Search

Porous carbon supports and antimony addition to palladium led to synergistic effects on the electrocatalytic performance for biomass-derived alcohol oxidation reactions.

Background Obesity is protective of bone health; however, abdominal obesity is associated with a higher fracture risk. Little is known about whether body composition protects or adversely affects osteoporotic fractures because of practical issues regarding assessment tools. This study aimed to evaluate the association of predicted body composition with fracture risk to determine the distinctive and differing effects of muscle or fat mass on bone health outcomes in the general population. Methods This population‐based, longitudinal cohort study used 2009–2010 Korean National Health Insurance Service data and follow‐up data from 1 January 2011 to 31 December 2013, to determine the incidence of osteoporotic fracture (total, spine, and non‐spine) defined using the International Classification of Diseases, Tenth Revision codes. The study participants were aged ≥50 years (men, 158 426; women, 131 587). The predicted lean body mass index (pLBMI), appendicular skeletal muscle index (pASMI), and body fat mass index (pBFMI) were used to assess body composition, using anthropometric prediction equations. Results Over a 3 year follow‐up, we identified 2350 and 6175 fractures in men and women, respectively. The mean age of the participants was 60.2 ± 8.3 and 60.7 ± 8.4 years in men and women, respectively. In a multivariable‐adjusted Cox proportional hazards regression model, increasing pLBMI or pASMI was significantly associated with a decreased risk of total fractures in men and women. When comparing individuals in the lowest pLBMI and pASMI (reference groups), men with the highest pLBMI and pASMI had adjusted hazard ratios of 0.63 [95% confidence interval (CI) 0.47–0.83] and 0.62 (95% CI 0.47–0.82), and women with the highest pLBMI and pASMI had adjusted hazard ratios of 0.72 (95% CI 0.60–0.85) and 0.71 (95% CI 0.60–0.85), respectively, for total fractures. The pBFMI had no significant association with total fractures in men or women. Regarding sex‐specific or site‐specific differences, the protective effects of the pLBMI and pASMI on fractures were greater in men and reduced the risk of spinal fractures. An increased pBFMI was associated with an increased risk of spinal fractures in women. Conclusions An increased pLBMI or pASMI was significantly associated with decreased total osteoporotic fracture risk; however, the pBFMI showed no statistically significant association. Muscle mass was more important than fat mass in preventing future osteoporotic fractures based on anthropometric prediction equations.

Human neurotropic immunodeficiency virus (HIV) ingress into the brain and its subsequent replication after infection results in viral reservoirs in the brain. The infected cells include microglia, perivascular macrophages, and astrocytes. HIV-associated neurocognitive disorders (HAND) affect glial cells by activating microglia and macrophages through neuroinflammation, as well as astrocytes through mitochondrial dysfunctions and the onset of oxidative stress, impairing the ability of these cells to engage in neuroprotection. Furthermore, the risk of neuroinflammation associated with HAND is magnified by recreational drug use in HIV-positive individuals. Most of the therapeutic options for HIV cannot be used to tackle the virus in the brain and treat HAND due to the inability of currently available combination antiretroviral therapies (ARTs) and neuroprotectants to cross the blood–brain barrier, even if the barrier is partially compromised by infection. Here, we report a strategy to deliver an optimized antiretroviral therapy combined with antioxidant and anti-inflammatory neuroprotectants using biodegradable brain-targeted polymeric nanoparticles to reduce the burden caused by viral reservoirs in the brain and tackle the oxidative stress and inflammation in astrocytes and microglia. Through in vitro coculture studies in human microglia and astrocytes as well as an in vivo efficacy study in an EcoHIV-infected, methamphetamine-exposed animal model, we established a nanoparticle-based therapeutic strategy with the ability to treat HIV infection in the central nervous system in conditions simulating drug use while providing enhanced protection to astrocytes, microglia, and neurons.

Background: In hemodialysis patients, brachial-ankle pulse wave velocity (baPWV) levels are affected by particulate matter with an aerodynamic diameter of 10 μm or less (PM10). We conducted this study to determine whether there is an association between short- and long-term PM10 exposure and baPWV in apparently healthy adults aged 40 years and older.Methods: A total of 1,628 subjects who underwent health examinations between 2006 and 2009 were included in the study. On the basis of the day of medical screening, the 1–3-day and 365-day moving averages of PM10 concentrations were used to evaluate the association between short- and long-term exposure to PM10 and high baPWV (≥the third quartile of baPWV, 1,534 cm/s) using logistic regression models. Additional subgroup analyses were conducted according to age, sex, obesity (body mass index ≥25.0 kg/m2), and comorbidities such as metabolic syndrome.Results: No statistically significant associations were identified between short-term and long-term exposure to PM10 and baPWV in any of the subjects and subgroups. A 10-μg/m3 increase in the 2-day moving average of PM10 exposure was marginally associated with high baPWV in non-obese subjects (odds ratio, 1.059; P=0.058). This association in non-obese subjects was significantly different from that in obese subjects (P=0.038).Conclusion: This study did not show statistically significant associations between short-term and long-term exposure to PM10 and baPWV in apparently healthy subjects. With short-term exposure to PM10, non-obese subjects showed a marginally unfavorable association with baPWV. Further studies are necessary to validate and elucidate the mechanism underlying the effect of PM10 on baPWV.

Repeated weight fluctuation has been proposed as a potential risk factor for increasing morbidity and mortality including cancer. We aimed to investigate the association between body weight variability (BWV) and all cancer and site-specific cancer incidence and the impact of smoking on these associations. A total of 1,759,848 cancer-free male subjects who had their weight measured at least 5 times from the National Health Insurance Service-Health Screening Cohort from 2002 to 2011 were included and followed up until 2015. BWV was defined as the average absolute difference between successive values (ASV). The risk of cancer and site-specific cancer from BWV was identified using Cox proportional hazards regression analysis using hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for potential confounders including weight, and stratified analysis was also conducted according to smoking status. During the 7,015,413 person-years of follow-up, 11,494 patients (0.65%) developed new-onset cancers. BWV was associated with a higher risk of all cancers after adjustment for confounders. The highest BWV quintile group compared to the lowest had greater risks of all cancers and site-specific cancers including lung, liver, and prostate cancer (HR 1.22, 95% CI 1.15–1.30; HR 1.22, 95% CI 1.07–1.39; HR 1.46, 95% CI 1.19–1.81; HR 1.36, 95% CI 1.15–1.62, in all cancers, lung, liver and prostate cancer, respectively). Due to small number of cancer occurrence, the risk of kidney cancer was increased, but statistically insignificant (HR 1.38, 95% CI 0.91–2.10). Similar results were observed in noncurrent smokers. However, in current smokers, the risks of all cancers and only prostate cancer were significantly increased in the highest BWV quintile group (HR 1.19, 95% CI 1.09–1.31; HR 1.51, 95% CI 1.08–2.11). The risk of kidney cancer also increased in this group, although the finding was not statistically significant (HR 1.77, 95% CI 0.87–3.63) This study suggested BWV is an independent risk factor for cancer in men, especially in lung, liver, and prostate cancer, but evidence was weaker in kidney cancer. This association remained significant only in prostate cancer in current smokers.

We prepared a highly active and stable cathode catalyst for a solid oxide electrolysis cell (SOEC), decorated with in situ exsolved Fe nanoparticles (NPs) socketed on La1.2Sr0.8Mn0.4Fe0.6O4−α (R.P.LSMF), toward the CO2 electrolysis reaction to produce CO selectively. This catalyst was derived from the perovskite structure of La0.6Sr0.4Mn0.2Fe0.8O3−δ (LSMF) by simple annealing in a H2 atmosphere and showed high current densities of 2.04, 1.43, and 0.884 A cm−2 at 850, 800, and 750 °C, respectively, at a voltage of 1.5 V with corresponding total polarization resistance values of 0.205, 0.326, and 0.587 Ω cm2, respectively, at an open circuit voltage. The highly improved performance should be ascribed to the in situ exsolved Fe NPs anchored on Ruddlesden–Popper oxide and to the increased contents of oxygen vacancies in R.P.LSMF. More importantly, this active catalyst also exhibited a stable voltage profile for 100 h operation at an constant current density of 1.8 A cm−2, suggesting that the catalyst Fe–R.P.LSMF proposed in this study is a highly promising candidate for use in an efficient SOEC cathode for CO2 electrolysis processes.

HIV‐1 enters the brain by altering properties of the blood‐brain barrier (BBB). Recent evidence indicates that among cells of the BBB, pericytes are prone to HIV‐1 infection. Occludin (ocln) and caveolin‐1 (cav‐1) are critical determinants of BBB integrity that can regulate barrier properties of the BBB in response to HIV‐1 infection. Additionally, Alix is an early acting endosomal factor involved in HIV‐1 budding from the cells. The aim of the present study was to evaluate the role of cav‐1, ocln, and Alix in HIV‐1 infection of brain pericytes. Our results indicated that cav‐1, ocln, and Alix form a multi‐protein complex in which they cross‐regulate each other's expression. Importantly, the stability of this complex was affected by HIV‐1 infection. Modifications of the complex resulted in diminished HIV‐1 infection and alterations of the cytokine profile produced by brain pericytes. These results identify a novel mechanism involved in HIV‐1 infection contributing to a better understanding of the HIV‐1 pathology and the associated neuroinflammatory responses.

BACKGROUND Sarcopenia is an important health problem, the risk factors of which a few studies have reported on. The purpose of this study was to evaluate the correlation between sarcopenia and the ratio of total energy intake to basal metabolic rate (BMR) as well as physical activity, and determine whether the relationship was different between younger and older age groups using data from the 2008-2011 Korea National Health and Nutrition Examination Survey. METHODS We analyzed 16,313 subjects older than 19 years who had dual energy X-ray absorptiometry data. Sarcopenia was defined as an appendicular lean mass/weight (%) ratio of 1 standard deviation below the sex-specific mean value for a younger reference group, and BMR was calculated using the Harris-Benedict equation. A chi-squared test and logistic regression analyses were performed to evaluate the factors associated with sarcopenia. RESULTS In this study, 15.2% of males and 15.4% of females had sarcopenia. Energy intake/BMR as well as physical activity was negatively related to sarcopenia risk. In stratified analysis by age and sex, strength exercises showed an inverse association with sarcopenia only in males under the age of 50 years (odds ratio, 0.577; P

The neurovascular units (NVU) are the minimal functional units of the blood–brain barrier (BBB), composed of endothelial cells, pericytes, astrocytes, microglia, neurons, and the basement membrane. The BBB serves as an important interface for immune communication between the brain and peripheral circulation. Disruption of the NVU by the human immunodeficiency virus-1 (HIV-1) induces dysfunction of the BBB and triggers inflammatory responses, which can lead to the development of neurocognitive impairments collectively known as HIV-1-associated neurocognitive disorders (HAND). Methamphetamine (METH) use disorder is a frequent comorbidity among individuals infected with HIV-1. METH use may be associated not only with rapid HIV-1 disease progression but also with accelerated onset and increased severity of HAND. However, the molecular mechanisms of METH-induced neuronal injury and cognitive impairment in the context of HIV-1 infection are poorly understood. In this review, we summarize recent progress in the signaling pathways mediating synergistic impairment of the BBB and neuronal injury induced by METH and HIV-1, potentially accelerating the onset or severity of HAND in HIV-1-positive METH abusers. We also discuss potential therapies to limit neuroinflammation and NVU damage in HIV-1-infected METH abusers.

Although many prediction models for cardiovascular diseases (CVDs) have been developed and validated for Western populations, the development of CVD prediction models for Asians has been slow. Our cohort study retrospectively analyzed the incidence of CVD that occurred between January 1, 2009, and December 31, 2016, in all Koreans who underwent national health screening. This dataset included 21,581,796 adults between the ages of 40 and 79 years (10,412,947 men, 11,168,849 women) without CVD at baseline. The primary outcome, CVD, was defined as the development of any of the following: acute coronary syndrome, cerebral infarction, and cerebral hemorrhage, as defined with health insurance claims data. The prediction model was constructed by Cox proportional hazard regression and validated with tenfold cross-validation. The performance of the models was evaluated through Harrell’s C-index and Brier score. The discrimination of the models was assessed by the area under the receiver operating characteristic curve (AUROC). Our model showed an AUROC of 0.762 in men and 0.811 in women. The Brier score of our model was 0.018 in men and 0.010 in women, which was better than the pooled cohort equation (PCE). Our novel model performed better than the FRS and PCE for Koreans.

Many state governments impose tuition regulations on public colleges in pursuit of college affordability. How effective are these regulations? We use a modified event study design to study how colleges' ``sticker price'' and institutional financial aid change during and after tuition caps and freezes in the United States from 1990 to 2013. While tuition regulations lower sticker prices during the regulation, colleges recoup losses through lowering institutional financial aid and more rapidly increasing tuition after the regulation has ended. Four-year colleges take advantage of the discrepancy between sticker price and net price - we estimate that regulations lower sticker price by 6.3 percentage points but at the same time lower institutional aid by nearly twice as much (11.3 percentage points). The gap widens over time: two years after the regulation has been lifted, sticker prices are 7.3 percentage points lower, and aid is 19.5 percentage points lower, than they would have been in the absence of the regulation. Two-year colleges rapidly increase tuition after the regulation - while there is a negative effect of 9.3 percentage points on sticker price during the cap/freeze, the negative effect disappears within three years of the end of the regulation. Net tuition discounts from caps and freezes vary widely across types of students; we find that while some students experience discount rates of up to 5.9 percentage points over four years in college, others must pay up to 3.8 percentage points more than they would have without the regulation. Students who receive financial aid, enter college right after the regulation is lifted, or attend colleges that are more dependent on tuition benefit less.

Methamphetamine (METH) abusers are prone to develop a variety of comorbidities, including cognitive disabilities, and the immunological responses have been recognized as an important component involved in the toxicity of this drug. Cytokines are among the key mediators between systemic inflammatory status and tissue responses. One of these, interleukin 1 (IL-1), has been hypothesized to be involved in cognitive functions and also appears to play a pivotal role among inflammatory molecules. In the present study, we demonstrate that exposure of mice to METH markedly increased the protein level of IL-1β in hippocampal tissue. Additionally, METH administration induced a decline in spatial learning as determined by the Morris water maze test. We next evaluated the hypothesis that blocking IL-1β signaling can protect against METH-induced loss of cognitive functioning. The results indicated that METH-induced impaired spatial learning abilities were attenuated by co-administration of mouse IL-1 Trap, a dimeric fusion protein that incorporates the extracellular domains of both of the IL-1 receptor components required for IL-1 signaling (IL-1 receptor type 1 and IL-1 receptor accessory protein), linked to the Fc portion of murine IgG2a. This effect was associated with a decrease in hippocampal IL-1β level. The current study indicates for the first time that the loss of METH-related cognitive decline can be attenuated by neutralizing IL-1 signaling. Our findings suggest a potential new therapeutic pathway for treatment of altered cognitive abilities that occur in METH abusing individuals.

Worldwide outbreaks of infectious diseases necessitate the development of rapid and accurate diagnostic methods. Colorimetric assays are a representative tool to simply identify the target molecules in specimens through color changes of an indicator (e.g., nanosized metallic particle, and dye molecules). The detection method is used to confirm the presence of biomarkers visually and measure absorbance of the colored compounds at a specific wavelength. In this study, we propose a colorimetric assay based on an extended form of double-stranded DNA (dsDNA) self-assembly shielded gold nanoparticles (AuNPs) under positive electrolyte (e.g., 0.1 M MgCl2) for detection of Middle East respiratory syndrome coronavirus (MERS-CoV). This platform is able to verify the existence of viral molecules through a localized surface plasmon resonance (LSPR) shift and color changes of AuNPs in the UV-vis wavelength range. We designed a pair of thiol-modified probes at either the 5' end or 3' end to organize complementary base pairs with upstream of the E protein gene (upE) and open reading frames (ORF) 1a on MERS-CoV. The dsDNA of the target and probes forms a disulfide-induced long self-assembled complex, which protects AuNPs from salt-induced aggregation and transition of optical properties. This colorimetric assay could discriminate down to 1 pmol/μL of 30 bp MERS-CoV and further be adapted for convenient on-site detection of other infectious diseases, especially in resource-limited settings.

Au and Pt are well-known catalysts for electrocatalytic oxidation of biomass-derived glycerol. Although some nonprecious-metal-based materials to replace the costly Au and Pt are used for this reaction, the fundamental question of how the nonprecious catalysts affect the reaction chemistry and mechanism compared to Au and Pt catalysts is still unanswered. In this work, both experimental and computational methods are used to understand how and why the reaction performance and chemistry for the electrocatalytic glycerol oxidation reaction (EGOR) change with electrochemically-synthesized CuCo-oxide, Cu-oxide, and Co-oxide catalysts compared to conventional Au and Pt catalysts. The Au and Pt catalysts generate major glyceric acid and glycolic acid products from the EGOR. Interestingly, the prepared Cu-based oxides produce glycolic acid and formic acid with high selectivity of about 90.0%. This different reaction chemistry is related to the enhanced ability of CC bond cleavage on the Cu-based oxide materials. The density functional theory calculations demonstrate that the formic acids are mainly formed on the Cu-based oxide surfaces rather than in the process of glycolic acid formation in the free energy diagram. This study provides critical scientific insights into developing future nonprecious-based materials for electrochemical biomass conversions.

Maintaining an intact pool of neural progenitor cells (NPCs) is crucial for generating new and functionally active neurons. Methamphetamine (METH) can exacerbate the HIV-induced deficit of adult neurogenesis; however, potential mechanisms of this influence are still poorly understood. In the present study, we present evidence that chronic exposure to METH combined with brain infection by EcoHIV results in enhanced proliferation of NPCs in the subventricular zone (SVZ) in mice. This effect was long-lasting as it was preserved ex vivo in NPCs isolated from the exposed mice over several passages in the absence of additional treatments. Increased proliferation in response to METH plus HIV was associated with dysregulation of cyclin B1 and cyclin D. Transcriptomic studies indicated that 27 out of the top 30 differentially expressed genes in response to METH plus EcoHIV were targets of the forkhead box O transcriptional factor (FOXO) and primarily FOXO3. Additional ex vivo studies and in vitro experiments using human NPCs exposed to METH and infected with HIV revealed upregulation of the CXCL12-CXCR4 axis, leading to activation of downstream pAkt and pErk, the pathways that can phosphorylate FOXO3 and force its exports from the nuclei into the cytoplasm. Indeed, nuclear expulsion of FOXO3 was demonstrated both in mice exposed to METH and infected with EcoHIV and in cell cultures of human NPCs. These results provide novel information that exposure to METH combined with HIV infection can induce aberrant proliferation of SVZ-derived NPCs and identifies CXCL12-CXCR4-Akt-1-mediated phosphorylation of FOXO3 as the mechanism responsible for this effect. Supplementary Information The online version contains supplementary material available at 10.1007/s12035-021-02407-9.

BackgroundMaintaining an intact pool of neural progenitor cells (NPCs) is crucial for generating new and functionally active neurons. As intrinsic and microenvironments tightly control developmental processes of adult neurogenesis, Methamphetamine (METH) and HIV-1-mediated impairment of the blood-brain barrier and development of neuroinflammation may induce alterations in functions of NPCs; however, the combined effects of METH and HIV-1 on the NPCs are still poorly understood.MethodsTo elucidate the possible mechanisms for the enhanced proliferation of NPCs by METH exposure and HIV infection, Male C57BL/6 mice were injected with METH with an escalating dose regimen for 6 days, followed by infusion with a chimeric HIV-NDK (EcoHIV) into the left internal carotid artery to infect brains. NPCs were isolated from the subventricular zone (SVZ) and used for RNA sequencing and differential expression analysis two weeks after infection. ReNcell VM, an immortalized human NPC line were used for in vitro exposure to METH and HIV infectionResultsChronic exposure to METH combined with brain infection by EcoHIV enhanced the proliferation of NPCs in the SVZ in mice. This effect was long-lasting as it was preserved ex vivo in NPCs isolated from the exposed mice over several passages in the absence of additional treatments. Transcriptomic studies indicated that 27 out of the top 30 differentially expressed genes response to METH plus EcoHIV were targets of the Forkhead box O transcriptional factor (FOXO), and primarily FOXO3. Additional ex vivo studies and in vitro experiments revealed the upregulation of the CXCL12-CXCR4 axis, leading to activation of downstream pAkt and pErk, the pathways that can phosphorylate FOXO3 and force its exports from the nuclei into the cytoplasm. Indeed, nuclear expulsion of FOXO3 was demonstrated both in mice exposed to METH and infected with EcoHIV and in cell culture of human NPCs.ConclusionsThese results provide novel information that exposure to METH combined with HIV infection can induce aberrant proliferation of SVZ-derived NPCs. Upregulation of CXCL12-CXCR4-Akt-1 signaling pathway exported FOXO3 into the cytoplasm, which changed the mRNA expression of FOXO3-target genes and induced the proliferation alteration as a result.

Sarcopenia is a common health issue that is not limited to only elderly patients. However, many studies have reported factors to prevent sarcopenia only in susceptible groups. This study evaluates the relationship of the total energy intake to basal metabolic rate ratio (EI/BMR) and physical activity (PA) with sarcopenia. A second aim was to analyze the interaction between EI/BMR and PA by sex and age. We analyzed 16,313 subjects aged ≥ 19 years who had dual‒energy X-ray absorptiometry data. Sarcopenia was defined as appendicular lean mass/weight (%) that was 1 standard deviation below the sex-specific mean value for a young reference group. Multivariate logistic regression analysis was used to examine the interaction between EI/BMR and PA. In this study, as EI/BMR increased, the risk of sarcopenia decreased, particularly in the older groups. Both high PA and high EI/BMR were independently related to the reduced risk of sarcopenia and showed additive effects on reducing the risk in young male and older groups. However, high PA was associated with an increased risk of sarcopenia in the young female group with low energy intake. Our findings suggest that an adequate balance between energy intake and PA is related to a low risk of sarcopenia, especially in young females.

The Tax Cuts and Jobs Act of 2017 established a new program called Opportunity Zones (OZs) that created tax advantages for investing in businesses or real estate in a limited number of low-income Census tracts. We use a census of establishment-level data on employment to identify the effect of the program on job creation. We show that in metropolitan areas, the OZ designation increased employment growth relative to comparable tracts by between 3.0 and 4.5 percentage points and new jobs were created across many different industries and education levels. The OZ designation did not create jobs in rural areas.

This paper evaluates the impact of a student-centered teaching pedagogy program by a local education authority on cooperative behaviors of 610 students in five middle schools. We measure changes of students’ cooperation with lab-in-the-field experiments, implemented before and after the program. Relying on a classroom-level fixed effect strategy, we show that the program has a positive effect on cooperation in a linear public goods experiment by way of remediating a negative time trend of contribution. Our findings support the idea that teaching practices stimulating interpersonal interaction affect the formation of cooperative norms among students.

HIV-infected brains are characterized by increased amyloid beta (Aβ) deposition. It is believed that the blood-brain barrier (BBB) is critical for Aβ homeostasis and contributes to Aβ accumulation in the brain. Extracellular vesicles (ECV), like exosomes, recently gained a lot of attention as potentially playing a significant role in Aβ pathology. In addition, HIV-1 hijacks the exosomal pathway for budding and release. Therefore, we investigated the involvement of BBB-derived ECV in the HIV-1-induced Aβ pathology in the brain. Our results indicate that HIV-1 increases ECV release from brain endothelial cells as well as elevates their Aβ cargo when compared to controls. Interestingly, brain endothelial cell-derived ECV transferred Aβ to astrocytes and pericytes. Infusion of brain endothelial ECV carrying fluorescent Aβ into the internal carotid artery of mice resulted in Aβ fluorescence associated with brain microvessels and in the brain parenchyma. These results suggest that ECV carrying Aβ can be successfully transferred across the BBB into the brain. Based on these observations, we conclude that HIV-1 facilitates the shedding of brain endothelial ECV carrying Aβ; a process that may increase Aβ exposure of cells of neurovascular unit, and contribute to amyloid deposition in HIV-infected brain.

To evaluate the association between alcohol intake and incident chronic kidney disease measures as well as the sex differences in this association, we analyzed health screening data of 14,190,878 adults who underwent health screening ≥3 times and had glomerular filtration rate (eGFR) ≥60 mL/min/1.73 m2 and normal proteinuria at baseline. eGFR was calculated with the Chronic Kidney Disease Epidemiology Collaboration equation. Proteinuria was defined as ≥1+ dipstick proteinuria and low eGFR as

Background: Although guidelines recommend regular glycated hemoglobin (HbA1c) testing every 6 months for type 2 diabetes patients, whether adherence to these guidelines leads to improved health outcomes is unclear. We aimed to determine the association of HbA1c testing intervals on stroke and cardiovascular disease (CVD) risk among newly diagnosed type 2 diabetes patients. Methods: The study population consisted of 31,041 newly diagnosed type 2 diabetes patients during 2003-2011 from the Korean National Health Insurance Service. Average HbA1c testing interval was calculated during 3 years after type 2 diabetes diagnosis. Participants were categorized into average HbA1c testing intervals of ≤6, >6 to ≤12, >12 to ≤18, and >18 months, after which they were followed-up for stroke and CVD until 2015. Adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs) were determined by Cox proportional hazards regression for the risk of stroke and CVD according to HbA1c testing interval. Results: Compared to patients with HbA1c testing intervals of ≤6 months, patients with >6 to ≤12 (aHR 1.40, 95% CI 1.10-1.78), >12 to ≤18 (aHR 1.43, 95% CI 1.12-1.84), and >18 (aHR 1.64, 95% CI 1.32-2.04) month intervals had elevated risk for stroke ( p trend 12 to ≤18 (aHR 1.28, 95% CI 1.10-1.50), and >18 (aHR 1.38, 95% CI 1.21-1.58) month intervals had increased risk for CVD ( p trend 3 to ≤6 months on stroke and CVD risk. The risk-increasing effect of stroke and CVD by longer HbA1c testing intervals was preserved among subgroups divided by fasting serum glucose, initial diabetes medication, outpatient department visits, and Charlson comorbidity index. Conclusions: HbA1c testing interval of more than 6 months was associated with increased risk of stroke and CVD among newly diagnosed type 2 diabetes patients. Type 2 diabetes patients who undergo biannual HbA1c testing may benefit from reduced stroke and CVD risk.