MAPKAP1 orchestrates macrophage polarization and lipid metabolism in fatty liver-enhanced colorectal cancer.

Various factors, including fatty liver and macrophage alterations, influence colorectal cancer (CRC). This study explores the mechanistic role of fatty liver in CRC progression, focusing on macrophage polarization and lipid metabolism. A murine fatty liver model was created with a high-fat diet (HFD), and CRC was induced using AOM and DSS. Single-cell transcriptome sequencing (scRNA-seq) identified MAPKAP1 as a critical gene promoting CRC via M2 macrophage polarization and lipid metabolism reprogramming. Prognosis analysis on the TCGA-CRC dataset confirmed MAPKAP1's significance. In vitro and in vivo experiments demonstrated that EVs from fatty liver cells enhanced MAPKAP1 expression, accelerating CRC development and metastasis. HFD exacerbated CRC, but fatty acid inhibitors delayed progression. Fatty liver upregulates MAPKAP1, driving M2 macrophage polarization and lipid metabolism changes, worsening CRC. These findings suggest potential therapeutic strategies for CRC, particularly targeting lipid metabolism and macrophage-mediated tumor promotion.

Morus alba L. (Sangzhi) alkaloids mitigate atherosclerosis by regulating M1/M2 macrophage polarization.

BACKGROUND: Atherosclerosis (AS) is an important cause of cardiovascular disease, posing a substantial health risk. Recognized as a chronic inflammatory disorder, AS hinges on the pivotal involvement of macrophages in arterial inflammation, participating in its formation and progression. Sangzhi alkaloid (SZ-A) is a novel natural alkaloid extracted from the mulberry branches, has extensive pharmacological effects and stable pharmacokinetic characteristics. However, the effects and mechanisms of SZ-A on AS remain unclear. PURPOSE: To explore the effect and underlying mechanisms of SZ-A on inflammation mediated by macrophages and its role in AS development. METHODS: Atherosclerosis was induced in vivo in apolipoprotein E-deficient mice through a high-fat and high-choline diet. We utilized macrophages and vascular endothelial cells to investigate the effects of SZ-A on macrophage polarization and its anti-inflammatory properties on endothelial cells in vitro. The transcriptomic analyses were used to investigate the major molecule that mediates cell-cell interactions and the antiatherogenic mechanisms of SZ-A based on AS, subsequently validated in vivo and in vitro. RESULTS: SZ-A demonstrated a significant inhibition in vascular inflammation and alleviation of AS severity by mitigating macrophage infiltration and modulating M1/M2 macrophage polarization in vitro and in vivo. Moreover, SZ-A effectively reduced the release of the proinflammatory mediator C-X-C motif chemokine ligand (CXCL)-10, predominantly secreted by M1 macrophages. This reduction in CXCL-10 contributed to improved endothelial cell function, reduced recruitment of additional macrophages, and inhibited the inflammatory amplification effect. This ultimately led to the suppression of atherogenesis. CONCLUSION: SZ-A exhibited potent anti-inflammatory effects by inhibiting macrophage-mediated inflammation, providing a new therapeutic avenue against AS. This is the first study demonstrating the efficacy of SZ-A in alleviating AS severity and offers novel insights into its anti-inflammatory mechanism.

Clinical and cardiac characteristics of primary bilateral macronodular adrenal hyperplasia.

Background: Cardiovascular disease is the leading cause of death in Cushingzs syndrome (CS). Primary bilateral macro-nodular adrenal hyperplasia (PBMAH), is a rare cause of CS that is clinically distinct from the other common types of CS, but cardiac characteristics have been poorly studied. Methods: The clinical data, steroid hormones and echocardiographic variables of 17 patients with PBMAH were collected. Twenty-one CS patients with cortisol-producing adenoma (CPA) were collected as controls. The similarities and differences of clinical and cardiac features between the two groups were compared.

Astragaloside IV induces the protective effect of bone marrow mesenchymal stem cells derived exosomes in acute myocardial infarction by inducing angiogenesis and inhibiting apoptosis.

Bone marrow mesenchymal stem cells (BMECs)-derived exosomes (MSC-Exo) can improve acute myocardial infarction (AMI). Astragaloside IV (AS-IV) has also been reported to have cardioprotective pharmacological effects. However, it is not entirely clear whether AS-IV can improve AMI by inducing MSC-Exo. BMSCs and MSC-Exo were isolated and identified, and we also established the AMI rat model and the OGD/R model with H9c2 cells. After MSC-Exo or AS-IV-mediated MSC-Exo treatment, cell angiogenesis, migration, and apoptosis were evaluated by tube formation, wound healing, and TUNEL staining. The cardiac function of the rats was measured by echocardiography. The pathological changes and collagen deposition in rats were also assessed with Masson and Sirius red staining. The levels of α-SMA, CD31 and inflammatory factors were determined by immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). In vitro, AS-IV-mediated MSC-Exo can significantly enhance the angiogenesis and migration of H9c2 cells induced by OGD/R, and significantly reduce their apoptosis. In vivo, AS-IV-mediated MSC-Exo can improve the cardiac function of rats, and attenuate pathological damage and collagen deposition in AMI model rats. In addition, AS-IV-mediated MSC-Exo can also promote angiogenesis and reduce inflammatory factors in rats with AMI. AS-IV-stimulated MSC-Exo can improve myocardial contractile function, myocardial fibrosis and angiogenesis, reduce inflammatory factors and induce apoptosis in rats after AMI.

Theoretical Study on the Swelling Mechanism and Structural Stability of Ni3Al-LDH Based on Molecular Dynamics.

layered double hydroxide (LDH) as a kind of 2D layer material has a swelling phenomenon. Because swelling significantly affects the adsorption, catalysis, energy storage, and other application properties of LDHs, it is essential to study the interlayer spacing, structural stability, and ion diffusion after swelling. In this paper, a periodic computational model of Ni3Al-LDH is constructed, and the supramolecular structure, swelling law, stability, and anion diffusion properties of Ni3Al-LDH are investigated by molecular dynamics theory calculations. The results show that the interlayer water molecules of Ni3Al-LDH present a regular layered arrangement, combining with the interlayer anions by hydrogen bonds. As the number of water molecules increases, the hydrogen bond between the anion and the basal layer gradually weakens and disappears when the number of water molecules exceeds 32. The hydrogen bond between the anion and the water molecule gradually increases, reaching an extreme value when the number of water molecules is 16. The interlayer spacing of Ni3Al-LDH is not linear with the number of water molecules. The interlayer spacing increases slowly when the number of water molecules is more than 24. The maximum layer spacing is stable at around 19 Å. The interlayer spacing, binding energy, and hydration energy show an upper limit for swelling: the number of water molecules is 32. When the number of interlayer water molecules is 16, the water molecules' layer structure and LDH interlayer spacing are suitable for anions to obtain the maximum diffusion rate, 10.97 × 10-8 cm2·s-1.

First-Principles Study on Interlayer Spacing and Structure Stability of NiAl-Layered Double Hydroxides.

Interlayer spacing and structure stability of layered double hydroxides (LDHs) on their application performance in adsorption, ion exchange, catalysis, carrier, and energy storage is important. The effect of different interlayer anions on the interlayer spacing and structure stability of LDHs has been less studied, but it is of great significance. Therefore, based on density functional theory (DFT), the computational model with 10 kinds of anions intercalated Ni3Al-A-LDHs (A = Cl-, Br-, I-, OH-, NO3 -, CO3 2-, SO4 2-, HCOO-, C6H5SO3 -, C12H25SO3 -) and four Ni R Al-Cl-LDH models with different Ni2+/Al3+ ratios (R = 2, 3, 5, 8) were constructed to calculate and analyze interlayer spacing, structural stability, and their influence factors. It was found that the interlayer spacing order of Ni3Al-A-LDHs intercalated with different anions is OH- < CO3 2- < Cl- < Br- < I- < HCOO- < SO4 2- < NO3 - < C6H5SO3 - < C12H25SO3 -. The hydrogen bond network between the base layer and the interlayer anions affects the arrangement structure of the interlayer anions, which affects the interlayer spacing. For interlayer monatomic anions Cl-, Br-, and I- and the anion of comparable size in each direction SO4 2-, the interlayer spacing is positively correlated with the interlayer anion diameter. The larger difference between the long-axis and short-axis dimensions of the polyatomic anions results in the long axis of the anion being perpendicular to the basal layer, increasing interlayer spacing. The long-chain anion C12H25SO3 - intercalation system exhibits the largest layer spacing of 24.262 Å. As R value increases from 2 to 8, the interlayer spacing of Ni R Al-Cl-LDHs gradually increases from 7.964 to 8.124 Å. The binding energy order between the interlayer anion and basal layer is CO3 2- > SO4 2- > OH- > Cl- > Br- > I- > HCOO- > NO3 - > C12H25SO3 - > C6H5SO3 -. The smaller the interlayer spacing, the higher the binding energy and the stronger the structural stability of LDHs. The factors affecting structural stability mainly include the bond length and bond angle of the hydrogen bond and the charge interaction between the basal layer and interlayer anion. In the CO3 2- intercalated system, the hydrogen bond length exhibits the shortest of 1.95 Å and the largest bond angle of 163.68°. The density of states and energy band analysis show that the higher the number of charges carried by the anion, the stronger its ability to provide electrons to the basal layer.

Association of Metabolic Dysfunction-Associated Fatty Liver Disease With Left Ventricular Diastolic Function and Cardiac Morphology.

Background and Aim: Non-alcoholic fatty liver disease (NAFLD) is closely related to cardiovascular diseases (CVD). A newly proposed definition is metabolic dysfunction-associated fatty liver disease (MAFLD), which was changed from NAFLD. The clinical effect of this change on abnormalities of cardiac structure and function is yet unknown. We aimed to examine whether MAFLD is associated with left ventricular (LV) diastolic dysfunction (LVDD) and cardiac remolding and further identify the impact of different subgroups and severity of MAFLD. Method: We evaluated 228 participants without known CVDs. Participants were categorized by the presence of MAFLD and the normal group. Then, patients with MAFLD were subclassified into three subgroups: MAFLD patients with diabetes (diabetes subgroup), overweight/obesity patients (overweight/obesity subgroup), and lean/normal-weight patients who had two metabolic risk abnormalities (lean metabolic dysfunction subgroup). Furthermore, the severity of hepatic steatosis was assessed by transient elastography (FibroScan®) with a controlled attenuation parameter (CAP), and patients with MAFLD were divided into normal, mild, moderate, and severe hepatic steatosis groups based on CAP value. Cardiac structure and function were examined by echocardiography. Results: LVDD was significantly more prevalent in the MAFLD group (24.6% vs. 60.8%, p < 0.001) compared to the normal group. The overweight subgroup and diabetes subgroup were significantly associated with signs of cardiac remolding, including interventricular septum thickness, LV posterior wall thickness, left atrial diameter (all p < 0.05), relative wall thickness, and LV mass index (all p < 0.05). Additionally, moderate-to-to severe steatosis patients had higher risks for LVDD and cardiac remolding (all p-values < 0.05). Conclusion: MAFLD was associated with LVDD and cardiac remolding, especially in patients with diabetes, overweight patients, and moderate-to-to severe steatosis patients. This study provides theoretical support for the precise prevention of cardiovascular dysfunction in patients with MAFLD.

Cholesterol Metabolic Markers for Differential Evaluation of Patients with Hyperlipidemia and Familial Hypercholesterolemia.

The cholesterol metabolism in humans can be indirectly reflected by measuring cholesterol metabolism marker levels. We aimed to investigate the association of cholesterol homeostasis markers on standard lipid profiling components in familial hypercholesteremia and hyperlipidemia patients. A total of 69 hyperlipidemia patients, 25 familial hypercholesteremia (FHC) patients, and 64 healthy controls were enrolled in this study. We performed routine testing of blood lipid water. Gas chromatography was used to determine the changes in the concentration of cholesterol synthesis (squalene, desmosterol, and lathosterol) and absorption markers (campesterol, sitosterol, and stigmasterol) in the blood. Baseline hyperlipidemia patients displayed significantly higher total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels in comparison to the control group, which was reflected in the increased levels of squalene, desmosterol, campesterol, and sitosterol observed (P < 0.05) in the hyperlipidemia patients. The desmosterol, lathosterol, campesterol, stigmasterol, and sitosterol were statistically different in the FHC group than the hyperlipidemic group (P < 0.05). The proportions of squalene/cholesterol, lathosterol/cholesterol, stigmasterol/cholesterol, and sitosterol/cholesterol in the FHC group were lower than those in the hyperlipidemic group; only desmosterol/cholesterol was higher than that in the hyperlipidemic group. Correlation studies between lipid metabolic factors showed that the proportion of moderate and strong correlations was much higher in the FHC group than in the other two groups (76.92% vs. 32.50% and 31.25%). Logistic regression analysis showed that the concentrations of glucose, LDL-C, lactosterol, and sitosterol were all independent risk factors for developing hyperlipidemia. This result was further confirmed by the ROC curve. These results indicated that the study of cholesterol synthesis and decomposition markers can serve as a reference index for related diseases caused by changes in its concentration.

Ultrasound cardiogram-based diagnosis of cardiac hypertrophy from hypertension and analysis of its relationship with expression of autophagy-related protein.

BACKGROUND: Ultrasound cardiogram is commonly used in the diagnosis of cardiac hypertrophy from hypertension. This study aimed to investigate the correlation between the occurrence of cardiac hypertrophy from hypertension with the expression of autophagy-related protein 9A (ATG9a). METHODS: In this study, 168 patients with hypertension in the Guizhou Medical University from February 2020 to September 2021 were selected. The patients were divided into an experimental group (cardiac hypertrophy group) and a normal group according to the results of ultrasound cardiogram examination, and serum ATG9a levels in the two groups were detected. The association between ATG9a and cardiac hypertrophy from hypertension and the relationship between serum ATG9a and ultrasound cardiogram indicators were analyzed. And a receiver operating characteristic (ROC) curve was drawn to analyze the value of ATG9a in the diagnosis of cardiac hypertrophy from hypertension. RESULTS: The results showed that there were no significant differences in age, diastolic blood pressure, hypertension course, body mass index (BMI), smoking history, and drinking history between the experimental and normal groups (P>0.05). Binary logistic regression analysis showed that compared with the normal control group, ATG9a increased significantly (P<0.05) and systolic blood pressure decreased significantly in the experimental group. The results showed that the area under the curve (AUC) of serum ATG9a was 0.736, the sensitivity was 76.54%, and the specificity was 78.42% in the diagnosis of cardiac hypertrophy from hypertension. Pearson correlation analysis showed that ATG9a was positively correlated with left ventricular posterior wall thickness (LVPWT) and interventricular septal thickness (IVST) in patients with cardiac hypertrophy from hypertension, and was negatively correlated with left ventricular ejection fraction (LVEF) (P<0.05). CONCLUSIONS: Serum ATG9a may be involved in the formation of cardiac hypertrophy in hypertensive patients. Our results, which showed that serum ATG9a level increased in cardiac hypertrophy patients, were consistent with the clinical ultrasonic cardiogram diagnosis result, and ATG9a is expected to be a marker for early ultrasonic cardiogram diagnosis.

Gas Chromatography and Flame-Ionization Detection of Non-Cholesterol Sterols as Indicators of Cholesterol Absorption and Synthesis in 158 Chinese Individuals with Normolipidemia, Hyperlipidemia, and Familial Hypercholesterolemia.

BACKGROUND There are limited studies on the effects of cholesterol homeostasis in populations at high risk for cardiovascular disease. We aimed to use gas chromatography and flame-ionization detection (GC-FID) of non-cholesterol sterols as indicators of cholesterol absorption and synthesis. Sterol indicators of cholesterol absorption included campesterol, stigmasterol, and sitosterol. Sterol indicators of cholesterol synthesis included squalene, 7-lathosterol, and desmosterol. MATERIAL AND METHODS A total of 158 participants were enrolled in 3 groups: healthy control (n=64), hyperlipidemia (n=69), and familial hypercholesterolemia (FH, n=25). Age, sex, blood pressure, blood glucose, and lipoprotein were collected, and cholesterol absorption and synthesis markers were determined by GC-FID. RESULTS All 6 cholesterol concentration indicators, except squalene, were significantly different among the 3 groups (all P<0.05); whereas in the ratio to cholesterol (%, sterols/cholesterol), only desmosterol and lathosterol were significantly different (P<0.05). Multifactorial regression analysis showed that triglycerides, total cholesterol, and desmosterol were independent risk factors affecting the development of hyperlipidemia (P<0.05). The efficacy of the ROC curve for the diagnosis of dyslipidemia was also higher for all 3 indices (Model 1, AUC=0.960). Model 1 was superior to Model 2 for the 6 indicators of cholesterol. For the FH and dyslipidemia groups, the 6-indicator model (Model 3) was shown to have a good diagnostic value (AUC=1.000). CONCLUSIONS The 6 sterol indicators of cholesterol absorption and synthesis had a dynamic course in all study participants. Desmosterol was an indicator of dyslipidemia. The combined use of the 6 sterol indicators differentiated between healthy individuals and patients with dyslipidemia and FH.

The importance of genetic counseling and genetic screening: a case report of a 16-year-old boy with resistant hypertension and severe hypokalemia.

Liddle's syndrome, an autosomal dominant form of monogenic hypertension, is characterized by salt-sensitive hypertension with early penetrance, hypokalemia, metabolic alkalosis, suppression of plasma rennin activity and aldosterone secretion, and a clear-cut response to epithelial sodium channel blockers but not spironolactone therapy. Here, we describe the case of a 16-year-old boy patient with resistant hypertension (maintain 170-180/100-110 mm Hg after administration four kinds of antiypertensive drugs) and severe hypokalemia. After a series of checks, we exclude primary aldosteronism and renal artery stenosis and other diseases. Finally, the Liddle syndrome was diagnosed because of the DNA sequencing found that the proband's mother and himself had mutations P616L (c.1847 C>T) in the SCNN1B gene. Liddle syndrome should be considered as a cause of hypertension in children or adolescents particularly with suppressed renin activity. Early diagnosis and appropriately tailored treatment avoid complications of long-term unrecognized or inappropriately managed hypertension. Genetic testing has made it possible to make accurate diagnoses and develop tailored therapies for mutation carriers. The role of genetic testing and genetic counseling in establishing the early diagnosis of Liddle's syndrome is important.

[Change of ambulatory blood pressure-related parameters for different levels of renal function in resistant hypertension].

OBJECTIVE: To explore the predictive values of ambulatory blood pressure-related parameters for moderate renal impairment in resistant hypertension (RH). METHODS: The clinical data were retrospectively analyzed for 401 hospitalized patients with hypertension at our hospital from October 2010 to October 2013. They were divided into RH (n = 263) and non-RH (n = 138). The modified estimating equation of glomerular filtration rate (GFR) for Chinese patients was used to assess renal functions. The standardization of moderate renal impairment was when GFR below 60 ml · min⁻¹ · 1.73 m⁻². The ambulatory blood pressure-related parameters were obtained by 24 h ambulatory blood pressure monitoring. The important prediction of these parameters for moderate renal impairment was accessed by receiver operating characteristic (ROC) curve. And the related risk factors for renal function impairment were tested by multiple stepwise Logistic regression analysis. RESULTS: Ambulatory arterial stiffness index (AASI), 24 h mean pulse pressure (24 hPP), sleeptime relative systolic blood pressure (SBP) decline and 24 h systolic blood pressure (24 hSBP) had important predictive values for moderate renal impairment in RH. GFR was significantly lower in those with AASI ≥ 0.485, 24 hPP ≥ 47.5 mmHg, sleeptime relative SBP decline ≤ -1.75% and 24 hSBP ≥ 130.5 mmHg (P < 0.05). Area under curve of ROC curve of AASI, 24 hPP, sleeptime relative SBP decline and 24 hSBP were 0.804, 0.644, 0.602 and 0.623 respectively. Multiple Logistic regression analysis showed that AASI (OR 1 268.5, P = 0.000), low density lipoprotein (OR 0.7, P = 0.01) and sleeptime relative SBP decline (OR 1.3, P = 0.01) were independent risk factors for GFR < 60 ml · min⁻¹ · 1.73 m⁻² in RH. CONCLUSION: AASI, 24 hPP, sleeptime relative SBP decline and 24 hSBP are the most significant ambulatory blood pressure-related parameters in predicting renal impairment in resistant hypertension.

Carotid atherosclerosis is associated with hypertension in a hospital-based retrospective cohort.

OBJECTIVE: We aim to investigate the association between carotid artery plaque and blood pressure variation, as well as other cardiovascular risk factors. MATERIALS AND METHODS: We retrospectively analyzed clinical data of inpatients with high blood pressure treated in the Department of Hypertension from April 2009 to June 2010. Results from carotid ultrasonography, demographic characteristics, and other clinical data were obtained from 408 patients. RESULTS: (1) The rate of positive plaque in carotid artery was 55.1%, and there was no difference between men and women. However, this rate was positively correlated with the age of the patients. (2) The rate of positive plaque in carotid artery was associated with the duration of the disease, fasting blood-glucose levels, total cholesterol, and low-density lipoprotein-cholesterol (LDL-C). (3) The prevalence of carotid artery plaque increased in accordance with the coefficient of systolic pressure variation (X(2) = 15.83, P = 0.001), whereas no correlation existed between prevalence of carotid artery plaque and coefficient of diastolic pressure variation and the plaque prevalence (X(2) = 0.24, P = 0.97). Mean systolic blood pressure (MSBP) was positively correlated with prevalence of carotid artery plaque (X(2) = 10.47, P = 0.005). (4) Multivariate regression analysis indicated that carotid plaque was associated with the age, duration of hypertension, high-density lipoprotein-cholesterol (HDL-C), LDL-C, 24 h MSBP, and coefficient of systolic pressure variation, whereas no associations were found with the coefficient of diastolic pressure variation, 24 h average diastolic blood pressure (AvDP), and 24 h mean arterial pressure (MAP) (P > 0.05). CONCLUSION: Carotid atherosclerosis was independently associated with variation of blood pressure, especially with coefficient of systolic blood pressure variation.

Urinary KIM-1, IL-18 and Cys-c as early predictive biomarkers in gadolinium-based contrast-induced nephropathy in the elderly patients.

BACKGROUND/AIMS: This study was designed to investigate whether urinary kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18) and cystatin C (Cys-C) are early predictive biomarkers for gadolinium-based contrast-induced nephropathy (Gd-CIN) in the elderly patients undergoing gadolinium-enhanced magnetic resonance imaging (MRI). METHODS: 60 elderly patients undergoing enhanced MRI using gadolinium-based contrast media were enrolled. Urine samples were collected before and 24 hours and 48 hours after the procedure, and KIM-1, IL-18 and Cys-C levels were measured by using an ELLSA kit respectively. Serum samples before and 24 hours and 48 hours after the procedure were also collected, and creatinine was measured by automatic biochemical analyzer. RESULTS: Gd-CIN was diagnosed in 8 of 60 (13.3%) patients. At 24 hours after MRI with gadolinium administration in the Gd-CIN group, the urinary KIM-1, IL-18 and Cys-C were significantly increased. Logistic regression analysis showed that urinary KIM-1 and IL-18 at 24 hours after gadolinium injection were independent predictive markers of Gd-CIN. The predictable time of acute kidney injury (AKI) onset determined by urinary KIM-1, IL-18 and Cys-C was 24 hours earlier than by serum creatinine. CONCLUSIONS: Urinary KIM-1, IL-18 and Cys-C could be early predictive biomarkers of Gd-CIN in the elderly patients, which showed a good performance in early diagnosis of Gd-CIN as compared with serum creatinine.

Application of plasma lipidomics in studying the response of patients with essential hypertension to antihypertensive drug therapy.

Hypertension is a key risk factor in the progression of cardiovascular disease (CVD). Dyslipidemia, a strong predictor of CVD, frequently coexists with hypertension. Therefore, the control of hypertension and dyslipidemia may help reduce CVD morbidity and mortality. In the present study, the therapeutic effects of antihypertensive agents on blood pressure control and plasma lipid metabolism were evaluated. The plasma lipid profiles of patients with treated (n = 25) or untreated (n = 30) essential hypertension as well as of subjects with normotension (n = 28) were analyzed using liquid chromatography mass spectrometry. Principal component analysis of the lipidomics data revealed distinct clusters among studied subjects across three human populations. Phosphatidylcholines and triacylglycerols (TG) dominated the pattern of hypertension-influenced plasma lipid metabolism. Discriminatory lipid metabolites were analyzed using one-way analysis of variance followed by a post hoc multiple comparison correction. TG lipid class was significantly increased by 49.0% (p < 0.001) in hypertensive vs. normotensive groups while tended to decrease (-21.2%, p = 0.054) in hypertensive patients after treatment. Total cholesteryl esters were significantly decreased by -16.9% (p < 0.001) in hypertensive patients after treatment. In particular, a large number of individual neutral lipid species were significantly elevated in hypertensive subjects but significantly decreased after treatment with antihypertensive agents. The present study applied, for the first time, a systems biology based lipidomics approach to investigate differentiation among plasma lipid metabolism of patients with treated/untreated essential hypertension and subjects with normotension. Our results demonstrate that antihypertensive medications to lower blood pressure of hypertensive patients to target levels produced moderate plasma lipid metabolism improvement of patients with hypertension.

[Association of carotid atherosclerosis and blood pressure variation].

OBJECTIVE: To investigate the relationship of carotid artery plaque and blood pressure variation and cardiovascular risk factors. METHODS: We retrospectively analyzed clinical data of in-patients treated in the department of hypertension between April 2009 and June 2010. Information on carotid ultrasonography and other clinical date were obtained from 408 patients. All patients were monitored by ambulatory blood pressure. RESULTS: (1) Carotid artery determined in plaque was 55.3%, there was no differences between men and women. However, the carotid artery plague was associated positively with age. Increased age was associated with a significantly increased positive rate. (2) Cardiovascular risk factors and carotid artery plaque: carotid artery plaque was associated with duration of disease, fasting blood sugar, total cholesterol, and low density lipoprotein-cholesterol. (3) 24 h ambulatory blood pressure and carotid artery plaque: the prevalence of carotid artery plaque increased with increasing coefficient of systolic variation (P = 0.001). There was no correlation between the coefficient of diastolic variation and the prevalence (P = 0.644).(4) Multivariate regression analysis indicated that carotid artery plaque was associated with duration of hypertension, 24 h mean systolic blood pressure, and coefficient of variation of 24 h blood pressure (P < 0.05). CONCLUSION: Carotid atherosclerosis is independently associated with coefficient of variation of blood pressure, especially with coefficient of variation of systolic blood pressure.

[Incidence of impaired glucose tolerance in hospitalized essential hypertension patients without diabetes mellitus history and with normal fasting glucose].

OBJECTIVE: To observe the incidence of impaired glucose tolerance in hospitalized patients with essential hypertension without diabetes mellitus history and with normal fasting glucose. METHODS: A total of 586 hospitalized patients with essential hypertension and without known diabetes mellitus (DM) and with normal fasting blood glucose (FBG < 5.6 mmol/L) were included in this epidemiologic cross-sectional survey and screening study and received oral glucose tolerance test (OGTT). Associations between postprandial blood sugar and age, gender, body mass index, blood pressure level, blood lipid level, carotid arterial sclerosis were analyzed. RESULTS: (1) Among 586 patients, the number of impaired glucose tolerance (IGT) was 159, the number of newly diagnosed DM was 41 and the prevalence rates of newly diagnosed DM and impaired glucose tolerance (IGT) were 7.0% and 27.1% respectively. (2) Incidence of carotid arterial sclerosis was 67.5% in patients with impaired glucose tolerance and 59.6% in patients with normal glucose tolerance (P > 0.05). CONCLUSION: Our results showed that incidence of newly diagnosed disturbed glucometabolic status is common among patients with essential hypertension without DM history and normal FBG. OGTT should be used as a routine procedure in these patients for the purpose of early intervention in hypertensive patients with abnormal glucometabolic status.