retrospective character of this research, particularly the significant number of patients who were eliminated due to incomplete data. Therefore, our results should be interpreted with caution and need to be further verified by a prospective, multicentre study.

    In conclusion, our study examined risk factors for all-cause and cardiovascular mortality in patients with coronary heart disease and diabetes. The individual’s frailty, life expectancy, diabetes duration and coronary stenosis should be considered in the decision of glycaemic control.

    Ethics Statement

    Registry and the registration no. of the study/trial: X2Y202352, on 2022/05/02.

    Approval of the research protocol: The protocol for this research project was approved by the Ethics Committee of the Second Affiliated Hospital of Xi’an Medical University. All available data were completely anonymous with no personal information.

    Informed Consent

    The participants were telephoned with their consent and informed of the purpose of the study. The verbal consent was recorded by audio recording. The reasons are as follows: 1. This study is a retrospective study and all data are anonymized during the analysis process, which does not involve the privacy of patients; 2. This study has a long time span and retrospective analysis of hospitalized patients 10 years ago. Some patients died or were unable to sign informed consent due to complications during the follow-up. All specimens involving participants were approved by the Ethics Committee of the Institutional Review Board of The Second Affiliated Hospital of Xi’an Medical University (No. X2Y202352).

    Funding

    This study was funded by grants from National Natural Science Foundation of China (No. 82470388, 82300407), the Nature Foundation of Xi’an Administration of Science &Technology (No. 22YXYJ0157), National Postdoctoral Researcher Funding Program (GZC20233580), Health Science and Technology Innovation Capacity Improvement Program of Shaanxi Province (No. 2024TD-09, 2024JC-YBQN-0813).

    Disclosure

    The authors declared no conflicts of interest concerning the authorship or publication of this article.

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    13. Golub IS, Termeie OG, Kristo S, et al. Major global coronary artery calcium guidelines. JACC Cardiovasc Imaging. 2023;16(1):98–117. doi:10.1016/j.jcmg.2022.06.018

    14. Shi K, Zhang G, Fu H, et al. Glycemic control and clinical outcomes in diabetic patients with heart failure and reduced ejection fraction: insight from ventricular remodeling using cardiac MRI. Cardiovasc Diabetol. 2024;23(1):148. doi:10.1186/s12933-024-02243-w

    15. Yang T, Fu P, Chen J, et al. Increased risk of adverse cardiovascular events by strict glycemic control after percutaneous coronary intervention (HbA1c < 6.5% at 2 years) in type 2 diabetes mellitus combined with acute coronary syndrome: a 5-years follow-up study. Curr Med Res Opin. 2021;37(9):1517–1528. doi:10.1080/03007995.2021.1947219

    16. Kavanagh ME, Back S, Chen V, et al. The portfolio diet and HbA1c in adults living with type 2 diabetes mellitus: a patient-level pooled analysis of two randomized dietary trials. Nutrients. 2024;16(17):2817. doi:10.3390/nu16172817

    17. von Elm E, Altman DG, Egger M, et al. The strengthening the reporting of observational studies in epidemiology (STROBE) statement: guidelines for reporting observational studies. Ann Intern Med. 2007;147(8):573–577. doi:10.7326/0003-4819-147-8-200710160-00010

    18. Wang KY, Zheng YY, Wu TT, et al. Predictive value of gensini score in the long-term outcomes of patients with coronary artery disease who underwent PCI. Front Cardiovasc Med. 2022;8:778615. doi:10.3389/fcvm.2021.778615

    19. El-Battrawy I, Demmer J, Abumayyaleh M, et al. The impact of sacubitril/valsartan on outcome in patients suffering from heart failure with a concomitant diabetes mellitus. ESC Heart Fail. 2023;10(2):943–954. doi:10.1002/ehf2.14239

    20. Peeters WM, Gram M, Dias GJ, et al. Changes to insulin sensitivity in glucose clearance systems and redox following dietary supplementation with a novel cysteine-rich protein: a pilot randomized controlled trial in humans with type-2 diabetes. Redox Biol. 2023;67:102918. doi:10.1016/j.redox.2023.102918

    21. Reynolds HR, Shaw LJ, Min JK, et al. Outcomes in the ISCHEMIA trial based on coronary artery disease and ischemia severity. Circulation. 2021;144(13):1024–1038. doi:10.1161/CIRCULATIONAHA.120.049755

    22. Einarson TR, Acs A, Ludwig C, et al. Prevalence of cardiovascular disease in type 2 diabetes: a systematic literature review of scientific evidence from across the world in 2007-2017. Cardiovasc Diabetol. 2018;17(1):83. doi:10.1186/s12933-018-0728-6

    23. Herrington WG, Alegre-Díaz J, Wade R, et al. Effect of diabetes duration and glycaemic control on 14-year cause-specific mortality in Mexican adults: a blood-based prospective cohort study. Lancet Diabetes Endocrinol. 2018;6(6):455–463. doi:10.1016/S2213-8587(18)30050-0

    24. Losito A, Nunzi E, Pittavini L, et al. Cardiovascular morbidity and long term mortality associated with in hospital small increases of serum creatinine. J Nephrol. 2018;31(1):71–77. doi:10.1007/s40620-017-0413-y

    25. Filippatos G, Anker SD, August P, et al. Finerenone and effects on mortality in chronic kidney disease and type 2 diabetes: a FIDELITY analysis. Eur Heart J Cardiovasc Pharmacother. 2023;9(2):183–191. doi:10.1093/ehjcvp/pvad001

    26. Alicic RZ, Rooney MT, Tuttle KR. Diabetic kidney disease: challenges, progress, and possibilities. Clin J Am Soc Nephrol. 2017;12(12):2032–2045. doi:10.2215/CJN.11491116

    27. Jain V, Ghosh RK, Bandyopadhyay D, et al. Serum bilirubin and coronary artery disease: intricate relationship, pathophysiology, and recent evidence. Curr Probl Cardiol. 2021;46(3):100431. doi:10.1016/j.cpcardiol.2019.06.003

    28. Nano J, Muka T, Cepeda M, et al. Association of circulating total bilirubin with the metabolic syndrome and type 2 diabetes: a systematic review and meta-analysis of observational evidence. Diabetes Metab. 2016;42(6):389–397. doi:10.1016/j.diabet.2016.06.002

    29. Wang J, Wu X, Li Y, et al. Serum bilirubin concentrations and incident coronary heart disease risk among patients with type 2 diabetes: the Dongfeng-Tongji cohort. Acta Diabetol. 2017;54(3):257–264. doi:10.1007/s00592-016-0946-x

    30. American Diabetes Association. Older adults: standards of medical care in diabetes-2018. Diabetes Care. 2018;41(Suppl 1):S119–S125. doi:10.2337/dc18-S011.

    31. Salehidoost R, Mansouri A, Amini M, et al. Diabetes and all-cause mortality, a 18-year follow-up study. Sci Rep. 2020;10(1):3183. doi:10.1038/s41598-020-60142-y

    32. Christiaens A, Henrard S, Zerah L, et al. Individualisation of glycaemic management in older people with type 2 diabetes: a systematic review of clinical practice guidelines recommendations. Age Ageing. 2021;50(6):1935–1942. doi:10.1093/ageing/afab157

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  • WhatsApp, Apple warn of highly targeted attacks with zero-day vulnerability

    WhatsApp, Apple warn of highly targeted attacks with zero-day vulnerability

    WhatsApp on Friday announced it patched a zero-day vulnerability it believes was used to launch sophisticated attacks against specific individuals.

    The Meta-owned messaging platform said in a security advisory that the bug, labeled CVE-2025-55177, involves “incomplete authorization of linked device synchronization messages.”

    The issue “could have allowed an unrelated user to trigger processing of content from an arbitrary URL on a target’s device,” the advisory says. 

    WhatsApp believes the vulnerability could have been combined with a separate OS-level vulnerability on Apple devices (CVE-2025-43300) to potentially launch sophisticated attacks against “specific targeted users,” the advisory says.

    Apple, which patched CVE-2025-43300 on August 20, has described it as an “out-of-bounds write issue.” 

    The tech giant said it is “aware of a report that this issue may have been exploited in an extremely sophisticated attack against specific targeted individuals.”

    CVE-2025-43300 affected Apple’s iOS, iPadOS and macOS products.

    No technical details were released by either company.

    In 2019, WhatsApp was exploited with a zero-day attack carried out by the NSO Group, which manufactures the zero-click spyware known as Pegasus. That attack impacted some 1,400 Apple users and resulted in a court finding holding NSO Group liable. 

    In January WhatsApp accused a separate spyware company, Paragon, of targeting about 90 of its users with spyware. Digital forensic experts from the Citizen Lab subsequently verified some of those attacks occurred.

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  • Pakistan, Bahrain discuss matters of mutual interest – RADIO PAKISTAN

    1. Pakistan, Bahrain discuss matters of mutual interest  RADIO PAKISTAN
    2. Defence Minister and Bahrain Defence Forces Chief of Staff agree to enhance defence cooperation  ptv.com.pk
    3. Bahrain Defence Chief, Naval Chief pledge stronger maritime and defence cooperation  Pakistan Today
    4. BDF Chief of Staff meets Pakistan Defence Minister  وكالة أنباء البحرين
    5. Pakistan, Bahrain discuss multi-domain warfare and joint training plans  Dunya News

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  • Cricket World Cup qualifiers: ‘Special’ Jersey targeting history

    Cricket World Cup qualifiers: ‘Special’ Jersey targeting history

    The Challenge League campaign, which concludes in 2026, features five matches in each round, with Jersey also beating Kenya by seven wickets, Denmark by 89 runs and Papua New Guinea by 160 runs, as well as sharing a tie with Kuwait.

    Hosting the round, seven of Jersey’s starting side against Qatar were under 26, including 20-year-old Richardson and 21-year-old Asa Tribe, who scored 53 off 40 balls.

    “The talent levels are through the roof and the desire is great to see,” added Perchard, who was their oldest player involved by two years at the age of 33.

    “These young lads bring in so much energy. They’re always asking questions and trying to get better.

    “The sky is the limit for the guys. I’ve got so much confidence that this team are going to achieve something special.

    “Without a shadow of a doubt, the talent level is within this group to qualify for a World Cup and achieve something truly remarkable.”

    A debutant in 2010, Perchard is part of a team who have consistently overachieved since the island of around 100,000 became International Cricket Council (ICC) associate members in 2007.

    “It’s changed a lot,” said the veteran known by the nickname ‘Chuggy’. “We’re a lot more well-versed and well-travelled.

    “We understand conditions and experiences a whole lot better. The professionalism’s gone through the roof and the training intensity has risen.

    “Some of these sides we’re playing against have more registered cricketers in their country than there are people in Jersey. The level we’re consistently playing at is amazing.

    “We’re not just team-mates – we’re mates as well. The group has grown up together and trained two or three times a week.

    “One of the beauties of being part of a small nation is you really have to work hard for each other.”

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  • Monoclonal antibody maker sees opportunity as COVID-19 vaccines fall off

    Monoclonal antibody maker sees opportunity as COVID-19 vaccines fall off

     

    As access to COVID-19 vaccines dwindles in the US, one company seems to be positioning its products as an alternative way of preventing the disease.

    Invivyd is the manufacturer of pemivibart, a monoclonal antibody sold under the name Pemgarda. The US Food and Drug Administration has authorized Pemgarda for emergency use in adults who are moderately or severely immunocompromised. So far, it’s authorized only as a pre-exposure prophylactic, despite Invivyd’s attempts to get the FDA to OK its use as a treatment.

    The agency rebuffed those efforts in February, saying it could not “reasonably conclude that the known and potential benefits of pemivibart . . . outweigh the known and potential risks,” according to a press release from Invivyd.

    Nonetheless, Invivyd has pressed forward with a strategy to make monoclonal antibodies part of the COVID-19 arsenal. The Waltham, Massachusetts–based company has another drug candidate waiting in the wings: VYD2311, an antibody that the company describes as having around 99% structural similarity to pemivibart. In press releases and interviews, Invivyd executives describe VYD2311 as a medicine that could eventually provide an alternative to vaccination.

    “There has been recent talk about how, where vaccine has been used in the past, it might not be used in the future,” Invivyd chief scientific officer Robert Allen tells C&EN. “In those settings, there is the potential for monoclonal antibody to provide some protection.” He adds that data from additional clinical trials would likely be needed.

    In a press release dated Aug. 14, Marc Elia, chair of Invivyd’s board of directors, is more blunt. “We believe monoclonal antibodies such as VYD2311 can serve as a powerful alternative to vaccines for COVID-19 prevention, and represent an important potential paradigm shift to move American medicine beyond the real and perceived limitations of COVID-19 vaccines,” Elia says in the statement. “Amidst declining public trust in vaccines, we want to offer Americans a new, non-vaccine choice.”

    In keeping with this stance, the company filed a citizen petition in May encouraging the federal government to switch its focus from vaccines to monoclonal antibodies as a preventive strategy for high-risk groups, writing that the medicines “have several inherent advantages over serial vaccination.”

    A few weeks later, when FDA leaders said they’d ask COVID-19 vaccine manufacturers to run placebo-controlled trials for their shots in young people without certain health conditions, Invivyd applauded the decision, even as bioethicists pointed out the pitfalls of giving people a placebo when an effective intervention is available.

    What remains to be seen is whether the firm’s efforts will bear fruit. VYD2311 has been tested only in a 40-person Phase 1 clinical trial. Invivyd says the study shows that the antibody has a long half-life, from which it infers that the drug candidate will have a long-term protective effect. Invivyd is planning a Phase 2/3 study that, if it succeeds, would be enough for the FDA to decide whether to approve VYD2311 as a preventive.

    But not everyone is convinced by the strategy. Monoclonal antibodies have failed to treat COVID-19 before—many times. By their nature, the drugs target specific viral epitopes, and if SARS-CoV-2, the virus that causes the disease, mutates such that the epitope no longer fits the antibody, the drugs stop working.

    “[VYD]2311 is almost certain to be rendered obsolete by the virus as the evolution of the virus continues,” says University of California, San Francisco, immunologist Warner C. Greene. “I view it as a flawed strategy, a weak strategy from the beginning.”

    Viral evolution

    Invivyd began life as Adagio Therapeutics. Spun offof Adimab in mid-2020, the start-up had a lofty goal of creating antibodies that would be able to “neutralize SARS-CoV-2 and all its known variants,” as founder and then-CEO Tillman Gerngross said at the time. Adagio went public in a stock offering a year later, raising $309 million.

    As it turned out, a lot hinged on “known variants.” In 2021, SARS-CoV-2 made its genetic leap to omicron, a new and powerful variant whose descendants still rule the viral landscape 4 years later. Adagio’s lead drug candidate collapsed, no longer able to effectively tackle the newly shaped virus. Gerngross left the company, along with several other executives and laid-off staffers.

    The company rebranded in 2022 as Invivyd, and new executives aimed to put Adagio firmly in the rearview mirror, prioritizing discovery and early-stage research instead of rejiggering its earlier antibodies. Those efforts eventually yielded pemivibart, a new antibody that held up well against omicron and its various spinoffs. The FDA issued an emergency use authorization (PDF) for pemivibart in March 2024.

    Invivyd says it expects both Pemgarda and VYD2311 to maintain their antiviral activity against new SARS-CoV-2 lineages, including the currently dominating Stratus variant.

    “Pemgarda was built on the basis of its ability to bind and neutralize those variants that occurred right at the time of the omicron emergence,” Allen says. “[VYD]2311 was updated against spike antigens that had followed the omicron variant emergence. . . . As time passes, the virus evolves, and what we could consider to be evolutionary drift is occurring. The antibody still maintains activity and binds well to those variants that emerge.”

    Pemgarda is currently the only monoclonal antibody on the market for COVID-19 in any capacity. By the end of 2022, the FDA had pulled marketing authorizations for every single other antibody for COVID-19 because they no longer worked.

    The last one to fall was AstraZeneca’s Evusheld, which, like Pemgarda, was designed as a preventive for people who are at especially high risk of complications from COVID-19. AstraZeneca attempted to develop a newer version of Evusheld called sipavibart, but it discontinued those efforts in the last year, after resistance emerged in a late-stage trial.

    “Invivyd is sort of, in the US, the lone monoclonal antibody company, and they’ve done a great job of tweaking a basic structure that works,” says David Sullivan, an infectious diseases specialist at the Johns Hopkins Bloomberg School of Public Health. He says that Pemgarda could eventually fall by the wayside but that VYD2311 has an opportunity to take its place.

    Broad population

    According to Allen, Invivyd has “no active plans” to expand the use of its antibodies beyond the immunocompromised population, where the FDA has so far shown a clear path to market. But the company is certainly looking.

    “With all the space that is still to be realized within immunocompromised individuals in different stages of development, there’s plenty to prospect on,” Allen says. “In cases where we saw that there was a clear need and a disease burden outside that context, we would at least entertain that.”

    It appears that window may be opening. Last week, the FDA approved updated COVID-19 vaccines for the 2025–26 season, but only for select groups: people 65 and older, and people with health conditions that make them susceptible to worse outcomes from COVID-19, which the US Centers for Disease Control and Prevention (CDC) has yet to clearly define. Invivyd raised $57.5 million in a stock offering as confusion about vaccine access began swirling.

    Monoclonal antibodies provide a kind of protection different from that of vaccines. Whereas vaccines stimulate the body’s immune system to form its own protective antibodies, a process known as active immunity, monoclonals simply are the antibodies. That approach is called passive immunity. Immunocompromised people don’t get as much active immunity from vaccines because their immune systems are weaker to begin with, but “it’s not a black-and-white issue,” says Johns Hopkins immunologist Arturo Casadevall.

    “My advice to the person at high risk is to get vaccinated,” he adds. “I don’t see this as either-or.”

    Should monoclonals like Pemgarda and VYD2311 be used as a replacement for COVID-19 vaccines? The answer from infectious disease specialists, so far, is a resounding no.

    “There is a role for monoclonals. I’ll leave it at that,” Sullivan says. “Honestly, I do not see monoclonal antibodies replacing vaccines.”

    Greene agrees. “I don’t think it’s a great plan to try and introduce this type of passive protection into a normally immune-responsive population,” he says. “I don’t think that would fly.”

    Chemical & Engineering News

    ISSN 0009-2347

    Copyright ©
    2025 American Chemical Society

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  • YOUNG PEOPLE MORE WILLING TO COMMIT INSURANCE FRAUD – Insurance News

    YOUNG PEOPLE MORE WILLING TO COMMIT INSURANCE FRAUD – Insurance News

    The following information was released by the University of Georgia:

    By

    Savannah Peat

    Millennials, Gen Z may not know they’re committing fraud or they may just not care

    If you’re under the age of 34, you may be more willing to commit insurance fraud, according to new University of Georgia research.

    The new study suggests that the younger you are, the more likely you may be to deceive a company or adjuster to get desired funds or outcomes.

    But some fraudsters might not realize they’re committing a crime when they do.

    “Many people, especially younger people, have an adversarial relationship with insurance companies,” said Brenda Cude, lead author of the study and a professor emerita in the UGA College of Family and Consumer Sciences. “If you’re pushed into a position of thinking you need to fight, maybe that pushes people into actions that they wouldn’t otherwise consider, especially if they’re not aware that it’s technically illegal. There are lots of major consequences that could come from that.”

    2 out of 5 in younger generations unfazed by insurance fraud

    The researchers relied on data from the Coalition Against Insurance Fraud, which surveyed almost 1,500 adults about their thoughts on insurance claims.

    Among other questions, the survey asked respondents if they would:

    Consider or had included damages that happened before a car accident on a claim (or if they had done so in the past).

    Leave out information or provide false information on an insurance application to get better coverage or a lower premium.

    Help a medical provider bill for treatment they hadn’t actually received and more.

    Respondents were also asked if they knew anyone who had committed one of these crimes.

    Two out of five respondents between the ages of 25 to 34 said they were OK with the fraudulent actions taken in the scenarios.

    They saw it as a smart way to save money or a way to help a friend out of a tough situation.

    “Age was significant. Part of that may be the impersonal way that younger adults relate to insurance companies,” Cude said. “They think, ‘I’m not hurting a person if I commit fraud. This is just a website.’ They might think it’s a good idea to tell the insurer their car is parked at their parents’ house when it’s actually in downtown Atlanta. But that’s technically fraud.”

    Generational divide may reflect ethical, moral differences

    Younger generations’ more carefree attitudes may affect their willingness to engage in insurance fraud, the researchers said.

    Only about 5% of those 55 and older signaled that they were OK with fraud. Cude suggested that there might be a connection between age and ethics, with older respondents reflecting a stronger moral compass.

    Millennials and Gen Z only changed their minds on insurance fraud if they perceived serious consequences; quick, wide-scale harm from their actions or felt bad about it.

    “The younger generation just might have a weaker connection to morality and have a situation-based code of ethics. It doesn’t bother them to do things, even if they know that they’re wrong, because they think they’re getting cheated and in the right,” she said.

    People don’t like insurance companies or understand what constitutes fraud

    Overall, the way people felt about insurance companies was unanimously bad regardless of age. That feeling is unlikely to change and won’t impact whether people commit fraud, Cude said.

    But one possible explanation for younger generations’ apathy toward insurance fraud may be that they don’t know what actually qualifies as fraud or how fraudulent claims may impact others.

    “We need to think more about how to approach younger folks in terms of insurance fraud. Part of that solution might be experience, but maybe part of that solution is also education,” said Cude. “I don’t think people really understand their insurance very well or the difference between a legit claim practice and something that is actually considered fraudulent.”

    Education might include learning how insurance works as well as why insurers make the decisions they do.

    This study was published in the Journal of Consumer Affairs and was co-authored by Hanchun Zhang.


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  • PEPITEM Molecule Shows Promise in Fighting Osteoporosis

    PEPITEM Molecule Shows Promise in Fighting Osteoporosis

    Birmingham researchers have identified bioactive peptide sequences in PEPITEM molecule, and demonstrated the biological of activity of the full PEPITEM molecule in counteracting key changes caused by osteoporosis.

    The latest study published in Biomedicine & Pharmacotherapy shows the whole PEPITEM molecule not only reduces bone resorption and increases bone formation, and but also promotes angiogenesis (the growth of capillaries from pre-existing blood vessels) in bone.

    The study was led by Professor Helen McGettrick and Dr Amy Naylor, including Dr Kathryn Frost, from the Department of Inflammation and Ageing at the University of Birmingham and Dr James Edwards from Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences at the University of Oxford.

    “The results show PEPITEM holds promise as a new therapeutic for osteoporosis and other disorders featuring bone loss. The dual action of promoting bone formation, and reducing bone breakdown, has distinct advantages over existing drugs. Excitingly, we are now closer to finding the mechanism for PEPITEM regulation of bone formation, angiogenesis and remodelling.” Professor Helen McGettrick, University of Birmingham


    PEPITEM (Peptide Inhibitor of Trans-Endothelial Migration) is a naturally occurring peptide (short protein), first identified at the University of Birmingham in 2015. Since then, the PEPITEM research team has investigated its role in the body and the potential for novel therapeutics, revealing its role in immune function and immune-mediated disorders.

    While previous studies have shown short sequences from the PEPITEM molecule can influence immune cells and inflammation, the latest study suggests the full PEPITEM molecule would offer the maximum efficacy in osteoporosis.

    Osteoporosis results from disruption to a tightly orchestrated process, involving a complex interplay between two cell types – osteoblasts, which form bone, and osteoclasts, which break down bone.

    The researchers used cell studies to identify peptide sequences from both ends of the PEPITEM molecule that influenced anabolic (construction) and catabolic (break down) processes in bone and identified four peptide sequences for further study.

    Investigations in cell and tissue culture showed the two different halves of the PEPITEM molecule were responsible for different functional responses, with direct effects on maturation or inhibition of osteoclast activity. Testing on bone organoids showed two smaller fragments, consisting of three amino acids from each end of the PEPITEM molecule, regulate the maturation of osteoblast cells and cause the release of a protein known to inhibit the formation of osteoclasts.

    “These findings build on our current understanding of PEPITEM biology in bone and clearly point to the next steps in research.” Professor McGettrick


    The researchers then used animal models of osteoporosis to evaluate the effects of these sequences and compared their effects to the whole PEPITEM molecule.

    Here the results showed that while the shorter versions of PEPITEM stimulate microscopic changes in bone architecture, the full-length peptide is essential to drive the multitude of functional changes in bone formation.

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  • Oil rises 1% ahead of OPEC+ meeting – Reuters

    1. Oil rises 1% ahead of OPEC+ meeting  Reuters
    2. Oil edges higher ahead of OPEC+ meeting By Reuters  Investing.com
    3. OPEC+ May Unwind 1.65MM Bpd of Cuts at Next Meeting, Analyst Warns  Rigzone
    4. Oil Gains as Technical Buying Bolsters Rally on Market Tightness  Yahoo Finance
    5. Oil Drifts as Traders Wait for OPEC+ and Next US Move on Russia  Bloomberg.com

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  • Rachel Scott talks Proenza Schouler: “There’s a beautiful legacy here. I think it has to move forward”

    Rachel Scott talks Proenza Schouler: “There’s a beautiful legacy here. I think it has to move forward”

    I have the ultimate respect for them for what they built, and to have had such an important role in fashion in this country.

    Talk a little bit more about balancing these two brands. To be upfront about it, I see it as a real challenge to manage two distinct design teams. How do you plan on nurturing both labels?

    Most of my career, I worked for other designers. Most of my career, I was crafting brands that were not my perspective. That’s my training. But also because of how specific Diotima is, I actually find [managing both brands] not that challenging. It’s actually quite fun: I can be really ridiculous over at Diotima, I can be really more radical over there if I want to be. Not that I’m not going to have interesting ideas here. But there is a formality here that doesn’t exist over at Diotima. I like this kind of push and flow. This is a really long-winded way to say it, but one of my favourite filmmakers is Raoul Peck. He made two films about Haiti after the earthquake. One is a documentary, and one is a film, and it’s kind of loosely based on Teorema [by Pier Paolo Pasolini], which is my favourite film. I saw him speak at the Metrograph, and he said that he made both films at the same time, because where he found limitations in the documentary form, he moved to the film, and where he found limitations there, he moved back. And I always found that so inspiring.

    Are you working with a stylist?

    Yes, Marika-[Ella Ames], who styles with Diotima. It’s unspoken at this point, we understand each other, and she’s so, so, so talented. I’ve just been so lucky over at Diotima to work with people I really admire. And I’m just so excited by this show; I have Julia Lange casting and Betak is producing it, and Marika styling it. I’ve been really lucky over there. And I’m really excited to have her here and continue our creative dialogue, but in a new world.

    Will it feel like a Proenza cast? Or will it have a little bit more Rachel in it?

    I think it will be a little bit of a mix. I think that’s more than anything, where I hope to point to the future.

    I’d like you to talk just a little bit more about what you think you can do here that you can’t do at Diotima?

    Like?

    Like, oh, are you really excited to dress somebody for a red carpet? Jack and Lazaro would often dress celebrities, It-girls.

    Maybe one day I’ll dress Isabelle Huppert. That would be goals. What I’m more excited about… you know, I love craft so much. But I hate when people think about it as an aesthetic, like crafty or nostalgic, or whatever. For me, it’s not an aesthetic, it’s a practice. What’s nice about craft here is that it can be really quite technical. It can be a technique that’s made by a very specialised machine that maybe I don’t have access to with my resources at Diotima. I could develop insane textiles that maybe I couldn’t do over there. Here, there’s really so much I can do. So that’s really exciting, more than anything.

    Comments, questions or feedback? Email us at feedback@voguebusiness.com.

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