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Guideline Clinical practice parameters for hemodynamic support of pediatric and neonatal septic shock: 2007 update from the American College of Critical Care Medicine. 2009
Brierley J, Carcillo JA, Choong K, Cornell T, Decaen A, Deymann A, Doctor A, Davis A, Duff J, Dugas MA, Duncan A, Evans B, Feldman J, Felmet K, Fisher G, Frankel L, Jeffries H, Greenwald B, Gutierrez J, Hall M, Han YY, Hanson J, Hazelzet J, Hernan L, Kiff J, Kissoon N, Kon A, Irazuzta J, Irazusta J, Lin J, Lorts A, Mariscalco M, Mehta R, Nadel S, Nguyen T, Nicholson C, Peters M, Okhuysen-Cawley R, Poulton T, Relves M, Rodriguez A, Rozenfeld R, Schnitzler E, Shanley T, Kache S, Skache S, Skippen P, Torres A, von Dessauer B, Weingarten J, Yeh T, Zaritsky A, Stojadinovic B, Zimmerman J, Zuckerberg A. · No affiliation provided · Crit Care Med. · Pubmed #19325359 No free full text.
Abstract: BACKGROUND: The Institute of Medicine calls for the use of clinical guidelines and practice parameters to promote "best practices" and to improve patient outcomes. OBJECTIVE: 2007 update of the 2002 American College of Critical Care Medicine Clinical Guidelines for Hemodynamic Support of Neonates and Children with Septic Shock. PARTICIPANTS: Society of Critical Care Medicine members with special interest in neonatal and pediatric septic shock were identified from general solicitation at the Society of Critical Care Medicine Educational and Scientific Symposia (2001-2006). METHODS: The Pubmed/MEDLINE literature database (1966-2006) was searched using the keywords and phrases: sepsis, septicemia, septic shock, endotoxemia, persistent pulmonary hypertension, nitric oxide, extracorporeal membrane oxygenation (ECMO), and American College of Critical Care Medicine guidelines. Best practice centers that reported best outcomes were identified and their practices examined as models of care. Using a modified Delphi method, 30 experts graded new literature. Over 30 additional experts then reviewed the updated recommendations. The document was subsequently modified until there was greater than 90% expert consensus. RESULTS: The 2002 guidelines were widely disseminated, translated into Spanish and Portuguese, and incorporated into Society of Critical Care Medicine and AHA sanctioned recommendations. Centers that implemented the 2002 guidelines reported best practice outcomes (hospital mortality 1%-3% in previously healthy, and 7%-10% in chronically ill children). Early use of 2002 guidelines was associated with improved outcome in the community hospital emergency department (number needed to treat = 3.3) and tertiary pediatric intensive care setting (number needed to treat = 3.6); every hour that went by without guideline adherence was associated with a 1.4-fold increased mortality risk. The updated 2007 guidelines continue to recognize an increased likelihood that children with septic shock, compared with adults, require 1) proportionally larger quantities of fluid, 2) inotrope and vasodilator therapies, 3) hydrocortisone for absolute adrenal insufficiency, and 4) ECMO for refractory shock. The major new recommendation in the 2007 update is earlier use of inotrope support through peripheral access until central access is attained. CONCLUSION: The 2007 update continues to emphasize early use of age-specific therapies to attain time-sensitive goals, specifically recommending 1) first hour fluid resuscitation and inotrope therapy directed to goals of threshold heart rates, normal blood pressure, and capillary refill <or=2 secs, and 2) subsequent intensive care unit hemodynamic support directed to goals of central venous oxygen saturation >70% and cardiac index 3.3-6.0 L/min/m.
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Review Systemic and localized scleroderma. 2006
Chung L, Lin J, Furst DE, Fiorentino D. · Department of Dermatology, Stanford University School of Medicine, CA 94305, USA. · Clin Dermatol. · Pubmed #16966019 No free full text.
Abstract: Sclerosing conditions of the skin are manifested by a full spectrum of presentations that includes skin-limited forms as well as those which can involve internal organs and result in death. At this point, we are just beginning to understand the mechanisms of tissue fibrosis, and it is likely that the fibrotic processes are a heterogeneous group of disorders in which perturbation of multiple molecular pathways, including vascular and immunologically mediated pathways, can lead to fibrosis. We now have some moderately effective therapies for vascular aspects of systemic sclerosis (eg, bosentan for pulmonary arterial hypertension, calcium-channel blockers for Raynaud's, or angiotensin-converting enzyme inhibitors for renal crisis). We also are beginning to find treatments interrupting the immunologic pathways that manifest as systemic sclerosis (eg, methotrexate for the skin or cyclophosphamide for the lungs). The basic process of fibrosis, however, awaits proven, effective therapy.
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Clinical Conference Mycophenolate mofetil (MMF) vs placebo in patients with moderately advanced IgA nephropathy: a double-blind randomized controlled trial. free! 2005
Frisch G, Lin J, Rosenstock J, Markowitz G, D'Agati V, Radhakrishnan J, Preddie D, Crew J, Valeri A, Appel G. · New York Presbyterian Hospital, Columbia University, New York, NY, USA. · Nephrol Dial Transplant. · Pubmed #16030050 links to free full text
Abstract: BACKGROUND: IgA nephropathy (IgAN) is the most common form of glomerulonephritis worldwide. Up to 40% progress to end-stage renal disease (ESRD) over 10-20 years. Currently, treatment is limited. We studied the use of mycophenolate mofetil (MMF) vs placebo in a group of North American IgAN patients at high risk for progressive disease. METHODS: Included were 32 patients aged 18-75 years from multiple centres who had their biopsies read at Columbia and who had at least 1 g of proteinuria per day plus at least two of the following risk factors: (i) male sex; (ii) hypertension >150/90 mmHg or requiring antihypertensive medications; (iii) creatinine clearance, measured by 24 h urine collection, <80 and >20 ml/min at time of enrolment; and (iv) presence of glomerulosclerosis or tubulointerstitial atrophy and fibrosis on renal biopsy. Patients were randomized to either 1 year of MMF, titrated up to a dose of 1000 mg bid, or placebo. Total follow-up was 2 years. All patients received angiotensin inhibition medication. The primary outcome was a 50% increase in baseline serum creatinine (SCr). Secondary outcomes were an increase of 0.5 mg/dl SCr, ESRD and a 50% reduction in proteinuria. RESULTS: The mean baseline SCr was 2.4 mg/dl. No statistically significant differences were observed for any outcome. Five of 17 who received MMF vs two of 15 patients in the placebo group reached a 50% increase in SCr (P = 0.4). In both groups, all patients who reached the primary outcome also reached ESRD. Ten who received MMF vs seven who received placebo had a 0.5 mg/dl increase in SCr (P = 0.7) Only three MMF and two placebo patients had a 50% reduction in 24 h proteinuria. No serious adverse events occurred in either group. CONCLUSION: No benefit was seen in patients who received MMF in this high risk group, probably reflecting the relatively advanced stage of disease of our population. We conclude that MMF is probably not effective in patients with IgAN who already have moderate renal insufficiency.
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Clinical Conference [Greater reduction of urinary albumin excretion in hypertensive patients with perindopril than nifedipine] 1999
Lin J, Chen D, Wu K. · Department of Cardiology, Fujian Institute of Hypertension, The First Affiliated Hospital of Fujian Medical University, Fuzhou 350005. · Zhonghua Nei Ke Za Zhi. · Pubmed #11798658 No free full text.
Abstract: OBJECTIVE: To examine the effect of perindopril and nifedipine on renal function in patients with essential hypertension (EH). METHODS: 52 cases with EH were divided randomly into two groups: perindopril group (4mg qd, n = 26); nifedipine group (10 mg tid, n = 26). Treatment period lasted for 24 weeks. Parameters of renal function were measured before and after treatment. RESULTS: (1) After treatment, the arterial pressure decreased in a similar way in the two groups, urinary albumin excretion was significantly less after treatment in the perindopril group [urinary albumin excretion/24 h (mg/24 h): 66.7 +/- 25.9 vs 104.5 +/- 41.8, P < 0.01; urine protein/24h (g/L): 0.17 +/- 0.039 vs 0.24 +/- 0.064, P < 0.01], GFR (ml/min) was higher in the perindopril group after treatment (125.5 +/- 15.2 vs 112.2 +/- 13.2, P < 0.05). No significant changes were observed with nifedipine (P < 0.05). (2) No significant correlation between the decrement of urinary albumin excretion and of SBP, DBP was found in both groups (P > 0.05). CONCLUSION: It is shown that perindopril, but not nifedipine, is able to reduce urinary excretion of albumin in patients with essential hypertension independently of its effective antihypertensive property. It is probable that the positive effect of perindopril on microalbuminuria is attributable to modification in intrarenal hemodynamics or to change in glomerular permeability.
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Article Fulminant idiopathic intracranial hypertension in a pediatric patient following a minor head trauma. free! 2009
Lin J, Fernandes JK, Faria EC, Pinho RS, Masruha MR, Vilanova LC. · Division of Child Neurology, Department of Neurology and Neurosurgery, Federal University of São Paulo, São Paulo, SP, Brazil. · Arq Neuropsiquiatr. · Pubmed #19623458 links to free full text
This publication has no abstract.
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Article [Prevention and treatment of hypertension after renal transplantation] 2009
Ma LL, Xie ZL, Tang YW, Sun W, Guo HB, Zhang L, Lin J, Tian Y. · Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China. · Zhongguo Yi Xue Ke Xue Yuan Xue Bao. · Pubmed #19621505 No free full text.
Abstract: Hypertension is a common complication after renal transplantation. Among post-transplantation patients died of cardiovascular diseases, about 41% have hypertension. Hypertension is an independent risk factor for kidney transplant failure. Post-transplantation hypertension can be caused by many factors, including the use of immunosuppressants. When the blood pressure exceeds 130/90 mmHg in a kidney transplant recipient, it is reasonable to provide active medical intervention. In summary, prevention and treatment of hypertension is important to prolong the survival of kidney transplant recipients.
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Article Genetic polymorphisms of angiotensin-2 type 1 receptor and angiotensinogen and risk of renal dysfunction and coronary heart disease in type 2 diabetes mellitus. free! 2009
Lin J, Hu FB, Qi L, Curhan GC. · Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. · BMC Nephrol. · Pubmed #19327134 links to free full text
Abstract: BACKGROUND: Increased activation of the renin-angiotensin system (RAS) may be important in promoting coronary heart disease (CHD) and renal dysfunction, but limited data are available on associations between angiotensin type 1 receptor (AGT1R) and angiotensinogen (AGT) genotypes in type 2 diabetes. METHODS: Study participants were diabetics from the Health Professionals Follow-Up Study (HPFS) and the Nurses' Health Study (NHS). We analyzed single nucleotide polymorphisms (SNPs) associated with cardiovascular pathophysiology (including AGT1R T573C, AGT1R A1166C, and AGT M235T) and presence of renal dysfunction (eGFR<60 ml/min/1.73 m2) or history of CHD. RESULTS: The AGT1R 1166 C-allele was associated with eGFR<60 ml/min/1.73 m2 (multivariable OR 1.63 [1.01, 2.65]) in the HPFS men (n = 733) and in the combined dataset (n = 1566) (OR 1.42 [1.02, 1.98]). The AGT1R 1166 C-allele was also associated with CHD in men (OR 1.57 [1.10, 2.24]). In NHS women (n = 833), AGT 235T-allele was associated with CHD (OR 1.72 [1.20, 2.47]). Removal of hypertension from the fully adjusted models did not influence results, suggesting that the associations may not be mediated by hypertension. There were significant interactions between sex and AGT1R 1166 C-allele (p = 0.008) and AGT M235T (p = 0.03) in models for CHD. No significant associations were seen between AGT1R T573 C-allele and renal dysfunction or CHD. CONCLUSION: Polymorphisms in AGT1R and AGT genes are associated with renal dysfunction and CHD in type 2 diabetes and further support the important role of the RAS in these complications. Sex may modify associations between AGT1R 1166 C-allele and AGT 235T and CHD in type 2 diabetes.
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Article Association between C-reactive protein and pre-diabetic status in a Chinese Han clinical population. 2009
Lin J, Zhang M, Song F, Qin J, Wang R, Yao P, Ying C, Hu FB, Liu L. · Department of Nutrition and Food Hygiene, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan, 430030, PR China. · Diabetes Metab Res Rev. · Pubmed #19116941 No free full text.
Abstract: BACKGROUND: C-reactive protein (CRP) has been showed to be associated with type 2 diabetes mellitus, but whether CRP underlies glucose disorders in Asian people is still unclear, for they have much lower body mass index (BMI) levels than these Westerns in previous studies. METHOD: In this clinical-based cross-sectional study, the association between CRP and hyperglycaemia in different BMI levels and different gender was compared among 1730 Chinese Han men and women, including 1258 subjects with normal glucose tolerance (NGT), 126 subjects with impaired fasting glucose (IFG) and 346 subjects with impaired glucose tolerance (IGT). Subjects with isolated IFG or IGT were all newly diagnosed and did not use anti-diabetic drugs. RESULTS: Compared with subjects with NGT, BMI, fasting blood glucose, homoeostasis model assessment insulin resistance (HOMA-IR), blood pressure, dyslipidemia, and serum CRP levels were increased in subjects with IGT and IFG. In stratified analyses, increasing CRP levels were strongly associated with prevalence of IGT and IFG in different BMI strata. After adjustment for sex, age, BMI, education, alcohol consumption, smoking, hypertension status, recreational physical activity and occupational physical activity, the ORs across quartiles of CRP were 1.00, 1.43, 2.14 and 2.29 for IFG (P for trend: 0.025) and 1.00, 1.85, 2.32 and 2.79 for IGT (P for trend: 0.012). CONCLUSION: These results support the hypothesis that chronic inflammation may be involved in the development of hyperglycaemia, even though in a thinner and healthy population.
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Article [Living related donor kidney transplantation: analysis of 117 cases] 2008
Tian Y, Zhang L, Xie ZL, Tang YW, Sun W, Guo HB, Lin J, Ji ZG. · Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China. · Zhonghua Yi Xue Za Zhi. · Pubmed #19080494 No free full text.
Abstract: OBJECTIVE: To summarize the clinical experience in living related donor kidney transplantation. METHODS: 117 patients with different nephropathies underwent transplantation of kidneys donated by their collateral relative in three generations. All donor kidneys were removed by open nephrectomy. Immunosuppressive protocols which consisting of cyclosporine A/tacrolimus, mycophenolate mofetil/azathioprine/rapamycin, and steroid were used in all patients as immunosuppressors. Follow-up was conducted for 1-44 months. RESULTS: Delayed graft function recovery occurred in 2 patients. Acute rejection episodes occurred in 18 patients, and the condition was reversed by high intravenous dose of methyl-prednisolone or polyclonal anti-T-cell antibodies. Follow-up showed that all the patients survived with normal kidney function, and the donors kept good kidney function with normal life quality. Hypertension was found in 2 donors and diabetes mellitus was found in 1 donor. CONCLUSION: Careful evaluation of both psychological and physical status of the donors and optimal physical status of recipients before operation are critical for successful kidney transplantation. Injury of graft kidney should be reduced and recipients should be treated with sufficient immunosuppressive regimen in early stage after transplantation.
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Article Prevalence and risk factors associated with chronic kidney disease in an adult population from southern China. 2009
Chen W, Chen W, Wang H, Dong X, Liu Q, Mao H, Tan J, Lin J, Zhou F, Luo N, He H, Johnson RJ, Zhou SF, Yu X. · Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China. · Nephrol Dial Transplant. · Pubmed #18952699 No free full text.
Abstract: BACKGROUND: Population-based studies evaluating the prevalence of kidney damage in different communities have been limited in developing countries. We conducted a population-based screening study in the southern Chinese city of Guangzhou that aimed to identify the prevalence and associated risk factors of chronic kidney disease (CKD) in southern Chinese populations. METHODS: We interviewed 6311 residents (>20 years) from six districts of Guangzhou from July 2006 to June 2007 and tested for haematuria, albuminuria and reduced renal function. Associations between age, gender, smoking, diabetes mellitus, hypertension, hyperuricaemia and kidney damage were examined. RESULTS: There were 6311 subjects enrolled in this study. After adjustment for age and gender, the prevalence of albuminuria, haematuria and reduced estimated glomerular filtration rate (eGFR) was 6.6% [95% confidence interval (CI): 5.5-7.6%], 3.8% (95% CI: 3.4%, 4.3%) and 3.2% (95% CI: 2.4%, 3.3%), respectively. Approximately 12.1% (95% CI: 11.3%, 12.9%) of the sample population had at least one indicator of kidney damage. Age, diabetes mellitus, hypertension, central obesity, hyperlipidaemia and use of nephrotoxic medications were independently associated with albuminuria; hyperuricaemia, age, gender, hypertension and use of nephrotoxic medications were independently associated with reduced eGFR, and female gender was independently associated with haematuria. CONCLUSIONS: In the general adult population from southern China, 12.1% has either proteinuria, haematuria and/or reduced eGFR, indicating the presence of kidney damage, with an awareness of only 9.6%. The high prevalence and low awareness of CKD in this population suggest an urgent need for CKD prevention programmes in China.
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Article Effects of early and late chronic pressure overload on extracellular matrix remodeling. 2008
Lin J, Davis HB, Dai Q, Chou YM, Craig T, Hinojosa-Laborde C, Lindsey ML. · Department of Medicine, Division of Cardiology, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229-3900, USA. · Hypertens Res. · Pubmed #18716372 No free full text.
Abstract: The left ventricle (LV) remodels with age and in response to pressure overload. While aging and pressure overload are superimposed in the clinical context, the structural and functional consequences of the individual processes are not well-understood. Accordingly, the objective of this study was to compare the effects of both early and late chronic hypertension on extracellular matrix (ECM) remodeling. The following groups of Dahl rats were studied: 1) young salt-resistant (control, n=6); 2) young salt-sensitive (early phase of chronic hypertension, n=6); 3) middle-aged salt-resistant (aging, n=5); and 4) middle-aged salt-sensitive (late phase of chronic hypertension, n=6). We measured LV mass (LVM) and body weight (BW) and immunoblotted a panel of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs), and ECM proteins. Total collagen increased, several MMPs decreased, and TIMP-1 increased in the early phase of hypertension, consistent with fibrosis. Active MMP-8 decreased from 8,010+/-81 U in young salt-resistant to 5,260+/-313 U in young salt-sensitive (p<0.05) rats. During the late phase, chronic hypertension decreased total collagen levels and increased MMP-8 and MMP-14 (all p<0.05). Based on good-fit modeling analysis, MMP-14 (45 kDa) correlated positively with changes in LVM/BW during the early phase. In conclusion, this is the first study to evaluate MMP levels during both early and late chronic phases of hypertension. Our results highlight that ECM remodeling in response to pressure overload is a dynamic process involving excessive ECM accumulation and degradation.
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Article Case-control analysis of nucleotide excision repair pathway and the risk of renal cell carcinoma. 2008
Lin J, Pu X, Wang W, Matin S, Tannir NM, Wood CG, Wu X. · Department of Epidemiology, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA. · Carcinogenesis. · Pubmed #18711149 No free full text.
Abstract: In this population-based case-control study with 325 Caucasian renal cell carcinoma (RCC) patients and 335 controls matched to cases by age, gender and county of residence, we evaluated the associations between 13 potential functional polymorphisms in nine major nucleotide excision repair (NER) genes and RCC risk. In individual single nucleotide polymorphism analysis, after adjustment for multiple comparisons, a significantly decreased RCC risk was observed for the heterozygous genotype of XPD Asp312Asn [odds ratio (OR) = 0.62; 95% confidence interval (CI): 0.43-0.90] and for the heterozygous and homozygous variant genotypes combined in a dominant model (OR = 0.64; 95% CI: 0.46-0.89). The heterozygous AG genotype of XPA 5'untranslated region was at 1.78-fold increased risk (95% CI: 1.18-2.69) and the risk reached 2.43-fold (95% CI: 1.57-3.75) for the homozygous variant GG genotype; the risk was significant both in the dominant model and in the recessive model. In joint analysis, compared with individuals with fewer than five adverse alleles, individuals with five (OR = 1.17; 95% CI: 0.71-1.93), six (OR = 1.66; 95% CI: 1.03-2.67), seven or more (OR = 1.85; 95% CI: 1.16-2.95) exhibited a progressively increased risk of RCC (P for trend = 0.004). Further, there were significant interactions between NER pathway genes and sex, hypertension and obesity (all P for interaction <0.05). Our results strongly support that common sequence variants of the NER pathway genes predispose susceptible individuals to increased risk of RCC and that the association may be modified by gender, history of hypertension and obesity. These results need to be replicated in larger studies.
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Article Fluvastatin decreases cardiac fibrosis possibly through regulation of TGF-beta(1)/Smad 7 expression in the spontaneously hypertensive rats. 2008
Zhai Y, Gao X, Wu Q, Peng L, Lin J, Zuo Z. · Department of Cardiology, First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China. · Eur J Pharmacol. · Pubmed #18430418 No free full text.
Abstract: Statins ameliorate myocardial fibrosis after myocardial infarction. We designed this study to determine whether fluvastatin reduced hypertension-induced myocardial hypertrophy and fibrosis and whether these fluvastatin effects involved transforming growth factor beta1 (TGF-beta1) and Smad 7, factors known to play a role in the myocardial hypertrophy and fibrosis. We randomized 14 week old spontaneously hypertensive rats (SHRs) to receiving vehicle or 5-20 mg/kg/day fluvastatin for 8 weeks. Wistar Kyoto (WKY) rats receiving vehicle or 10 mg/kg/day fluvastatin were also studied. SHRs had an increased blood pressure, left ventricular hypertrophy and fibrosis compared with WKY rats. SHRs also had an elevated TGF-beta1 expression and a decreased Smad 7 expression. These changes in SHRs were dose-dependently attenuated by fluvastatin. For example, the hydroxyproline content was 3.2+/-0.1, 4.0+/-0.1 and 3.5+/-0.1 microg/mg heart and the Smad 7 protein expression was 5.1+/-0.6, 1.0+/-0.1 and 4.1+/-0.7 arbitrary units for WKY rats, SHRs and SHRs receiving 20 mg/kg/day fluvastatin, respectively. The hydroxyproline content in the SHRs treated with or without fluvastatin was positively correlated with the left ventricular mass index, systolic blood pressure and the amount of TGF-beta1 proteins and negatively correlated with the Smad 7 expression level. The left ventricular mass index was positively correlated with the systolic blood pressure. Fluvastatin did not alter the blood pressure, left ventricular mass index and collagen content of WKY rats. These results suggest that fluvastatin reduces hypertension-induced myocardial hypertrophy and fibrosis. These effects may involve an increased expression of Smad 7 and a decreased expression of TFG-beta1. Our results call for clinical studies to evaluate these fluvastatin effects in hypertensive patients.
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Article Estrogen effects on MMP-13 and MMP-14 regulation of left ventricular mass in Dahl salt-induced hypertension. 2008
Dai Q, Lin J, Craig T, Chou YM, Hinojosa-Laborde C, Lindsey ML. · Department of Medicine/Cardiology, University of Texas Health Science Center, San Antonio,TX 78229-3900, USA. · Gend Med. · Pubmed #18420168 No free full text.
Abstract: BACKGROUND: Female Dahl salt-sensitive (DS) rats fed a low-salt diet develop hypertension at 6 months of age. Ovariectomy at 2 months of age accelerates the development of hypertension, and estrogen replacement delays it. Although acute pressure overload induces structural changes in the left ventricle (LV) further effects of gradual hypertension on LV remodeling have not been examined in the DS rat model. OBJECTIVE: The purpose of this study was to test the hypothesis that aging and estrogen loss in hypertensive DS rats are accompanied by changes in LV remodeling. METHODS: Four groups of DS rats were examined: young intact, middle-aged (MA) intact, MA ovariectomized (MA-OVX), and MA-OVX with 17beta-eestradiol (E(2)) supplementation (MA-OVX+E(2)). Myocardial matrix metalloproteinases (MMPs),tissue inhibitors of metalloproteinases (TIMPs),and extracellular matrix (ECM) proteins were assessed by immunoblotting. RESULTS: Each of the 4 groups comprised 6 animals. Mean (SEM) LV mass was significantly greater in the MA-intact and the MA-OVX groups (1257 [31] mg and 1199 [25] mg, respectively; both, P < 0.05) compared with the young-intact group (697 [6] mg). LV mass in the MA-OVX+E(2) group was significantly lower compared with the MA-intact and MA-OVX groups (both, P < 0.05), suggesting that estrogen may attenuate LV remodeling. Fibronectin and collagen III and IV concentrations increased significantly in the MA-intact and MA-OOVX groups (all, P < 0.05),indicating increased fibrosis. Multiple MMPs also increased in the MA-intact an nd MA-OVX rats, including MMP-3, -7, -99, -113, and -114, and all TIMPs. In contrast, estrogen attenuated fibrosis by increasing MMP-8 concentrations and increasing collagen III fragments. From good-fit regression modeling, MMP-13 and MMP-14 concentrations correlated positively with LV mass for the MA-intact and MA-OVX groups, respectively. CONCLUSIONS: Gradual hypertension stimulated ECM turnover by increasing both MMP/TIMP production and ECM degradation.Estrogen loss or gain resulted in a shift in MMP profiles, suggesting that MMP-13 and MMP-14 may be differentially regulated in postmenopausal hypertension.
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Article Kidney function decline and physical function in women. 2008
Lin J, Curhan GC. · Renal Division, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. · Nephrol Dial Transplant. · Pubmed #18398018 No free full text.
Abstract: BACKGROUND: Cross-sectional analyses of kidney function and physical function have identified profound quality of life impairments in people with advanced kidney dysfunction. No data are currently available, however, on how kidney function decline may be associated with physical function. METHODS: We undertook a study of kidney function decline and physical function in 2544 women participating in the Nurses' Health Study. Glomerular filtration rates (GFR) were estimated using the four-variable MDRD equation from plasma creatinine measured in blood collected in 1989 and 2000. Physical function was assessed by the Physical Function Sub-Scale (PFS) score of the Short Form 36 (SF-36) in a questionnaire administered in the year 2000. PFS scores have been shown to correlate well with direct measures of physical function. RESULTS: In the year 2000, the median age was 67 years, median body mass index (BMI) was 25.6 kg/m(2), 48.5% had hypertension and 5.8% had diabetes. There were 427 women (16.8%) who experienced an >/=25% decline in eGFR between 1989 and 2000. Median PFS in 2000 for those with an eGFR decline of >/=25% was 80 compared to a PFS score of 85 for those without (P < 0.001). In fully adjusted models, the presence of an eGFR decline of >/=25% was independently associated with a 3.5-point lower PFS score (95% CI -5.4 to -1.5). Also, an eGFR decline of >/=25% was independently associated with an increased odds ratio of being in the lowest quartile of PFS score (OR 1.37; 95% CI 1.04-1.81). CONCLUSIONS: We conclude that an eGFR decline of >/=25% over 11 years is independently associated with lower physical function in women.
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Article Paroxysmal hypertension in a 48-year-old woman. 2008
Hunt J, Lin J. · Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. · Kidney Int. · Pubmed #18305464 No free full text.
This publication has no abstract.
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Article Age-related cardiac muscle sarcopenia: Combining experimental and mathematical modeling to identify mechanisms. free! 2008
Lin J, Lopez EF, Jin Y, Van Remmen H, Bauch T, Han HC, Lindsey ML. · Department of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA. · Exp Gerontol. · Pubmed #18221848 links to free full text
Abstract: Age-related skeletal muscle sarcopenia has been extensively studied and smooth muscle sarcopenia has been recently described, but age-related cardiac sarcopenia has not been previously examined. Therefore, we evaluated adult (7.5+/-0.5 months; n = 27) and senescent (31.8+/-0.4 months; n = 26) C57BL/6J mice for cardiac sarcopenia using physiological, histological, and biochemical assessments. Mice do not develop hypertension, even into senescence, which allowed us to decouple vascular effects and monitor cardiac-dependent variables. We then developed a mathematical model to describe the relationship between age-related changes in cardiac muscle structure and function. Our results showed that, compared to adult mice, senescent mice demonstrated increased left ventricular (LV) end diastolic dimension, decreased wall thickness, and decreased ejection fraction, indicating dilation and reduced contractile performance. Myocyte numbers decreased, and interstitial fibrosis was punctated but doubled in the senescent mice, indicating reparative fibrosis. Electrocardiogram analysis showed that PR interval and QRS interval increased and R amplitude decreased in the senescent mice, indicating prolonged conduction times consistent with increased fibrosis. Intracellular lipid accumulation was accompanied by a decrease in glycogen stores in the senescent mice. Mathematical simulation indicated that changes in LV dimension, collagen deposition, wall stress, and wall stiffness precede LV dysfunction. We conclude that age-related cardiac sarcopenia occurs in mice and that LV remodeling due to increased end diastolic pressure could be an underlying mechanism for age-related LV dysfunction.
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Article Refinement of survival prediction in patients undergoing lower extremity bypass surgery: stratification by chronic kidney disease classification. 2007
Owens CD, Ho KJ, Kim S, Schanzer A, Lin J, Matros E, Belkin M, Conte MS. · Division of Vascular Surgery, Brigham and Women's Hospital, Boston, MA 02115, USA. · J Vasc Surg. · Pubmed #17391900 No free full text.
Abstract: OBJECTIVE: End-stage renal disease (ESRD) imparts a significant survival disadvantage to individuals undergoing lower extremity revascularization; however, the influence of lesser degrees of renal impairment remains unclear. This study examined the prognostic significance of the chronic kidney disease (CKD) classification on survival, limb salvage, and graft patency in patients undergoing lower extremity arterial reconstruction. METHODS: A prospective registry was evaluated for consecutive patients between January 31, 1995, and December 21, 2004, undergoing first-time, lower extremity vein bypass surgery. Glomerular filtration rate (GFR) was estimated with the Modification of Diet in Renal Disease equation using each patient's preoperative creatinine concentration. CKD categories were taken from current National Kidney Foundation Kidney Disease Outcomes Quality Initiative staging criteria. RESULTS: The cohort included 456 subjects, with a mean (+/- SD) age of 68.1 +/- 10.8 years. There were 274 men (60%) and 378 Caucasians (82.5%). Comorbidities included diabetes mellitus in 270 (59.0%), hypertension in 333 (72.7%), coronary artery disease in 242 (52.8%), and dyslipidemia in 203 (44.5%). The surgical indication was critical limb ischemia in 384 (83.8%). Among the variables examined, diabetes and critical ischemia as the indication for bypass were significantly skewed toward higher CKD classifications (P < .001). The 5-year survival rates by CKD class were, CKD 1 and 2, 57%; CKD 3, 46%; CKD 4, 23%; and CKD 5, 9.5%. On univariate analysis, age, coronary artery disease, diabetes mellitus, hypertension, critical ischemia, and CKD were significant predictors of mortality. After adjustment, however, only age (hazard ratio [HR], 1.05, 95% confidence interval [CI], 1.03 to 1.06) and CKD stages 4 (HR, 4.23; 95% CI, 2.04 to 8.75) and 5 (HR, 3.27; 95% CI, 1.96 to 5.45) retained significance. Subjects within the CKD 5 classification were more likely to have a major amputation (P = .018) compared with all other CKD classes. Notably, no relationship was detected between CKD category and graft patency. CONCLUSION: CKD staging adequately differentiates survival curves and risk for major amputation among patients with renal impairment who are undergoing lower extremity bypass surgery. This may help in clinical decision analysis as well as in the refinement of stratification in future clinical trial design where survival is an end point.
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Article Inhibition of NAD(P)H oxidase reduces fibronectin expression in stroke-prone renovascular hypertensive rat brain. 2007
Cui C, Chen AF, Jiang Z, Wu Q, Lin J, Wen H, Zeng J. · Stroke Center and Department of Neurology, First Affiliated Hospital, Sun Yat-Sen University, No. 58 Zhongshan 2 Road, Guangzhou 510080, China. · Clin Exp Pharmacol Physiol. · Pubmed #17324142 No free full text.
Abstract: 1. The aim of the present study was to test the hypothesis that in vivo chronic inhibition of NAD(P)H oxidase reduces cerebrovascular fibronectin expression in stroke-prone renovascular hypertensive rats (RHRSP). 2. The RHRSP model was induced by two clips and NAD(P)H oxidase was inhibited with apocynin. The mRNA and protein expression of NAD(P)H oxidase subunit p22(phox) in brains of RHRSP and Sprague-Dawley (control) rats was determined using real-time reverse transcription-polymerase chain reaction, western blot and immunohistochemistry. The expression of fibronectin protein was localized immunohistochemically in cerebral vessels and then quantified by western blot. 3. Cerebrovascular fibronectin levels in RHRSP (n = 6) were significantly higher than control (n = 5) levels 8 weeks after operation (1.29 +/- 0.04 vs 1.15 +/- 0.02, respectively; P = 0.007). The p22(phox) immunopositive reactivity was localized in the cerebral vasculature of control rats and RHRSP. Furthermore, chronic treatment of RHRSP with apocynin, a selective NAD(P)H oxidase inhibitor, in the drinking water for 4 weeks (1.5 mmol/L, 5 weeks after operation) resulted in a significant decrease in the expression of p22(phox) protein (0.85 +/- 0.01 vs 0.93 +/- 0.01 in non-treated RHRSP; n = 5; P = 0.002), with a concomitant reduction of fibronectin levels in the cerebral vasculature (1.31 +/- 0.03 vs 1.56 +/- 0.05 in non-treated RHRSP; n = 5; P = 0.002). No significant differences were detected in the expression of p22(phox) mRNA and protein between RHRSP (4 and 8 weeks after renal artery constriction) and the control group. 4. These findings suggest that the chronic inhibition of NAD(P)H oxidase in vivo by apocynin reduces cerebrovascular fibronectin levels, which may lessen hypertensive cerebrovascular fibrosis.
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Article Etiologic factors associated with symptomatic achilles tendinopathy. 2006
Holmes GB, Lin J. · Department of Orthopaedic Surgery, Rush University Medical School, 800 South Wells, M30, Chicago, IL 60607, USA. · Foot Ankle Int. · Pubmed #17144959 No free full text.
Abstract: BACKGROUND: The purpose of this study was to determine if a statistical association exists between Achilles tendinopathy (also referred to as tendinosis) and obesity, diabetes mellitus, hypertension, the supplemental use of estrogen, and exposure to local or systemic steroids. METHODS: From July, 1997, to February, 2003, 82 patients with a diagnosis of Achilles tendinopathy were identified. The diagnosis of Achilles tendinopathy was confirmed by a review of medical records, radiographs, and MRI. There were 44 women and 38 men with an average age of 50 (range 27 to 77) years. For the parameters of obesity, hypertension, diabetes, steroid exposure, and the use of estrogen compounds, all patients were analyzed both cumulatively and stratified into subgroups by gender and age. Chi-square 2 x 2 tables were used to compare the observed prevalence of the parameters in patients with Achilles tendinopathy to the expected prevalence of these disorders and exposures in the population at large. RESULTS: Cumulatively, 98% percent (43 of 44 women; 29 of 38 men) had hypertension, diabetes, obesity, and steroid or estrogen exposure. Seventy-six percent of men (29) had hypertension, diabetes, and obesity, or steroid exposure. Sixty-eight percent of women (15 of 22) had a history of hormone replacement therapy and 44% (8 of 15) had a positive history for use of oral contraceptives. When compared with published national data using Chi-square analysis, the association between tendinopathy and hormone replacement therapy and oral contraceptives was found to be statistically significant with p-values of 0.01 and 0.001, respectively. For both women and men, obesity was statistically associated with Achilles tendinopathy with p-values of 0.025 and. 001, respectively. Hypertension was statistically associated with Achilles tendinopathy only for women. Diabetes mellitus and Achilles tendinopathy were found to have a statistical association only for men younger than 44 years old CONCLUSIONS: Obesity, hypertension, and steroids have as their end-organ effect a diminution of local microvascularity. The significant correlation of these factors with Achilles tendinopathy suggests the importance of their effect on microvascularity in the development of Achilles tendinopathy.
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Article Photodynamic therapy increases brain edema and intracranial pressure in a rabbit brain tumor model. 2006
Li F, Zhu G, Lin J, Meng H, Wu N, Du Y, Feng H. · Department of Neurosurgery, Southwest Hospital, The Third Military Medical University, Shapingpa, Chongqing, China. · Acta Neurochir Suppl. · Pubmed #16671498 No free full text.
Abstract: The objective of this study was to evaluate the effect of a single photodynamic therapy (PDT) on brain edema and intracranial pressure (ICP) in a rabbit model of brain tumor. A total of 57 adult New Zealand rabbits were assigned to 3 groups: the PDT group, the tumor group, and the tumor plus PDT group. Rabbits in the PDT group (n = 9) received PDT but no tumor implantation; rabbits in the tumor group (n = 18) received VX2 carcinoma implantation but no PDT; rabbits in the tumor plus PDT group (n = 30) received tumor implantation with subsequent PDT 16 days later. Brain edema and ICP levels were then evaluated. We found that ICP in the PDT group was 7.43 +/- 0.50 mmHg. After tumor implantation, ICP increased rapidly (18.43 +/- 1.10 mmHg, 21 days later). PDT alone did not increase ICP, but compared with that in the tumor group, ICP increased significantly in the tumor plus PDT group (9.55 +/- 1.32 vs. 13.31 +/- 1.13 mmHg, p < 0.01) 24 hours after treatment. Brain water content in the tumor group increased rapidly after tumor implantation. PDT again increased perineoplastic brain edema 24 hours after treatment (81.09 +/- 0.97% vs. 78.32 +/- 0.49%, p < 0.01). It should be noted that PDT alone did not induce brain edema. In conclusion, PDT causes transient brain edema and increases ICP in a rabbit brain tumor model.
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Article Predicting survival in patients requiring renal replacement therapy after cardiac surgery. 2006
Leacche M, Winkelmayer WC, Paul S, Lin J, Unic D, Rawn JD, Cohn LH, Byrne JG. · Division of Cardiac Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. · Ann Thorac Surg. · Pubmed #16564277 No free full text.
Abstract: BACKGROUND: We sought to develop and internally validate a prediction score for all-cause in-hospital mortality in patients who have acute renal failure and require renal replacement therapy after cardiac surgery. METHODS: From January 1992 to July 2001, 136 of 14,000 patients (0.9%) had acute renal failure requiring renal replacement therapy after cardiac surgery. Multivariate logistic regression analysis, based on pre-renal replacement therapy variables, was used to construct a predictive score for all causes of in-hospital mortality. Subsequently, the score was validated in 27 patients who underwent surgery between August 2001 and March 2003. RESULTS: In-hospital mortality was 58% (79 of 136). From the logistic regression model, we assigned a score (range, 0 to 6) based on the presence of independent predictors of operative mortality (preoperative creatinine < or = 1.5 mg/dL [odds ratio (OR) = 5.0], hypertension [OR = 4.4], predialysis coma [OR = 9.6], sepsis [OR = 6.4], and total bilirubin > or = 2 mg/dL [OR = 5.6]). Higher scores strongly predicted mortality: patients who scored 3 or higher before the initiation dialysis (n = 54), had a mortality rate of 94% (51 of 54). In contrast, patients who scored 1 or less on this scale (n = 36), had a mortality of 16% (6 of 36). In the validation cohort, the sensitivity of the new score at the cutoff of 2 or fewer points versus 3 or more points was 0.71, the specificity was 0.90, the positive predictive value was 0.92, and the negative predictive value was 0.64. CONCLUSIONS: The prediction score represents a simple and accurate tool for predicting in-hospital mortality associated with renal replacement therapy for cardiac surgery patients before the institution of this resource-intensive treatment.
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Article [Analysis of risk factors about stress urinary incontinence in female] 2003
Song YF, Lin J, Li YQ, He XY, Xu B, Hao L, Song J. · Department of Obstetrics and Gynecology, Fuzhou General Hospital, Najing Military Command, Fuzhou 350025, China. · Zhonghua Fu Chan Ke Za Zhi. · Pubmed #14728844 No free full text.
Abstract: OBJECTIVE: The aim was to assess the prevalence of stress urinary incontinence (SUI) in community dwelling women and to assess the relationship between the various risk factors and this disease. METHODS: Selecting the community of Gulou at random and sending questionnaires to 6,066 women who living there. The questionnaire was designed to investigate the lower urinary tract symptoms, especially urinary incontinence. The questionnaire included some questions such as: age, weight, occupation, the level of education, menopause pregnancy and delivery, delivery through vagina or by cesarean section, the maximum body weight of fetus, chronic disease (hypertension, diabetes mellitus, cough, constipation), operation in abdomen and pelvis, the behaviour of life (smoking, alcohol abuse, exercise), the prevalence and frequency of urinary incontinence, the quality of life and the recognition of this disease. RESULTS: The collecting rate was 92.1% (5,587/6,066). The prevalence of urinary incontinence was 18.1% and the prevalence of SUI was 8.8%. Age (OR: 1.010, 95% CI: 1.001 - 1.025), higher body mass index (OR: 1.092, 95% CI: 1.054 - 1.132), hypertension (OR: 2.342, 95% CI: 1.026 - 5.349), constipation (OR: 1.448, 95% CI: 1.216 - 1.725), multiple abortion (OR: 1.306, 95% CI: 1.113 - 1.533), multipara (OR: 1.205, 95% CI: 1.009 - 1.440), using abdominal pressure in laboring (OR: 1.684, 95% CI: 1.140 - 2.489), straight cutting of perineum (OR: 2.244, 95% CI: 1.162 - 4.334), perineum tear (OR: 2.576, 95% CI: 1.724 - 3.851), infection of perineal incision (OR: 5.988, 95% CI: 1.936 - 18.616) were risk factors of SUI in women. CONCLUSION: Many risk factors can cause urinary incontinence, among them age, pregnancy and childbirth are most important ones.
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Article [Association of single nucleotide polymorphism in human SCN7A gene with essential hypertension in Chinese] 2003
Zhang KX, Zhu DL, He X, Zhang Y, Zhang H, Zhao R, Lin J, Wang GL, Zhang KY, Huang W. · Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Second Medical University, Shanghai, 200025 PR China. · Zhonghua Yi Xue Yi Chuan Xue Za Zhi. · Pubmed #14669210 No free full text.
Abstract: OBJECTIVE: To identify the single nucleotide polymorphisms (SNPs) in the regulatory and coding regions of human SCN7A (sodium channel, voltage-gated, type VII, alpha polypeptide) gene and to investigate the association of some of these SNPs with essential hypertension (EH) in Chinese. METHODS: The promoter region, exons, as well as part of the introns of SCN7A gene were sequenced by a fluorescent labeling automatic sequencing method to identify and characterize the SNPs in Chinese population. SNP genotyping was performed by PCR-RFLP or direct DNA sequencing in unrelated EH patients and normotensive controls from a Chinese Han population residing in Shanghai area. Case-control studies on seven SNPs were first carried out in 96 patients and 96 normotensive controls. The positive finding was further verified in an extended study containing 288 patients and 288 controls. RESULTS: Thirty-two SNPs were identified through a 13,132 bp sequencing of SCN7A gene. Among them, seven were in regulatory region, ten in coding regions, one in 3'UTR and fourteen in introns. Thirty SNPs were novel SNPs, and a cSNP in exon 18 (SNP021) was associated with hypertension. CONCLUSION: The SNP021 in the gene SCN7A is associated with essential hypertension of Chinese Han population in Shanghai and the role of SCN7A gene in hypertension deserves to be further analyzed.
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Article 3D contrast-enhanced MR portography and direct X-ray portography: a correlation study. 2003
Lin J, Zhou KR, Chen ZW, Wang JH, Yan ZP, Wang YX. · Department of Radiology, ZhongShan Hospital, Fudan University, Shanghai, China. · Eur Radiol. · Pubmed #12764642 No free full text.
Abstract: Our objective was to compare 3D contrast-enhanced MR portography (3D CE MRP) on a 1.5-T MR imager with direct X-ray portography. Twenty-six consecutive patients underwent 3D CE MRP with in-plane resolution of 1.4 or 1.8 mm, and direct X-ray portography. The findings of these two methods were evaluated and compared. The main portal vein (PV), right PV with its anterior and posterior segmental branches, and left PV including its sagittal segment were shown clearly without diagnostic problem in all cases on MRP. The main PV appearance was accordant with MRP and X-ray. For intrahepatic PVs, the results agreed in 21 patients but disagreed in 5 patients. In 1 patient with a huge tumor in right liver, the right posterior PV was classified as occluded at MRP, but diffusely narrowed at X-ray. The findings of left intrahepatic PV were discordant in 3 patients with hepatocelluar carcinoma in the left lobe. The MRP demonstrated complete occlusion of the left PVs, whereas X-ray showed proximal narrowing and distal occlusion. In another patient with hepatocelluar carcinoma, a small non-occlusive thrombus involving the sagittal segment of the left PV was seen on MRP but not on X-ray. With demonstration of varices and portosystemic shunts, MRP showed results similar to those of X-ray, except one recanalized para-umbilical vein was excluded from the field of view at MRP due to the patient's limited ability of breathholding. The 3D CE MRP correlated well with direct X-ray portography in most cases, it was limited in distinguishing narrowing of an intrahepatic PV from occlusion, but it showed advantage in demonstrating small thrombus within PV.
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