219 research outputs found

    The compression type of coronary artery motion in patients with ST-segment elevation acute myocardial infarction and normal controls: a case-control study

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    <p>Abstract</p> <p>Background</p> <p>Prediction of the location of culprit lesions responsible for ST-segment elevation myocardial infarctions may allow for prevention of these events. A retrospective analysis of coronary artery motion (CAM) was performed on coronary angiograms of 20 patients who subsequently had ST-segment elevation myocardial infarction treated by primary or rescue angioplasty and an equal number of age and sex matched controls with normal angiograms.</p> <p>Findings</p> <p>There was no statistically significant difference between the frequency of CAM types of the ST-segment elevation acute myocardial infarction and control patients (p = 0.97). The compression type of CAM is more frequent in the proximal and mid segments of all three coronary arteries. No statistically significant difference was found when the frequency of the compression type of CAM was compared between the ST-segment elevation acute myocardial infarction and control patients for the individual coronary artery segments (p = 0.59).</p> <p>Conclusion</p> <p>The proportion of the compression type of coronary artery motion for individual artery segments is not different between patients who have subsequent ST-segment elevation myocardial infarctions and normal controls.</p

    Conversion of Urine Protein-Creatinine Ratio or Urine Dipstick Protein to Urine Albumin-Creatinine Ratio for Use in Chronic Kidney Disease Screening and Prognosis : An Individual Participant–Based Meta-analysis

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    Financial Support: The CKD-PC Data Coordinating Center is funded in part by a program grant from the U.S. National Kidney Foundation and the National Institute of Diabetes and Digestive and Kidney Diseases (R01DK100446). Various sources have supported enrollment and data collection, including laboratory measurements and follow-up, in the collaborating cohorts of the CKD-PC. These funding sources include government agencies, such as national institutes of health and medical research councils, as well as the foundations and industry sponsors listed in Supplemental Appendix 3 (available at Annals.org).Peer reviewedPostprin

    Prevalence of chronic kidney disease in population-based studies: Systematic review

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    which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Chronic kidney disease (CKD) is becoming a major public health problem worldwide. This article reviews the published evidence of prevalence of CKD in population-based study samples that used the standardized definition from the Kidney Disease Outcomes Quality Initiative of the National Kidney Foundation (K/DOQI) practice guideline, and particularly focus on performance of serum-creatinine based equations for GFR estimation. We provide a summary of available data about the burden of CKD in various populations. Methods: We performed a systematic review of available published data in MEDLINE. A combination of various keywords relevant to CKD was used in this research. Related data of included studies were extracted in a systematic way. Results: A total of 26 studies were included in this review. The studies were conducted in different populations, and the number of study participants ranged from 237 to 65181. The median prevalence of CKD was 7.2 % in persons aged 30 years or older. In persons aged 64 years or older prevalence of CKD varied from 23.4 % to 35.8%. Importantly, the prevalence of CKD strongl

    Inflammation gene variants and susceptibility to albuminuria in the U.S. population: analysis in the Third National Health and Nutrition Examination Survey (NHANES III), 1991-1994

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    <p>Abstract</p> <p>Background</p> <p>Albuminuria, a common marker of kidney damage, serves as an important predictive factor for the progression of kidney disease and for the development of cardiovascular disease. While the underlying etiology is unclear, chronic, low-grade inflammation is a suspected key factor. Genetic variants within genes involved in inflammatory processes may, therefore, contribute to the development of albuminuria.</p> <p>Methods</p> <p>We evaluated 60 polymorphisms within 27 inflammatory response genes in participants from the second phase (1991-1994) of the Third National Health and Nutrition Examination Survey (NHANES III), a population-based and nationally representative survey of the United States. Albuminuria was evaluated as logarithm-transformed albumin-to-creatinine ratio (ACR), as ACR ≥ 30 mg/g, and as ACR above sex-specific thresholds. Multivariable linear regression and haplotype trend analyses were conducted to test for genetic associations in 5321 participants aged 20 years or older. Differences in allele and genotype distributions among non-Hispanic whites, non-Hispanic blacks, and Mexican Americans were tested in additive and codominant genetic models.</p> <p>Results</p> <p>Variants in several genes were found to be marginally associated (uncorrected P value < 0.05) with log(ACR) in at least one race/ethnic group, but none remained significant in crude or fully-adjusted models when correcting for the false-discovery rate (FDR). In analyses of sex-specific albuminuria, <it>IL1B </it>(rs1143623) among Mexican Americans remained significantly associated with increased odds, while <it>IL1B </it>(rs1143623), <it>CRP </it>(rs1800947) and <it>NOS3 </it>(rs2070744) were significantly associated with ACR ≥ 30 mg/g in this population (additive models, FDR-P < 0.05). In contrast, no variants were found to be associated with albuminuria among non-Hispanic blacks after adjustment for multiple testing. The only variant among non-Hispanic whites significantly associated with any outcome was <it>TNF </it>rs1800750, which failed the test for Hardy-Weinberg proportions in this population. Haplotypes within <it>MBL2</it>, <it>CRP</it>, <it>ADRB2, IL4R</it>, <it>NOS3</it>, and <it>VDR </it>were significantly associated (FDR-P < 0.05) with log(ACR) or albuminuria in at least one race/ethnic group.</p> <p>Conclusions</p> <p>Our findings suggest a small role for genetic variation within inflammation-related genes to the susceptibility to albuminuria. Additional studies are needed to further assess whether genetic variation in these, and untested, inflammation genes alter the susceptibility to kidney damage.</p

    Fungal diversity notes 253–366: taxonomic and phylogenetic contributions to fungal taxa

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    Notes on 113 fungal taxa are compiled in this paper, including 11 new genera, 89 new species, one new subspecies, three new combinations and seven reference specimens. A wide geographic and taxonomic range of fungal taxa are detailed. In the Ascomycota the new genera Angustospora (Testudinaceae), Camporesia (Xylariaceae), Clematidis, Crassiparies (Pleosporales genera incertae sedis), Farasanispora, Longiostiolum (Pleosporales genera incertae sedis), Multilocularia (Parabambusicolaceae), Neophaeocryptopus (Dothideaceae), Parameliola (Pleosporales genera incertae sedis), and Towyspora (Lentitheciaceae) are introduced. Newly introduced species are Angustospora nilensis, Aniptodera aquibella, Annulohypoxylon albidiscum, Astrocystis thailandica, Camporesia sambuci, Clematidis italica, Colletotrichum menispermi, C. quinquefoliae, Comoclathris pimpinellae, Crassiparies quadrisporus, Cytospora salicicola, Diatrype thailandica, Dothiorella rhamni, Durotheca macrostroma, Farasanispora avicenniae, Halorosellinia rhizophorae, Humicola koreana, Hypoxylon lilloi, Kirschsteiniothelia tectonae, Lindgomyces okinawaensis, Longiostiolum tectonae, Lophiostoma pseudoarmatisporum, Moelleriella phukhiaoensis, M. pongdueatensis, Mucoharknessia anthoxanthi, Multilocularia bambusae, Multiseptospora thysanolaenae, Neophaeocryptopus cytisi, Ocellularia arachchigei, O. ratnapurensis, Ochronectria thailandica, Ophiocordyceps karstii, Parameliola acaciae, P. dimocarpi, Parastagonospora cumpignensis, Pseudodidymosphaeria phlei, Polyplosphaeria thailandica, Pseudolachnella brevifusiformis, Psiloglonium macrosporum, Rhabdodiscus albodenticulatus, Rosellinia chiangmaiensis, Saccothecium rubi, Seimatosporium pseudocornii, S. pseudorosae, Sigarispora ononidis and Towyspora aestuari. New combinations are provided for Eutiarosporella dactylidis (sexual morph described and illustrated) and Pseudocamarosporium pini. Descriptions, illustrations and / or reference specimens are designated for Aposphaeria corallinolutea, Cryptovalsa ampelina, Dothiorella vidmadera, Ophiocordyceps formosana, Petrakia echinata, Phragmoporthe conformis and Pseudocamarosporium pini. The new species of Basidiomycota are Agaricus coccyginus, A. luteofibrillosus, Amanita atrobrunnea, A. digitosa, A. gleocystidiosa, A. pyriformis, A. strobilipes, Bondarzewia tibetica, Cortinarius albosericeus, C. badioflavidus, C. dentigratus, C. duboisensis, C. fragrantissimus, C. roseobasilis, C. vinaceobrunneus, C. vinaceogrisescens, C. wahkiacus, Cyanoboletus hymenoglutinosus, Fomitiporia atlantica, F. subtilissima, Ganoderma wuzhishanensis, Inonotus shoreicola, Lactifluus armeniacus, L. ramipilosus, Leccinum indoaurantiacum, Musumecia alpina, M. sardoa, Russula amethystina subp. tengii and R. wangii are introduced. Descriptions, illustrations, notes and / or reference specimens are designated for Clarkeinda trachodes, Dentocorticium ussuricum, Galzinia longibasidia, Lentinus stuppeus and Leptocorticium tenellum. The other new genera, species new combinations are Anaeromyces robustus, Neocallimastix californiae and Piromyces finnis from Neocallimastigomycota, Phytophthora estuarina, P. rhizophorae, Salispina, S. intermedia, S. lobata and S. spinosa from Oomycota, and Absidia stercoraria, Gongronella orasabula, Mortierella calciphila, Mucor caatinguensis, M. koreanus, M. merdicola and Rhizopus koreanus in Zygomycota

    Estimated Glomerular Filtration Rate, Albuminuria, and Adverse Outcomes. An Individual-Participant Data Meta-Analysis

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    IMPORTANCE: Chronic kidney disease (low estimated glomerular filtration rate [eGFR] or albuminuria) affects approximately 14% of adults in the US. OBJECTIVE: To evaluate associations of lower eGFR based on creatinine alone, lower eGFR based on creatinine combined with cystatin C, and more severe albuminuria with adverse kidney outcomes, cardiovascular outcomes, and other health outcomes. DESIGN, SETTING, AND PARTICIPANTS: Individual-participant data meta-analysis of 27 503 140 individuals from 114 global cohorts (eGFR based on creatinine alone) and 720 736 individuals from 20 cohorts (eGFR based on creatinine and cystatin C) and 9 067 753 individuals from 114 cohorts (albuminuria) from 1980 to 2021. EXPOSURES: The Chronic Kidney Disease Epidemiology Collaboration 2021 equations for eGFR based on creatinine alone and eGFR based on creatinine and cystatin C; and albuminuria estimated as urine albumin to creatinine ratio (UACR). MAIN OUTCOMES AND MEASURES: The risk of kidney failure requiring replacement therapy, all-cause mortality, cardiovascular mortality, acute kidney injury, any hospitalization, coronary heart disease, stroke, heart failure, atrial fibrillation, and peripheral artery disease. The analyses were performed within each cohort and summarized with random-effects meta-analyses. RESULTS: Within the population using eGFR based on creatinine alone (mean age, 54 years [SD, 17 years]; 51% were women; mean follow-up time, 4.8 years [SD, 3.3 years]), the mean eGFR was 90 mL/min/1.73 m2 (SD, 22 mL/min/1.73 m2) and the median UACR was 11 mg/g (IQR, 8-16 mg/g). Within the population using eGFR based on creatinine and cystatin C (mean age, 59 years [SD, 12 years]; 53% were women; mean follow-up time, 10.8 years [SD, 4.1 years]), the mean eGFR was 88 mL/min/1.73 m2 (SD, 22 mL/min/1.73 m2) and the median UACR was 9 mg/g (IQR, 6-18 mg/g). Lower eGFR (whether based on creatinine alone or based on creatinine and cystatin C) and higher UACR were each significantly associated with higher risk for each of the 10 adverse outcomes, including those in the mildest categories of chronic kidney disease. For example, among people with a UACR less than 10 mg/g, an eGFR of 45 to 59 mL/min/1.73 m2 based on creatinine alone was associated with significantly higher hospitalization rates compared with an eGFR of 90 to 104 mL/min/1.73 m2 (adjusted hazard ratio, 1.3 [95% CI, 1.2-1.3]; 161 vs 79 events per 1000 person-years; excess absolute risk, 22 events per 1000 person-years [95% CI, 19-25 events per 1000 person-years]). CONCLUSIONS AND RELEVANCE: In this retrospective analysis of 114 cohorts, lower eGFR based on creatinine alone, lower eGFR based on creatinine and cystatin C, and more severe UACR were each associated with increased rates of 10 adverse outcomes, including adverse kidney outcomes, cardiovascular diseases, and hospitalizations

    A systematic review of clinical trials of pharmacological interventions for acute ischaemic stroke (1955-2008) that were completed, but not published in full

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    <p>Abstract</p> <p>Background</p> <p>We assessed the prevalence, and potential impact of, trials of pharmacological agents for acute stroke that were completed but not published in full. Failure to publish trial data is to be deprecated as it sets aside the altruism of participants' consent to be exposed to the risks of experimental interventions, potentially biases the assessment of the effects of therapies, and may lead to premature discontinuation of research into promising treatments.</p> <p>Methods</p> <p>We searched the Cochrane Stroke Group's Specialised Register of Trials in June 2008 for completed trials of pharmacological interventions for acute ischaemic stroke, and searched MEDLINE and EMBASE (January 2007 - March 2009) for references to recent full publications. We assessed trial completion status from trial reports, online trials registers and correspondence with experts.</p> <p>Results</p> <p>We identified 940 trials. Of these, 125 (19.6%, 95% confidence interval 16.5-22.6) were completed but not published in full by the point prevalence date. They included 16,058 participants (16 trials had over 300 participants each) and tested 89 different interventions. Twenty-two trials with a total of 4,251 participants reported the number of deaths. In these trials, 636/4251 (15.0%) died.</p> <p>Conclusions</p> <p>Our data suggest that, at the point prevalence date, a substantial body of evidence that was of relevance both to clinical practice in acute stroke and future research in the field was not published in full. Over 16,000 patients had given informed consent and were exposed to the risks of therapy. Responsibility for non-publication lies with investigators, but pharmaceutical companies, research ethics committees, journals and governments can all encourage the timely publication of trial data.</p
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