This study was aimed to evaluate the relationship between the changes of plasma intermedin (IMD) and atrial fibrosis in hypertensive patients with atrial fibrillation. During the period from 2010 to 2011, appropriate 150 subjects of out-patients (female 50%, male 50%) were selected in West China Hospital, Sichuan University, and were divided into three groups: the hypertension-only group, the hypertension combined with paroxysmal atrial fibrillation group and the hypertension combined with persistent atrial fibrillation group. Firstly, we collected the Physical examination results and medical history records of the patients. We then performed ultrasound cardiogram and blood biochemical tests on the patients. We also detected the plasma IMD and transforming growth factor β1 (TGF-β1) using ELISA. The results showed that compared with the hypertensive group, the plasma level of IMD, TGF-β1 and left atrium director (LAD) in the hypertensive combined with atrial fibrillation group were higher significantly. Compared with the paroxymal atrial fibrillation group, the levels of IMD, TGF-β1 and LAD were higher significantly in persistent atrial fibrillation group. Analysis of correlation and partial correlation showed that IMD was positively correlated with TGF-p1 (r=0.51, P<0. 001), IMD was positively correlated with LAD(r=0.59, P< 0.001), and TGF-β1 was positively correlated with LAD (r = 0.57, P < 0.001). The results suggest that IMD might suppress the pathophysiological process of atrial fibrillation.
Atrial Fibrillation ; physiopathology ; Female ; Humans ; Hypertension ; physiopathology ; Male ; Peptide Hormones ; blood ; Transforming Growth Factor beta1 ; blood

BACKGROUND: Urinary TGF-beta1 reflects intrarenal TGF-beta1 production and is increased in patients with progressive nephropathies. We studied the effects of angiotensin receptor blocker (ARB) on serum and urinary TGF-beta1 excretion in chronic glomerulonephritis patients with proteinuria. Also the role of urinary TGF-beta1 in ARB induced antiproteinuric responses was evaluated. METHODS: Patients with non-diabetic chronic renal disease with proteinuria of 1 g or more were enrolled in this open, prospective study. After four weeks of washout period, the patients received losartan 50 mg daily followed by 100 mg in two treatment periods each lasting 12 weeks. Clinical parameters and urinary indices including proteinuria and urinary TGF-beta1 were measured at baseline and after each 12 week treatment period. RESULTS: Among the 42 patients who completed the study, 31 responded to ARB therapy determined as a decrease in proteinuria by 30% (responders), and 11 did not respond (non-responders). ARB treatment controlled blood pressure to a similar degree in both responders and non-responders. Renal function and other biochemical parameters did not change during the study period. Both doses of losartan significantly lowered proteinuria and urinary TGF-beta1 excretion in responders (50 mg: 33.4% and 29.0%, 100 mg: 64.1% and 45.8%, respectively, p<0.05). In contrast, non-responders showed no significant reduction in proteinuria and no further decrease in urinary TGF-beta1 after 100 mg treatment. Urinary TGF-beta1 excretion lacked any correlation between clinical parameters such as proteinuria or renal function. Responders were younger, showed lower baseline proteinuria and urinary TGF-beta1 excretion and greater reduction in urinary TGF-beta1 excretion after ARB treatment. However, lower baseline urinary TGF-beta1 excretion was the only significant predictor of response to ARB therapy. CONCIUSION: Our data suggest that ARB therapy in nondiabetic proteinuric chronic glomerulonephritis patients reduces proteinuria and urinary TGF-beta1 excretion and baseline urinary TGF-beta1 excretion may predict antiproteinuric response to ARB therapy.
Angiotensins ; Blood Pressure ; Glomerulonephritis* ; Humans* ; Losartan* ; Prospective Studies ; Proteinuria* ; Renal Insufficiency, Chronic ; Transforming Growth Factor beta1

OBJECTIVETo analyze the polymorphism at -509C/T site of TGF-β1 gene in patients with keloids, and to explore its relationship with the occurrence of keloid and its influence on the plasma level of TGF-β1.

METHODSOne hundred and sixty-nine patients with keloids and hospitalized from June 2011 to April 2014 were included as keloid group, and 119 healthy blood donors were enrolled as healthy control group. Venous blood of study subjects was collected. The -509C/T genotype of TGF-β1 gene was determined with PCR-restriction fragment length polymorphism technique combined with DNA sequence analysis, and the frequency of allele C or T was calculated. The theoretical frequency of the 3 genotypes CC, CT, and TT was calculated according to the theory of Hardy-Weinberg equilibrium to determine whether the gene frequency of the study subject was group representative or not. The distribution of -509C/T genotype of TGF-β1 gene among patients in keloid group was analyzed by grouping in gender, age, with or without family history of keloid, and the number of keloid respectively. Plasma level of TGF-β1 of all study subjects was determined with ELISA, and the plasma level TGF-β1 of patients with various -509C/T genotypes of TGF-β1 gene in keloid group was analyzed. The relative risk of allele frequency of patients in keloid group was analyzed by Logistic regression analysis, and the other data were processed with chi-square test and t test.

RESULTSAmong the -509C/T genotypes of TGF-β1 gene between subjects in the two groups, the distribution of genotypes CC, CT, and TT was quite similar, and they were respectively 38 cases (22.5%), 79 cases (46.7%), and 52 cases (30.8%) in keloid group and 39 persons (32.8%), 52 persons (43.7%), and 28 persons (23.5%) in healthy control group (χ² = 4.225, P>0.05). The distribution frequency of alleles C and T in the two groups were obviously different, and they were respectively 45.9% and 54.1% in keloid group and 54.6% and 45.4% in healthy control group (χ² = 4.291, P<0.05). The theoretical frequency values of the three kinds of genotypes of CC, CT, and TT were respectively 35 cases (21.0%), 84 cases (49.7%), and 50 cases (29.3%) in keloid group, and 35 persons (29.8%), 59 persons (49.6%), and 25 persons (20.6%) in healthy control group. There were no statistically significant differences between the actual genotype frequency and the theoretical values (with χ² values respectively 0.581 and 1.672, P values above 0.05), showing that the research group reached Hardy-Weinberg equilibrium. Relative risk analysis of allele frequency showed that the risk of suffering from keloid of patients carrying allele C was 1.421 times of that of patients without carrying allele C (odds ratio = 1.421, with 95% confidence interval 1.109-1.983, P < 0.05). The distribution of -509C/T genotypes of TGF-β1 gene among patients in keloid group was similar by grouping in gender, age, and number of keloid (with χ² values 0.895-5.008, P values above 0.05). Between patients with or without family history of keloid, the differences of distribution frequencies of genotypes CC and CT were significantly different, which were respectively 61.8% (21/34) and 37.8% (51/135) in patients with family history of keloid and 14.7% (5/34) and 34.1% (46/135) in patients without a family history of keloid, with χ² values respectively 6.391 and 4.835, P values below 0.05; the distribution frequency of genotype TT was close (χ² = 0.292, P > 0.05). The plasma level of TGF-β1 of patients in keloid group was (42 ± 9) µg/L, which was significantly higher than that of people in healthy control group \[(34 ± 8) µg/L, t = 4.408, P < 0.05\]. In keloid group, the plasma level of TGF-β1 in patients with genotype CC and that of patients with genotype CT was quite similar, which were respectively (43 ± 9) and (40 ± 9) µg/L (t = 0.680, P > 0.05), and they were significantly higher than that of patients with genotype TT \[(34 ± 8) µg/L, with t values respectively 2.676 and 2.137, P values below 0.05\].

CONCLUSIONSTGF-β1 gene -509C/T polymorphism was shown to be present in patients with keloids who were admitted to our hospital. It was shown to influence the plasma level of TGF-β1 in patients. The individuals who carry TGF-β1 allele C may increase the risk of developing keloid by promoting the expression of TGF-β1.

Alleles ; Gene Frequency ; Genotype ; Humans ; Keloid ; genetics ; Polymorphism, Genetic ; Transforming Growth Factor beta1 ; blood ; genetics

Adult ; Female ; Hepatitis B, Chronic ; blood ; pathology ; Humans ; Liver Cirrhosis ; blood ; pathology ; Liver Function Tests ; Male ; Middle Aged ; Transforming Growth Factor beta ; blood ; Transforming Growth Factor beta1

OBJECTIVETo probe into the mechanisms of thread implantation at Zusanli(ST 36) and Chinese herbs in treatment of chronic renal failure(CRF).

METHODSCRF rat model was made by Platt subtotal nephrectomy. They were divided into 5 groups, sham operation group, model group, Chinese herbs group, thread implantation group and thread implantation plus Chinese herbs group. After treatment of 8 weeks, serum parathyroid hormone (PHT), transforming growth factor beta1 (TGF-beta1) expression in residual renal cells, malondialdehyde(MDA) content in the residual renal tissue, serum urea nitrogen(BUN) and creatinine(Scr), protein in urine and pathological changes were investigated.

RESULTSThe above indexes after treatment by thread implantation at acupoint, Chinese herbs, and acupoint thread implantation plus Chinese herbs showed begin reversion, especially, the most obviously improvement in the acupoint thread implantation plus Chinese herbs treatment group.

CONCLUSIONThe mechanism of acupoint thread implantation and Chinese herbs in improvement of CRF is related with decrease of PTH, inhibition of TGF-beta1 expression, decrease of MDA content and resisting lesion of renal fibrosis.

Acupuncture Points ; Animals ; Drugs, Chinese Herbal ; pharmacology ; Kidney Failure, Chronic ; blood ; therapy ; Male ; Parathyroid Hormone ; blood ; Rats ; Rats, Wistar ; Transforming Growth Factor beta ; blood ; Transforming Growth Factor beta1

Humans ; Leptin ; blood ; Liver Cirrhosis ; blood ; etiology ; metabolism ; Liver Diseases, Alcoholic ; complications ; Male ; Transforming Growth Factor beta ; metabolism ; Transforming Growth Factor beta1

OBJECTIVEThis study examined the changes of serum levels of interleukin 12 ( IL-12), transforming growth factor beta 1 (TGFbeta 1) and immunoglobulin E ( IgE) in children with asthma as well as the correlation of IL-12 and TGFbeta 1 with IgE in order to investigate their roles in asthma.

METHODSSerum levels of IL-12 , TGFbeta 1 and IgE were detected using ELISA in 85 asthmatic children at the acute and the remission stages. Thirty healthy children served as control group.

RESULTSCompared with the control group, serum IL-12 and TGFbeta 1 levels were significantly lower and serum IgE levels were significantly higher in the asthmatic group through the acute to the remission stages. Serum IL-12 and TGFbeta 1 levels (40.42+/-15.26 ng/L and 65.41+/-22.38 pg/mL) significantly increased in the asthmatic group at the remission stage compared with those at the acute stage (28.42+/-10.73 ng/L and 40.25+/-11.73 pg/mL) (P<0.01), but remained lower levels than those in the control group (67.42+/-20.58 ng/L and 178.54+/-90.56 pg/mL) (P<0.01). The asthmatic patients at the remission stage showed significantly decreased serum IgE levels (145.67 +/-51.25 IU/mL) compared with those at the acute stage (280.35 +/-80.54 IU/mL) (P<0.01), but the IgE level in the remission stage was obviously higher than in the control group (53.61+/-13.32 IU/mL) (P<0.01). Serum IL-12 and TGFbeta 1 levels were negatively correlated with serum IgE level in asthmatic children.

CONCLUSIONSThere might be an imbalance in serum IL-12, TGFbeta 1 and IgE levels in asthmatic children. IL-12, TGFbeta 1 and IgE may play an important role in the pathogenesis of asthma. They may be useful in the diagnosis and severity evaluation of asthma.

Asthma ; etiology ; immunology ; Child ; Child, Preschool ; Female ; Humans ; Immunoglobulin E ; blood ; Interleukin-12 ; blood ; Male ; Transforming Growth Factor beta1 ; blood

Adult ; Case-Control Studies ; Humans ; Interleukin-12 ; blood ; Liver Diseases, Alcoholic ; blood ; Male ; Middle Aged ; Transforming Growth Factor beta1 ; blood

The expression of transforming growth factor-beta1 (TGF-beta1) in placental tissue of pregnancy-induced hypertension (PIH) and the relationship between the level of expression of TGF-beta1 and the amount of vascular cell adhesion molecule-1 (VCAM-1) in serum was studied. Immunohistochemistry ABC was used to detect the expression and distribution of TGF-beta1 in placental tissues in 40 PIH women and 20 normal pregnancy women. High resolution pathological image analysis system was used to determine the quality of TGF-beta1. The VCAM-1 in serum was examined by enzyme linked immunoabsorbent assay (ELISA). The results showed that TGF-beta1 could be express in syncytiotrophoblast. The levels of TGF-beta1 expression in placental tissues of the patients with moderate and severe PIH were significantly higher (P < 0.05), while the serum VCAM-1 was significantly lower than in normal group (P < 0.01). There was a significant positive correlation between the expression of TGF-beta1 in placental tissues and the serum VCAM-1 (r = 0.969, P < 0.01). It was concluded that the level of TGF-beta1 expression in PIH was increased and was positively correlated with the amount of serum VCAM-1, indicating that they might be involved in the pathogenesis of PIH.
Hypertension, Pregnancy-Induced/*metabolism ; Placenta/metabolism ; Transforming Growth Factor beta/*metabolism ; Transforming Growth Factor beta1 ; Vascular Cell Adhesion Molecule-1/*blood

OBJECTIVE: To analyze the influence of serum levels of transforming growth factor-β1 (TGF-β1) and epidermal growth factor receptor (EGFR) on the therapeutic effect of high-dose cytarabine (HD-AraC) in patients with acute myeloid leukemia (AML). METHODS: 98 patients with AML treated in our hospital from January 2019 to June 2020 were selected as the research subjects, all patients were treated with HD-AraC for 1 course of treatment every week. The effect of 2 groups were evaluated during after one course of treatment and divided into effective group and ineffective group, statistical table of baseline data was designed, the baseline data of 2 groups were counted in detail, the baseline data and serum levels of TGF-β1 and EGFR of 2 groups were compared, Logistic regression analysis was used to examine the relationship between the levels of serum TGF-β1, EGFR and the therapeutic effect of HD-AraC in patients with AML, the value of serum TGF-β1 and EGFR levels in predicting the therapeutic effect of HD-AraC in AML patients was analyzed based on ROC curve and decision curve. RESULTS: After 1 course of treatment, among the 98 patients, 26 cases had complete remission, 38 cases had partially remission and 34 cases no remission, the total effective rate was 65.31% (64/98); after comparing data of 2 groups, Logistic regression analysis showed that the overexpression of serum EGFR before treatment might be a risk factor for the ineffective treatment of HD-AraC in AML patients (OR>1, P<0.05), overexpression of serum TGF-β1 before treatment might be a protective factor for the ineffective treatment of HD-AraC in AML patients (OR<1, P<0.05); the ROC curve results showed that the AUC of serum EGFR and TGF-β1 before treatment in predicting the risk of ineffective HD-AraC treatment in AML patients were >0.70, which had certain predictive value. The decision curve results showed that in the threshold range of 0.15-044, the prediction model combined with serum EGFR and TGF-β1 levels in predicting the net benefit rate of HD-AraC treatment in AML patients was better than that of serum EGFR or serum TGF-β1 alone. CONCLUSION The levels of serum TGF-β1 and EGFR affect the therapeutic effect of HD-AraC in patients with AML and increase the risk of ineffective treatment, serum TGF-β1 and EGFR can be used to predict the risk of ineffective HD-AraC treatment in AML patients, and the combined prediction of net benefit rate is higher.
Cytarabine/therapeutic use* ; ErbB Receptors/blood* ; Humans ; Leukemia, Myeloid, Acute/drug therapy* ; Remission Induction ; Transforming Growth Factor beta1/blood*