-
[show abstract]
[hide abstract]
ABSTRACT: Treatment of uremia is now dominated by dialysis, in some cases, patients are treated with dialysis for decades, but overall outcomes are disappointing. A number of studies have confirmed the relevance of several experimental insights to the pathogenesis of uremia, but the specific biomarkers of uremia have not been fully elucidated. Studies of the epigenome have attracted little interest in nephrology, especially in uremia. However, to date, our knowledge about the alterations in histone methylation in uremia is unclear. H3K9me3 variations were analyzed in peripheral blood mononuclear cells from 10 uremia patients and 10 healthy subjects, using chromatin immunoprecipitation followed by high-throughput sequencing (ChIP-seq). There were 96 genes with significantly different expressions in the uremia patients compared with the normal controls. Forty-two increased and 54 decreased H3K9me3 genes displaying significant differences were found in uremia patients compared with healthy subjects. Five positive genes, ras-related C3 botulinum toxin substrate 3 (RAC3), polycomb group ring finger 2 (PCGF2), myosin heavy chain 3 (MYH3), noggin (NOG), serpin peptidase inhibitor 8 (SERPINB8), were selected and quantified. Our studies indicate that there are significant alterations of H3K9me3 in uremia patients; these significant H3K9me3 candidates may help to explain the immunological disturbance and high cardiovascular complications in uremia patients. Such novel findings show the significance of H3K9me3 as a potential biomarker or promising target for epigenetic-based uremia therapies.
Hemodialysis International 04/2013; · 1.54 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The aim of this study was to investigate the differential expression characteristics and the roles of the genome-wide microRNAs (miRNAs) in immunoglobulin A nephropathy (IgAN) kidney tissues. We used Illumina high-throughput sequencing technology to evaluate the miRNAs expression of six biopsy tissues from IgAN and six normal renal cortex specimens from patients with renal cell carcinoma. We observed a total of 85 miRNAs that were differentially expressed in the six IgAN patients, of which 11 miRNAs were up-regulated and 74 miRNAs were down-regulated in patients' tissues compared with control tissues. Additionally, we identified 55 candidate novel miRNAs in our study, which comprised seven candidates who were detected in the IgAN group and 49 candidates who were detected in the control group. Only one candidate (miR-n-9) was expressed in both groups. The bioinformatics showed that the regulated target genes of differentially expressed miRNAs were associated with immune and renal pathological changes. The identification of specific tissue miRNAs in our study not only helped clarify the genetics or immunology mechanisms involved in the pathogenesis of IgAN but also helped explain the pathological changes in the kidney tissues. We hypothesize that some significant miRNAs might potentially serve as novel diagnostic biomarkers in IgAN patients.
Genome 03/2013; 56(3):161-9. · 1.65 Impact Factor
-
Weiguo Sui,
Minglin Ou,
Jinlong Liang,
Min Ding,
Jiejing Chen,
Wei Liu,
Ruo Xiao,
Xiaohua Meng,
Lijuan Wang,
Xiaohua Pan,
Peng Zhu,
Wen Xue,
Yue Zhang,
Hua Lin,
Fengyan Li,
Jianguo Zhang,
Yong Dai
[show abstract]
[hide abstract]
ABSTRACT: Osteopetrosis is a rare genetically heterogeneous disorder of bone metabolism characterized by increased skeleton density. In the past, standard methods for genetic diagnosis of osteopetrosis have primarily been performed by candidate genes screening and positional cloning. However, these methods are time and labor consumptive; and the genetic basis of approximately 30% of cases is yet to be elucidated. Here, we employed whole exome sequencing of two affected individuals from an osteopetrosis family to identify a candidate mutation in CLCN7 (Y99C). It was identified from a total of 1,757 and 1,728 genetic variations found in either patient, which were then distilled using filtering strategies and confirmed using Sanger sequencing. We identified this mutation in six family members, while not in population matched controls. This mutation was previous found in osteopetrosis patients by other researchers, our evolutionary analysis also indicated it is under extremely high selective pressure, and is likely to be critical for the correct function of ClC-7, and thus is likely to be the responsible cause of disease. Collectively, our data further indicated that mutation (Y99C) may be a cause of osteopetrosis, and highlights the use of whole exome sequencing as a valuable approach to identifying disease mutations in a cost and time efficient manner.
Gene 01/2013; · 2.34 Impact Factor
-
Weiguo Sui,
Minglin Ou,
Jiejing Chen,
Huan Li,
Hua Lin,
Yue Zhang,
Wuxian Li,
Wen Xue,
Donge Tang,
Weiwei Gong,
Ruohan Zhang,
Fengyan Li,
Yong Dai
[show abstract]
[hide abstract]
ABSTRACT: microRNAs are a type of small non-coding RNAs which play important roles in post-transcriptional gene regulation, and the characterization of microRNA expression profiling in peripheral blood mononuclear cells (PBMCs) from patients with Klinefelter syndrome requires further investigation. In this study, PBMCs were obtained from patients with Klinefelter syndrome and normal controls. After preparation of small RNA libraries, the two groups of samples were sequenced simultaneously using next generation high-throughput sequencing technology, and novel and known microRNAs were analyzed. A total of 9,772,392 and 9,717,633 small RNA reads were obtained; 8,014,466 (82.01%) and 8,104,423 (83.40%) genome-matched reads, 64 and 49 novel microRNAs were identified in the library of Klinefelter syndrome and the library of healthy controls, respectively. There were 71 known microRNAs with differential expression levels between the two libraries. Clustering of over-represented gene ontology (GO) classes in predicted targets of novel microRNAs in the Klinefelter syndrome library showed that the most significant GO terms were genes involved in the endomembrane system, nucleotide binding and kinase activity. Our data revealed that there are a large number of microRNAs deregulated in PBMCs taken from patients with Klinefelter syndrome, of which certain novel and known microRNAs may be involved in the pathological process of Klinefelter syndrome. Further studies are necessary to determine the roles of microRNAs in the pathological process of Klinefelter syndrome in the future.
Experimental and therapeutic medicine 11/2012; 4(5):825-831.
-
[show abstract]
[hide abstract]
ABSTRACT: Background: Long noncoding RNAs (lncRNAs) are transcripts longer than ~200 nucleotides with little or no protein-coding capacity. There is evidence that the lncRNAs are involved in a variety of biological functions and are associated with human diseases. The aim of this study was to reveal any potential lncRNA regulatory mechanism in uremia. Methods: Blood samples were obtained from 20 uremic patients not on dialysis and 20 healthy volunteers. The genome-wide analysis of lncRNA expression in peripheral blood mononuclear cells was completed by microarray assay and validated by quantitative real-time reverse transcriptase polymerase chain reaction (real-time qRT-PCR) analysis. Differentially expressed lncRNAs and mRNAs were identified through fold-change filtering. Gene ontology analysis and pathway analysis were performed with the standard enrichment computation method. The relationship between lncRNAs and adjacent protein-coding genes was determined by complex transcriptional loci analysis. Results: We identified thousands of lncRNAs and mRNA that were differentially expressed in uremic patients. Some lncRNAs are transcribed in complex loci with overlapping and antisense patterns relative to adjacent protein-coding genes. Differential expression of ZAP70 and BC133674 (ZAP70-ncRNA) was confirmed by RT-PCR. Conclusions: Some lncRNAs and their associated protein-coding genes are closely related and may be part of a potential regulatory mechanism of uremia, and lncRNAs will provide additional opportunities to advance our understanding of the basic biology of uremia.
Journal of nephrology 10/2012; · 1.65 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: OBJECTIVE: To investigate the expression of matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metallopropteinase-1 (TIMP-1) in the renal allografts of patients with chronic active antibody-mediated rejection (AMR), and to explore their role in the pathogenesis of AMR. METHODS: Immunohistochemistry assay and computer-assisted image analysis were used to detect the expression of MMP-2 and TIMP-1 in the renal allografts with interstitial fibrosis and tubular atrophy (IF/TA) in 46 transplant recipients and 15 normal renal tissue specimens as the controls. The association of the expression level of either MMP-2 or TIMP-1 with the pathological grade of IF/TA in AMR was analyzed. RESULTS: The expression of either MMP-2 or TIMP-1 was significantly increased in the renal allografts of the recipients as compared with the normal renal tissue (P < 0.05). MMP-2 expression tended to decrease, while TIMP-1 and serum creatinine increased along with the increase of pathological grade of IF/TA (P < 0.05). In IF/TA groups, the expression of TIMP-1 was positively correlated to serum creatinine level (r = 0.718, P < 0.05). CONCLUSIONS: It is suggested by the results that abnormal expressions of MMP-2 and TIMP-1 might play roles in the development of renal fibrosis in chronic AMR.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1128474926172838.
Diagnostic Pathology 10/2012; 7(1):141. · 1.64 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Mesangial proliferative glomerulonephritis (MsPGN) is one of the most common immune-mediated renal diseases. The mesangium is expanded and hypercellular, immuno-globulin deposits can be found in the mesangium, but the mechanism underlying its cause remains largely unclear. There is a large amount of evidence suggesting that long ﹥200 nucleotide) non-coding RNAs (lncRNA) have important regulatory functions in the epigenetic control of gene expression. Multiple lines of evidence increasingly link mutations and dysregulations of lncRNAs to a diverse number of human diseases. Through microarray expression analysis, tests show that thousands of lncRNAs and protein-coding genes are significantly differentially expressed in IgA-negative MsPGN. Some lncRNAs and their neighboring protein-coding genes are closely related and are cooperatively expressed. This may be part of a potential regulatory mechanism. The malfunction of regulation in the network of lncRNAs may be a possible mechanism for the development of IgA-negative MsPGN. Our observations suggest that some lncRNAs are closely related to IgA-negative MsPGN and may be playing an important role in this disease.
International Journal of Molecular Medicine 07/2012; 30(1):173-8. · 1.98 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Background: Mesangial proliferative glomerulonephritis (MePGN) is characterized by excessive mesangial cell proliferation and mesangial matrix expansion, which lead to glomerular sclerosis and obliteration and, in turn, to deteriorating renal function. To identify and quantify the total proteins in renal tissues of MePGN patients, we used isobaric tags for relative and absolute quantification (iTRAQ) technology, and then looked for differentially expressed proteome profiles in MePGN patients. Methods: Eight-plex iTRAQ coupled with multiple chromatographic fractionation and tandem mass spectrometry was used to analyze total proteins in renal tissues of MePGN patients. Proteins were identified using Mascot, compared to show any differential expression. Results: Among 512 distinct proteins identified, 113 proteins were up-regulated or down-regulated with a onefold or more alteration in levels across groups. Among of them, there was significant variation in our present iTRAQ study, which contains lamin A, actin, profilin-1, annexin-A1 and A2 up-regulated, and antiquitin and aldolase B down-regulated. Conclusion: iTRAQ-based quantitative proteomic technology is efficiently applicable for protein identification and relative quantitation of proteomes of renal tissue. Differentially expressed proteome profiles of MePGN patients are determined. Further investigation of the molecular mechanism of the involved proteins may help to better understand the pathogenesis of MePGN and to discover novel biomarker candidates, which may enable the development of new approaches to diagnosis of MePGN.
Journal of nephrology 05/2012; · 1.65 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Transcription factors (TFs) play a central role in regulating gene expression and in providing interconnecting regulatory networks between related pathway elements. Systemic lupus erythematosus (SLE) is an organ-nonspecific autoimmune disorder characterized by the production of autoantibodies against a host of nuclear antigens.
The pathogenesis of lupus is incompletely understood. Understanding the mechanisms that contribute to SLE and finding effect biomarkers to anticipate SLE will be of great value.
To investigate possible mechanisms, we describe a comparison of TF activity profiles between SLE and controls. Through TF assay analysis and electrophoretic mobility shift assay (EMSA) confirmation, we identified different activities of TFs in SLE.
Three hundred and forty-five TFs were detected in both groups, with 92 of them differentially expressed by TF array in which 78 TFs up-regulated and 14 TFs down-regulated in SLE compared with the control group, while 253 TFs showed no significant expression levels. The array data was consistent with the EMSA verification results.
Our data indicated that TFs may be potentially involved in the pathogenesis of SLE, and can help to diagnose, treat and prevent SLE. The method could simplify the assay of multiple TFs and may facilitate high-throughput profiling of large numbers of TFs.
International Journal of Rheumatic Diseases 04/2012; 15(2):212-9. · 0.81 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: At present, the diagnosis of nephrotic syndrome (NS) requires a renal biopsy which is an invasive procedure. We undertook this pilot study to develop an alternative method and potential new biomarkers for diagnosis, and validated a set of well-integrated tools called ClinProt to investigate serum petidome in NS patients.
The fasting blood samples from 49 patients diagnosed with NS by renal biopsy, including 17 mesangial proliferative glomerulonephritis (MsPGN), 12 minimal change nephrotic syndrome (MCNS), 10 focal segmental glomerulosclerosis (FSGS) and 10 membranous nephropathy (MN), were collected and screened to describe their variability of the serum peptidome. The results in NS group were compared with those in 10 control healthy individuals. Specimens were purified with magnetic beads-based weak cation exchange chromatography and analyzed in a MALDI-TOF MS.
The results showed 43, 61, 45 and 19 differential peptide peaks in MsPGN, MCNS, MN and FSGS groups, respectively. A Genetic Algorithm was used to set up the classification models. Cross validation of healthy controls from MsPGN, MCNS, MN and FSGS was 96.18, 100, 98.53 and 94.12 per cent, respectively. The recognition capabilities were 100 per cent.
Our results showed that proteomic analysis of serum with MALDI-TOF MS is a fast and reproducible approach, which may give an early idea of the pathology of nephrotic syndrome.
The Indian journal of medical research 03/2012; 135:305-11. · 1.84 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The purpose of the present study was to investigate the aberrance of histone H3 lysine 4 trimethylation (H3K4me3) in patients with IgA Nephropathy (IgAN).
In this study, H3K4me3 variations in peripheral blood mononuclear cells (PBMCs) from 15 IgAN patients and 15 healthy subjects were analyzed using chromatin immunoprecipitation linked to microarrays analysis (ChIP-chip). ChIP real-time PCR was used to validate the microarray results. Expression analysis by quantitative real-time PCR (qRT-PCR) revealed correlations between mRNA and H3K4me3 levels. DNA methylation status was analyzed by quantitative methylation-specific PCR.
We found that 321 probes displayed significant H3K4me3 differences in IgAN patients compared with healthy controls. Among these probes, 154 probes displayed increased H3K4me3 and 167 probes demonstrated decreased H3K4me3. For further validation, we selected 4 key relevant genes (FCRL4, GALK2, PTPRN2 and IL1RAPL1) to study. The results of ChIP real-time PCR coincided well with the microarray data. Quantitative RT-PCR revealed the correlations between the mRNA expression and the methylation levels of H3K4me3. Different degrees of DNA methylation alterations appeared on the selected positive genes.
Our studies indicated that there were significant alterations in H3K4me3 in IgAN patients. These findings may help to explain the disturbed immunity and abnormal glycosylation involved in IgAN patients.
Yonsei medical journal 03/2012; 53(2):377-85. · 0.77 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To explore the expression of Glycogen synthase kinase 3 beta (GSK-3β) in renal allograft tissue and its significance in the pathogenesis of chronic allograft dysfunction.
Renal allograft biopsy was performed in all of the renal allograft recipients with proteinuria or increased serum creatinine level who came into our hospital from January 2007 to December 2009. Among them 28 cases was diagnosed as chronic allograft dysfunction based on pahtological observation, including 21 males with a mean age of 45 ± 10 years old and 7 females with a mean age of 42 ± 9 years old. The time from kidney transplantation to biopsy were 1-9 (3.5) years. Their serum creatinine level were 206 ± 122 umol/L. Immunohistochemical assay and computer-assisted genuine color image analysis system (imagepro-plus 6.0) were used to detect the expression of GSK-3β in the renal allografts of 28 cases of recipients with chronic allograft dysfunction. Mean area and mean integrated optical density of GSK-3β expression were calculated. The relationship between expression level of GSK-3β and either the grade of inflammatory cell infiltration or interstitial fibrosis/tubular atrophy in renal allograft was analyzed. Five specimens of healthy renal tissue were used as controls.
The expression level of the GSK-3β was significantly increased in the renal allograft tissue of recipients with chronic allograft dysfunction, compared to normal renal tissues, and GSK-3β expression became stronger along with the increasing of the grade of either inflammatory cell infiltration or interstitial fibrosis/tubular atrophy in renal allograft tissue.
There might be a positive correlation between either inflammatory cell infiltration or interstitial fibrosis/tubular atrophy and high GSK-3β expression in renal allograft tissue. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here:http://www.diagnosticpathology.diagnomx.eu/vs/9924478946162998.
Diagnostic Pathology 01/2012; 7:5. · 1.64 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Immunoglobulin A nephropathy is the most common cause of chronic renal failure among primary glomerulonephritis patients. The ability to diagnose immunoglobulin A nephropathy remains poor. However, renal biopsy is an inconvenient, invasive, and painful examination, and no reliable biomarkers have been developed for use in routine patient evaluations. The aims of the present study were to identify immunoglobulin A nephropathy patients, to identify useful biomarkers of immunoglobulin A nephropathy and to establish a human immunoglobulin A nephropathy metabolic profile.
Serum samples were collected from immunoglobulin A nephropathy patients who were not using immunosuppressants. A pilot study was undertaken to determine disease-specific metabolite biomarker profiles in three groups: healthy controls (N = 23), low-risk patients in whom immunoglobulin A nephropathy was confirmed as grades I-II by renal biopsy (N = 23), and high-risk patients with nephropathies of grades IV-V (N = 12). Serum samples were analyzed using proton nuclear magnetic resonance spectroscopy and by applying multivariate pattern recognition analysis for disease classification.
Compared with the healthy controls, both the low-risk and high-risk patients had higher levels of phenylalanine, myo-Inositol, lactate, L6 lipids ( = CH-CH2-CH = O), L5 lipids (-CH2-C = O), and L3 lipids (-CH2-CH2-C = O) as well as lower levels of β -glucose, α-glucose, valine, tyrosine, phosphocholine, lysine, isoleucine, glycerolphosphocholine, glycine, glutamine, glutamate, alanine, acetate, 3-hydroxybutyrate, and 1-methylhistidine.
These metabolites investigated in this study may serve as potential biomarkers of immunoglobulin A nephropathy. Point scoring of pattern recognition analysis was able to distinguish immunoglobulin A nephropathy patients from healthy controls. However, there were no obvious differences between the low-risk and high-risk groups in our research. These results offer new, sensitive and specific, noninvasive approaches that may be of great benefit to immunoglobulin A nephropathy patients by enabling earlier diagnosis.
Clinics (São Paulo, Brazil) 01/2012; 67(4):363-73. · 1.59 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: In clinical practice, it is difficult to monitor the repeating relapse in patients suffering from systemic lupus erythematosus (SLE), who usually associated with some potential complications, for example, lupus nephritis (LN), repetition renal biopsy is necessary to determine LN flares. To identify and quantify the total proteins in renal tissue of LN patients, isobaric tags for relative and absolute quantification (iTRAQ) technology was performed. Eight-plex iTRAQ coupled with multiple chromatographic fractionation and tandem mass spectrometry were used to analyze total proteins in renal tissue of LN patients and healthy controls. Proteins were identified by mascot, which expressed differentially were noted. A total of 490 distinct proteins were identified, 113 proteins were up-regulation or down-regulation at one fold or more alteration in levels. Among of them, there was significant deviation of four proteins between our present iTRAQ study, which are up-regulated heterogeneous nuclear ribonucleoprotein (hnRNP-), Annexins and down-regulated Argininosuccinate synthetase (ASS), aldolase. iTRAQ-based quantitative proteomic technology is efficiently applicable for identification and relative quantitation of proteome of renal tissue. Differentially expressed proteome profiles of LN patients are determined. And further investigation is necessary using large cohorts of patient samples with long-term clinical follow-up data, to assess the usefulness of the pathogenesis and novel biomarker candidates of LN, which may develop a new way for diagnosis of LN.
Rheumatology International 11/2011; · 1.88 Impact Factor
-
Saudi medical journal 12/2010; 31(12):1378-9. · 0.52 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To investigate the expression of integrin-linked kinase (ILK) and collagen IV in renal allografts with interstitial fibrosis and tubular atrophy (IF/TA) in kidney transplant recipients, and explore its relationship with transforming growth factor-beta(1) (TGF-beta(1)) expression and the pathogenesis of IF/TA.
Immunohistochemical assay and computer-assisted genuine colored image analysis system were used to detect the expression of ILK, TGF-beta(1) and collagen IV in the renal allografts with IF/TA. The association between TGF-beta(1), collagen IV and ILK, as well as the relationship between their expressions and the pathological class of IF/TA, was analyzed. 10 specimens of healthy renal tissue were used as controls.
The expression levels of ILK, TGF-beta(1) and collagen IV in renal allografts were significantly higher, compared to normal renal tissues (P<0.001), and the expressions tended to increase along with the increase of pathological class of IF/TA. In IF/TA group, the expression of ILK was positively correlated with the expression of TGF-beta(1) and collagen IV (r=0.976 and r=0.912, respectively; P<0.001 for both).
It is suggested that by the data that ILK might mediate the mechanism through which TGF-beta(1) promote the abnormal deposition of ECM in renal allografts with IF/TA. ILK might play an important role in the progression of the interstitial fibrosis and tubular atrophy of human renal allografts and the development of chronic renal allograft dysfunction.
Transplant Immunology 05/2010; 23(1-2):1-5. · 1.46 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Proteomics is one of the emerging techniques for biomarker discovery. Biomarkers can be used for early noninvasive diagnosis and prognosis of diseases and treatment efficacy evaluation. In the present study, the well-established research systems of ClinProt Micro solution incorporated unique magnetic bead sample preparation technology, which, based on matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS), have become very successful in bioinformatics due to its outstanding performance and reproducibility for discovery disease-related biomarker. We collected fasting blood samples from patients with biopsy-confirmed acute renal allograft rejection (n = 12), chronic rejection (n = 12), stable graft function (n = 12) and also from healthy volunteers (n = 13) to study serum peptidome patterns. Specimens were purified with magnetic bead-based weak cation exchange chromatography and analyzed with a MALDI-TOF mass spectrometer. The results indicated that 18 differential peptide peaks were selected as potential biomarkers of acute renal allograft rejection, and 6 differential peptide peaks were selected as potential biomarkers of chronic rejection. A Quick Classifier Algorithm was used to set up the classification models for acute and chronic renal allograft rejection. The algorithm models recognize 82.64% of acute rejection and 98.96% of chronic rejection episodes, respectively. We were able to identify serum protein fingerprints in small sample sizes of recipients with renal allograft rejection and establish the models for diagnosis of renal allograft rejection. This preliminary study demonstrated that proteomics is an emerging tool for early diagnosis of renal allograft rejection and helps us to better understand the pathogenesis of disease process.
Clinical and Experimental Medicine 04/2010; 10(4):259-68. · 1.58 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Uremia is a term used to loosely describe the illness accompanying renal failure, in particular the nitrogenous waste products associated with the failure of this organ. At present, the diagnosis of uremia could be implemented by clinical symptoms, laboratory examinations, or image analysis. To develop alternative methods and potential new biomarkers for diagnosis, we employed a novel platform called ClinProt to investigate serum peptidome of uremia.
The first-morning serum samples from 30 patients, including 10 non-dialysis (ND), 10 peritoneal dialysis (PD), and 10 hemodialysis (HD) patients, were collected and screened to describe their variability of the serum peptidome. The results in uremia were compared to the findings in 13 normal controls. Specimens were purified with magnetic beads-based weak cation exchange chromatography and analyzed in a matrix-assisted laser desorption/ionization time-of-flight mass spectrometry.
Compared to normal controls, we screened 7, 7, and 9 significantly expressed polypeptides in ND, PD, and HD groups, respectively. Group comparisons were done by means of t-tests, the statistical significance was set at p < 0.05. A genetic algorithm was used to set up the classification models between uremia groups and normal controls. Cross-validation of normal controls from ND, PD, and HD was 99.30%, 95.12%, and 98.61%, respectively. The recognition capabilities were 100%.
We were able to identify serum protein fingerprints in small sample sizes of recipients with uremia and establish the models for diagnosis of uremia. This preliminary study demonstrated that proteomics is an emerging tool for early diagnosis of uremia and helps us to better understand the pathogenesis of the disease process.
Renal Failure 01/2010; 32(10):1153-9. · 0.82 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: This study investigated the gain of the human telomerase RNA gene TERC at 3q26 in patients with uterine cervix disease in the southern part of China and assessed the relationship between TERC gain and cervical pathological findings. One hundred ten cervical specimens, which were collected from patients with various kinds of uterine cervix disease that was subsequently diagnosed as chronic cervicitis and with examination results negative for intraepithelial lesion or malignancy (NILM, n = 23), mild dysplasia (cervical intraepithelial neoplasia type 1 [CIN1], n = 37), moderate dysplasia (CIN2, n = 12), severe dysplasia (CIN3, n = 10), and squamous cell carcinoma (SCA, n = 28) confirmed by histologic diagnosis, were analyzed for the proportion of abnormal cells with TERC gain using a commercially available 2-color fluorescence in situ hybridization (FISH) probe. The cases with a higher proportion of abnormal cells than the threshold evaluated by NILM were recorded as positive TERC gain. The chi and Kruskal-Wallis tests were used to assess the associations between FISH findings and diagnoses. The incidence of positive TERC gain in the cases diagnosed as NILM or CIN1 was significantly lower than that in cases diagnosed as CIN2, CIN3, or SCA (P < 0.01). In addition, a significantly higher proportion of abnormal cells with TERC gain was found as a pathological change from CIN1 to SCA (P < 0.01). We conclude that the TERC gain seems to be an important associated genetic event in CIN and carcinoma; FISH is a potential tool for the diagnoses of uterine cervix disease.
International Journal of Gynecological Cancer 11/2009; 19(8):1303-6. · 1.65 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The concordance rate between IHC and FISH according to clinical performance is still controversial. We report a prospective study to reflect the concordance between IHC and FISH in Guilin city, People's Republic of China.
Fifty cases of invasive ductal carcinoma of breast tested by IHC and scored as 0, 1+, 2+ and 3+ by pathologists were further analyzed by FISH using a commercially available double-color probe, and the FISH findings were compared with IHC test results.
A total concordance of 82.0% was observed with a Kappa coefficient of 0.640 (P<0.001). A high discordance was observed in 30.0% of the patients with IHC 2+, 7.1% in IHC 3+, 19.2% overall in IHC 0 and 1+.
The IHC can be used firstly to screen the HER-2 status, and FISH can be used as a supplementary role to IHC and 2+ and some negative cases. And only those cases with Her-2 status of IHC 3+ or FISH positive should be treated with Herceptin.
World Journal of Surgical Oncology 11/2009; 7:83. · 1.12 Impact Factor
