OBJECTIVE: To analysis the specific protein markers of essential thrombocythemia (ET) based on proteomics technology, to explore and verify the differential protein related to platelet activation. METHODS: Blood samples were obtained from ET patients and healthy people and a certain protein mass spectrometry was detected using label-free quantitative technology. The proteins relative abundance increased or down-regulated by 1.3 times in the disease group compared with the control group, and the protein abundance in the two groups t test P＜0.05 were defined as differential proteins. Bioinformatics analysis of the differential proteins was performed using GO and KEGG. The difference in the average protein abundance between the two groups was analyzed by t test and P＜0.05 was considered statistically significant. Differential proteins were selected for verification by parallel reaction monitoring (PRM) technology. RESULTS: A total of 140 differential proteins were found, of which 72 were up-regulated and 68 were down-regulated. KEGG enrichment showed that the differential protein expression was related to the platelet activation pathway. The differential proteins related to platelet activation were GPV, COL1A2, GP1bα, COL1A1 and GPVI. Among them, the expressions of GPV, GP1bα and GPVI were up-regulated, and the expressions of COL1A2 and COL1A1 were down-regulated. PRM verification of COL1A1, GP1bα, GPVI and GPV was consistent with LFP proteomics testing. CONCLUSION Differential proteins in ET patients are related to platelet activation pathway activation.Differential proteins such as GPV, GPVI, COL1A1 and GP1bα can be used as new targets related to ET platelet activation.
Blood Platelets/metabolism* ; Humans ; Platelet Activation ; Platelet Membrane Glycoproteins/metabolism* ; Technology ; Thrombocythemia, Essential

Aged ; Aged, 80 and over ; Alzheimer Disease/diagnosis* ; Animals ; Biomarkers/blood* ; Cognitive Dysfunction ; Female ; Humans ; Male ; Membrane Glycoproteins/blood* ; Mental Status and Dementia Tests ; Mice ; Middle Aged ; Models, Animal ; Morris Water Maze Test ; Parkinson Disease/diagnosis* ; ROC Curve ; Receptors, Immunologic/blood* ; Sensitivity and Specificity

Blood Platelets ; Humans ; Platelet Membrane Glycoproteins ; Thrombosis

ObjectiveRapid eye movement sleep behavior disorder (RBD) is characterized by dream enactment and loss of muscle atonia during rapid eye movement sleep. RBD is closely related to α-synucleinopathies including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Many studies have investigated the markers of imaging and neurophysiological, genetic, cognitive, autonomic function of RBD and their predictive value for neurodegenerative diseases. This report reviewed the progress of these studies and discussed their limitations and future research directions.

Data SourcesUsing the combined keywords: "RBD", "neurodegenerative disease", "Parkinson disease", and "magnetic resonance imaging", the PubMed/MEDLINE literature search was conducted up to January 1, 2018.

Study SelectionA total of 150 published articles were initially identified citations. Of the 150 articles, 92 articles were selected after further detailed review. This study referred to all the important English literature in full.

ResultsSingle-nucleotide polymorphisms in SCARB2 (rs6812193) and MAPT (rs12185268) were significantly associated with RBD. The olfactory loss, autonomic dysfunction, marked electroencephalogram slowing during both wakefulness and rapid eye movement sleep, and cognitive impairments were potential predictive markers for RBD conversion to neurodegenerative diseases. Traditional structural imaging studies reported relatively inconsistent results, whereas reduced functional connectivity between the left putamen and substantia nigra and dopamine transporter uptake demonstrated by functional imaging techniques were relatively consistent findings.

ConclusionsMore longitudinal studies should be conducted to evaluate the predictive value of biomarkers of RBD. Moreover, because the glucose and dopamine metabolisms are not specific for assessing cognitive cognition, the molecular metabolism directly related to cognition should be investigated. There is a need for more treatment trials to determine the effectiveness of interventions of RBD on preventing the conversion to neurodegenerative diseases.

Biomarkers ; blood ; Humans ; Lysosome-Associated Membrane Glycoproteins ; genetics ; Neurodegenerative Diseases ; blood ; genetics ; physiopathology ; Parkinson Disease ; blood ; genetics ; physiopathology ; Polymorphism, Single Nucleotide ; genetics ; REM Sleep Behavior Disorder ; blood ; genetics ; physiopathology ; Receptors, Scavenger ; genetics ; tau Proteins ; genetics

OBJECTIVETo determine the diagnostic values of plasma CD64 and soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) in children with pneumonia.

METHODSSixty children with pneumonia between August 2014 and October 2015 were classified into bacterial pneumonia group (25 cases), viral pneumonia group (17 cases), and Mycoplasma pneumonia group (18 cases) according to their clinical manifestations, pathogen cultures, and X-ray findings. Another 30 healthy children who underwent physical examination during the same period were selected as the control group. The concentrations of CD64 and sTREM-1 in blood samples were determined using ELISA. The receiver operating characteristic (ROC) curve was used to evaluate the diagnostic sensitivity and specificity of plasma CD64 and/or sTREM-1 for bacterial pneumonia.

RESULTSThe expression of CD64 and sTREM-1 in the bacterial pneumonia group was significantly higher than that in the viral pneumonia, Mycoplasma pneumonia, and control groups (P<0.05). The areas under the ROC curves of CD64, sTREM-1, and a combination of the two markers for diagnosing bacterial pneumonia were 0.878, 0.805, and 0.956, respectively. The sensitivity and specificity of CD64 for diagnosing bacterial pneumonia were 81.30% and 92.32%, respectively, when the cut-off value was 641 pg/mL. The sensitivity and specificity of sTREM-1 for diagnosing bacterial pneumonia were 78.65% and 84.67%, respectively, when the cut-off value was 1 479 pg/mL. The sensitivity and specificity of a combination of the two markers for diagnosing bacterial pneumonia were 93.15% and 91.54%, respectively.

CONCLUSIONSPlasma CD64 and sTREM-1 can be used as markers for diagnosing pediatric bacterial pneumonia, and a combination of the two markers results in better diagnosis.

Biomarkers ; blood ; Child ; Female ; Humans ; Male ; Membrane Glycoproteins ; blood ; Pneumonia ; blood ; diagnosis ; ROC Curve ; Receptors, IgG ; blood ; Receptors, Immunologic ; blood ; Triggering Receptor Expressed on Myeloid Cells-1

OBJECTIVETo study the role of triggering receptor expressed on myeloid cells-1(TREM-1) in the pathogenesis of Kawasaki disease (KD).

METHODSBased on color Doppler examination results, 45 children with KD were classified into two groups: coronary artery lesions (CAL group) and no coronary artery lesions (NCAL group). Fifteen children with fever caused by respiratory infection (fever control group) and fifteen healthy children (normal control group) served as controls. Real-time fluorescence quantitative PCR was used to detect the expression of TREM-1 mRNA and DNAX-activating protein 12 (DAP12) mRNA in peripheral blood mononuclear cells (PBMC). ELISA was used to detect the expression of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1), DAP12, monocyte chemoattractant protein-1(MCP-1), interleukin-8 (IL-8) proteins levels.

RESULTSThe mean serum protein concentrations of sTREM-1 and DAP12 and the expression levels of TREM-1 mRNA and DAP12 mRNA in PBMC in 45 children with KD (KD group) were significantly higher than in the two control groups (P<0.05). The levels of sTREM-1 protein and TREM-1 mRNA in the CAL subgroup were significantly higher than in the NCAL subgroup (P<0.05). The serum protein concentrations of MCP-1 and IL-8 in the KD group were significantly higher than in the two control groups (P<0.05). The MCP-1 protein level in the CAL subgroup was significantly higher than in the NCAL subgroup (P<0.05). In children with KD, there was a positive correlation between serum sTREM-1 and MCP-1 levels (r=0.523, P<0.05).

CONCLUSIONSTREM-1 activation may be involved in the development of KD.

Chemokine CCL2 ; blood ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Interleukin-8 ; blood ; Male ; Membrane Glycoproteins ; blood ; genetics ; physiology ; Mucocutaneous Lymph Node Syndrome ; etiology ; immunology ; RNA, Messenger ; analysis ; Receptors, Immunologic ; blood ; genetics ; physiology ; Triggering Receptor Expressed on Myeloid Cells-1

OBJECTIVETo explore the dynamic variation rule of kidney injury makers of molecule 1 (KIM-1), Cystatinc (Cys-C), Blood urea nitrogen (BUN) and Creatinine (Cr) in kidney injury in rats with acute paraquat poisoning.

METHODSHealthy adult rats were randomly divided into control group (normal saline solution) and exposure group (2% paraquat solution 40 mg/kg), and 90 in each group. Six rats in each group were randomly sacrificed at one, one point five, two, three, six, twelve, twenty four, seventy two or one hundred and sixty eight hours after different administration, abdominal aortic blood and the kidney tissue were collected. The concenstrations of kidney injury makers of molecule 1 (KIM-1), cystatinc (Cys-C), blood urea nitrogen (BUN) and creatinine (Cr) were determined by ELASA. The concenstrations of paraquat were determined by HPLC. Pathological changes of kidney tissue that stained by HE were axamined by optical microscopy. The cell apoptosis in kidney tissue were analyzed by TUNEL assay. The ptotein expression of KIM-1 was determined by immunohistochemistry.

RESULTSSerum levels of KIM-1 were significantly increased in exposure group as compared with control group at two, three, six, twelve, twenty four, seventy two or one hundred and sixty eight hours, and the peak level was at twenty four hours, and there was a statistical significance between control group and exposure group (P < 0.01). Serum levels of Cys-C were significantly increased in exposure group as compared with control group at six, twelve, twenty four, seventy two or one hundred and sixty eight hours, the peak level was at twenty four hours, and there was a statistical significance between control group and exposure group (P < 0.01). Serum levels of BUN were significantly increased in exposure group as compared with control group at twelve, twenty four, seventy two or one hundred and sixty eight hours, and the peak level was at seventy two hours, and there was a statistical significance between control group and exposure group (P < 0.01). Compared with control group, there was mild tubular epithelial cells edema in exposure group of three hours, serious epithelial cells edema and few slightly increased glomeruli in exposure group of six hours, severe epithelial cells swelling, tube formation, and interstitial lesions including edema, congestionin and increased inflammatory cell infiltration in exposure group of twelve hours, these pathologic changes gradually reached the peak at twenty four hours, the pathologic injury score was 5.56 ± 0.0349 (P < 0.01), and then the pathological lesion was more palliative. Apoptosis rate of kidney tissue were significantly increased in exposure group as compared with control group at three, six, twelve, twenty four, seventy two or one hundred and sixty eight hours, and the peak level was at twenty four hours, and there was a statistical significance between control group and exposure group (P < 0.01). The immunohistochemical assay indicated that KIM-1 of control group were weakly positive expressed in tubular epithelial cell membrane, but the positive expression of KIM-1 were slightly increased in exposure group of two hours, the.immunohistochemistry score was 5.47 ± 0.1033 (P < 0.05), the positive expression of KIM-1 were gradually increased in exposure group of three, six and twelve hours, it reached peak at twenty four hours, the.immunohistochemistry score was 11.73 ± 0.4676 (P < 0.01), then the positive expression of KIM-1 decreased, but there was still positive expression at one hundred and sixty eight hours.

CONCLUSIONSerum levels of KIM-1 and Cys-C were significantly increased in the kidney injury in rats with acute paraquat poisoning in early stage, earlier than the changes of BUN and Cr. KIM-1 had relation with apoptosis rate. Cys-C had relation with pathological lesion changes.

Animals ; Blood Urea Nitrogen ; Creatinine ; blood ; Cystatin C ; blood ; Immunohistochemistry ; Kidney ; drug effects ; pathology ; Membrane Glycoproteins ; blood ; Paraquat ; poisoning ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the protective effect of ulinastatin against the activation of tourniquet-induced platelet mitochondria apoptotic signaling.

METHOD44 patients with unilateral lower limb operation and tourniquet application were randomly divided into normal saline group and ulinastatin group, and were treated with normal saline and ulinastatin respectively. 12 patents with unilateral lower limb operation but without tourniquet application were enrolled in control group. Lipid hydroperoxide (LPO) in serum was detected by LPO assay kit, the content of ATP was examined by fluorescein-luciferase assay kit; the change of mitochondrial membrane potential (Δ ψm) was detected by JC-1 mitochondrial membrane potential kit; the content of cytoplasmic cytochrome C was examined by Cytochrome C ELISA kit; Caspase-3 activity was detected by Caspase-3 fluorometric assay kit.

RESULTSAs compared with control group, the patients in normal saline group exhibited significant platelet mitochondrial dysfunction which characterized by low ATP level and low mitochondrial membrane potential (Δ ψm) (P < 0.05). Tourniquet application resulted in the activation of the mitochondria apoptotic signaling in platelet, displaying increase in the serum LPO level, release of mitochondrial cytochrome C into the cytoplasm, and activation of caspase-3 (P < 0.05). These alterations above-mentioned were obviously improved by ulinastatin treatment (P < 0.05).

CONCLUSIONTourniquet induces platelet mitochondrial dysfunction and mitochondria-dependent apoptotic signaling activation, which can be improved by ulinastatin treatment.

Apoptosis ; Blood Platelets ; Caspase 3 ; Cytochromes c ; Glycoproteins ; Humans ; Membrane Potential, Mitochondrial ; Mitochondria ; Signal Transduction ; Tourniquets

OBJECTIVETo investigate whether the plasma level of platelet auto- antibodies in ITP patients is related to that of co-stimulatory molecules sB7-H2 and sB7-H3.

METHODSA total of 61 ITP patients and 25 healthy controls from the First Affiliated Hospital of Soochow University from June 2012 to August 2013 were enrolled in this study. The expression levels of platelet auto-antibodies against 5 glycoproteins (GPIX, GP Ib, GP IIIa, GPIIb and P-selectin) in plasma were detected by flow cytometric immuno-beads array, and the expression of soluable co-stimulatory molecules sB7-H2 and sB7-H3 was measured by ELISA.

RESULTSThe plasma levels of 5 auto-antibodies against platelet membrance glycoproteins significantly increased in ITP patiens (P < 0.01). Compared with healthy controls, sB7-H2 levels increased (P < 0.05), while the sB7-H3 level did not significantly change (r = 0.13, P > 0.05). However, the correlation analysis showed that sB7-H3 negatively correlated with platelet P-selectin auto-antibody (r = -0.46, P < 0.05), and sB7-H2 and sB7-H3 significantly reduced in ITP patients with positive P-selectin auto-antibody (P < 0.01). In ITP patients, platelet counts negatively correlated with sB7-H2 (r = -0.3907, P < 0.01), but did not correlate with sB7-H3.

CONCLUSIONSoluble costimulatory molecule sB7-H2 elevates in ITP patients, and the level of sB7-H3 is associated with auto-antibodies against P-selectin, suggesting that costimulatory molecules B7-H2 and B7-H3 may be involved in the pathogenesis of immune regulation abnormality in ITP.

Autoantibodies ; B7 Antigens ; Blood Platelets ; Enzyme-Linked Immunosorbent Assay ; Flow Cytometry ; Humans ; Platelet Membrane Glycoproteins ; Purpura, Thrombocytopenic, Idiopathic

OBJECTIVETo study whether infantile wheezing pneumonia has similar immune mechanisms to asthma by determining the levels of serum inflammatory factors in wheezing infants with community-acquired pneumonia (CAP).

METHODSForty-two infants with CAP but without wheezing, 47 infants with CAP and wheezing, and 30 healthy infants as a control were recruited in the study. The peripheral blood levels of C-reactive protein, procalcitonin, soluble triggering receptor expressed on myeloid cell-l, interferon-γ, interleukin-4, interleukin-10, and periostin were compared in the three groups.

RESULTSThe serum levels of procalcitonin, soluble triggering receptor expressed on myeloid cell-l, interleukin-4 and interleukin-10 in the two CAP groups were higher than in the control group (P<0.05). The ratio of interferon-γ/interleukin-4 in the wheezing pneumonia group was lower than in the non-wheezing pneumonia and control groups (P<0.05). The serum level of periostin in the wheezing pneumonia group was higher than in the non-wheezing pneumonia and control groups (P<0.05).

CONCLUSIONSThe unbalanced ratio of interferon-γ/interleukin-4 and airway eosinophilic inflammation in wheezing infants with pneumonia suggest infantile pneumonia with wheezing may has similar immune mechanisms to asthma.

Child, Preschool ; Community-Acquired Infections ; immunology ; Female ; Humans ; Infant ; Interferon-gamma ; blood ; Interleukin-10 ; blood ; Interleukin-4 ; blood ; Male ; Membrane Glycoproteins ; blood ; Pneumonia ; immunology ; Receptors, Immunologic ; blood ; Respiratory Sounds ; immunology ; Triggering Receptor Expressed on Myeloid Cells-1