Validation of the ANDON KD-595 automated upper-arm blood pressure monitor according to the universal standard.

OBJECTIVE: To validate the ANDON KD-595 automated upper-arm blood pressure monitor for clinical use and self-measurement blood pressure measurement according to the Association for the Advancement of Medical Instrumentation/European Society of Hypertension/International Organization for Standardization (AAMI/ESH/ISO) Universal Standard. METHODS: Same left-arm blood pressure was sequentially measured in 90 qualified adult participants and compared with a standard mercury sphygmomanometer. A total of 270 comparison pairs were obtained and analyzed according to the universal standard. RESULTS: For the validation Criterion 1 of the universal standard, the mean ± SD of the differences between the test device and reference blood pressure readings was 0.96 ±â€…5.35 and 0.82 ±â€…5.08 mmHg for SBP and DBP, respectively. For Criterion 2, the SDs of the averaged blood pressure differences between the test device and reference blood pressure per subject were 4.84 and 4.64 mmHg (with maximum allowed SDs of 6.87 and 6.89 mmHg) for SBP and DBP, respectively. CONCLUSION: The ANDON KD-595 automated upper-arm blood pressure monitor passed all the validation requirements according to the AAMI/ESH/ISO Universal Standard and can be recommended for clinical use and self-measurement blood pressure measurement in the general population.

Validation of the Wellvii VitalDetect blood pressure monitor in general population according to the International Standardization Organization 81060-2:2018.

OBJECTIVE: To evaluate the accuracy of the Wellvii VitalDetect automated oscillometric finger blood pressure monitor (single cuff size) for self/home blood pressure measurement according to the AAMI/ESH/ISO Universal Standard (ISO 81060-2:2018). METHODS: According to the universal standard, a total of 92 participants were recruited and finally blood pressure of 85 eligible participants was sequentially measured and compared with a standard mercury sphygmomanometer. RESULTS: A total of 255 comparison pairs were obtained and analyzed based on the universal standard. For the validation criterion 1 of the ISO 81060-2:2018 universal standard, the mean ± SD of the differences between the test device and reference blood pressure readings was 1.66 ±â€…7.67 and 1.04 ±â€…6.45 mmHg for systolic and diastolic blood pressure, respectively. For criterion 2, the SD of the averaged blood pressure differences between the test device and reference blood pressure per subject was ± 6.49 mmHg (pass ≤ 6.73 mmHg) and ± 5.67 mmHg (pass ≤ 6.86 mmHg) for systolic and diastolic blood pressure, respectively. CONCLUSION: The Wellvii VitalDetect automated finger blood pressure monitor passed all the requirements for validation by the ISO 81060-2:2018 universal standard and can be recommended for self/home blood pressure measurement in general population.

Role of microglial metabolic reprogramming in Parkinson's disease.

Parkinson's disease (PD) is a common age-related neurodegenerative disorder characterized by damage to nigrostriatal dopaminergic neurons. Key pathogenic mechanisms underlying PD include alpha-synuclein misfolding and aggregation, impaired protein clearance, mitochondrial dysfunction, oxidative stress, and neuroinflammation. However, to date, no study has confirmed the specific pathogenesis of PD. Similarly, current PD treatment methods still have shortcomings. Although some emerging therapies have proved effective for PD, the specific mechanism still needs further clarification. Metabolic reprogramming, a term first proposed by Warburg, is applied to the metabolic energy characteristics of tumor cells. Microglia have similar metabolic characteristics. Pro-inflammatory M1 type and anti-inflammatory M2 type are the two types of activated microglia, which exhibit different metabolic patterns in glucose, lipid, amino acid, and iron metabolism. Additionally, mitochondrial dysfunction may be involved in microglial metabolic reprogramming by activating various signaling mechanisms. Functional changes in microglia resulting from metabolic reprogramming can cause changes in the brain microenvironment, thus playing an important role in neuroinflammation or tissue repair. The involvement of microglial metabolic reprogramming in PD pathogenesis has been confirmed. Neuroinflammation and dopaminergic neuronal death can effectively be reduced by inhibiting certain metabolic pathways in M1 microglia or reverting M1 cells to the M2 phenotype. This review summarizes the relationship between microglial metabolic reprogramming and PD and provides strategies for PD treatment.

Recent research progress on metabolic syndrome and risk of Parkinson's disease.

Parkinson's disease (PD) is one of the most widespread neurodegenerative diseases. PD is associated with progressive loss of substantia nigra dopaminergic neurons, including various motor symptoms (e.g., bradykinesia, rigidity, and resting tremor), as well as non-motor symptoms (e.g., cognitive impairment, constipation, fatigue, sleep disturbance, and depression). PD involves multiple biological processes, including mitochondrial or lysosomal dysfunction, oxidative stress, insulin resistance, and neuroinflammation. Metabolic syndrome (MetS), a collection of numerous connected cerebral cardiovascular conditions, is a common and growing public health problem associated with many chronic diseases worldwide. MetS components include central/abdominal obesity, systemic hypertension, diabetes, and atherogenic dyslipidemia. MetS and PD share multiple pathophysiological processes, including insulin resistance, oxidative stress, and chronic inflammation. In recent years, MetS has been linked to an increased risk of PD, according to studies; however, the specific mechanism remains unclear. Researchers also found that some related metabolic therapies are potential therapeutic strategies to prevent and improve PD. This article reviews the epidemiological relationship between components of MetS and the risk of PD and discusses the potentially relevant mechanisms and recent progress of MetS as a risk factor for PD. Furthermore, we conclude that MetS-related therapies are beneficial for the prevention and treatment of PD.

Angiopoietin-like protein 8 deficiency attenuates thoracic aortic aneurysm/dissection development in ß-aminopropionitrile monofumarate-induced model mice.

Thoracic aortic aneurysm/dissection (TAAD) is a life-threatening cardiovascular disorder. Endoplasmic reticulum stress (ERS) and vascular smooth muscle cell (VSMC) apoptosis are involved in TAAD progression. The Protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) pathway is associated with VSMC apoptosis. Serum Angiopoietin-Like Protein 8 (ANGPTL8) levels are associated with aortic diameter and rupture rate of TAAD. However, a direct role of ANGPTL8 in TAAD has not been determined. ß-Aminopropionitrile monofumarate (BAPN) was used to induce TAAD in C57BL/6 mice. ANGPTL8 knockout mice were used to detect the effects of ANGPTL8 on TAAD development. ANGPTL8knockdown in vitro was used to analyze the role of ANGPTL8 in VSMCs and ERS. In addition, over-expression of ANGPTL8 in VSMCs and a PERK inhibitor were used to assess the effect of ANGPTL8 on the PERK pathway. ANGPTL8 levels were increased in the aortic wall and VSMCs of BAPN-induced TAAD mice. Compared with BAPN-treated wild-type mice, ANGPTL8 knockout significantly reduced the rupture rate of TAAD to 0 %. In addition, the protein levels of proinflammatory cytokines and matrix metalloproteinase 9 (MMP9) and ERS proteins were decreased in the aorta wall. Angptl8 shRNA decreased MMP9 and ERS protein levels in VSMCs in vitro. Overexpression of ANGPTL8 significantly increased the levels of ERS proteins and MMPs, while a PERK inhibitor significantly decreased the effects of ANGPTL8 in VSMCs. ANGPTL8 contributed to TAAD development by inducing ERS activation and degradation of extracellular matrix in the aorta wall. Inhibition of ANGPTL8 may therefore represent a new strategy for TAAD therapy.

Update on the application of mesenchymal stem cell-derived exosomes in the treatment of Parkinson's disease: A systematic review.

Parkinson's disease (PD) has become the second largest neurodegenerative disease after Alzheimer's disease, and its incidence is increasing year by year. Traditional dopamine replacement therapy and deep brain stimulation can only alleviate the clinical symptoms of patients with PD but cannot cure the disease. In recent years, stem cell therapy has been used to treat neurodegenerative diseases. Many studies have shown that stem cell transplantation has a therapeutic effect on PD. Here, we review recent studies indicating that exosomes derived from mesenchymal stem cells also have the potential to treat PD in animal models, but the exact mechanism remains unclear. This article reviews the mechanisms through which exosomes are involved in intercellular information exchange, promote neuroprotection and freely cross the blood-brain barrier in the treatment of PD. The increase in the incidence of PD and the decline in the quality of life of patients with advanced PD have placed a heavy burden on patients, families and society. Therefore, innovative therapies for PD are urgently needed. Herein, we discuss the mechanisms underlying the effects of exosomes in PD, to provide new insights into the treatment of PD. The main purpose of this article is to explore the therapeutic potential of exosomes derived from mesenchymal stem cells and future research directions for this degenerative disease.

Validation of the KANG KC-2850 oscillometric upper-arm ambulatory blood pressure monitor in general population according to the Association for the Advancement of Medical Instrumentation/European Society of Hypertension/International Organization for Standardization universal standard.

OBJECTIVE: To evaluate the accuracy of the KANG KC-2850 ambulatory blood pressure monitor (ABPM) for clinical blood pressure (BP) measurement according to the Association for the Advancement of Medical Instrumentation/European Society of Hypertension/International Organization for Standardization (AAMI/ESH/ISO) universal standard (ISO 81060-2:2018). METHODS: BP was sequentially measured and compared with a standard mercury sphygmomanometer in 85 eligible participants. A standard adult cuff (22-3232 cm) was used for test device measurements. A total of 255 comparison pairs were obtained and analyzed according to the Association for the Advancement of Medical Instrumentation/European Society of Hypertension/International Organization for Standardization (AAMI/ESH/ISO universal standard. RESULTS: The standard requirements were followed precisely. For the validation Criterion 1, the mean ± SD of the differences between the test device and reference BP readings was -1.12 ± 5.01 and -0.33 ± 4.52 mmHg for SBP and DBP, respectively. For Criterion 2, the SD of the averaged BP differences between the test device and reference BP per subject was 3.59 and 3.60 mmHg for SBP and DBP, respectively. CONCLUSION: The KANG KC-2850 ABPM met all the requirements for validation by the AAMI/ESH/ISO universal standard and can be recommended for clinical use in general population.

Validation of the G.LAB MD41A0 upper arm blood pressure monitor in patients with diabetes mellitus according to the AAMI/ESH/ISO 81060-2:2018 Universal Standard.

OBJECTIVE: The objective of this study is to determine the accuracy of the G.LAB MD41A0 upper-arm oscillometric blood pressure (BP) monitor for self/home BP measurement in patients with diabetes according to the Association for the Advancement of Medical Instrumentation /European Society of Hypertension /International Organization for Standardization (AAMI/ESH/ISO) Universal Standard (ISO 81060-2:2018). METHODS: Patients with diabetes were recruited according to AAMI/ESH/ISO Universal Standard using the same arm sequential BP measurement method. The standard cuff of the test device was used for arm circumference 22-44 cm. RESULTS: A total of 92 patients with diabetes were recruited and 85 were analyzed with an average age of 55.1 ± 17.7 years, 48 men, and arm circumference of 32.0 ± 6.0 cm. For the validation Criterion 1, the mean ± SD of the differences between the test device and reference BP readings was 0.89 ± 6.04/-0.84 ± 5.11 mmHg (systolic/diastolic). For Criterion 2, the SD of the averaged BP differences between the test device and reference BP per subject was 4.23/4.19 mmHg (systolic/diastolic). CONCLUSION: The G.LAB MD41A0 upper arm BP monitor fulfilled all the requirements of the AAMI/ESH/ISO Universal Standard (ISO 81060-2:2018) in patients with diabetes and can be recommended for self/home use.

Laryngeal Squamous Cell Carcinoma: Clinical Significance and Potential Mechanism of Cell Division Cycle 45.

Background: Cell division cycle 45 (CDC45) plays an important role in the occurrence and development of numerous carcinomas, but its effect in laryngeal squamous cell carcinoma (LSCC) remains unclear. Materials and Methods: The messenger RNA and protein expression levels of CDC45 in LSCC were evaluated with a t test and the standard mean difference (SMD). The ability of CDC45 expression to distinguish the LSCC was assessed through receiver operating characteristic (ROC) curves. Gene set enrichment analysis (GSEA), protein-protein interaction, public databases, and online tools were used to explore the potential molecular mechanism of CDC45 in LSCC. Results: A high expression of CDC45 was identified in LSCC (SMD = 2.61, 95% confidence interval [1.62-3.61]). Through ROC curves, the expression of CDC45 makes it feasible to distinguish the LSCC group from the non-LSCC counterpart. CDC45 was relevant to the progression-free interval of LSCC patients (log-rank p = 0.03). GSEAs show that CDC45 is related to the cell cycle. CDC45, CDC6, KIF2C, and AURKB were identified as hub genes of LSCC. E2F1 may be the regulatory transcription factor of CDC45. Conclusions: High expression of CDC45 likely demonstrates carcinogenic effects in LSCC, and CDC45 is a potential target in screening and treatment of LSCC.

Controlled Synthesis, Mechanism and Degradation Property of Birnessite-MnO2 Nanoflowers and Nanoflakes.

Birnessite-MnO2 nanoflakes were synthesized via an aqueous oxidation method at 90 °C using Mn(CH3COO)2, NaOH, and KMnO4. The samples' morphology, crystalline structure, and optical property were determined by field emission scanning electron microscopy, X-ray powder diffraction and UV-Vis spectrophotometry. The birnessite-MnO2 nanoflakes were converted to KxMn8O16 and Mn suboxides following a decrease in the concentration of KMnO4 in the reaction. The amount of NaOH in the reaction determined the type of precursor. Without NaOH, the precursor was converted from Mn(OH)2 to Mn2+ (from Mn(CH3COO)2), thereby enabling the synthesis of birnessite-MnO2 nanoflowers. The formation mechanism of birnessite-MnO2 nanoflowers and nanoflakes was clarified via the corresponding simulated crystal structures. Evaluation of the synthesized samples confirmed that the birnessite-MnO2 nanoflakes and nanoflowers exhibited excellent degradation properties.

Angiopoietin-like proteins 8 knockout reduces intermittent hypoxia-induced vascular remodeling in a murine model of obstructive sleep apnea.

OBJECTIVE: Obstructive sleep apnea (OSA) is a major risk factor for cardiovascular mortality. Apnea-induced chronic intermittent hypoxia (CIH) is a primary pathophysiological manifestation of OSA that promotes various cardiovascular alterations, such as aortic vascular remodeling. In this study, we investigated the association between angiopoietin-like proteins 8 (ANGPTL8) and CIH-induced aortic vascular remodeling in mice. METHODS: C57BL/6J male mice were divided into four groups: Normoxia group, ANGPTL8-/- group, CIH group, CIH + ANGPTL8-/- group. Mice in the normoxia group and ANGPTL8-/- group received no treatment, while mice in the CIH and CIH + ANGPTL8-/- group were subjected to CIH (21%-5% O2, 180 s/cycle, 10 h/day) for 6 weeks. At the end of the experiments, intima-media thickness (IMT), elastin disorganization, and aortic wall collagen abundance were assessed in vivo. Immunohistochemistry and Western-blot were used to detect endoplasmic reticulum stress (ERS) and aortic vascular smooth muscle cell proliferation. ANGPTL8 shRNA and ANGPL8 overexpression were used in aortic vascular smooth muscle cells to investigate the mechanism of ANGPTL8 in CIH. RESULTS: Compared to the control group, CIH exposure significantly increased intima-media thickness (IMT), elastic fibers disorganization, and aortic wall collagen abundance. CIH also significantly increased blood pressure, induced hyperlipidemia, as well as the expression of ERS protein activating transcription factor-6 (ATF6) and aortic vascular smooth muscle cell proliferation. Contrary, ANGPTL8-/- significantly mitigated the CIH-induced vascular remodeling; ANGPTL8-/- decreased CIH-induced hypertension and hyperlipidemia, inhibited the protein expression of ATF6, and aortic vascular smooth muscle cell proliferation. Moreover, our in vitro study suggested that CIH could induce ANGPTL8 expression via hypoxia-inducible factor (HIF-1α); ANGPTL8 induced proliferation of aortic vascular smooth muscle cells via the ERS pathway. CONCLUSION: ANGPTL8-/- can prevent CIH-induced aortic vascular remodeling, probably through the inhibition of the ERS pathway. Therefore, ANGPTL8 might be a potential target in CIH-induced aortic vascular remodeling.

Associations between insecurity and stress among Chinese university students: The mediating effects of hope and self-efficacy.

BACKGROUND: In the context of the pandemic, exploration on the association between insecurity and stress among university students is limited. The current study aims to investigate the parallel mediation role of hope and self-efficacy in the relationship between insecurity and stress among university students during the COVID-19 pandemic. METHODS: We employed a cross-sectional research design in a university by distributing questionnaires online. 5286 participants were recruited (mean age = 19.65; SD = 1.13). Items were from the Security Questionnaire, Depression Anxiety and Stress Scale-21, and the Positive Psychology Capital (Psycap) Questionnaire (PPQ). Parallel mediation analysis was performed using PROCESS macro in SPSS. RESULTS: The results indicate that insecurity predicted students' stress positively and that students with high-level perceived insecurity are more likely to perceive stress. Moreover, hope and self-efficacy mediated the relationship between insecurity and stress, indicating that hope and self-efficacy could buffer the negative effects of insecurity on stress. LIMITATIONS: This study examines the mediating model between insecurity and stress among Chinese university students. The generalizability of the findings in other regions remains to be explored. Additionally, the roles of other positive self-beliefs including optimism and resilience in relieving stress can be further explored in future research. CONCLUSIONS: This research provides direct evidence of insecurity effects on stress among university students, enriching relevant theories in the field of stress. Moreover, this research suggests that enhancing positive self-beliefs such as hope, and self-efficacy helps to relieve students' stress during COVID-19.

Intermittent Hypoxia Alleviates ß-Aminopropionitrile Monofumarate Induced Thoracic Aortic Dissection in C57BL/6 Mice.

OBJECTIVE: Thoracic aortic dissection (TAD) has a high mortality rate. Intermittent hypoxia (IH) triggers both harmful and beneficial effects in numerous physiological systems. The effects of IH on TAD development were explored in a mouse model. METHODS: ß-Aminopropionitrile monofumarate (BAPN) was used to induce TAD in C57BL/6 mice. Three week old male mice were treated with 1 g/kg/day BAPN in drinking water for four weeks and simultaneously subjected to IH (n = 30) (21%-5% O2, 90 s/cycle, 10 h/day, IH + BAPN group) or normoxia (n = 30) (21% O2, 24 h/day, BAPN group). Human VSMCs (HUASMCs) exposed to IH (30 min, 5% O2)/re-oxygenation (30 min, 21% O2) cycles with a maximum of 60 min/cycle to detect the effect of IH on HIF-1α and LOX via HIF-1α-siRNA. RESULTS: It was found that BAPN administration significantly increased the lumen size and wall thickness of aortas compared with the normal group, but was significantly reversed by IH exposure. Additionally, IH exposure significantly increased the survival rate of BAPN induced TAD (70% vs. 40%). Furthermore, IH exposure reduced BAPN induced elastin breaks and apoptosis of vascular smooth muscle cells. IH exposure also reversed BAPN induced upregulation of inflammation and extracellular matrix (ECM) degradation. Real time polymerase chain reaction (RT-PCR) confirmed that IH inhibited inflammation and ECM degradation related genes interleukin (IL)-1ß, IL-6, cathepsin S (Cat S), and matrix metalloproteinase 9 (MMP-9), but upregulated the ECM synthesis related genes lysyl oxidase (LOX) and collagen type I alpha2 (Col1a2) compared with the BAPN group. In vitro results suggest that IH promotes the expression of LOX via HIF-1α. CONCLUSION: The results suggest that IH alleviates BAPN induced TAD in C57BL/6 mice.

Effects of continuous positive airway pressure on cardiovascular biomarkers in patients with obstructive sleep apnea: a meta-analysis of randomized controlled trials.

PURPOSE: Obstructive sleep apnea (OSA) is associated with increased levels of systemic inflammatory markers, increased arterial stiffness, and endothelial dysfunction, which may lead to increased cardiovascular risk. We aimed to quantify the effects of continuous positive airway pressure (CPAP) on cardiovascular biomarkers and to establish predictors of response to CPAP. METHODS: We searched PubMed and the Cochrane Library from inception to May 31, 2017. Randomized controlled trials (RCTs) assessing the efficacy of CPAP on high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), tumor necrosis factor- alpha (TNF-α), augmentation index (AIx), pulse wave velocity (PWV), and flow-mediated dilatation (FMD) in patients with OSA were selected by consensus. RESULTS: We included 15 RCTs comprising 1090 patients in the meta-analysis. The pooled standard mean difference (SMD) of effect of CPAP on hs-CRP was - 0.64 (95% confidence interval (CI) - 1.19 to - 0.09; P = 0.02). CPAP was associated with a reduction in AIx of 1.53% (95% CI, 0.80 to 2.26%; P < 0.001) and a significant increase in FMD of 3.96% (95% CI 1.34 to 6.59%; P = 0.003). Subgroup analyses found CPAP was likely to be more effective in improving FMD levels in severe OSA patients or patients with effective CPAP use ≥ 4 h/night. CONCLUSIONS: Among patients with OSA, CPAP improves inflammatory marker hs-CRP, arterial stiffness marker AIx, and endothelial function marker FMD. These biomarkers may provide information related to response to treatment. Future studies will need to clarify the efficacy of these biomarkers in assessing cardiovascular risk reduction among OSA treated with CPAP.

[Effects of thyroid hormone on macrophage dysfunction induced by oxidized low-density lipoprotein].

It has been recognized that patients with hypothyroidism have higher risks of atherosclerosis and coronary heart disease, however, the mechanisms are largely unknown. Considering that macrophage dysfunction plays an important role in the formation and development of atherosclerosis plaques, this study aimed to investigate the direct effects of thyroid hormone on macrophage functions and to provide new insight for the mechanism of hypothyroid atherosclerosis. RAW264.7 cells (mouse leukaemic monocyte macrophage cell line) were incubated with oxidized low-density lipoprotein (oxLDL) to establish macrophage foam cells model in vitro, and the protective effects of different concentration of thyroxine (T4) on the macrophage foam cells function were explored. The proliferation, migration and cell aging of macrophages were detected by MTT method, scratch test and ß-galactosidase staining respectively. The ELISA method was used to detect the secretion of tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and interleukin-1ß (IL-1ß). Western blot analysis was applied to measure the phosphorylation of focal adhesion kinase (FAK), which was required for the process of proliferation and migration of macrophages. The results showed that oxLDL significantly inhibited the macrophage proliferation and migration, induced cell senescence, and promoted the secretion of TNF-α, MCP-1, and IL-1ß; while T4 reversed those effects of oxLDL on macrophage in a concentration-dependent manner. Moreover, oxLDL increased the phosphorylation of FAK in macrophage, while T4 concentration-dependently reversed the effect. These results suggest that T4 modulates macrophage proliferation, migration, senescence, and secretion of inflammation factors in a concentration-dependent way.

One-pot synthesis and characterization CdTe:Zn2+ quantum dots and its molecular interaction with calf thymus DNA.

Tremendous research efforts have been dedicated to fabricating high-quality Zn-doped CdTe quantum dots (QDs) for any potential biomedical applications. In particular, the correlation of issues regarding how QDs interact with DNA is of greatest importance. Herein, a pH-responsive study of the interactions between CdTe:Zn2+ quantum dots with 4 different sizes and calf thymus DNA (ctDNA) was conducted using multispectroscopic techniques and electrochemical investigation. Fluorescence studies revealed that this interaction process is predominantly a static process and groove binding was the main binding mode for CdTe:Zn2+ QDs to ctDNA. The calculated negative values of enthalpy (-45.06 kJ mol-1 ) and entropy (-133.62 J mol-1  K-1 ) with temperature changes indicated that the hydrogen bonds and van der Waals interactions played major roles in the reaction. Furthermore, circular dichroism spectroscopy and Fourier transform infrared spectrometry analyses indicate that the normal conformation of ctDNA is discombobulated by CdTe:Zn2+ QDs. In addition, the electrochemical behavior of the affinity of CdTe:Zn2+ QDs for ctDNA agreed well with the results obtained from fluorescence experiments. This study might be meaningful for understanding the molecular binding mechanism of QDs for DNA and provides a basis for QD-labeled systems.

Validation of the Grandway MD2301 digital automatic blood pressure monitor according to the European Society of Hypertension International Protocol.

OBJECTIVE: The aim of the present study was to validate the Grandway MD2301 digital automatic blood pressure monitor according to the European Society of Hypertension International Protocol (ESH-IP) revision 2010. METHODS: The ESH-IP revision 2010 for the validation of blood pressure-measuring devices in adults was followed precisely. Systolic and diastolic blood pressure (SBP and DBP, respectively) were measured sequentially in 33 adult patients and compared with a standard mercury sphygmomanometer (two observers). A total of 99 comparison pairs were obtained. RESULTS: The device produced 78, 95 and 99 measurements within 5, 10, and 15 mmHg for SBP and 83, 96, and 99 for DBP, respectively. The average device-observer difference was -1.81±4.22 mmHg for SBP and -0.15±3.93 mmHg for DBP. All of the data were within the standards requirements to pass the testing. CONCLUSION: The Grandway MD2301 digital automatic blood pressure monitor meets the standards of the ESH-IP revision 2010 and can be recommended for self/home measurement in the general population.

A refined-JinQi-JiangTang tablet ameliorates prediabetes by reducing insulin resistance and improving beta cell function in mice.

ETHNOPHARMACOLOGICAL RELEVANCE: Refined-JQ (JQ-R) is a mixture of refined extracts from three major herbal components of JinQi-JiangTang tablet: Coptis chinensis (Ranunculaceae), Astragalus membranaceus (Leguminosae), and Lonicera japonica (Caprifoliaceae). Our previous studies have indicated that JQ-R could decrease fasting blood glucose levels in diabetic mice and insulin resistance mice. Investigating the hypoglycemic effect of JQ-R on prediabetes has practical application value for preventing or delaying insulin resistance, impaired glucose tolerance and possibly the development of clinical diabetes. MATERIALS AND METHODS: The anti-diabetic potential of JQ-R was investigated using a high fat-diet (HFD)-induced obesity mouse model. C57BL/6J mice (HFD-C57 mice) were fed with high-fat diet for 4 months. HFD-C57 mice were treated with either JQ-R (administered intragastrically once daily for 4 weeks) or metformin (as positive control), and the effects of JQ-R on body weight, blood lipids, glucose metabolism, insulin sensitivity, and beta cell function were monitored. RESULTS: The body weight, serum cholesterol, and the Homeostasis Model Assessment ratio (insulin resistance index) were significantly reduced in JQ-R or metformin-treated mice, and the glucose tolerance was enhanced and insulin response was improved simultaneously. Moreover, both JQ-R and metformin could activate liver glycogen syntheses even under a relatively high glucose loading. Although glyconeogenesis was inhibited in the metformin treated mice, it was not observed in JQ-R treated mice. Similar to metformin, JQ-R could also improve the glucose infusion rate (GIR) in hyperglycemic clamp test. JQ-R was also shown to increase the levels of phosphorylated AMPKα and phosphorylated acetyl CoA carboxylase (ACC), similar to metformin. CONCLUSION: JQ-R could reduce HFD-induced insulin resistance by regulating glucose and lipid metabolism, increasing insulin sensitivity through activating the AMPK signaling pathway, and subsequently improving ß cell function. Therefore, JQ-R may offer an alternative in treating disorders associated with insulin resistance, such as prediabetes and T2DM.

Long-term treatment with EXf, a peptide analog of Exendin-4, improves ß-cell function and survival in diabetic KKAy mice.

EXf is a C-terminally truncated fragment of Exendin-4 with two amino acid substitutions. Previous studies showed that EXf controls plasma glucose level acting as a glucagon-like peptide 1 (GLP-1) receptor agonist. The purpose of this study was to evaluate the effects of EXf on ß-cell function and survival in diabetic KKAy mice. EXf treatment significantly improved the glucose intolerance and reduced non-fasting and fasting plasma glucose levels, as well as plasma triglyceride levels in diabetic KKAy mice. In hyperglycemic clamp test, EXf-treated mice displayed an increased glucose infusion rate and first-phase insulin secretion. Treatment with EXf also led to a significant restoration of islet morphology, an increase in Ki67 expression in ß-cells, and a reduction in the number of TUNEL positive ß-cells. In the pancreas, comparative transcription analysis showed up-regulation of Akt1. The up-regulation of phosphorylated Akt1 was confirmed by Western blot, and changes in the protein levels of members of the Akt1 pathway, such as PI3K, Bim, Bcl-2, Bax, Caspase-3, and Caspase-9, PDX-1, were observed as well. Therefore, EXf treatment could improve ß-cell function and survival in diabetic KKAy mice, likely as a result of islet morphology restoration, stimulation of ß-cell proliferation, and inhibition of ß-cell apoptosis.

Long-term fenofibrate treatment impaired glucose-stimulated insulin secretion and up-regulated pancreatic NF-kappa B and iNOS expression in monosodium glutamate-induced obese rats: is that a latent disadvantage?

BACKGROUND: Fenofibrate, a PPAR alpha agonist, has been widely used in clinics as lipid-regulating agent. PPAR alpha is known to be expressed in many organs including pancreatic beta cells and regulate genes involved in fatty acid metabolism. Some reports based on cell lines or animals have provided evidences that PPAR alpha agonists may affect (increased or suppressed) beta cell insulin secretion, and several studies are producing interesting but still debated results. METHODS: In this research, we investigated the long term effects of fenofibrate on beta cell function in a metabolic syndrome animal model, monosodium glutamate (MSG) induced obese rats. Obese MSG rats were administered by gavage with fenofibrate at a dose of 100 mg/kg for 12 weeks. Oral glucose tolerance and insulin tolerance tests were performed to evaluate glucose metabolism and insulin sensitivity. We have used the hyperglycemic clamp technique to evaluate the capacity of beta cell insulin secretion. This technique provides an unbiased approach to understand the beta cell function in vivo. The changes of gene and protein expression in the pancreas and islets were also analyzed by Real-Time-PCR, Western blot and immunostaining. RESULTS: Fenofibrate reduced the plasma lipid levels within a few days, and showed no beneficial effects on glucose homeostasis or insulin sensitivity in obese MSG rats. But the animals treated with fenofibrate exhibited significantly decreased fasting plasma insulin and impaired insulin secretory response to glucose stimulation. Further studies confirmed that fenofibrate increased MDA level and decreased total ATPase activity in pancreatic mitochondrion, accompanied by the upregulation of iNOS and NF-kappa B and TNF alpha expression in pancreatic islets of obese MSG rats. CONCLUSIONS: Long-term fenofibrate treatment disrupted beta cell function, and impaired glucose-stimulated insulin secretion in obese MSG rats, perhaps to some extent associated with the activated inflammatory pathway and increased formation of oxidative products, especially the up-regulation of NF-kappa B and iNOS expression in islets.