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2.  A case report of acute severe paraquat poisoning and long-term follow-up 
In the present study, the successful management of severe paraquat (PQ) poisoning with multiple organ dysfunction syndrome is described. A 42-year-old female ingested >100 ml PQ (20% weight/volume) in an attempted suicide. After 22 h the patient was admitted to hospital with serious liver, kidney and lung damage. Comprehensive therapy that maximized poison elimination was administered, along with appropriate glucocorticoids and medication for anticoagulation and protection of the liver and kidney. The patient was successfully treated and recovered after 40 days. However, pulmonary damage was aggravated when the glucocorticoid treatment was stopped after 2 months; the lungs recovered again following systematic therapy. Subsequent to a 8-month follow-up, the patient was able to look after herself in her daily life. To the best of our knowledge, successful treatment following severe PQ poisoning is rare.
PMCID: PMC4061211  PMID: 24944627
acute paraquat poisoning; treatment; long-term follow
3.  Chromophobe renal cell carcinoma associated with eosinophilia: A report of three cases 
Eosinophilia is typically associated with allergic reactions, parasitic infestations, certain forms of vasculitis, the use of certain medications and hematologic malignancies. In addition to eosinophilia associated with gastrointestinal tumors, lung cancer and thyroid carcinoma in solid malignancies, there are a limited number of cases describing peripheral hypereosinophilia in urologic tumors. The present study reports three cases of eosinophilia in patients with chromophobe renal cell carcinoma (CRCC) and investigates the association between excessive eosinophilia and the recurrence and prognosis of renal carcinoma. This is the first report of CRCC associated with excessive eosinophilia. Eosinophilia following tumor resectioning may indicate a poor prognosis, tumor recurrence and rapid disease progression.
PMCID: PMC4061223  PMID: 24944603
chromophobe renal cell carcinoma; eosinophilia; recurrence
4.  Expression of hypoxia-inducible factor-1α, endothelin-1 and adrenomedullin in newborn rats with hypoxia-induced pulmonary hypertension 
Hypoxia-inducible factor (HIF)-1α is associated with hypoxia-induced pulmonary hypertension (HPH) in adults. In the present study, the expression levels of HIF-1α, endothelin (ET)-1 and adrenomedullin (ADM) were analyzed during HPH in neonates. In total, 96 newborn rats were subjected to hypoxia or normoxia for 3, 5, 7, 10, 14 or 21 days (n=8 per subgroup). HIF-1α, ET-1 and ADM expression levels were measured by quantitative polymerase chain reaction. In addition, the intima-media thickness/external diameter ratio (MT%) and medial wall cross-sectional area/vessel total cross-sectional area ratio (MA%) were calculated to evaluate pulmonary vascular remodeling. The mean pulmonary arterial pressure (mPAP) increased with exposure to hypoxia. Furthermore, the expression levels of HIF-1α, ET-1 and ADM in the lungs were shown to increase after three and five days of hypoxia, while the MT% and MA% increased after seven days of hypoxia, as compared with the controls (P<0.05). Therefore, the expression of HIF-1α, ET-1 and ADM is upregulated in the lungs of newborn rats during early HPH. At later stages, the mPAP increases, vascular remodeling occurs and HIF-1α, ET-1 and ADM expression levels restore to normal levels.
PMCID: PMC4061228  PMID: 24944643
hypoxia-inducible factor-1; endothelin-1; adrenomedullin; pulmonary hypertension; rat
5.  Anti-inflammatory effect of sodium butyrate preconditioning during myocardial ischemia/reperfusion 
High mobility group box 1 protein (HMGB1) has an important role in myocardial ischemia/reperfusion (I/R) injury. Sodium butyrate, an inhibitor of histone deacetylase, has been shown to inhibit HMGB1 expression. In the present study, the effect of sodium butyrate on myocardial I/R injury in rats was investigated. Anesthetized male rats were intraperitoneally administered sodium butyrate (100 or 300 mg/kg) 30 min prior to the induction of ischemia. The rats were then subjected to ischemia for 30 min followed by reperfusion for 4 h. Infarct size, lactate dehydrogenase (LDH), creatine kinase (CK) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were then measured. The expression of HMGB1 was assessed using western blot analysis. The results demonstrated that pretreatment with sodium butyrate (300 mg/kg) significantly reduced the infarct size, as well as the levels of LDH and CK (P<0.05). In addition, sodium butyrate (300 mg/kg) was shown to significantly inhibit the I/R-induced increase in the level of MDA and reduction in the level of SOD (P<0.05). Furthermore, treatment with sodium butyrate (300 mg/kg) was found to significantly inhibit the expression of TNF-α, IL-6 and HMGB1 induced by I/R injury (P<0.05). In conclusion, the results from the present study suggest that preconditioning with sodium butyrate may attenuate myocardial I/R injury by inhibition of the expression of inflammatory mediators during myocardial I/R.
PMCID: PMC4061237  PMID: 24944626
sodium butyrate; high mobility group box 1 protein; myocardial ischemia; reperfusion
6.  Green tea catechin, epigallocatechin-3-gallate, attenuates the cell viability of human non-small-cell lung cancer A549 cells via reducing Bcl-xL expression 
Clinical and epidemiological studies have indicated that the consumption of green tea has a number of beneficial effects on health. Epigallocatechin-3-gallate (EGCg), the major polyphenolic compound present in green tea, has received much attention as an active ingredient. Among the numerous promising profiles of EGCg, the present study focused on the anticancer effects. Apoptosis induced by EGCg and subsequent cell growth suppression have been demonstrated in a number of cell culture studies. However, the underlying mechanism of apoptotic cell death remains unclear. Thus, the aim of the present study was to identify the major molecule that mediates proapoptotic cell death by EGCg. The effect of EGCg on cell proliferation and the induction of mRNA that modulates apoptotic cell death was evaluated in the A549 human non-small-cell lung cancer cell line. In addition, morphological changes were assessed by microscopy in A549 cells that had been treated with 100 μM EGCg for 24 h. The MTT assay revealed that cell proliferation was significantly reduced by EGCg in a dose-dependent manner (3–100 μM). The mRNA expression level of B-cell lymphoma-extra large (Bcl-xL) was decreased in A549 cells following 24 h incubation with 100 μM EGCg. Therefore, the results indicated that the inhibition of cell proliferation by EGCg may be achieved via suppressing the expression of the cell death-inhibiting gene, Bcl-xL.
PMCID: PMC4061191  PMID: 24944597
epigallocatechin-3-gallate; A549 cells; B-cell lymphoma-extra large; apoptosis
7.  SOD3 and eNOS genotypes are associated with SOD activity and NOx 
Oxidative stress, characterized by increased reactive oxygen species production and/or decreased antioxidant enzyme activity, plays an important role in the pathogenesis of hypertension. The identification of molecular markers corresponding to the oxidative stress status of hypertension may assist in the antioxidant therapy of hypertension. In the present study, superoxide dismutase (SOD) and endothelial nitric oxide synthase (eNOS) were analyzed as markers of hypertension responding to oxidative stress. The plasma SOD activity and mononitrogen oxides (NOx) concentration were measured, and the SOD3 Ala58Thr and eNOS Glu298Asp polymorphisms were genotyped in hypertensive patients and normotensive controls. Further association experiments were replicated in an extended population, including 343 hypertensive patients and 290 controls. The results demonstrated that no statistically significant differences in the total SOD activity and NOx concentration were identified between the hypertensive patients and controls. However, the plasma SOD activity levels in the SOD3 Ala/Ala homozygote carriers (80.51±27.68 U/ml) were significantly lower compared with the Thr allele carriers (92.18±16.37 U/ml; P=0.031). In addition, the plasma NOx concentration in the eNOS Glu/Glu homozygote carriers (129.66±59.15 μmol/l) was significantly lower compared with the Asp allele carriers (169.84± 55.18 μmol/l; P=0.010). Notably, the altered SOD activity levels and NOx concentration were in concordance in 56.3% of the 80 participants. Therefore, the concordance of decreased SOD activity and NOx concentration, combined with genotypes of SOD3 Ala/Ala and/or eNOS Glu/Glu in hypertensive patients, may be useful in directing the antioxidant therapy of hypertension.
PMCID: PMC4061193  PMID: 24944642
nitric oxide synthase; oxidative stress; polymorphism; superoxide dismutase; hypertension
8.  Qianliening capsule inhibits benign prostatic hyperplasia angiogenesis via the HIF-1α signaling pathway 
Angiogenesis plays an important role in the progression and development of benign prostatic hyperplasia (BPH), and has become a promising target for BPH treatment. The hypoxia-inducible factor-1α (HIF-1α) signaling pathway promotes the process of angiogenesis, contributing to the growth and progression of a number of hyperplasia diseases, including BPH. Qianliening capsule (QC) is a traditional Chinese formula that has been used clinically in China to treat BPH for a number of years. Recently, QC was demonstrated to inhibit prostatic cell growth and induce apoptosis in vivo and in vitro via regulating the epidermal growth factor/signal transducer and activator of transcription 3 signaling pathway and mitochondrion-dependent apoptosis pathway. However, the mechanisms underlying the anti-BPH effect remain largely unknown. To further elucidate the mechanism of QC activity in BPH treatment, a rat BPH model established by injecting testosterone following castration was established and the effect of QC on prostatic tissue angiogenesis was evaluated, as well as the underlying molecular mechanisms. QC was shown to reduce the prostatic index in BPH rats, but without affecting the body weight, demonstrating that QC is effective in the treatment of BPH and without apparent toxicity. In addition, QC treatment significantly reduced the intraprostatic microvessel density, indicating antiangiogenesis activity in vivo. In addition, treatment with QC inhibited the expression of HIF-1α in BPH rats, as well as the expression of vascular endothelial growth factor and basic fibroblast growth factor. Therefore, for the first time, the present study hypothesized that QC inhibits angiogenesis in prostatic tissue of BPH rats via the inhibition of the HIF-1α signaling pathway, which may be one of the mechanisms in which QC treats BPH.
PMCID: PMC4061199  PMID: 24944609
qianliening capsule; benign prostatic hyperplasia; angiogenesis; hypoxia-inducible factor-1α; vascular endothelial growth factor; basic fibroblast growth factor
9.  Clinical improvement following therapy for periodontitis: Association with a decrease in IL-1 and IL-6 
Although a number of inflammatory cytokines have been shown to be associated with periodontal pathogenesis, it is important to investigate further whether these biomarkers are associated with the degree of success in nonsurgical treatment of chronic periodontitis. The aim of the present study was to quantify the total levels of interleukin (IL)-1α, -1β, -6, -10 and tumour necrosis factor (TNF)-α in gingival crevicular fluid (GCF) of chronic periodontitis patients prior to and following nonsurgical periodontal therapy. In total, 52 GCF samples from disease sites of patients with chronic periodontitis, prior to and following periodontal therapy, and ten non-disease sites from non-periodontitis subjects, were collected and cytokine concentrations were determined using a multiplex method. Periodontal parameters, including bleeding on probing, probing pocket depth and the clinical attachment level, in all the sites were recorded. Untreated disease sites exhibited higher cytokine levels in the GCF when compared with the non-disease sites. Nonsurgical periodontal therapy resulted in a statistically significant decrease in the total levels of IL-1α, -1β and -6 in the GCF, but not in IL-10 or TNF-α. The results support the hypothesis that proinflammatory cytokines, including IL-1α, IL-1β and IL-6, are likely to be involved in the pathogenesis of periodontitis and are good markers to evaluate the success of nonsurgical therapy in disease sites of patients with periodontitis.
PMCID: PMC4061202  PMID: 24944641
periodontal therapy; biomarkers; cytokines; gingival crevicular fluid; multiplex immunoassay
10.  Atorvastatin increases lipopolysaccharide-induced expression of tumour necrosis factor-α-induced protein 8-like 2 in RAW264.7 cells 
RAW264.7 cells are one of the major sources of productive inflammatory biomediators, including tumour necrosis factor-α (TNF-α) and interleukin (IL)-6. TNF-α-induced protein 8-like 2 (TIPE2) is an essential negative regulator of Toll-like and T-cell receptors, and the selective expression in the immune system prevents hyper-responsiveness and maintains immune homeostasis. The aim of the present study was to investigate whether atorvastatin upregulates the expression of TIPE2 and further regulates the inflammatory response and oxidation emergency response in RAW264.7 cells. RAW264.7 cells were incubated in Dulbecco’s modified Eagle’s medium containing lipopolysaccharide (LPS) in the presence or absence of atorvastatin. Following incubation, the medium was collected and the levels of TNF-α and IL-6 were measured using an enzyme-linked immunosorbent assay. The cells were harvested, and the mRNA and protein expression levels of TIPE2, macrophage migration inhibitory factor (MIF), IκB and nuclear factor (NF-κB)-κB were analysed using quantitative polymerase chain reaction and western blotting analysis, respectively, the expression of NOS, COX-2 and HO-1 protein were essayed by western blotting analysis, NO and ROS activities were determined. The results revealed that LPS increased the mRNA and protein expression levels of TIPE2, MIF and NF-κB, as well as the production of IL-6 and TNF-α, in a dose and time dependent manner in RAW264.7 cells. Meanwhile, LPS enhanced the expression of NOS and COX-2 protein, blocked HO-1 protein expression, increased NO and PGE2 production and ROS activity in a dose dependent manner in RAW264.7 cells. Atorvastatin significantly increased LPS induced expression of TIPE2, downregulated the expression of NOS, COX-2, MIF and NF-κB and the production of PGE2, NO, IL-6 and TNF-α in a time and dose dependent manner, and increased HO-1 protein expression, reduced ROS production in a dose dependent manner. The observations indicated that atorvastatin upregulated LPS induced expression of TIPE2 and consequently inhibited MIF, NF-κB, NOS and COX-2 expression and the production of NO, PGE2, TNF-α and IL-6, increased HO-1 expression, and inhibited ROS activity in cultured RAW264.7 cells.
PMCID: PMC4061217  PMID: 24944625
atorvastatin; RAW264.7 cells; tumour necrosis factor-α-induced protein 8-like 2; macrophage migration inhibitory factor; nuclear factor-κB
11.  TGF-β1 induces the formation of vascular-like structures in embryoid bodies derived from human embryonic stem cells 
Human embryonic stem cells (ESCs) can differentiate into endothelial cells in response to stimuli from extracellular cytokines. Transforming growth factor (TGF)-β1 signaling is involved in stem cell renewal and vascular development. Previously, human ESCs were isolated from inner cell mass and a stable ESC line was developed. In the present study, the effects of extracellular TGF-β1 were investigated on human ESC-derived embryoid bodies (EB) in suspension. The structures of the EBs were analyzed with light and electron microscopy, while the cellular composition of the EBs was examined via the expression levels of specific markers. Vascular-like tubular structures and cardiomyocyte-like beating cells were observed in the EBs at day 3 and 8, respectively. The frequencies of vascular-like structures and beating cells in the TGF-β1 treated group were significantly higher compared with the control group (84.31 vs. 12.77%; P<0.001; 37.25 vs. 8.51%; P<0.001, respectively). Electron microscopy revealed the presence of lumens and gap junctions in the sections of the tubular structures. Semiquantitative polymerase chain reaction revealed elevated expression levels of CD31 and fetal liver kinase-1 in EBs cultured with TGF-β1. In addition, extensive staining of von Willebrand factor was observed in the vascular-like structures of TGF-β1-treated EBs. Therefore, the results of the present study may aid the understanding of the underlying mechanisms of human ESC differentiation and improve the methods of propagating specific cell types for the clinical therapy of cardiovascular diseases.
PMCID: PMC4061233  PMID: 24944596
human embryonic stem cell; transforming growth factor-β; embryoid body; endothelial cell
12.  A novel NF-κB inhibitor, DHMEQ, ameliorates pristane-induced lupus in mice 
Nuclear factor (NF)-κB is strongly associated with the development of immune regulation and inflammation. The aim of the present study was to identify whether a NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), ameliorates systemic lupus erythematosus (SLE) in a pristane-induced mouse model. SLE was induced in 8-week-old female BALB/c mice by the injection of 0.5 ml pristane. The therapeutic effect of 12 mg/kg DHMEQ on the pristane-induced BALB/c mouse model of lupus was investigated to elucidate the effects on SLE. The intraperitoneal administration of DHMEQ three times per week was initiated when the mice were 16 weeks-old (8 weeks following the pristane injection) and the treatment was continued for 16 weeks. Serum IgG autoantibodies against nucleosomes, dsDNA and histones were detected at weeks 8, 16 and 32. In addition, the expression levels of interleukin (IL)-1β, 6 and 17, as well as tumor necrosis factor (TNF)-α, were analyzed at week 32. Renal lesions were also observed. DHMEQ was shown to antagonize the increasing levels of anti-nucleosome, anti-dsDNA and anti-histone autoantibodies, as well as the increasing levels of IL-1β, 6 and 17 and TNF-α. In addition, DHMEQ reduced the number of renal lesions caused by pristane, as reflected by milder proteinuria and reduced renal pathology. The renal expression levels of phosphorylated-p38 mitogen-activated protein kinase (MAPK), phosphorylated-c-Jun N-terminal kinase (JNK) and NF-κB p65 were significantly downregulated. Therefore, the results of the present study indicate that DHMEQ has a beneficial effect on pristane-induced lupus through regulating cytokine levels and the MAPK/JNK/NF-κB signaling pathway.
PMCID: PMC4061236  PMID: 24944605
systemic lupus erythematosus; nuclear factor-κB; dehydroxymethylepoxyquinomicin; lupus model; pristane
13.  Piperine potentiates the hypocholesterolemic effect of curcumin in rats fed on a high fat diet 
It has previously been demonstrated that curcumin possesses a hypocholesterolemic effect and potentiates numerous pharmacological effects of curcumin, however, the mechanisms underlying this hypocholesterolemic effect and the interaction between curcumin and piperine remain to be elucidated. In the present study, male Sprague-Dawley rats were fed on a high-fat diet (HFD) to establish a hyperlipidemia (HLP) model. Co-administration of curcumin plus piperine was found to decrease the levels of total cholesterol (TC), triglyceride (TG) and low-density lipoprotein cholesterol in the serum and liver, as well as increase the levels of fecal TC, TG and total bile acid, compared with administration of curcumin alone. Curcumin plus piperine also markedly increased the levels of high-density lipoprotein cholesterol. Furthermore, compared with administration of curcumin alone, administration of curcumin plus piperine resulted in a significant upregulation of the activity and gene expression of apolipoprotein AI (ApoAI), lecithin cholesterol acyltransferase (LCAT), cholesterol 7α-hydroxylase (CYP7A1) and low-density lipoprotein receptor (LDLR). In conclusion, these results indicated that co-administration of curcumin plus piperine potentiates the hypocholesterolemic effects of curcumin by increasing the activity and gene expression of ApoAI, CYP7A1, LCAT and LDLR, providing a promising combination for the treatment of HLP.
PMCID: PMC4061201  PMID: 24944632
curcumin; piperine; cholesterol; rat; mRNA
14.  Arsenic trioxide induces apoptosis in the THP1 cell line by downregulating EVI-1 
Acute leukemia is a malignant clonal hematopoietic stem cell disease. In the current study, the effects of arsenic trioxide (ATO) on the ecotropic viral integration site-1 (EVI-1) gene were investigated in the THP1 cell line. THP-1 cells were treated with different concentrations of ATO (0, 1, 3 and 5 μM) for 24, 48 or 72 h, then tested for cell viability by CCK-8 kit, cell morphology by cytospin smear, cell apoptosis by flow cytometry, EVI-1 mRNA expression by reverse transcription polymerase chain reaction (RT-PCR) and protein quantity by western blot. ATO treatment was shown to inhibit proliferation and induce apoptosis in THP1 cells in a dose- and time-dependent manner. ATO downregulated the mRNA and protein expression of EVI-1 in the THP1 cell line. In addition, ATO significantly decreased the expression of antiapoptotic proteins, B-cell lymphoma 2 (Bcl-2) and B cell lymphoma-extra large (Bcl-xL), but markedly increased the expression of proapoptotic proteins, including c-Jun N-terminal kinase (JNK), phosphorylated-JNK, Bax, full length caspase-3 and cleaved caspase-3. These results indicated that ATO inhibited the proliferation and induced apoptosis in THP1 cells partially via blocking the inhibitory effects of EVI-1 on the JNK signaling pathway with the involvement of apoptosis-associated proteins, including Bax, Bcl-2, Bcl-xL and caspase-3. These novel observations may be used to elucidate the mechanism by which ATO induces apoptosis in acute leukemia cells, and provide rationales to develop a personalized medicine strategy for ATO via targeting EVI-1 positive neoplasm.
PMCID: PMC4061239  PMID: 24944602
arsenic trioxide; THP1; ecotropic viral integration site-1; apoptosis
15.  Preventive effect of polysaccharides from the large yellow croaker swim bladder on HCl/ethanol induced gastric injury in mice 
In the present study the preventive effect of polysaccharides from the large yellow croaker swim bladder (PLYCSB) on HCl/ethanol-induced gastric injury in ICR mice was investigated. A high dose of PLYCSB (50 mg/kg) was found to reduce the levels of the serum proinflammatory cytokines interleukin (IL)-1β, IL-6, IL-8, as well as increase the levels of IL-4 compared with those in mice treated with a low dose of PLYCSB (25 mg/kg) and control mice. The somatostatin and vasoactive intestinal peptide serum levels in PLYCSB-treated mice were higher compared with those in control mice, whilst motilin and substance P serum levels were lower compared with those in control mice. The extent of the gastric injury in the mice treated with PLYCSB was lower compared with that in the control mice; however, the results obtained for mice treated with a high dose of PLYCSB were similar to those for omeprazole-treated mice. In addition, the superoxide dismutase and glutathione peroxidase activities of PLYCSB-treated mice were higher compared with those of the control mice, and similar to those observed in normal and omeprazole-treated mice. Furthermore, PLYCSB-treated mice showed levels of nitric oxide and malondialdehyde that were similar to those in the normal group. Using PCR and western blot analysis, it was demonstrated that PLYCSB significantly inhibited inflammation in the tissues of the HCl/ethanol induced gastric injury mice by downregulating the expression of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α and IL-1β. These results suggest that PLYCSB has an inhibitory effect against gastric injury that is comparable to that of the gastric injury drug omeprazole. Therefore, PLYCSB has the potential to be used as a natural therapeutic drug.
PMCID: PMC4061197  PMID: 24944640
polysaccharide; large yellow croaker; gastric injury; cytokine; ICR mice
16.  High dosage of agmatine alleviates pentylenetetrazole-induced chronic seizures in rats possibly by exerting an anticonvulsive effect 
The aim of the present study was to investigate the mechanism underlying the effects of different doses of agmatine in rats with chronic epilepsy. To generate chronic epilepsy models, rats pretreated with different doses of agmatine (20, 40 and 80 mg/kg) were intraperitoneally injected with pentylenetetrazole (35 mg/kg) for 28 consecutive days. Epileptic behavior was observed using behavioral measurements of convulsion for 1 h after each treatment with pentylenetetrazole. Morphological alterations of the hippocampal neurons were also observed using hematoxylin and eosin staining. In addition, the expression levels of glial fibrillary acidic protein and inducible nitric oxide synthase (iNOS) in the hippocampus were detected by immunohistochemistry. Furthermore, reverse transcription polymerase chain reaction was performed to detect the mRNA expression of two subunits (NR1 and NR2B) of the N-methyl-D-aspartic acid (NMDA) receptor in the rat hippocampus. The results demonstrated that administration of agmatine (80 mg/kg) significantly decreased the daily average grade of epileptic seizures and also reduced neuronal loss and astrocyte hyperplasia in the hippocampal area. Furthermore, agmatine (80 mg/kg) affected the mRNA expression levels of the NR1 subunit of the NMDA receptor, however, agmatine had no effect on the expression of iNOS in the hippocampus. Higher doses of agmatine inhibited the effect of pentylenetetrazole in rats, reduced astrocytic hyperplasia and neuronal damage in the hippocampus caused by seizures and selectively reduced the expression of the NR1 subunit of NMDA. Our results suggest that agmatine has an anticonvulsive effect in chronic epilepsy.
PMCID: PMC4061208  PMID: 24944600
agmatine; chronic seizures; pentylenetetrazole; N-methyl-D-aspartic acid receptor
17.  CXCL9 and CXCL10 accelerate acute transplant rejection mediated by alloreactive memory T cells in a mouse retransplantation model 
C-X-C motif chemokine ligand (CXCL) 9 and CXCL10 play key roles in the initiation and development of acute transplant rejection. Previously, higher levels of RANTES expression and secretion were demonstrated in retransplantation or T-cell memory-transfer models. In the present study, the effect of the chemokines, CXCL9 and CXCL10, were investigated in a mouse retransplantation model. BALB/c mice were used as donors, while C57BL/6 mice were used as recipients. In the experimental groups, a heterotopic heart transplantation was performed six weeks following skin grafting. In the control groups, a heterotopic heart transplantation was performed without skin grafting. Untreated mice served as blank controls. The mean graft survival time of the heterotopic heart transplantations was 7.7 days in the experimental group (n=6), as compared with 3.25 days in the control group (n=6; P<0.001). On day three following cardiac transplantation, histological evaluation of the grafts revealed a higher International Society for Heart & Lung Transplantation grade in the experimental group as compared with the control group. In addition, gene expression and serum concentrations of CXCL9, CXCL10, interferon-γ, and interleukin-2 were markedly higher in the experimental group when compared with the control group. Differences between the levels of CXCL9 and CXCL10 in the pre- and post-transplant mice indicated that the chemokines may serve as possible biomarkers to predict acute rejection. The results of the present study demonstrated that CXCL9 and CXCL10 play a critical role in transplantation and retransplantation. High levels of these cytokines during the pre-transplant period may lead to extensive acute rejection. Thus, the observations enhance the understanding of the mechanism underlying the increased expression and secretion of CXCL9 and CXCL10 by alloreactive memory T cells.
PMCID: PMC4061216  PMID: 24944628
C-X-C motif chemokine ligand 9; C-X-C motif chemokine ligand 10; retransplantation; memory T cells; heart transplantation
18.  Possible factors affecting thyroid dysfunction in hepatitis C virus-infected untreated patients 
The present study investigated the association of thyroid dysfunction (TD) with the distribution of chronic hepatitis C virus (HCV) infection in untreated patients. A total of 1,012 cases of HCV-infected patients were collected from different regions, of which 209 patients demonstrated a type of TD (chronic thyroiditis complicated with hyperthyroidism, chronic thyroiditis complicated with hypothyroidism, subclinical hyperthyroidism, subclinical hypothyroidism, hyperthyroidism, hypothyroidism or chronic thyroiditis). The results showed the existence of geographical differences in the types of TD present with HCV infection. The female patients had a higher incidence of autoimmune-related TD than the male patients. High levels of HCV RNA expression were most common in all HCV-infected patients, regardless of the presence of TD. High and medium expression levels of HCV RNA were more prevalent in the patients with autoimmune-related TD. Relative analysis of the HCV RNA levels showed that the pathogenesis of TD was not correlated with the HCV RNA expression levels; however, it may have been associated with autoimmunity. The HCV-infected patients with TD were most commonly middle-aged, whereas young adults were the largest group of patients with HCV and normal thyroid function. Among all HCV genotypes, type 1b was the most common HCV genotype and type 2 was the second most common. Types 3 and 6 were scarce in this study population. No associations were identified between HCV genotypes and thyroid disease. The data of liver function showed that HCV-infected patients with TD had a higher liver dysfunction rate compared with that of the patients with normal thyroid function. Therefore, liver dysfunction may be associated with thyroid disease. This study supports the potential of individualized treatment for HCV-infected patients.
PMCID: PMC4061218  PMID: 24944611
thyroid dysfunction; liver dysfunction; hepatitis type C; Chinese population
19.  Expression of circulating vascular endothelial growth factor-antagonizing cytokines and vascular stabilizing factors prior to and following bypass surgery in patients with moyamoya disease 
The aim of the present study was to investigate the levels of vascular endothelial growth factor (VEGF)-antagonizing cytokines and VEGF-influenced vascular stabilizing cytokines in patients with moyamoya disease (MMD) and the association with postoperative collateral vessel formation. The study population included 53 MMD patients that had undergone indirect bypass surgery and 50 healthy controls. Serum levels of VEGF, thrombospondin-1 (TSP-1), TSP-2, soluble VEGF receptor-1 (sVEGFR-1), sVEGFR-2, endostatin, angiopoietin-1 (Ang-1) and Ang-2 were measured at the baseline (preoperative) and at day seven following surgery. Postoperative collateralization assessment was conducted upon the six-month follow-up cerebral angiography. Cytokine levels were compared between patients with good or poor collateral formation. Compared with the healthy controls, MMD patients exhibited lower baseline levels of sVEGFR-1 (P<0.0001) and sVEGFR-2 (P<0.0001), but higher VEGF expression (P<0.0001). Ang-1 and Ang-2 levels did not exhibit any difference between the two groups. On day seven following surgery, MMD patients exhibited an almost unchanged sVEGFR-1 and sVEGFR-2 expression level, but upregulated expression of VEGF (P<0.0001), Ang-1 (P<0.0001) and TSP-2 (P<0.0001). The six-month follow-up angiographies revealed that 21 patients (45.65%) that had undergone the same surgical procedure achieved good collateralization. Patients with good collateral formation appeared to have lower sVEGFR-1 and sVEGFR-2 levels prior to (P=0.029 and P=0.045, respectively) and at day seven (P=0.044 and P=0.047, respectively) following bypass surgery when compared with the patients with worse collateralization. Therefore, sVEGFR-1 and sVEGFR-2 may play a role in the pathogenesis of MMD. Lower levels of sVEGFR-1 and sVEGFR-2 indicated better postoperative collateralization in the six months following indirect bypass surgery. However, Ang-1 and Ang-2 may not be specifically involved in the course of MMD.
PMCID: PMC4061224  PMID: 24944638
moyamoya disease; vascular endothelial growth factor; soluble vascular endothelial growth factor receptor; angiopoietin
20.  Clinical findings of 40 patients with nocardiosis: A retrospective analysis in a tertiary hospital 
To the best of our knowledge, no Chinese case studies concerning Nocardia infection have been published to date. Therefore, the present study aimed to retrospectively evaluate the risk factors, clinical features, imaging results, laboratory abnormalities, treatments and outcomes of nocardiosis in a Chinese tertiary hospital. Data collected from patients with laboratory-confirmed nocardiosis were retrospectively analyzed. A total of 40 patients who had a positive culture of Nocardia were included. The median time between the onset of symptoms and diagnosis was 42 days. Underlying diseases were identified in 72.5% of the patients of which diabetes was the most common (32.5%). The most important risk factor was corticosteroid administration. Fever and cough were common clinical symptoms. The pleuropulmonary (85%) were the most frequently involved sites and the disseminated disease rate was 30.0%. Frequent chest computed tomography scans revealed the presence of airspace opacities, nodules and masses, in addition to cavitary lesions that were particularly common among the study group. Brain images revealed lesions associated with abscesses. The majority of the patients (71.1%) were treated with trimethoprim sulfamethoxazole alone or in combination with other drugs. The in-hospital mortality rate was 15.0%. Disseminated disease, immunocompromised patients, an older age, brain involvement and concomitant infections were associated with a poor prognosis. Nocardiosis is an uncommon but emerging disease. The present study reports the first case series on nocardiosis from China and provides important information on the clinical features and risk factors of nocardiosis. Early recognition of the disease and the initiation of appropriate treatment are essential for a good prognosis.
PMCID: PMC4061227  PMID: 24944592
Nocardia; corticosteroids; opportunistic disease; pulmonary nocardiosis; brain abscess
21.  In vivo determination of muscle-derived stem cells in the rat corpus cavernosum 
The aim of the present in vivo study was to determine the presence of muscle-derived stem cells (MDSCs) in the corpus cavernosum of rats. Immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR) were performed to detect the expression of the stem cell markers stem cell antigen-1 (Sca-1), Oct4 and Desmin in Sprague-Dawley rats aged 2, 5 and 20 months. Sca-1 was mainly expressed in the blood vessels and cavernous sinus and staining revealed that Sca-1 was predominantly expressed in the cytoplasm. Desmin was primarily expressed in muscular tissues and staining demonstrated that it was mainly expressed in the cytoplasm, however, Desmin was also partially expressed in the nuclei. A small number of double positive cells, expressing Sca-1 and Desmin, were also detected near the cavernous sinus. It was found that the expression of the markers was negatively correlated with the age of the rats (P<0.05). The results from the RT-PCR demonstrated that the expression levels of Sca-1 and Desmin significantly decreased with age (P<0.05). In addition, the correlation analysis indicated that the expression of Sca-1 and Desmin were negatively correlated with the age of the rats (r=−−0.929; P<0.05). In conclusion, the present study provided evidence for the presence of MDSCs in the rat corpus cavernosum. MDSCs may be a potential therapeutic treatment for organic erectile dysfunction.
PMCID: PMC4061231  PMID: 24944634
muscle-derived stem cells; rat corpus cavernosum; stem cell markers; erectile dysfunction
22.  Association between IL-21 gene rs907715 polymorphisms and Graves’ disease in a Southern Chinese population 
Interleukin-21 (IL-21) is a pleiotropic cytokine linking innate and adaptive immune responses, which has been reported to play a key role in multiple autoimmune diseases. The aim of the present case-control study was to investigate the genetic association between single nucleotide polymorphisms (SNPs) of rs907715 within the IL-21 gene and Graves’ disease (GD) in a Southern Chinese population. A total of 211 patients with GD and 212 control subjects were recruited for the study. IL-21 gene rs907715 polymorphisms were detected by direct DNA sequencing. The results indicated that the frequencies of the GG genotype and the G allele in GD patients were significantly increased when compared with the frequencies in the controls (P=6.7×10−3 and P=2.0×10−5, respectively). In addition, the frequency of the AA genotype was much lower in the patient group when compared with the control group (16.6 vs. 34.0%; P=4.0×10−5). Furthermore, the G allele of rs907715 was associated with relapse in GD patients. These observations indicated that polymorphisms of IL-21/rs907715 may affect the susceptibility to GD in a Southern Chinese population. The G allele was significantly associated with an increased risk of GD development, whereas the A allele may lower the susceptibility to GD.
PMCID: PMC4061203  PMID: 24944624
interleukin-21; Graves’ disease; gene polymorphisms
23.  MicroRNA-203 inhibits malignant melanoma cell migration by targeting versican 
MicroRNA (miR)-203 has been demonstrated to function as a suppressor in tumorigenesis. Recently, miR-203 was reported to play a role in malignant melanoma (MM); however, the detailed function of miR-203 in MM remains unclear. In the present study, the expression of miR-203 was shown to be significantly downregulated in MM tissues when compared with normal adjacent tissues. Based on a bioinformatic prediction, versican was further identified as a novel target of miR-203, and the expression of versican was markedly increased in MM tissues. Inhibition of miR-203 increased the protein expression of versican, while upregulation of miR-203 inhibited the protein expression of versican in MM A375 cells. In addition, the upregulation of versican significantly promoted A375 cell migration; however, upregulation of miR-203 suppressed A375 cell migration. The present study further investigated whether miR-203 was involved in versican-mediated A375 cell migration, and the results indicated that upregulation of miR-203 significantly inhibited A375 cell migration, which was impaired by overexpression of versican. These observations indicated that versican functions as a downstream effector in miR-203-mediated MM cell migration. Therefore, the results demonstrated that miR-203 exhibited an inhibitory effect on MM cell migration via directly targeting versican, thus, may become an effective inhibitor for MM metastasis.
PMCID: PMC4061213  PMID: 24944639
malignant melanoma; microRNA-203; versican; migration
24.  Eosinophilic cystitis in a patient with hypereosinophila syndrome: A case report 
Hypereosinophilic syndrome (HES) is a rare disorder that is characterized by hypereosinophilia and organ damage, caused by the infiltration of eosinophils. In rare cases, the urinary bladder may also be involved. The current case report presented a 56-year-old male with gross hematuria and hypereosinophilia. The diagnosis of eosinophilic cystitis associated HES was established. Oral prednisone with a slow tapering regimen was administered as the primary treatment for the patient, which achieved partial hematological remission and complete relief of cystitis during a six-month follow-up period. Although eosinophilic cystitis is not commonly the primary manifestation of HES, eosinophilic cystitis should be taken into consideration following the onset of urinary symptoms in patients with HES.
PMCID: PMC4061232  PMID: 24944595
hypereosinophilic syndrome; eosinophilic cystitis
25.  Direct identification of Mycobacterium abscessus through 16S rDNA sequence analysis and a citrate utilization test: A case report 
A growing number of nontuberculous mycobacteria infection cases, especially those caused by rapidly growing mycobacteria (RGM), have been reported in the past decade. Conventional methods for mycobacteria diagnosis are inefficient and easily lead to misdiagnosis. New detection methods, such as gene sequencing, have been reported but are not widely used. The aim of the present case report was to provide a quick and exact method of identifying Myobacterium abscessus (M. abscessus) infections. The particular case reported in this study initially manifested as hyperglycemia and papules in the right leg. Routine cultures for fungus were repeatedly negative. However, cultures of the purulent material under aerobic cultivation for five days yielded a rapidly growing, nontuberculous mycobacterium. A Ziehl-Neelsen staining of this mycobacterium revealed the presence of acid-fast bacilli that were finally identified as M. abscessus through 16S rDNA sequence analysis and a citrate utilization test. The current report may help other clinicians to make a quick and accurate diagnosis of RGM infection.
PMCID: PMC4061238
diabetes; rapidly growing mycobacteria; Mycobacterium abscessus; 16S rDNA sequence analysis; citrate utilization test

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