Method for real-time prediction of cutter wear during shield tunnelling: A new wear rate index and MCNN-GRU.

Cutter wear is one of the key factors influencing construction efficiency during shield tunnelling. Prediction of cutter wear can improve construction efficiency by reducing the times of cutter inspections in engineering practice. Evaluation of cutter life is vital for cutter wear prediction, however, existing cutter life indices can only estimate the health condition of all cutters on cutterhead on a holistic basis. A new index was proposed to evaluate cutter wear located at a specific installation position on cutterhead. A deep learning model integrating the index was developed for the estimation of accumulated cutter wear during real time shield tunnelling. The new index can be obtained by monitored field parameters and can predict cutter wear with historical wear patterns. The input and output data samples were reshaped for multi-step prediction. A shield tunnelling section in Guangzhou weathered granite was used for validation. The proposed method can help reduce the cost of cutter replacement by reducing the times of machine interventions. The method article is a companion paper to the original article [1].•Proposed index for prediction of cutter wear rate.•Deep learning model of 1D-CNN and GRU.•Multi-step cutter wear prediction.

Evaluation of environmental impact of red tide around Pearl River Estuary, Guangdong, China.

This paper presents a case study of red tide hazards around the Pearl River Estuary (PRE). Red tide hazards, meteorological data, and seawater monitoring data were collected from 1996 to 2020 at different locations around the PRE to investigate the internal and external factors influencing the occurrence of red tides. The enhancement of the assessment of estuarine trophic status (ASSETS) method enables us to evaluate the effects of meteorological factors and seawater eutrophication status on the red tide risk level. Using ASSETS, we established a framework for red tide risk assessment of the Pearl River Estuary. We analysed the external and internal factors causing the red tide based on meteorological data and seawater monitoring data in the PRE. The results show that the temperature was higher than the annual monthly average temperature of 1.265 °C, and east and north winds at velocities of 3-4 m/s could result in the formation of red tides. However, precipitation inhibits the formation of the red tide in PRE.

Doxazosin attenuates renal matrix remodeling mediated by anti-α1-adrenergic receptor antibody in a rat model of diabetes mellitus.

Diabetic nephropathy is a major complication of diabetes mellitus (DM). Recent studies suggest that immunological mechanisms have a key role in the pathogenesis of DM, therefore these mechanisms may be important targets for diabetes therapy. The present study evaluated the effects of anti-α1-adrenergic receptor antibody (α1-R Ab) mediation and doxazosin treatment in a rat model of DM. It was observed that levels of 24-h urinary protein, serum creatinine and transforming growth factor-ß1 in DM were significantly increased after α1-R Ab mediation (all P<0.05). In addition, electron microscopy identified severe damage in the renal tissue microstructures of DM rats following α1-R Ab mediation, while only mild abnormalities were observed in that of healthy rats mediated with α1-R Ab and of untreated DM rats. No marked abnormalities were observed in the renal tissue of healthy blank controls. Furthermore, in DM rats treated with α1-R Ab mediation + doxazosin intervention, the expression of TGF-ß1 significantly decreased, and renal functions and renal matrix remodeling were significantly improved, relative to untreated DM controls (P<0.01). These results suggest that α1-R Ab may be involved in renal matrix remodeling during DM, and that kidney protection during DM may be achieved through treatment with corresponding receptor antagonists.

[Regulatory effect of liraglutide on the expression of eNOS in the corpus cavernosum of diabetic rats].

UNLABELLED: OCTOBER: To explore the effects of the glucagon-like peptide 1 (GLP-1) liraglutide on the penile erectile function of rats with diabetic erectile dysfunction (DED) by observing the impact of liraglutide on the expression of eNOS in the corpus cavernosum of diabetic rats. METHODS: We randomly divided 30 six-week-old male SD rats into a normal control (n = 10) and an experimental group (n = 20) , established models of diabetes mellitus (DM) in the experimental rats, and subdivided them into a DM (n = 8) and a GLP-1 group (n = 8) to receive intramuscular injection of normal saline and liraglutide at 5 mg per kg of the body weight per day, respectively. After 12 weeks of intervention, we obtained the levels of FPG, FINS, TG, TC, HDL-C, LDL-C, testosterone, and IL-6 and the indexes of Homa-IR and Homa-ß, detected the expressions of Akt/p-Akt and eNOS/p-eNOS in the corpus cavernosum by Western blot, and compared the erectile function between different groups. RESULTS: The frequency and rate of penile erection were significantly lower in the DM group than in the GLP-1 and normal control groups (P < 0.05) and also lower in the GLP-1 group than in the normal controls (P < 0.05). Immunofluorescence staining showed the expression of eNOS mainly in the cytoplasm of the cavernosal vessels and sinusoidal endothelial cells, markedly lower in the DM and GLP-1 groups than in the normal rats (P < 0.05), but higher in the GLP-1 than in the DM group (P < 0.05). The level of eNOS/p-eNOS in the penile tissue was significantly decreased in the DM and GLP-1 groups in comparison with the normal controls (P < 0.01 or P < 0.05), while that of p-eNOS was markedly increased in the GLP-1 group as compared with the DM group (P < 0.05). No statistically significant differences were observed in the Akt level among the three groups of animals (P > 0.05). The expression of p-Akt was remarkably reduced in the DM and GLP-1 groups in comparison with the control rats (P < 0.01 or P < 0.05), but higher in the GLP-1 than in the DM group (P < 0.05). CONCLUSION: GLP-1 can protect the function of endothelial cells in the corpus cavernosum and improve the erectile function of DED rats by regulating the Akt/ eNOS signaling pathway, which indicates that GLP-1 could be an important option for the treatment and prevention of DED.

Effect of prazosin on diabetic nephropathy patients with positive α1-adrenergic receptor autoantibodies and refractory hypertension.

To investigate the effect of prazosin on patients with diabetic nephropathy (DN), α1-adrenergic receptor (α1-R) autoantibodies and refractory hypertension, a total of 126 patients with DN and hypertension were recruited. The patients were divided into a refractory hypertension group, (n=76) and a non-refractory hypertension group (n=50). The epitope of the second extracellular loop of the α1-R (192-218) was synthesized and an enzyme-linked immunosorbent assay (ELISA) was performed to detect serum autoantibodies. In the group with DN-associated refractory hypertension, the positive rate of autoantibodies against the α1-R was 80.3% (n=61). The 61 patients who were positive for α1-R autoantibodies were randomly divided into a treatment group (n=31) and a control group (n=30). The patients were given drugs at the same dosage and administration, with the exception of prazosin, which was provided only to the patients in the treatment group [1 mg, three times a day (tid)] for a duration of six weeks. Subsequently, prazosin was added (1 mg, tid) to the therapeutic schedule of the patients in the control group and the α1-R autoantibody-negative group for another six weeks. The analysis was carried out on an intention-to-treat basis. The prazosin treatment resulted in significant improvements in hypertension in the treatment group (P<0.05), while there was no marked improvement in the control group. The total effective rate of hypertension improvement was 90.3% in the treatment group, which was higher compared with that of the control group (33.3%). In conclusion, α1-R autoantibodies may play an important role in the pathogenesis of DN with refractory hypertension. Prazosin was demonstrated to be effective and safe in the treatment of DN with refractory hypertension.

Clinical evaluation of valsartan and metoprolol tartrate in treatment of diabetic nephropathy with positive ß1-adrenergic and anti-angiotensin II type 1 receptor antibody.

BACKGROUND: Studies have confirmed that angiotensin II receptor blocker (ARB) and angiotensin converting enzyme inhibitors (ACEI) in the treatment of diabetic nephropathy (DN) has special advantages. We observed the effects of valsartan and metoprolol tartrate hydrchloride in treatment of DN patients with positive ß1-adrenergic and anti-angiotensin II type 1 (AT1) receptor antibody. METHODS: The epitopes of the second extracellular loop of ß1 receptor (197 - 222) and AT1 receptor (165 - 191), were synthesized and used respectively to screen serum autoantibodies from patients with DN (n = 371, group A), diabetes mellitus (DM) without renal failure (n = 107, group B) and healthy blood donors (n = 47, control, group C) by enzyme-linked immunosorbent assay (ELISA). Metoprolol tartrate 25 - 50 mg, three times per day, valsartan 160 mg, once a day, aspirin 100 mg, once a day, and nitrendipine 10 - 20 mg, three times per day, were given to DN patients with positive or negative autoantibodies. The cystatin C level and 24-hour urinary protein were measured before and after treatment. RESULTS: In DN patients, the positive rate of the autoantibodies against ß1 receptors and AT1 receptor was 47.7% and 51.5%, respectively, which were significantly higher than those in DM patients and healthy controls (all P < 0.01). Patients with anormalous cystatin C had higher positive rates of the autoantibodies than patients with normal cystatin C. Valsartan and metoprolol tartrate reduced proteinuria significantly (P < 0.01) in DN patients with positive autoantibodies. CONCLUSIONS: The findings suggest that these autoantibodies against ß1 and AT1-receptor may play important roles in the pathogenesis of DN. Valsartan and metoprolol tartrate are effective and safe in the treatment of DN.

Postprandial lipaemia suppresses endothelium-dependent arterial dilation in patients with hypothyroidism.

Endothelial dysfunction represents an early step in the development of atherosclerosis. The purpose of this study was to investigate the relationship between postprandial lipaemia and endothelial dysfunction in patients with overt hypothyroidism (oHT) and subclinical hypothyroidism (sHT). Female subjects with oHT and sHT, as well as female healthy subjects with euthyroid state were enrolled (10 cases in each group). The examination of flow-mediated dilation (FMD) was performed before and after an oral fat-loading by high resolution ultrasound. Endothelial dysfunction after an oral fat challenge was related to the extent of hypertriglyceridemia and free radicals. FMD decreased significantly at 4-h point in 3 groups, (p < 0.05) and then FMD in control and sHT restored to baseline at 8-h point, it was lower than baseline in sHT group at 6-h point (p = 0.042). However, FMD continued to decrease at 6-h point (p < 0.001), and then increased toward to baseline at 8-h point, which was still lower than baseline (p = 0.039) in oHT. Spearman's analysis showed a negative correlation between FMD and triglyceride, a negative correlation between FMD and thiobarbituric acid reactive substances (TBARS), and a positive correlation between triglyceride and TBARS levels during oral lipid-loading test in hypothyroid patients (p < 0.001) and controls (p < 0.05). In hypothyroid subjects including oHT and sHT, even in healthy individuals, FMD was impaired after an oral fat challenge. The endothelial dysfunction observed after an oral fat challenge was related to the extent of hypertriglyceridemia and oxygen-derived free radicals.

[Positive rate of autoantibodies against adrenergic receptors beta1 and angiotensin II type 1 receptors in the type 2 diabetes mellitus with or without hypertension].

OBJECTIVE: To observe the positive rates of autoantibodies against beta1 adrenergic receptors (beta1-receptor) and angiotensin II type 1 receptors (AT(1)-receptor) in type 2 diabetes patients with or without hypertension. METHODS: The epitopes of the second extracellular loop of beta1-receptor (197 - 222) and AT(1) receptor (165 - 191) were synthesized and serum autoantibodies were determined in type 2 diabetes patients with hypertension (n = 171) or without hypertension (n = 106). Left ventricular dimension was determined by echocardiography. The 24-hour urinary protein was measured by ELISA. The risk factors for enlarged left ventricle were analyzed by multiple logistic regressions. RESULTS: The positive rates of the autoantibodies against beta1-receptors (45.0%) and AT(1)-receptor (46.2%) in patients with type 2 diabetes with hypertension were significantly higher than those in patients with type 2 diabetes without hypertension (16.0% and 10.4%, respectively, all P < 0.01). In type 2 diabetes patients with hypertension and enlarged left ventricle, the positive rates of the autoantibodies against beta1-receptor 61.4% (35/57) and against AT(1)-receptor 64.9% (37/57)were significantly higher than those in type 2 diabetes patients with normal left ventricular dimension (36.8%, 42/114 and 36.8%, 42/114, respectively, all P < 0.01). Regression analysis demonstrated that course of disease, systolic pressure, serum autoantibodies against beta1 adrenergic receptor and angiotensin II type 1 receptors sera autoantibodies were independent risk factors for left ventricular enlargement (all P < 0.05). CONCLUSION: The serum beta1 and AT(1)-receptor autoantibodies are related to enlarged left ventricle in type 2 diabetes patients with hypertension and suggest that autoantibodies against beta1 and AT(1)-receptor might play important roles in the pathogenesis of type 2 diabetes patients with hypertension and enlarged left ventricle.

1,5-Diamino-tetra-zolium chloride.

The title compound, CH(5)N(6) (+)·Cl(-), crystallized with two indepedent 1,5-diamino-tetra-zolium cations and two independent chloride anions in the asymmetric unit. In the crystal, there are a number of N-H⋯Cl hydrogen-bonding inter-actions, which generate a three-dimensional network.

[The relation between positive rate of autoantibodies against beta1 and M2-adrenergic receptors and urinary albumin excretion rate in the type 2 diabetes mellitus with refractory hypertension].

OBJECTIVE: To explore the relation between the positive rates of autoantibodies against beta(1) adrenergic receptor (beta1-receptor)and (M2-receptor) with urinary albumin excretion rate (UAER) in type 2 diabetes patients with refractory hypertension. METHODS: Autoantibodies against beta(1)- and M(2)-receptor as well as autoantibodies were determined in type 2 diabetes patients with (n = 136) or without (n = 111) refractory hypertension, hypertensive patients without renal failure (n = 60) and healthy control subjects (n = 40, control) by ELISA. RESULTS: The positive rates of the autoantibodies against beta1-receptors (44.9%) and M(2)-receptor (37.5%) in patients with type 2 diabetes with refractory hypertension were significantly higher than those in patients with type 2 diabetes without refractory hypertension (27.9% and 24.3%, respectively, all P < 0.05), in patients with hypertension without renal failure (11.7% and 15.0%, all P < 0.01) and in healthy controls (8.3% and 7.5%, all P < 0.01). In type 2 diabetes patients with refractory hypertension and renal failure (UAER > or = 200 microg/min), the positive rates of the autoantibodies against beta(1)-receptor (87.1%, 27/31) and against M(2)-receptor (67.7%, 21/31) were significantly higher than those in type 2 diabetes patients with refractory hypertension but without renal failure (UAER 20 - 199 microg /min, 46.7%, 28/60 and 41.7%, 25/60, respectively, all P < 0.05). CONCLUSION: The serum beta(1)- and M (2)-receptor autoantibodies are positively associated with the UAER level and suggest that these autoantibodies against beta(1) and M(2)-receptor may play important roles in the pathogenesis of the type 2 diabetes with refractory hypertension.

The antioxidant alpha-lipoic acid improves endothelial dysfunction induced by acute hyperglycaemia during OGTT in impaired glucose tolerance.

OBJECTIVE: Impaired glucose tolerance (IGT) is considered a transitional phase in the development of type 2 diabetes, and is also independently associated with the occurrence of cardiovascular disease. Endothelial dysfunction (ED) represents a very early step in the development of atherosclerosis. The aim of the present study was to examine ED in the fasting state and after a glucose challenge as well as after administration of an antioxidant agent. PATIENTS AND METHODS: The study subjects included 42 IGT patients and 26 healthy individuals (control group). The IGT patients were randomly divided into two groups, 21 in each group (the alpha-lipoic acid group and the placebo group). In the alpha-lipoic acid group, 300 mg of alpha-lipoic acid was administrated before an oral glucose tolerance test (OGTT); in the placebo group, 250 ml of 0.9% sodium chloride was administrated before the OGTT. In addition, 250 ml of 0.9% sodium chloride was also administrated to the control subjects before the OGTT (control group), and then vascular function was examined in the fasting state and repeated 1 and 2 h after the glucose load. High-resolution ultrasound was used to measure flow-mediated endothelium-dependent arterial dilation (FMD) and glyceryltrinitrate (GTN)-induced endothelium-independent arterial dilation. RESULTS: In the fasting state, and at 60 and 120 min, FMD in both the placebo and alpha-lipoic acid groups was significantly lower than in the controls (P < 0.01). In the control group, FMD tended to decrease at 60 min after glucose loading and returned to the baseline levels at 120 min (P > 0.05). In the placebo group, FMD decreased significantly at 60 min after glucose loading (P < 0.01) and increased markedly from 60 to 120 min (P < 0.01). The alpha-lipoic acid-treated patients showed FMD values intermediate between the control subjects and the IGT patients treated with placebo, at both 60 and 120 min, and the differences were significant (P < 0.01). In multiple regression analysis, FMD was significantly correlated to fasting blood glucose (FBG), low density lipoprotein cholesterol (LDL-C), lipoprotein (a) [Lp(a)], C-reactive protein (CRP), thiobarbituric acid reactive substances (TBARS) and age in IGT patients at baseline (P < 0.01). Spearman's analysis showed a significant negative correlation between FMD and plasma glucose levels, and between FMD and TBARS during the OGTT in IGT patients (placebo group) (P < 0.01). There was also a significant correlation between FMD and plasma glucose levels, and between FMD and TBARS during the OGTT in IGT patients treated with alpha-lipoic acid (P < 0.05), although the power of association decreased. CONCLUSION: In subjects with IGT, FMD was impaired both in the fasting state and after a glucose challenge, probably through increased production of oxygen-derived free radicals. The ED observed after a glucose challenge is related to the extent of hyperglycaemia and TBARS, and an antioxidant agent can improve the impairment of endothelial function induced by acute hyperglycaemia.

[Changes in plasma concentrations of osteoprotegerin before and after levothyroxine replacement therapy in hypothyroid patients].

OBJECTIVE: To investigate the alteration of plasma osteoprotegerin (OPG) concentration before and after levothyroxine (L-T4) replacement therapy and its association with endothelium-dependent arterial dilation in patients with overt hypothyroidism (oHT) and subclinical hypothyroidism (sHT). METHODS: L-T4 therapy was given to 20 oHT patients and 20 sHT patients, all female, till the free serum triiodothyronine (FT3), free thyroxin (FT4), and thyroid-stimulating hormone (TSH) were near or within the respective normal ranges. Twenty healthy women were used as controls. Sandwich ELISA was used to measure the plasma OPG concentration before and after treatment. RESULTS: The plasma OPG levels before treatment of the oHT and sHT patients were 3.13 ng/L +/- 0.27 ng/L and 2.95 ng/L +/- 0.24 ng/L respectively, both significantly higher than that of the controls (2.42 ng/L +/- 0.26 ng/L, both P = 0.000). Multivariate analysis showed that OPG was significantly associated with TSH (r = 0.306, P < 0.05) and endothelium-dependent arterial dilation (r = -0.675, P < 0.01) at baseline. After the normalization of thyroid function the OPG levels of the oHT and sHT patients decreased markedly to 2.53 ng/L +/- 0.28 ng/L and 2.54 ng/L +/- 0.21 ng/L respectively (both P = 0.000), very close to that in the controls. The absolute changes of OPG was significantly positively correlated with the changes of TSH (P < 0.05), negatively correlated with the changes of endothelium-dependent arterial dilation (P < 0.01), and not significantly correlated with other parameters in the hypothyroid patients during the course of treatment. CONCLUSION: OPG may act as an important regulatory molecule in the vasculature and, particularly, may be involved in the development of vascular dysfunction in hypothyroid patients.

[Changes of osteoprotegerin before and after insulin therapy in type 1 diabetic patients].

OBJECTIVE: To investigate the relationship between the plasma osteoprotegerin (OPG) level and endothelium-dependent arterial dilation in type 1 diabetic patients. METHODS: Sandwich ELISA method was used to detect the plasma OPG levels of 22 newly diagnosed type 1 diabetic patients before and 6 months after treatment and of 28 healthy subjects. All patients were then given insulin therapy for 6 months. High resolution ultrasound was used to measure the brachial artery diameter at rest, after reactive hyperemia and after sublingual administration of glyceryltrinitrate (GTN). RESULTS: The plasma OPG level of the patients before treatment was 3.09 ng/L +/- 0.70 ng/L, significantly higher than that of the healthy controls (2.07 ng/L +/- 0.75 ng/L, P < 0.001). After 6 months treatment, the OPG level of the patients decreased to 2.58 ng/L +/- 0.59 ng/L, significantly lower than that before treatment (P < 0.001). The flow-mediated endothelium-dependent arterial dilation in the patients before treatment was 3.35% +/- 0.67%, significantly lower than that of the healthy controls (5.17% +/- 0.83%, P < 0.001), and was increased to 4.27% +/- 0.63% after 6 months treatment, significantly higher than that before (P < 0.001). Multivariate analysis showed that OPG level was significantly associated with endothelium-dependent arterial dilation, fasting blood glucose (FBG), hemoglobin A1c (HbA1c), and ultra-sensitive C-reactive protein (CRP) at baseline (all P < 0.01). The absolute change in OPG level was significantly correlation with the changes in endothelium-dependent arterial dilation, FBG, HbA1c, and CRP in the diabetic patients during the course of treatment (all P < 0.01). CONCLUSION: Plasma OPG level is elevated in newly diagnosed diabetic patients, and the plasma OPG level is significantly associated with endothelial function.

Changes of osteoprotegerin before and after insulin therapy in type 1 diabetic patients.

OBJECTIVE: Osteoprotegerin (OPG) regulates osteoclast and immune functions and appears to represent a protective factor for vascular system. However, the role of OPG in endothelial dysfunction of type 1 diabetic patients has not been evaluated. The purpose of this study was to investigate the relationship between plasma OPG levels and endothelium-dependent arterial dilation in type 1 diabetic patients. RESEARCH DESIGN AND METHODS: This study subjects included 22 newly diagnosed type 1 diabetic patients and 28 healthy subjects. All patients were then given insulin therapy for 6 months. Plasma OPG concentration was measured in duplicate by a sandwich ELISA method, and high-resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperemia and after sublingual glyceryltrinitrate (GTN). RESULTS: Plasma OPG level in patients before treatment was 3.09+/-0.70 ng/L, which was significantly higher than that in control (2.07+/-0.75 ng/L) (p<0.001). After 6 months treatment, OPG levels decreased markedly (2.58+/-0.59 ng/L) (p<0.001). The flow-mediated endothelium-dependent arterial dilation in patients before treatment was 3.35+/-0.67%, which was significantly lower than that in control (5.17+/-0.83%) (p<0.001), and improved markedly after 6 months treatment (4.27+/-0.63%) (p<0.001). In multivariate analysis, OPG was significantly associated with endothelium-dependent arterial dilation, fasting blood glucose (FBG), hemoglobin A1c (HbA1c), and ultra sensitive C-reactive protein (CRP) at baseline (p<0.01). The absolute changes in OPG showed significant correlation with the changes in endothelium-dependent arterial dilation, FBG, HbA1c, and CRP in diabetic patients during the course of treatment (p<0.01). CONCLUSION: This study shows that plasma OPG levels are elevated in newly diagnosed type 1 diabetic patients, and that plasma OPG levels are significantly associated with endothelial function.

The relationship between plasma osteoprotegerin and endothelium-dependent arterial dilation in type 2 diabetes.

Osteoprotegerin is a recently identified inhibitor of bone resorption. Recent studies indicate that osteoprotegerin also acts as an important regulatory molecule in the vasculature. The purpose of this study was to investigate the relationship between plasma osteoprotegerin levels and endothelium-dependent arterial dilation in type 2 diabetic patients. The study subjects included 40 newly diagnosed type 2 diabetic patients and 46 healthy subjects. All patients were given insulin therapy for 6 months. Plasma osteoprotegerin concentration was measured in duplicate by a sandwich enzyme-linked immunosorbent assay method, and high-resolution ultrasound was used to measure brachial artery diameter at rest, after reactive hyperemia, and after sublingual glyceryltrinitrate. The plasma osteoprotegerin level in patients before treatment was 3.36 +/- 0.32 ng/l, which was significantly higher than that in control subjects (2.38 +/- 0.25 ng/l, P < 0.001). After 6 months of treatment, osteoprotegerin levels decreased markedly (2.83 +/- 0.34 ng/l, P < 0.001). Flow-mediated endothelium-dependent arterial dilation in patients before treatment was 3.21 +/- 0.52%, which was significantly lower than that in control subjects (4.46 +/- 0.56%, P < 0.01), and it improved markedly after 6 months of treatment (4.03 +/- 0.49%, P < 0.01). In multivariate analysis, osteoprotegerin was significantly associated with endothelium-dependent arterial dilation, fasting blood glucose (FBG), HbA(1c) (A1C), and ultrasensitive C-reactive protein (CRP) at baseline (P < 0.01). The absolute changes in osteoprotegerin showed significant correlation with changes in endothelium-dependent arterial dilation, FBG, A1C, and CRP in diabetic patients during the course of treatment (P < 0.01). This study shows that plasma osteoprotegerin levels are elevated in newly diagnosed diabetic patients and are significantly associated with endothelial function.

[Autoantibodies against beta1 and M2 receptor in diabetic patients with refractory hypertension].

OBJECTIVE: To explore the role of the autoantibodies against M(2)-muscarinic receptor (M(2)-receptor), beta(1)-adrenergic receptor (beta(1)-receptor) in the development of diabetic with refractory hypertension. METHODS: Serum autoantibodies against M(2) and beta(1) were detected by ELISA using synthesized epitopes of the second extracellular loop of M(2) receptor (169 - 193) and beta(1) receptor (197 - 222) in healthy controls (n = 40), diabetic patients (n = 62), diabetic patients with non-refractory hypertension (n = 55) and diabetic patients with refractory hypertension (n = 81). RESULTS: The positive rates of the autoantibodies against M(2) receptor and beta(1) receptor were similar among healthy controls (15.0% and 17. 5%), diabetes mellitus patients (17.7% and 14.5%) and diabetic patients with non-refractory hypertension (16.4% and 12.7%) but are significantly higher in diabetic patients with refractory hypertension (64.2% and 55.6%, P < 0.01 vs. other 3 groups). CONCLUSION: This finding suggests that autoimmune mechanisms might play a role in the pathogenesis of diabetic patients with refractory hypertension.