Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three oligonucleotide probes, complementary to tetM sequences, were labelled non-radiometrically using the DIG-oligonucleotide tailing kit and evaluated for their specificity for the detection of plasmid mediated tetracycline resistance in Neisseria gonorrhoeae. Only Probe 3, 5'-GCT CAA CAA TTC TGT TCC AGC-3', was specific for tetM. It hybridized with the tetM-containing 25.2-MDa plasmids from all of the 232 TRNG and the 130 PP/TRNG isolates used in the study. Its sensitivity, determined by dot-blot hybridization, was 0.1 pg of pJ13 plasmid DNA or 10(4) cells. It did not hybridize with the DNA from non-PPNG, CMRNG and tetracycline susceptible isolates from seven other Neisseria species (N. meningitidis, N. subflava, N. cinerea, N. lactamica, N. sicca, N. mucosa, and N. flavescens), Moraxella spp. and Haemophilus influenzae. Probe 3 also hybridized to DNA of three tetracycline resistant P. magnus (MIC = 16 micrograms ml-1) isolates which presumptively carried the tetM determinant. Therefore, probe 3 can be used by reference laboratories as a confirmatory test for TRNG, as well as isolates from other genera containing the tetM determinant.
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PMID:Detection of the tetM determinant in Neisseria gonorrhoeae using a non-radioactively labelled oligonucleotide probe. 796 93

The aim of this study was to establish reference intervals for cerum cystatin C and serum creatinine in adults. Blood samples were collected from 270 healthy blood donors (135 men and 135 women between 20 and 65 years old with 15 men and 15 women in each five-year-interval). Serum cystatin C was analyzed using an automated particle-enhanced immunoassay (DAKO Cystatin C PET kit) on the Cobas Mira S analyzer. Serum creatinine was analyzed using the Vitros Creatinine Slide, an enzymatic method on the Vitros 950 chemistry analyzer. The calculated reference intervals for serum cystatin C were 0.62-1.15 mg/l in women (median 0.84 mg/l, range 0.56-1.29 mg/l) and 0.51-1.25 mg/l in men (median 0.87 mg/l, range 0.42-1.39 mg/l). The Mann-Whithey U-test revealed no gender-related difference for cystatin C (p = 0.48). A common reference interval in women and men was calculated to be 0.54-1.21 mg/l (median 0.85 mg/l, range 0.42-1.39 mg/l). The non-parametric reference interval for serum creatinine was 57-95 mumol/l in women (median 72 mumol/l, range 44-105 mumol/l) and 69-111 mumol/l in men (median 89 mumol/l, range 58-123 mumol/l).
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PMID:Reference intervals for serum cystatin C and serum creatinine in adults. 971 28

The search for whether endogenous markers of changes in glomerular filtration rate (GFR) by serum cystatin C assay and serum cystatin C compare with creatinine clearance by the Cockeroft-Gault formula and the evaluation of its clinical significance as a marker of GFR is important in clinical practice at present. Serum cystatin C was determined by sandwich enzyme immunoassay using a kit. Control blood samples were collected from 70 healthy subjects and 168 patients with various kidney diseases. Creatinine clearance (Cockeroft-Gault formula) as a measure of GFR, in 168 patients with various kidney diseases, depends on the creatinine clearance; GFR parameters were used to divide patients into two groups. The GFR was >80 mL/min in 38 patients (group A) and <80 mL/min in 130 patients (group B). The two groups were analyzed by correlation coefficient and diagnostic sensitivity and specificity were assessed by the receiver-operating characteristic (ROC) plots (area under the curve). Of the 70 healthy control individuals, the serum level of cystatin C was measured as normal value range and a reference interval of 1.05+/-0.18 micro g/mL (mean+/-1.96 SD, 95% confidence limits for the upper references limit is 1.4 microg/mL). In group A, serum cystatin C had no correlation to the creatinine clearance (r=0.171, P>0.05) and in group B, serum cystatin C was closely correlated to the creatinine clearance (r=-0.771, P<0.001). Diagnostic sensitivity and specificity were assessed by the ROC plots for serum cystatin C (area under the curve=0.8461, SE=0.057) and creatinine clearance (area under the curve=0.7642, SE=0.068). These data suggest that combined measurement of serum cystatin C is useful to estimate GFR, especially to detect the reduction of GFR. Further studies are required to evaluate the whether serum cystatin C as a more sensitive marker of early renal injury might be extremely useful, particularly in nonproteinuric or unapparent renal disease.
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PMID:Clinical value of serum cystatin C by ELISA for estimation of glomerular filtration rate. 1506 9

Cystatin C, known as an inhibitor of the cathepsin family of cysteine proteases, has been evaluated in several cardiovascular disorders such as atherosclerosis and acute myocardial infarction. The potential interaction between transforming growth factor-beta1 and cystatin C has also been demonstrated in some cell types. Accordingly, we aimed to compare the plasma levels of cystatin C and transforming growth factor-beta1 in patients with coronary artery ectasia coexisting with coronary artery disease and those with coronary artery disease alone. Thirty-nine patients with coronary artery ectasia and coronary artery disease and 35 age and sex-matched patients with coronary artery disease alone were prospectively enrolled in the study. Blood samples of all patients and control participants for measuring plasma cystatin C and transforming growth factor-beta1 levels were drawn>or=24 h after the coronary angiography. Cystatin C concentrations in plasma were measured by latex-enhanced reagent on a Behring Nephelometer II. Plasma levels of transforming growth factor-beta1 were measured by using transforming growth factor-beta1 enzyme-linked immunosorbent assay kit (BioSource International, Inc., Camarillo, California, USA). Plasma level of cystatin C was significantly higher in patients with coronary artery ectasia+coronary artery disease than in patients with coronary artery disease alone (1.05+/-0.30 mg/dl vs. 0.92+/-0.18 mg/mdl, P=0.025, respectively). Transforming growth factor-beta1 was also found to be significantly higher in patients with coronary artery ectasia+coronary artery disease compared with those with coronary artery disease (2.47+/-0.43 vs. 2.22+/-0.43 pg/ml, P=0.02, respectively). The plasma level of cystatin C was significantly but weakly correlated with that of transforming growth factor-beta1 (r=0.217 P=0.02). We conclude that plasma levels of cystatin C and transforming growth factor-beta1 are significantly higher in patients with combined coronary artery ectasia and coronary artery disease than in those with coronary artery disease. Correlation between transforming growth factor-beta1 and cystatin C may also suggest that pathogenesis of coronary artery ectasia might have some different pathways from atherosclerosis with respect to the regulation of extracellular matrix remodeling. Therefore, the role of cystatin in the pathogenesis of coronary artery ectasia and its potential interaction with transforming growth factor-beta1 should be evaluated in further studies.
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PMID:Increased plasma levels of cystatin C and transforming growth factor-beta1 in patients with coronary artery ectasia: can there be a potential interaction between cystatin C and transforming growth factor-beta1. 1742 95

A human kit for cystatin C determination was evaluated for use with canine sera. A reference range was also established. The association between cystatin C and glomerular filtration rate (GFR) was evaluated in 60 dogs with various diseases, by using exogenous creatinine plasma clearance (ECPC) as a measure of GFR. The correlation between cystatin C and ECPC (correlation coefficient [r] = -0.630; P<0.001) was stronger than the correlation between serum creatinine and ECPC (r = -0.572; P<0.001). Nonrenal diseases (e.g., neoplasia, infection) did not influence serum cystatin C concentration. Test sensitivity was significantly better (P<0.001) for cystatin C (76%) than for creatinine (65%). Specificities for the two tests were 87% and 91%, respectively.
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PMID:Utility of serum cystatin C as a clinical measure of renal function in dogs. 1845 Oct 71

Amyotrophic lateral sclerosis (ALS) is diagnosed on the basis of progressive symptoms in both the upper and lower motor neurons. Because there are no specific biomarkers for ALS, it is difficult to diagnose this disease in its early stages. Cerebrospinal fluid (CSF) samples were obtained from 14 patients in the early stages of ALS, from 13 with polyneuropathy, and from 16 with other neurological disorders. The concentration of cystatin C in the CSF was measured using a sandwich enzyme-linked immunosorbent assay (ELISA) kit. The concentration of cystatin C in the CSF was significantly lower in ALS patients than in the control subjects who were patients with polyneuropathy or other neurological diseases (patients with ALS, polyneuropathy, and other diseases exhibited 5.5 +/- 0.3, 6.7 +/- 0.4, and 6.9 +/- 0.3 mg/L cystatin C, respectively; ALS patients vs. control subjects: p = 0.014 and ALS patients vs. polyneuropathy patients: p = 0.024). Cystatin C may be a useful biomarker of ALS and can be used to distinguish between ALS and polyneuropathy.
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PMID:Cystatin C in cerebrospinal fluid as a biomarker of ALS. 1944 52

Copeptin is cosynthesized with vasopressin, also known as antidiuretic hormone, with plasma levels similar to vasopressin. In the past 2 years, copeptin has been studied as a diagnostic and prognostic marker in infections and other diseases. In patients with destabilized heart failure, copeptin is an accurate prognostic marker for mortality. The aim of this study was to assess copeptin in orthotopic heart recipients in relation to New York Heart Association class and kidney function. The studies were performed on 139 prevalent patients after orthotopic heart transplantation-(OHT) including 105 males and 34 females. Glomerular filtration rate (GFR) was estimated using simplified Modification of Diet in Renal Disease (MDRD), Cockcroft-Gault, and new the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. In addition 24-hour creatinine clearances were performed on each patient. Complete blood count, urea, serum lipids, fasting glucose, creatinine, BNP were studied by standard laboratory method in the hospital central laboratory. Plasma copeptin was measured using a commercially available kit. Copeptin correlated with parameters of kidney function: creatinine (r = .39, P < .001), estimated GFR by MDRD (r = -.24, P < .01), estimated GFR by CKD-EPI (r = -.25, P < .01), creatinine clearance by Cockcroft-Gault (r = -.27, P < .01), 24-hour creatinine clearance (r = -.21, P < .05), cystatin C (r = .45, P < .001), and high-density lipoprotein (r = .18, P < .05), BNP (r = .25, P < .01), intraventricular septal diameter/thickness (IVS); r = -.30, P < .01), ejection fraction (r = -.17, P < .05), ferritin (r = .21, P < .05). Upon multiple regression analysis, predictors of copeptin were cystatin C and IVS, which explained 51% of copeptin variations (F = 3.21, P < .03 and Standard error of estimate was 0.57). Beta value for cystatin C was 0.51 (P = .024) and for IVS was -0.59 (P = .018). Copeptin in a heart transplant population was independently associated with kidney function and IVS.
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PMID:Copeptin in heart transplant recipients depends on kidney function and intraventricular septal thickness. 2062 May 28

Base editing is a promising technique, allowing precise single-base mutagenesis in genomes without double-strand DNA breaks or donor templates. Cytosine base editors (CBEs) convert cytosine to thymidine. In particular, CBEs can transform four codons, CAA, CAG, CGA, and TGG, into stop codons, providing a new means to rapidly inactivate a gene of interest and enabling loss-of-function study in recombination-deficient species and the construction of gene-inactivation libraries. However, designing single guide RNAs (sgRNAs) for gene inactivation is more complicated and more restricted in applicability than using the lustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated (CRISPR/Cas9) system only, especially for researchers who do not specialize in the bioinformatics skills needed to design and evaluate sgRNAs. Here, we present a new user-friendly designing tool kit, namely, CRISPR-CBEI (cytosine base editor-mediated gene inactivation), including a Web tool and a command-line tool. The Web tool is dedicated to the design of sgRNAs for CBE-mediated gene inactivation and integrates various functions, including open reading frame (ORF) identification, CBE customization, sgRNA designing, summarizing, and front-end off-target searching against user-defined unlimited-file-size local genome files without the necessity of uploading to the server. The command-line version serves the same purpose but for a larger number of coding DNA sequences (CDSs), for instance, for designing a CBE-inactivation library in a target species which provides comprehensive evaluations of CBEs and target genomes. We envision that this tool would contribute to CBE-inactivation design.IMPORTANCE Life science has been in pursuit of precise and efficient genome editing in living cells since the very beginning of the first restriction cloning attempt. The introduction of RNA-guided CRISPR-associated (Cas) nucleases contributed to this ultimate goal through their ability to deliver a double-strand break (DSB) to a precise target location in various species, obsoleting the preceding editing tools, such as zinc-finger nucleases (ZFNs) and transcription activator-like effector nucleases (TALENs). The derivative technology, base editing, combines the catalytically inactivated Cas nuclease and nucleotide deaminase and mediates the genetic modifications at single-nucleotide precision without introducing a DSB. Moreover, the cytosine base editors (CBEs) are able to transform multiple codons into stop codons, rapidly inactivating a gene of interest and enabling loss-of-function study in some recombination-deficient species. Here, we present the CRISPR-CBEI tool kit to assist the design of sgRNAs for CBE-mediated gene inactivation.
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PMID:CRISPR-CBEI: a Designing and Analyzing Tool Kit for Cytosine Base Editor-Mediated Gene Inactivation. 3296 98