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1.
Patients with chronic kidney disease (CKD) have an increased incidence of cancer. It is well known that long periods of hemodialysis
(HD) treatment are linked to DNA damage due to oxidative stress. In this study, we examined the effect of selenium (Se) supplementation
to CKD patients on HD on the prevention of oxidative DNA damage in white blood cells. Blood samples were drawn from 42 CKD
patients on HD (at the beginning of the study and after 1 and 3 months) and from 30 healthy controls. Twenty-two patients
were supplemented with 200 μg Se (as Se-rich yeast) per day and 20 with placebo (baker's yeast) for 3 months. Se concentration
in plasma and DNA damage in white blood cells expressed as the tail moment, including single-strand breaks (SSB) and oxidative
bases lesion in DNA, using formamidopyrimidine glycosylase (FPG), were measured. Se concentration in patients was significantly
lower than in healthy subjects ( P < 0.0001) and increased significantly after 3 months of Se supplementation ( P < 0.0001). Tail moment (SSB) in patients before the study was three times higher than in healthy subjects ( P < 0.01). After 3 months of Se supplementation, it decreased significantly ( P < 0.01) and was about 16% lower than in healthy subjects. The oxidative bases lesion in DNA (tail moment, FPG) of HD patients
at the beginning of the study was significantly higher ( P < 0.01) compared with controls, and 3 months after Se supplementation it was 2.6 times lower than in controls ( P < 0.01). No changes in tail moment was observed in the placebo group. In conclusion, our study shows that in CKD patients
on HD, DNA damage in white blood cells is higher than in healthy controls, and Se supplementation prevents the damage of DNA. 相似文献
2.
Cardiovascular diseases (CVD) constitute a significant risk and may, in part, explain the high morbidity and mortality rates
among haemodialysis (HD) patients. Several studies have implicated reduced insulin like growth factor (IGF-1) levels in the
development of CVD. However, it is not clear whether IGF-1, and its relationship with other hormones such as leptin, insulin,
and growth hormone (GH), as well as anthropometric variables may explain the high incidence of vascular complications in chronic
kidney disease (CKD) patients. This study was designed to measure total serum IGF-1, leptin, insulin and GH levels in CKD
patients and in age-matched control subjects and to elucidate the relationship between IGF-1 and GH, leptin, and insulin as
well as other known aetiological risk factors for CVD including blood pressure, body mass index (BMI), and age. The study
consisted of 50 CKD patients [36 M and 14 F; mean age; 41.8 ± 10.3 years) on maintenance haemodialysis and 50 healthy control
subjects (36 M and 14 F; mean age 41.6 ± 10.2 years) matched for age and sex. None of the subject among patients and controls
reported either smoking or history of diabetes mellitus. The circulating levels of IGF-1 were significantly lower ( P < 0.001) in both male and female patients compared to the control subjects. Moreover, IGF-1 was strongly and inversely correlated
with both systolic blood pressure (SBP) ( r = −0.360; P < 0.01) and diastolic blood pressure (DBP) ( r = −0.512; P < 0.001) in the CKD group, and when the two groups were combined SBP ( r = −0.396; P < 0.001) and DBP ( r = −0.296; P < 0.01). When adjusted for age, the correlation was more significant, however, when adjusted for BMI no significant correlation
was observed between IGF-1 and blood pressure. IGF-1 was inversely correlated with age ( r = −0.367; P < 0.01) and BMI ( r = −0.310; P < 0.05) in the control group, but not the patient group. In controls and patients, respectively, a positive correlation between
leptin and BMI ( r = 0.358; P < 0.01; r = 0.640, P < 0.001) was observed. The results show that circulating levels of IGF-1 were significantly lower in CKD patients as compared
to healthy normal subjects and were inversely correlated with SBP and DBP independent of age, but not BMI indicative of a
strong relationship between cardiovascular risk factors and low IGF-1 levels. Although, the data do not clearly indicate low
IGF-1 levels as a cause or an effect of these cardiovascular risk factors, they do point to an interesting relationship between
low IGF-1 levels and increased cardiovascular risk factors among CKD patients as compared to age-matched healthy control subjects. 相似文献
4.
Gout patients have a high incidence of atherosclerotic coronary heart disease. Low serum paraoxonase (PON) activity is considered
a risk factor for atherosclerosis. The relationships among paraoxonase-1 (PON1) activity, oxidative stress parameters, and
atherosclerosis in gout is not known. Therefore, we determined the plasma levels of malondialdehyde (MDA), oxidized low-density
lipoprotein (Ox-LDL), and activities of PON1/superoxide dismutase (SOD) activities in 49 gout patients (mean age 44.2 ± 7.0 years)
and 42 healthy, age-matched controls (mean age 45.0 ± 9.3 years). PON1 was measured spectrophotometrically, MDA by thiobarbituric
acid method, SOD by Griess reaction, and Ox-LDL by sandwich ELISA. Lipid and other biochemical parameters were determined
by routine laboratory methods. In gout patients, PON1/SOD activities and MDA/Ox-LDL levels were 131.3 ± 25.3/75.3 ± 28.9 kU l −1 and 6.12 ± 1.67 nmol ml −1/690.1 ± 180.2 μg l −1, respectively. In controls, these were 172.5 ± 27.8/94.0 ± 26.3 kU l −1 and 4.10 ± 1.25 nmol ml −1/452.3 ± 152.1 μg l −1, respectively. Thus, in gout patients, there was a significant decrease in PON1 ( P < 0.01) and SOD ( P < 0.05) activities, and an increase in MDA ( P < 0.01) and Ox-LDL ( P < 0.01) levels compared with controls. PON1 activity correlated positively with SOD ( P < 0.05), and negatively with MDA ( P < 0.01) and Ox-LDL ( P < 0.01). These results suggest that gout patients were in a state of oxidative stress and the protective effects of HDL against
atherosclerosis maybe dependent on PON1 activity. These findings may explain in part the reported increase in cardiovascular
mortality in gout patients. 相似文献
5.
We investigated, for the first time, the expression of I- and L-FABP in two very rare hereditary lipid malabsorption syndromes
as compared with normal subjects. Abetalipoproteinemia (ABL) and Anderson’s disease (AD) are characterized by an inability
to export alimentary lipids as chylomicrons that result in fat loading of enterocytes. Duodeno-jejunal biopsies were obtained
from 14 fasted normal subjects, and from four patients with ABL and from six with AD. Intestinal FABP expression was investigated
by immuno-histochemistry, western blot, ELISA and Northern blot analysis. In contrast to normal subjects, the cellular immunostaining
for both FABPs was clearly decreased in patients, as the enterocytes became fat-laden. In patients with ABL, the intestinal
contents of I- (60.7 ± 13.38 ng/mg protein) and L-FABP (750.3 ± 121.3 ng/mg protein) are significantly reduced (50 and 35%,
P < 0.05, respectively) as compared to normal subjects (I-135.3 ± 11.1 ng, L-1211 ± 110 ng/mg protein). In AD, the patients
also exhibited decreased expression (50%, P < 0.05; I-59 ± 11.88 ng, L-618.2 ± 104.6 ng/mg protein). Decreased FABP expression was not associated with decreased mRNA
levels. The results suggest that enterocytes might regulate intracellular FABP content in response to intracellular fatty
acids, which we speculate may act as lipid sensors to prevent their intracellular transport. 相似文献
6.
Blood platelets have been widely proposed as biomarkers in studies of mitochondrial function and aging-related and neurodegenerative diseases. Defects in mitochondrial function were found not only in the substantia nigra of Parkinson’s disease patients but also in their blood platelets. Similarly, it has also been described in the blood platelet mitochondria of Alzheimer’s disease patients. To study mitochondrial aerobic metabolism function and protein expression in platelets of multiple sclerosis (MS) patients and control subjects, mitochondrial aconitase, mitochondrial superoxide dismutases 1 and 2 (SOD1 and SOD2), and respiratory complex enzyme activities in platelets of MS patients and control subjects were determined. Likewise, mitochondrial lipid peroxidation and mitochondrial SOD1 and cytochrome c expressions were investigated. Mitochondrial aconitase activity was higher in MS patients than in controls ( P?<?0.05). A significant increase on all respiratory complex activities in MS patients was observed ( P?<?0.05). Mitochondrial lipid peroxidation was significantly higher in MS patients than in controls ( P?<?0.05). Significant changes of cytochrome c and mitochondrial SOD1 expressions were detected ( P?<?0.05), with a decrease of 44?±?5 % and an increase of 46?±?6 %, respectively. Our study reveals that significant changes in mitochondrial aerobic metabolism function and mitochondrial SOD1 and cytochrome c expressions are produced in platelets of MS patients. 相似文献
7.
Background/Aims: A close relationship exists between inflammation and vascular calcification. Although fetuin-A is known to be an inhibitor of calcification, studies correlating levels of this glycoprotein to markers of inflammation are limited. To understand these relationships, we investigated the relationship between serum fetuin-A and proinflammatory cytokine levels in patients with chronic renal failure (CRF). Methods: Thirty-two patients on haemodialysis (HD), 32 conservatively managed chronic kidney disease (CKD) patients and a control group of 25 subjects with normal renal function were enrolled in this study. Serum fetuin-A, IL-1β, IL-6 and TNF-α levels were measured by ELISA. Correlations between serum fetuin-A and IL-1β, IL-6 and TNF-α concentrations were investigated by the Spearman correlation test. Results: In 64 CRF patients (on HD and with CKD), serum fetuin-A was significantly and inversely related to IL-1β ( P < 0.001), IL-6 ( P = 0.025) and TNF-α levels ( P = 0.007), respectively. The serum fetuin-A levels of the control subjects were not significantly correlated to levels of the inflammatory markers IL-1β, IL-6 and TNF-α ( P = 0.551, 0.985 and 0.984, respectively). Conclusion: The negative correlation between serum fetuin-A and cytokine concentrations in CRF patients supports the hypothesis of inflammation-dependent down-regulation of fetuin-A expression. 相似文献
8.
Heat shock proteins play an important role as molecular chaperones of the cell. Inducible heat shock protein 70 is rapidly
synthesised in response to numerous stressors and monocytes are sensitive to changes in core temperature resulting in a circadian
variation of Hsp70 expression. Monocytes were isolated via density centrifugation from nine healthy male volunteers at 5 am,
1 pm and 9 pm, representing the nadir (5 am), peak (9 pm) and intermediate (1 pm) of Hsp70 expression in the 24-h cycle. Analysis
of freshly isolated monocytes for Hsp70 expression confirmed Hsp70 levels at the three selected time points. Monocytes were
subjected to in vitro heat shock at 40°C (±0.1) for 90 min with a 90 min 37°C (±0.1) exposure acting as a control. A significant
increase in Hsp70 was observed at 5 am ( p < 0.001) and 1 pm ( p = 0.028) at 40°C when compared to 37°C but not at 9 pm ( p = 0.19). A significant increase was also observed from the basal levels of Hsp70, measured on freshly isolated monocytes
and the levels detected after heat shock at 40°C at 5 am ( p < 0.001) and 1 pm ( p = 0.001), which was not observed at 9 pm ( p = 0.15). Furthermore, a significant correlation was observed in the heat shock response at 40°C and that obtained at 37°C
( p < 0.001). In conclusion, the heat shock response in monocytes is directly proportional to the amount of Hsp70 present in
the cells and the stress response may be much higher at different times of the day. 相似文献
10.
The primary aim of our study was to determine the influence of taking chromium plus carnitine on insulin resistance, with a secondary objective of evaluating the influences on lipid profiles and weight loss in overweight subjects with polycystic ovary syndrome (PCOS). In a 12-week randomized, double-blind, placebo-controlled clinical trial, 54 overweight women were randomly assigned to receive either supplements (200 μg/day chromium picolinate plus 1000 mg/day carnitine) or placebo (27/each group). Chromium and carnitine co-supplementation decreased weight (− 3.6 ± 1.8 vs. − 1.0 ± 0.7 kg, P < 0.001), BMI (− 1.3 ± 0.7 vs. − 0.3 ± 0.3 kg/m2, P < 0.001), fasting plasma glucose (FPG) (− 5.1 ± 6.0 vs. − 1.1 ± 4.9 mg/dL, P = 0.01), insulin (− 2.0 ± 1.4 vs. − 0.2 ± 1.2 μIU/mL, P < 0.001), insulin resistance (− 0.5 ± 0.4 vs. − 0.04 ± 0.3, P < 0.001), triglycerides (− 18.0 ± 25.2 vs. + 5.5 ± 14.4 mg/dL, P < 0.001), total (− 17.0 ± 20.3 vs. + 3.6 ± 12.0 mg/dL, P < 0.001), and LDL cholesterol (− 13.3 ± 19.2 vs. + 1.4 ± 13.3 mg/dL, P = 0.002), and elevated insulin sensitivity (+ 0.007 ± 0.005 vs. + 0.002 ± 0.005, P < 0.001). In addition, co-supplementation upregulated peroxisome proliferator-activated receptor gamma (P = 0.02) and low-density lipoprotein receptor expression (P = 0.02). Overall, chromium and carnitine co-supplementation for 12 weeks to overweight women with PCOS had beneficial effects on body weight, glycemic control, lipid profiles except HDL cholesterol levels, and gene expression of PPAR-γ and LDLR. Clinical trial registration number: http://www.irct.ir: IRCT20170513033941N38. 相似文献
11.
The quality of life of hemodialysis (HD) patients is hampered by reduced nocturnal sleep quality and excessive daytime sleepiness. In addition to the sleep/wake cycle, levels of circadian biomarkers (e.g. melatonin) are disturbed in end-stage renal disease (ESRD). This suggests impaired circadian clock performance in HD patients, but the underlying mechanism is unknown. In this observational study, diurnal rhythms of sleep, serum melatonin and cortisol concentrations and clock gene mRNA expression are compared between HD patients (n?=?9) and healthy control subjects (n?=?9). In addition, the presence of circulating factors that might affect circadian rhythmicity is tested in vitro with cell culture experiments. Reduced sleep quality (median sleep onset latency [interquartile range] of 23.9 [17.3]?min for patients versus 5.0 [10] minutes for controls, p?<?0.01; mean (± SD) sleep efficiency 70.2?±?8.1% versus 82.9?±?10.9%, p?=?0.02 and mean awake minutes after sleep onset 104.8?±?27.9 versus 54.6?±?41.6 minutes, p?= 0.01) and increased daytime sleepiness (mean Epworth Sleepiness Score of 10.0?±?4.8 versus 3.9?±?2.0, p?<?0.01) were confirmed in HD patients. Reduced nocturnal melatonin concentrations (1 AM: 98.1 [122.9] pmol/L versus 12.5 [44.2] pmol/L, p?= 0.019; 5 AM: 114.0 [131.6] pmol/L versus 11.8 [86.8] pmol/L, p?= 0.031) and affected circadian control of cortisol rhythm and circadian expression of the clock gene REV-ERBα were found. HD patient serum had a higher capacity to synchronize cells in vitro, suggesting an accumulated level of clock resetting compounds in HD patients. These compounds were not cleared by hemodialysis treatment or related to frequently used medications. In conclusion, the abovementioned results strongly suggest a disturbance in circadian timekeeping in peripheral tissues of HD patients. Accumulation of clock resetting compounds possibly contributes to this. Future studies are needed for a better mechanistic understanding of the interaction between renal failure and perturbation of the circadian clock. 相似文献
12.
The unicellular green alga Dunaliella salina is a recognized model for studying plant adaptation to high salinity. To isolate some salt-induced proteins at proteomics
levels and to identify their expressions at gene levels, algal cells at logarithmic phase cultured in 1.5 and 3.5 M NaCl media
were harvested for protein extraction. Solubilized proteins were applied to two-dimensional gel electrophoresis (2-DE) and
analyzed by ImageMaster 2D Platinum software. Twenty-one protein spots whose intensities were elevated threefold to 13-fold
at 3.5 M NaCl as compared to 1.5 M NaCl were analyzed by matrix-assisted laser desorption/ionization tandem time of flight
mass spectrometry. One salt-induced protein isolated from the 2-DE gels was identified as a glucose-6-phosphate isomerase
(GPI) from D. salina (DsGPI). A full-length cDNA of DsGPI was obtained using rapid amplification of cDNA end technique, and it was shown by heterologous
expression to encode a protein with a molecular weight consistent with the protein spot in the 2-DE gels. Real-time quantitative
RT-PCR demonstrated that the mRNA of DsGPI was induced up to eightfold ( P < 0.01) by 2.5 M and 14-fold higher ( P < 0.01) by 3.5 M NaCl than by 1.5 M NaCl, respectively. It is concluded that the protein isolated through 2-DE is indeed
DsGPI and that the DsGPI gene may be involved in adaptation to high salinity. 相似文献
13.
Occludin is an essential component of tight junctions, which are involved in controlling the integrity of the blood–brain
barrier and blood–spinal cord barrier (BSCB). Diabetes-induced alteration of occludin in rat BSCB and the relationship between
occludin level and disease course was examined. Diabetes was induced using streptozotocin. Occludin rat spinal cord mRNA levels
were assessed by real-time quantitative RT-PCR. Protein levels were examined by western blot. Occludin expression in 1-month
diabetic rats was significantly reduced compared to the controls (0.20 ± 0.01 vs 1.00 ± 0.01, respectively; P < 0.05). Expression was also significantly lower in the 3-month diabetic group (0.06 ± 0.02; P < 0.01). Occludin protein levels of 1-month (0.53 ± 0.01) and 3-month (0.31 ± 0.01) diabetic rats were also significantly
reduced compared to controls (0.91 ± 0.06; P < 0.01 for both). Diabetes decreased BSCB occludin expression at the mRNA and protein level. This down-regulation appears
to correlate with the course of the disease, and may be a causal factor of diabetes-induced increase of BSCB permeability. 相似文献
14.
Background Mannose-binding lectin (MBL) is a circulating collectin that is part of the innate immune response. We explored the serum
levels of MBL in persons with different forms of coccidioidomycosis.
Methods Serum MBL was measured by ELISA from samples obtained from healthy donors with immunity to Coccidioides, and those with various forms of active coccidioidomycosis. Blood cell specimens from a subgroup of subjects with active
coccidioidomycosis were examined for single nucleotide polymorphisms of the MBL gene and promoter regions.
Results The control group comprised 29 healthy immune subjects. Patient groups with active coccidioidomycosis consisted of 20 patients
with symptomatic primary pulmonary coccidioidomycosis, 26 with non-meningeal disseminated coccidioidomycosis, and nine with
coccidioidal meningitis. The group with active coccidioidomycosis was significantly older and more likely to be male than
the control group (for both, P < 0.001). The mean ± SEM level of serum MBL in the healthy controls was 169.4 ± 28.6 ng/ml, significantly higher than the
79.2 ± 10.9 ng/ml for all active groups ( P < 0.001). Moreover, the active coccidioidomycosis group was significantly more likely to have serum MBL level ≤70 ng/ml compared
to the control group ( P = 0.001). Genetic analysis in 27 subjects with active coccidioidomycosis revealed marked variation based on race and ethnicity.
Among a subgroup of 10 white, non-hispanic men with active coccidioidomycosis, there was a significant association between
the H and P haplotypes and MBL levels ≤70 ng/ml ( P < 0.036 and P < 0.035, respectively).
Conclusions These data suggest that there is an association between low serum MBL levels and symptomatic coccidioidomycosis. 相似文献
15.
The study of biomarkers in the cerebrospinal fluid (CSF) of patients with mild cognitive impairment (MCI) is a technique used
with increasing frequency in the early diagnosis of Alzheimers disease (AD). Our objectiv was to gain an own experience while
evaluating the reliability, sensitivity, and reproducibility of this technique in Spanish patients. Thirty-seven patients
with MCI and twenty-four control subjects were studied by means of AD biomarker analysis in CSF. xMAP Luminex and INNO-BIA
Alzbio3 reagents of Innogenetics were used. The study variables assessed were levels of Aβ 1–42, T-tau and P-tau 181p proteins as well as the ratios of T-tau/Aβ 1–42 and P-tau 181p/Aβ 1–42. Samples from nineteen patients were examined twice. Intra-class correlation coefficients for the three biomarkers used showed
values higher than 0.95. We observed significant differences between the control group and the MCI groups. In the 6 months
following lumbar puncture (LP), eleven (29%) patients with MCI developed AD. These patients showed significant lower levels
in Aβ 1–42 protein (276.35 ± 78 vs. 367.13 ± 123.49, P < 0.03) and higher ratios (T-tau/Aβ 1–42 [0.38 ± 0.2 vs. 0.22 ± 0.14, P < 0.01] and P-tau 181p/Aβ 1–42 [0.27 ± 0.13 vs. 0.16 ± 0.1, P < 0.008]) to those in the same group who remained stable. We obtained similar results to those in the most recent reliable
literature with our ROC curves, especially with our P-tau 181p values and T-tau/Aβ 1–42 ratio in order to differentiate between control and AD groups. Our experience showed that the analysis of CSF-AD biomarkers
in patients with MCI is reliable, sensitive and reproducible. In our knowledge, this is the first experience in Spanish patients. 相似文献
16.
The long-term effects (~3 weeks) of two Wnt inhibitors (dickkopf [DKK]-1 and secreted frizzled-related protein [sFRP]-1),
on the chondrogenic differentiation of human mesenchymal stem cells (hMSCs) was determined. Wnt inhibitors significantly increased
the amount of glycosaminoglycan (GAG) in treated pellets ( P < 0.05). The gene expression of COL2A1 increased and COL1A1 decreased while the gene expression of SOX-9 and COL10A1 did
not change significantly after three weeks of in vitro culture. The protein expression of type II collagen significantly increased
( P < 0.05) and that of type I collagen significantly decreased ( P < 0.05) while SOX-9 and type X collagen protein expression was unaffected. These findings suggest that Wnt inhibitors promote
the chondrogenic differentiation of hMSCs when treated for three weeks. 相似文献
17.
ObjectivePatients with impaired renal function, particularly those on dialysis, frequently exhibit high blood pressure and hemodynamic instability, which often lead to pheochromocytoma assessment. Our objective was to assess plasma free metanephrine (MN) and normetanephrine (NMN) in chronic kidney disease patients (CKD) with or without dialysis. MethodsIn this prospective observational study we performed enzyme-linked immunosorbent assays (ELISAs) to evaluate plasma free MN and NMN in 48 CKD patients (15 with stage 3-5 CKD without dialysis, 26 on hemodialysis [HD], and 7 continuous ambulatory peritoneal dialysis [CAPD]), 30 patients with histologically proven pheochromocytoma, and 43 hypertensive patients. Adrenal masses were ruled out by abdominal computed tomography (CT) scans in all CKD and control hypertensive patients. ResultsAll 3 CKD groups (HD, CAPD, and CKD without dialysis) had significantly higher plasma free MN and NMN levels than the control hypertensive group ( P < .0055). HD and CAPD patients had significantly lower plasma free NMN ( P < .0055), but free MN levels were not significantly different than those observed in pheochromocytoma patients. In patients with HD, CAPD, and CKD without dialysis, plasma free MN and NMN were higher than manufacturer’s upper limits of normal in 57.7% and 28.5%, 13.3% and 61.5%, and 85.7% and 26.6%, respectively. Regression models showed that the number of dialysis years was significantly correlated with plasma free MN ( r = 0.615, P < .001) but not free NMN. ConclusionPlasma free MN and NMN levels are frequently elevated in CKD patients, particularly in those on dialysis. Plasma free MN levels significantly overlap with the range in pheochromocytoma patients and correlate with the number of years on dialysis. (Endocr Pract. 2014;20:139-144) 相似文献
18.
The novel human gene, designated ubiquitin-conjugating enzyme E2Q family member 1 (UBE2Q1) maps to chromosome 1q21.3. The
gene has an open reading frame corresponding to 422 amino acids and contains a RWD domain and an E2 ubiquitin conjugating
enzyme domain. Here, we investigated the expression levels of both mRNA and protein of UBE2Q1 gene in cancerous versus normal
parts of breast specimens from 26 patients. Real-time PCR data showed that the relative expression level of UBE2Q1 mRNA was
significantly greater in cancers than in non-cancerous tissues of breast specimens (Mean ± SEM, 0.064 ± 0.015 for cancers
and 0.026 ± 0.01 for noncancerous tissues, P < 0.05 Mann–Whitney test). A rabbit polyclonal antibody was generated against an amino acid sequence predicted from the DNA
sequence of UBE2Q1 gene. This antibody was used to perform Western blotting on 21 cases in our cohort of breast specimens.
Thus, 13 (61.904%) of the cases showed an increase in the UBE2Q1 immunoreactivity in their cancerous tissues as compared with
the corresponding normal tissues. This result along with the real-time PCR data shows that the novel human gene, UBE2Q1, is
expressed in human breast and may have implications for pathogenesis of breast cancer. 相似文献
19.
We evaluated the changes in CD4 + CD25 high regulatory T (Treg) cells and FOXP3 mRNA expression in patients with advanced esophageal cancer as well as its clinical significance.
For this purpose, the frequencies of peripheral blood Treg cells in 68 patients with advanced esophageal cancer and 40 healthy
controls were determined by flow cytometry, and FOXP3 mRNA expression in Treg cells of 40 patients was determined by RT–PCR.
The data show that Treg cell numbers were significantly higher ( P < 0.01) in esophageal cancer patients (1.82 ± 0.54% of CD4 + T cells) as compared with healthy controls (1.52 ± 0.70% of
CD4 + T cells). Treg cell numbers in the patients were significantly higher ( P < 0.05) before chemotherapy (1.82 ± 0.54% of CD4 + T cells) than after chemotherapy (1.66 ± 0.58% of CD4 + T cells). Expression
of the FOXP3 mRNA in the patients was significantly lower ( P < 0.05) after chemotherapy (0.266 ± 0.028% of CD4 + T cells) than before chemotherapy (0.318 ± 0.027% of CD4 + T cells).
It was, therefore, concluded that Treg cell numbers as well as FOXP3 mRNA expression in advanced esophageal cancer patients
were significantly decreased after chemotherapy. Notably, FOXP3 gene may thus be involved in regulating the numbers and function
of Treg cells in advanced esophageal cancer patients receiving chemotherapy. 相似文献
20.
We examined CpG island methylation in p16 gene and its effect on p16 protein expression in tetralogy of Fallot (ToF) patients to explore its potential implications in the development and progression of ToF. The study subjects consisted of 75 healthy controls and 63 ToF patients recruited at Linyi People’s Hospital between January 2012 and June 2014. The 4 mL of peripheral venous blood of each subject was obtained and saved in ethylene diamine tetraacetic acid (EDTA) tubes. Methylation-specific polymerase chain reaction (MSP) was employed to detect CpG island methylation in p16 promoter region and Western blotting was used to detect p16 expression of all subjects. Real-time fluorescence quantitative polymerase chain reaction (FQ-PCR) was performed to test p16 mRNA expression. The results showed that p16-methylation rates in ToF group were significantly higher than the control group (ToF group, 58.73%; control group, 13.33%; P < 0.001). Remarkably, Western blotting and FQ-PCR results derived from RVOT revealed that p16 protein expression was significantly lower in ToF group compared to the control group (0.76 ± 0.21 versus 2.31 ± 0.35; P < 0.001), and p16 gene expression was also markedly decreased in ToF group (1.212 ± 0.152 versus 1.346 ± 0.191, P < 0.001). Additionally, our analysis suggested that CpG island methylation in p16 promoters in ToF patients was negatively correlated with p16 protein and gene expression (both P < 0.05). Our study reports that high CpG island methylation of p16 gene and loss of p16 protein expression associate with the development and progression of ToF, which may have significant therapeutic applications for ToF. 相似文献
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