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- MANAGEMENT OF ENDOCRINE DISEASE: Clinical management of paragangliomas. [JOURNAL ARTICLE]
- Eur J Endocrinol 2014 Jul 25.
Paragangliomas (PGLs) are rare vascular, neuroendocrine tumors of paraganglia, which derive from either sympathetic tissue in adrenal (pheochromocytomas or PCCs) and extraadrenal (sPGLs) locations, or parasympathetic tissue of the head and neck (HNPGLs). Since HNPGLs are usually benign and most tumors grow slowly, a wait-and-scan policy is often advised. However, their location in the close proximity to cranial nerves and vasculature may result in considerable morbidity due to compression or infiltration of the adjacent structures, necessitating balanced decisions between a wait-and-see policy and active treatment. The main treatment options for HNPGL are surgery and radiotherapy. In contrast to HNPGLs, the majority of sPGL/PCC produce catecholamines, in advanced cases resulting in typical symptoms and signs such as palpitations, headache, diaphoresis and hypertension. The state-of-the-art diagnosis and localization of sPGL/PCC is based on measurement of plasma and/or 24 h urinary excretion of (fractionated) metanephrines and methoxytyramine. sPGL/PCC can subsequently be localized by anatomical (computed tomography and/or magnetic resonance imaging) and functional imaging studies (123I-MIBG-scintigraphy, 111In-pentetreotide scintigraphy, or positron emission tomography with radiolabelled dopamine or dihydroxyphenylalanine). Although most PGL/PCC are benign, factors such as genetic background, tumor size, tumor location, and high methoxytyramine levels are associated with higher rates of metastatic disease. Surgery is the only curative treatment. Treatment options for patients with metastatic disease are limited. PGL/PCC have a strong genetic background, with at least one third of all cases linked to germline mutations in 11 susceptibility genes. As genetic testing becomes more widely available, the diagnosis of PGL/PCC will be made earlier due to routine screening of at-risk patients. Early detection of a familial PGL allows early detection of potentially malignant PGLs and early surgical treatment, reducing the complication rates of this operation.
- Effects of Xin-Ji-Er-Kang formula on 2K1C-induced hypertension and cardiovascular remodeling in rats. [JOURNAL ARTICLE]
- J Ethnopharmacol 2014 Jul 22.
Xin-Ji-Er-Kang(XJEK),a a Chinese herbal formula,is effective against hypertension induced coronary heart disease, viral myocarditis and toxic myocarditis.In this study,the effect of XJEK on cardiovasuclar system were investigated.To test the hypothesis that Xin-Ji-Er-Kang (XJEK) has an anti-hypertensive effect mediated through attenuation of cardiac remodeling，and amelioration of vascular endothelial dysfunction and oxidative stress.Hypertension was induced in Wistar rats by 2 kidney 1 clip (2K1C) treatment. The hypertensive rats were then randomly assigned into four groups and treated as follows: group 1 (Sham-operated [Sh-Op] group received only drinking water), group 2 (Induced hypertensive model+no treatment), and group 3 (Induced hypertensive+a single daily oral dose of 24g·kg(-1)XJEK treatment) and group 4 (Induced hypertensive+a single oral dose of 15mgkg(-1)Fosinopril treatment). The rats in all the defined groups were respectively treated for a period of 4 weeks. Cardiovascular parameter such as systolic blood pressure (SBP) was measured weekly by using tail-cuff apparatus; left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP) and the rate of the rise in left ventricular pressure (± dp/dt max) were measured by using PowerLab 8/30 apparatus (AD Instruments, Australia) at the end of the 8th week; heart weight/body weight (HW/BW) was determined as an index of myocardial hypertrophy (MH). Hematoxylin and eosin (H&E) and Van Gieson (VG) stain were used to assess the cardio-histological changes. Colorimetric analysis was used to assay serum superoxide dismutase (SOD) activity, malondialdehyde (MDA), nitric oxide (NO), and hydroxyproline (Hyp) contents in cardiac tissue. AngiotensinⅡ (Ang II) content in serum was assessed by radioimmunoassay; tetrahydrobiopterin (BH4) content in cardiac tissue,BNP and endothelial NOS(eNOS) in serum were determined by using ELISA, and the protein expressions of c-Jun NH2-terminal kinase (JNK), P-JNK, p38, P-p38,, and NADPH oxidases -2 (Nox-2) were measured by western blot.XJEK therapy could impaire the heart systolic and diastolic function, potently improve the heart weight index, inhibite the elevation of HW/BW ratio,markedly ameliorate hemodynamic indexes, vascular remodeling index. It has blunted the decrease of SOD, NO and the increase in MDA and AngⅡserum contents, myocardial cross-section area (CSA), collagen volume fraction (CVF) and perivascular circumferential collagen area (PVCA) compared to the hypertensive model group. It also reduced the serum content of Hyp while increased BH4 levels in cardiac tissue. In addition, the expressions of Nox-2, P-JNK and P-p38MAPK were all suppressed compared to the hypertensive model group.What's more, treatment with XJEK improved endothelial dysfunction (ED) manifested by promoting eNOS activities and enhancing the NO activity in serum.The results of the present study show that XJEK attenuates 2K1C-induced hypertension in rats, which confirms our hypothesis that XJEK has an anti-hypertensive and cardiovascular remodeling effect via attenuation of cardiac remodeling and improvement of endothelial dysfunction and oxidative stress.
- Role of Cognitive Enhancer Therapy in Alzheimer's Disease with Concomitant Cerebral White Matter Disease: Findings from a Long-Term Naturalistic Study. [JOURNAL ARTICLE]
- Drugs R D 2014 Jul 26.
Evidence is lacking for cognitive enhancer therapy in patients with Alzheimer's disease (AD) and concomitant cerebrovascular disease (mixed AD) as such patients would have been excluded from clinical trials. Earlier studies of mixed AD have focused on large vessel cerebrovascular disease. The influence of small vessel cerebrovascular disease (svCVD) in the form of white matter hyperintensity (WMH) on treatment outcomes in mixed AD has not been addressed.In this long-term naturalistic study, we evaluated the effectiveness of cognitive enhancers in patients with mixed AD with svCVD.We conducted a retrospective analysis of a prospective clinical database from a memory clinic of a tertiary hospital. Magnetic resonance imaging WMH was used as a marker of svCVD. Demographic, cognitive, and treatment data were analysed. Linear mixed models with patient-specific random effects were used to evaluate cognitive outcomes over time while adjusting for confounders.Patients with mixed AD (n = 137) or AD without svCVD (pure AD) (n = 28) were studied over a median duration of 28.7 months. Patients with mixed AD had a higher prevalence of hypertension (62.8 vs. 35.7 %, p = 0.011). The majority (75.2 %) of the study sample were managed with monotherapy. Mini Mental State Examination (MMSE) scores decreased over time (-0.04, p = 0.007), and the decrease was similar for both diagnosis groups (-0.03, p = 0.246). Annual estimated mean MMSE decline was 0.84 for pure AD and 0.48 for mixed AD. Similar trends were observed with Montreal Cognitive Assessment (MoCA) scores, with annual estimated mean reduction of 0.72 and 0.48 for pure AD and mixed AD, respectively.Cognitive enhancers are effective in slowing the rate of cognitive decline in patients with AD with svCVD. These findings would need to be confirmed in randomized clinical trials.
- Dissecting Histone Deacetylase Role in Pulmonary Arterial Smooth Muscle Cell Proliferation and Migration. [JOURNAL ARTICLE]
- Biochem Pharmacol 2014 Jul 22.
Pulmonary Arterial Hypertension (PAH) is a rare and devasting condition characterized by elevated pulmonary vascular resistance and pulmonary artery pressure leading to right-heart failure and premature death. Pathologic alterations in proliferation, migration and survival of all cell types composing the vascular tissue play a key role in the occlusion of the vascular lumen. In the current study, we initially investigated the action of selective class I and class II HDAC inhibitors on the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) after exposure to Platelet Derived Growth Factor (PDGF). Class I HDAC inhibitors were able to counteract the hyperproliferative response to PDGF, reducing both proliferation and migration in PASMCs, while class II were ineffective. Selective silencing with siRNAs targeted against different HDACs revealed a major role of class I, and within this class, of HDAC1 in mediating PDGF-induced Akt Phosphorylation and Cyclin D1 (CycD1) expression. These results from these combinatorial approaches were further confirmed by the ability of a specific HDAC1 inhibitor to antagonize the PDGF action. The finding that HDAC1 is a major conductor of PDGF-induced patterning in PAH-PASMCs prompts the development of novel selective inhibitors of this member of class I HDACs as a potential tool to control lung vascular homeostasis in PAH.
- Involvement of calcium-sensing receptors in hypoxia-induced vascular remodeling and pulmonary hypertension by promoting phenotypic modulation of small pulmonary arteries. [JOURNAL ARTICLE]
- Mol Cell Biochem 2014 Jul 26.
Phenotype modulation of pulmonary artery smooth muscle cells (PASMCs) plays an important role during hypoxia-induced vascular remodeling and pulmonary hypertension (PAH). We had previously shown that calcium-sensing receptor (CaSR) is expressed in rat PASMCs. However, little is known about the role of CaSR in phenotypic modulation of PASMCs in hypoxia-induced PAH as well as the underlying mechanisms. In this study, we investigated whether CaSR induces the proliferation of PASMCs in small pulmonary arteries from both rats and human with PAH. PAH was induced by exposing rats to hypoxia for 7-21 days. The mean pulmonary arterial pressure (mPAP), right ventricular hypertrophy index (RVI), the percentage of medial wall thickness to the external diameter (WT %), and cross-sectional total vessel wall area to the total area (WA %) of small pulmonary arteries were determined by hematoxylin and eosin (HE), masson trichrome and Weigert's staining. The protein expressions of matrix metalloproteinase (MMP)-2 and MMP-9, the tissue inhibitors of metalloproteinase (TIMP)-3, CaSR, proliferating cell nuclear antigen (PCNA), phosphorylated extracellular signal-regulated kinase (p-ERK), and smooth muscle cell (SMC) phenotype marker proteins in rat small pulmonary arteries, including calponin, SMα-actin (SMAα), and osteopontin (OPN), were analyzed by immunohistochemistry and Western blotting, respectively. In addition, immunohistochemistry was applied to paraffin-embedded human tissues from lungs of normal human and PAH patients with chronic heart failure (PAH/CHF). Compared with the control group, mPAP, RVI, WT % and WA % in PAH rats were gradually increased with the prolonged hypoxia. At the same time, the expressions of CaSR, MMP-2, MMP-9, TIMP-3, PCNA, OPN, and p-ERK were markedly increased, while the expressions of SMAα and calponin were significantly reduced in lung tissues or small pulmonary arteries of PAH rats. Neomycin (an agonist of CaSR) enhanced but NPS2390 (an antagonist of CaSR) weakened these hypoxic effects. We further found that the expression change of CaSR, PCNA, and SMC phenotypic marker proteins in PAH/CHF lungs was similar to those in PAH rats. Our data suggest that CaSR is involved in the pulmonary vascular remodeling and PAH by promoting phenotypic modulation of small pulmonary arteries.
- Risk factor analysis of pulmonary hemorrhage complicating CT-guided lung biopsy in coaxial and non-coaxial core biopsy techniques in 650 patients. [JOURNAL ARTICLE]
- Eur J Radiol 2014 Jul 5.
To evaluate the risk factors involved in the development of pulmonary hemorrhage complicating CT-guided biopsy of pulmonary lesions in coaxial and non-coaxial techniques.Retrospective study included CT-guided percutaneous lung biopsies in 650 consecutive patients (407 males, 243 females; mean age 54.6 years, SD: 5.2) from November 2008 to June 2013. Patients were classified according to lung biopsy technique in coaxial group (318 lesions) and non-coaxial group (332 lesions). Exclusion criteria for biopsy were: lesions <5mm in diameter, uncorrectable coagulopathy, positive-pressure ventilation, severe respiratory compromise, pulmonary arterial hypertension or refusal of the procedure. Risk factors for pulmonary hemorrhage complicating lung biopsy were classified into: (a) patient's related risk factors, (b) lesion's related risk factors and (d) technical risk factors. Radiological assessments were performed by two radiologists in consensus. Mann-Whitney U test and Fisher's exact tests for statistical analysis. p values <0.05 were considered statistically significant.Incidence of pulmonary hemorrhage was 19.6% (65/332) in non-coaxial group and 22.3% (71/318) in coaxial group. The difference in incidence between both groups was statistically insignificant (p=0.27). Hemoptysis developed in 5.4% (18/332) and in 6.3% (20/318) in the non-coaxial and coaxial groups respectively. Traversing pulmonary vessels in the needle biopsy track was a significant risk factor of the development pulmonary hemorrhage (incidence: 55.4% (36/65, p=0.0003) in the non-coaxial group and 57.7% (41/71, p=0.0013) in coaxial group). Other significant risk factors included: lesions of less than 2cm (p value of 0.01 and 0.02 in non-coaxial and coaxial groups respectively), basal and middle zonal lesions in comparison to upper zonal lung lesions (p=0.002 and 0.03 in non-coaxial and coaxial groups respectively), increased lesion's depth from the pleural surface (p=0.021 and 0.018 in non-coaxial and coaxial groups respectively), increased distance of traversed lung in the needle track of more than 2.5cm (p=0.001 in both groups). Insignificant risk factors were patient's age, gender or emphysema in both groups (p value >0.1 in both groups). Concomitant incidence of pneumothorax was 32.3% (21/65) in non-coaxial group and 36.6% (26/71) in coaxial group. Pulmonary hemorrhage in the majority of cases was treated conservatively.Pulmonary hemorrhage complicating CT-guided core biopsy of pulmonary lesions, showed insignificant difference between coaxial and non-coaxial techniques. Significant risk factors of pulmonary hemorrhage included small and basal lesions, increased lesion's depth from pleural surface, increased length of aerated lung parenchyma crossed by biopsy needle and passing through vessels within the lung during puncture.
- Protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats. [Journal Article]
- Asian Pac J Trop Med 2014 May; 7(5):402-6.
To observe the protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats.All rats were randomly divided into normal control group, cirrhosis and treatment group. Thioacetamide was used to establish rat model of cirrhotic portal hypertension. The necrotic tissue of gastric mucosa ulcer focus, degree of neutrophils infiltration at the ulcer margin, portal pressure, portal venous flow, abdominal aortic pressure, abdominal aortic blood flow at front end, gastric mucosal blood flow (GMBF), glycoprotein (GP) of gastric mucosa, basal acid secretion, H(+)back -diffusion, gastric mucosal damage index, NO, prostaglandin E2(PGE2) and tumor necrosis factor-α (TNF-α) were determined respectively, and the pathological changes of gastric mucosa were also observed by microscope.Compared with cirrhosis group and the control group, the ulcer bottom necrotic material, gastric neutrophil infiltration and UI of the treatment group were all decreased significantly (P<0.01), GMBF value, GP values, serum NO, PGE2, TNF-α were all significantly increased.Omeprazole has an important protective effect on gastric mucosal and it can increase gastric mucosal blood flow and related to many factors.
- Economic Impact of Heart Failure According to the Effects of Kidney Failure. [JOURNAL ARTICLE]
- Rev Esp Cardiol 2014 Jul 22.
To evaluate the use of health care resources and their cost according to the effects of kidney failure in heart failure patients during 2-year follow-up in a population setting.Observational retrospective study based on a review of medical records. The study included patients ≥ 45 years treated for heart failure from 2008 to 2010. The patients were divided into 2 groups according to the presence/absence of kidney failure. Main outcome variables were comorbidity, clinical status (functional class, etiology), metabolic syndrome, costs, and new cases of cardiovascular events and kidney failure. The cost model included direct and indirect health care costs. Statistical analysis included multiple regression models.The study recruited 1600 patients (prevalence, 4.0%; mean age 72.4 years; women, 59.7%). Of these patients, 70.1% had hypertension, 47.1% had dyslipidemia, and 36.2% had diabetes mellitus. We analyzed 433 patients (27.1%) with kidney failure and 1167 (72.9%) without kidney failure. Patients with kidney failure were associated with functional class III-IV (54.1% vs 40.8%) and metabolic syndrome (65.3% vs 51.9%, P<.01). The average unit cost was €10 711.40. The corrected cost in the presence of kidney failure was €14 868.20 vs €9364.50 (P=.001). During follow-up, 11.7% patients developed ischemic heart disease, 18.8% developed kidney failure, and 36.1% developed heart failure exacerbation.Comorbidity associated with heart failure is high. The presence of kidney failure increases the use of health resources and leads to higher costs within the National Health System. Full English text available from: www.revespcardiol.org/en.
- Progression of coronary artery calcification seems to be inevitable, but predictable - results of the Heinz Nixdorf Recall (HNR) study† [JOURNAL ARTICLE]
- Eur Heart J 2014 Jul 25.
Coronary artery calcification (CAC), as a sign of atherosclerosis, can be detected and progression quantified using computed tomography (CT). We develop a tool for predicting CAC progression.In 3481 participants (45-74 years, 53.1% women) CAC percentiles at baseline (CACb) and after five years (CAC5y) were evaluated, demonstrating progression along gender-specific percentiles, which showed exponentially shaped age-dependence. Using quantile regression on the log-scale (log(CACb+1)) we developed a tool to individually predict CAC5y, and compared to observed CAC5y. The difference between observed and predicted CAC5y (log-scale, mean±SD) was 0.08±1.11 and 0.06±1.29 in men and women. Agreement reached a kappa-value of 0.746 (95% confidence interval: 0.732-0.760) and concordance correlation (log-scale) of 0.886 (0.879-0.893). Explained variance of observed by predicted log(CAC5y+1) was 80.1% and 72.0% in men and women, and 81.0 and 73.6% including baseline risk factors. Evaluating the tool in 1940 individuals with CACb>0 and CACb<400 at baseline, of whom 242 (12.5%) developed CAC5y>400, yielded a sensitivity of 59.5%, specificity 96.1%, (+) and (-) predictive values of 68.3% and 94.3%. A pre-defined acceptance range around predicted CAC5y contained 68.1% of observed CAC5y; only 20% were expected by chance. Age, blood pressure, lipid-lowering medication, diabetes, and smoking contributed to progression above the acceptance range in men and, excepting age, in women.CAC nearly inevitably progresses with limited influence of cardiovascular risk factors. This allowed the development of a mathematical tool for prediction of individual CAC progression, enabling anticipation of the age when CAC thresholds of high risk are reached.
- Current concepts of the role of abdominal compartment syndrome in acute pancreatitis - An opportunity or merely an epiphenomenon. [REVIEW]
- Pancreatology 2014 July - August; 14(4):238-243.
The association of acute pancreatitis (AP) with intra-abdominal hypertension (IAH) and abdominal compartment syndrome (ACS) has only recently been recognized. The detrimental effects of raised intra-abdominal pressure in cardiovascular, pulmonary and renal systems have been well established. Although IAH was associated with a higher APACHE II score and multi-organ dysfunction syndrome (MODS) in severe acute pancreatitis, a causal relationship between ACS and MODS in SAP is yet to be established. It is therefore debatable whether IAH is a phenomenon causative of organ failure or an epiphenomenon seen in conjunction with other organ dysfunction. This review systemically examines the pathophysiological basis and clinical relevance of ACS in AP and summarizes all the available evidence in its management.