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Objective: This review examined the literature for evidence on the prognostic ability of systemic immune-inflammation index (SII) and pan-immune inflammation value (PIV) for predicting overall survival (OS) and disease-free survival (DFS) in breast cancer patients., Materials and Methods: PubMed, Embase, Scopus, and Web of Science were searched with Google Scholar for gray literature. All types of studies reporting the association between SII or PIV and OS or DFS of breast cancer were eligible., Results: 13 studies on SII and 4 studies on PIV were included. Meta-analysis showed that a high SII was a significant predictor of OS (HR: 1.97 95% CI: 1.54, 2.52 I2=76%) and DFS (HR: 2.07 95% CI: 1.50, 2.86 I2=79%) in breast cancer patients. These results did not change on sensitivity analysis and were more or less stable on multiple subgroup analyses. Pooled analysis showed that high PIV was also a significant predictor of poor OS (HR: 2.63 95% CI: 1.46, 4.74 I2=71%) and DFS (HR: 1.64 95% CI: 1.23, 2.17 I2=0%) in breast cancer patients., Conclusions: High SII and PIV can predict poor OS and DFS in breast cancer patients. High heterogeneity and the observational nature of data are important limitations of the review. Further studies are needed specifically on PIV to increase the strength of the evidence.

Objective: To compare the sedation profiles and the pharmacokinetic, pharmacodynamic and safety characteristics of ciprofol and propofol at 3 escalated dose levels in healthy Chinese male subjects., Patients and Methods: Eighteen subjects were planned to be enrolled into 3 dose groups in turn: group 1 (ciprofol-0.4 mg/kg vs. propofol-2.0 mg/kg), group 2 (ciprofol-0.6 mg/kg vs. propofol-3.0 mg/kg) and group 3 (ciprofol-0.8 mg/kg vs. propofol-4.0 mg/kg). They were randomly assigned into a ciprofol or propofol group in a ratio of 1:1, with sequences of ciprofol-propofol or propofol-ciprofol, separated with a washout period of at least 48 h., Results: A total of 19 subjects were enrolled and 18 completed the trial. The median time to being fully alert after induction by ciprofol was longer than for propofol. The bispectral index (BIS) recovered significantly slower with ciprofol than with propofol 5 min and 10 min after reaching its lowest points. Systolic blood pressure (group 1: p=0.041; group 2: p=0.015; group 3: p=0.004) and mean arterial pressures (group 1: p=0.026; group 2: p=0.015; group 3: p=0.004) measured by the area under the curve below the baseline during the 2 min after induction were significantly less for ciprofol compared to propofol, but a significant change in diastolic blood pressure was only observed in group 3 (p=0.002). Eighteen (100.0%) subjects experienced 47 ciprofol-related treatment emergent adverse events (TEAEs) and 17 (94.4%) subjects had 54 propofol-related TEAEs, which were mainly hypotension, involuntary movements, respiratory depression, and pain at the injection site with severity of grade 1 or 2., Conclusions: Ciprofol may be well tolerated at higher doses in the clinical practice and exhibited significantly different sedation profiles to propofol.

Objective: To explore the clinical and prognostic features of CVT caused by PROS1 gene mutations and to provide clinical experience for new oral anticoagulants, such as rivaroxaban, in the treatment of CVT with a high risk of thrombosis., Patients and Methods: The CVT patient's clinical symptoms were described, and the brain imaging and blood coagulation tests were performed to confirm the diagnosis of CVT. The patient's family members were recruited to receive blood coagulation tests and ultrasonic examination of lower limb vessels. Genetic analysis on the pedigree was carried out to identify the responsible gene for PS deficiency. We followed-up with this patient for 24 months to evaluate the clinical outcomes, laboratory results and imaging performances of CVT., Results: The patient presented with typical CVT symptoms, including headache and epilepsy. Brain CT showed hemorrhage in the bilateral frontal lobe and left occipital lobe, while MRV demonstrated that thrombus had occurred. It was reviewed that the patient and his mother had a history of bilateral leg deep vein thrombosis. Gene tests revealed that the patient and two family members carried a heterozygous mutation of PROS1 (c.751_752delAT, p.M251Vfs*17). During 24 months of follow-up study, the patient was treated with rivaroxaban continuously and recovered well, supported by an mRS score that remained below 2. Blood coagulation tests were within normal limits, and MRV revealed partial recanalization of the cerebral venous sinus., Conclusions: The frame shift mutation in the PROS1 gene (c.751_752delAT) may greatly affect the function of protein S and lead to a severe phenotype of CVT. Rivaroxaban showed a satisfying therapeutic effect in this CVT patient with hereditary thrombophilia.

Objective: We aimed at investigating the changes in the number of circulating tumor cells (CTCs) in patients with early breast cancer (BCa) before and after different treatments, and the influence of INHBA expression on patients' therapy efficacy and prognosis prediction was also evaluated., Patients and Methods: Treatment plans were formulated based on patient's condition and willingness. 160 patients with early BCa were divided into trastuzumab adjuvant group (80 cases) and surgery group (80 cases). The correlation between the number of CTCs and Inhibin, beta A (INHBA) level was assessed by Spearman correlation analysis. The cumulative survival curve was depicted using Kaplan-Meier method to evaluate the prognosis of patients in different groups., Results: The number of detected CTCs and INHBA expression in the two groups were both reduced as compared with those before chemotherapy. After 3 months of treatment, CTCs and INHBA level in the surgical group were detected lower than those in the trastuzumab group. The number of CTCs was positively correlated with INHBA level. The overall survival rate of patients in the surgery group was remarkably higher than those in the adjuvant trastuzumab group., Conclusions: The CTCs in the peripheral blood of patients with early BCa showed a great relevance to INHBA expression, which may thus serve as predictors of treatment effect and prognosis of BCa patients in early stage. Meanwhile, we demonstrate that surgery should be the first choice for early BCa patients after chemotherapy.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Over-expression of DJ-1 attenuates effects of curcumin on colorectal cancer cell proliferation and apoptosis, by H. Shang, T. Wang, F. Shang, M. Li, Y. Luo, K.-M. Huang, published in Eur Rev Med Pharmacol Sci 2019; 23 (7): 3080-3087-DOI: 10.26355/eurrev_201904_17591-PMID: 31002157" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17591.

Objective: Endoplasmic reticulum (ER) stress has an effect on cancer cell proliferation and survival. TMTC1 has been reported to be involved in cell proliferation and inflammation, and development of ER. Hsa_circRNA_101036 is an exon circRNA formed by splicing of TMTC1 mRNA precursor. This study intends to explore the effect of hsa_circRNA_101036 on the malignant behavior of oral squamous cell carcinoma through endoplasmic reticulum stress., Materials and Methods: We firstly evaluated the levels of Hsa_circRNA_101036 in human oral mucous fibroblasts (hOMF), and in several OSCC cell lines, including FaDu, OECM1, SAS, HSC3. Then, we studied the effects of overexpression of Hsa_circRNA_101036 on the cell proliferation, apoptosis, invasion, migration, and cytokine release in OSCC cells. Finally, we evaluated the levels of CHOP that are critical in ER and the ROS levels in OSCC cells., Results: We found that compared with hOMF, a significantly lower mRNA expression of Hsa_circRNA_101036 was found in OECM1 and HSC3 cells. In OECM1 and HSC3 cells, with overexpression of Hsa_circRNA_101036, a significant decrease in cell proliferation, apoptosis, invasion, migration, and cytokine release was found. A significantly increased ROS, as well as increased protein level of CHOP, P38 and Bcl-2, was found in cells with Hsa_circRNA_101036 overexpression., Conclusions: This study indicated that Hsa_circRNA_101036 may acts as a tumor suppressor in OSCC via regulating the ER in cancer cells.

Objective: Longnon-coding RNAs (lncRNAs) have been reported to participate in the regulatory mechanisms of various cancers. Therefore, the aim of this study was to investigate the functional role of lncRNA HLA complex group 11 (HCG11) in laryngeal carcinoma., Materials and Methods: The laryngeal carcinoma cell lines SNU46, SNU899, AMC-HN-8, and normal human nasopharyngeal epithelial cells NP69 were purchased. The expression of HCG11, miR-4469, and apolipoprotein M (APOM) was detected by quantitative Real Time-PCR (qRT-PCR) in tissues and cells. Cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay and colony formation assays. The protein expression of Bax and Bcl-2 was detected by Western blot. Besides, the mechanism assays were conducted to observe the interaction between miR-449 and HCG11 or APOM. The apoptosis in each group was detected by TUNEL assay., Results: In this research, low expression of HCG11 was discovered in laryngeal carcinoma tissues and cells. Overexpression of HCG11 retarded cell proliferation and enhanced cell apoptosis. Later, we found that APOM was also downregulated in laryngeal carcinoma tissues and cell lines, and inhibited laryngeal carcinoma progression. HCG11 positively regulated APOM at the post-transcriptional level. MiR-4469 was predicted to have the binding sites of HCG11 and APOM. Furthermore, it was demonstrated that HCG11 absorbed miR-4469 to upregulate APOM expression. Finally, it was indicated that the repression of APOM rescued the effects of HCG11 overexpression on cell proliferation and cell apoptosis., Conclusions: This study uncovered that HCG11 sponged miR-4469 to suppress laryngeal carcinoma progression by upregulating APOM expression.

Objective: Non-alcoholic fatty liver disease (NAFLD) has been proven to be the most common liver disease in the world, which is a sterile liver disease and is characterized by chronic hepatic steatosis and inflammation. The first step of the spectrum of the disease is the non-alcoholic fatty liver (NAFL). Based on hepatocellular necrosis and inflammation, NAFL will progress to non-alcoholic steatohepatitis (NASH), which may have the potential to progress cirrhosis, and even hepatocellular carcinoma (HCC) in a few years. Kupffer cells (KCs) are liver-resident macrophages and have been proven to play a crucial role in NAFLD development. Cardiolipin is reported to be effective to trigger the activation of NLRP3 inflammasome through a ROS-independent signaling pathway. However, the exact mechanism of NLRP3 inflammasome activated by cardiolipin in KCs is still unclear., Materials and Methods: To make clear of the specific mechanism mentioned above, we firstly used a MCD-induced NASH mice model to demonstrate that CLS1 suppression reduced hepatic steatosis and inflammation. Secondly, the results of IHC staining indicated that the expressions of CLS1 and NLRP3 in liver tissues were significantly upregulated in the NASH group compared to the ND group. On the contrary, CLS1 inhibition significantly downregulated NLRP3 expression in liver tissues, which indicated that CLS1 probably regulated the level of NLRP3 expression. Furthermore, we demonstrated that CLS1 suppression significantly ameliorated the liver function and decreased the TG level, and interleukin-1β (IL-1β) and IL-18 were markedly reduced upon CLS1 inhibition., Results: In this work, we reported that cardiolipin is involved in the development of NASH, and the suppression of the cardiolipin synthesis by shRNA-CLS1 could ameliorate the hepatic pathogenic manifestations, as well as the serum inflammatory biomarkers. We further showed that the protein expressions of CLS1, NLRP3, ASC, and Caspase-1 were all upregulated in the NASH liver tissues and palmitic stimulated KCs., Conclusions: Our study showed that the upregulation of NLRP3 inflammasome activated by cardiolipin is crucial in NASH pathogenesis, which might provide a novel potential role of cardiolipin blockade in the treatment of NASH.

Objective: The phosphatase and tensin homologue deleted on chromosome ten (PTEN) acts as a tumor suppressor gene by inhibiting the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. DJ-1, a negative regulator of PTEN, is associated with the pathogenesis of a variety of tumors. Curcumin (Cur) is a phenolic compound that is extracted from various plant rhizomes with various anti-tumor pharmacological effects. This study aimed to investigate the effects of Cur on proliferation and apoptosis of colorectal cancer cells., Materials and Methods: Human normal colorectal epithelial cell line (NCM460) and colorectal cancer cell line (SW480 and SW620) were cultured in vitro. Real-time quantitative PCR (RT-PCR) and western blot were used to detect DJ-1 and PTEN mRNA and protein, respectively. Cell apoptosis was determined with flow cytometry. SW480 cells were divided into control, 20 μM Cur treatment group, Cur+pcDNA3.1-Blank group and Cur+pcDNA3.1-DJ-1 group. Cell proliferation activity was evaluated with EdU staining., Results: Comparing with NCM460 cells, DJ-1 was significantly increased, while PTEN was significantly declined in SW480 and SW620 cells (p<0.05). Cur treatment significantly inhibited SW480 and SW620 cell proliferation and significantly induced apoptosis compared to control group (p<0.05) but showed no significant effects on NCM460 cells. Cur down-regulated DJ-1 level and enhanced PTEN expressions in SW480 cells with dose dependence. The pcDNA3.1-DJ-1 transfection significantly declined PTEN expression, enhanced p-AKT levels, reduced cell apoptosis, and strengthened cell proliferation in SW480 cells treated by Cur (p<0.05)., Conclusions: Cur can inhibit colorectal cancer cell proliferation and promote apoptosis by down-regulating DJ-1 expression to regulate the activity of PTEN/PI3K/AKT signaling pathway.

Objective: To investigate the effect of tacrolimus on the proliferation of fibroblasts after glaucoma surgery., Materials and Methods: Biopsy was applied in this study. Under aseptic conditions, tissues were collected from rabbits, cut into small pieces and cultured. Morphology of fibroblasts was observed under a microscope. Features of fibroblasts were identified via immunocytochemistry and reverse transcription-polymerase chain reaction (RT-PCR). Western blotting and RT-PCR were performed to detect the expressions of related proteins after treatment. Flow cytometry and cell counting kit-8 (CCK-8) assay were employed to examine the proliferation of human Tenon's capsule fibroblasts (HTFs) after tacrolimus treatment., Results: Tacrolimus decreased the levels of survivin and α-smooth muscle actin (α-SMA) after transforming growth factor-β (TGF-β) treatment. Besides, it inhibited proliferation and induced apoptosis of HTFs., Conclusions: Tacrolimus reduces proliferation and promotes apoptosis of HTFs by inhibiting the expression of survivin, which may be a strategy for treating hypertrophic scar after glaucoma surgery.

Objective: Accumulating evidence suggests that SPARC/osteonectin, cwcv, and kazal-like domain proteoglycan 1 (SPOCK1) contributes to the initiation and progression of human cancers. However, little is known about the function mechanisms of SPOCK1 in non-small cell lung cancer (NSCLC). The aim of this study was to investigate the molecular mechanism of SPOCK1 in NSCLC., Patients and Methods: The expression levels of SPOCK1 in NSCLC tissues and cell lines were analyzed by qRT-PCR and Western blotting. The proliferative activity of NSCLC cells was determined by MTT and colony formation assays. The transwell assay was used to examine the cell migration and invasive ability. To study the impact of SPOCK1 on Wnt/β‑catenin signaling, we further performed Western blotting for related proteins in this pathway., Results: We observed that the expression of SPOCK1 at both protein and mRNA levels was also increased in human NSCLC tissues and cell lines. Functionally, down-regulation of SPOCK1 in NSCLC cells markedly suppressed cell proliferation, colony formation, migration and invasion in vitro. Mechanistically, we found that indicated the activation of Wnt/β-catenin pathway was suppressed by SPOCK1 silencing., Conclusions: The expression of SPOCK1 served as a tumor promoter, possibly through the Wnt/β-catenin signaling pathway in NSCLC. Targeting SPOCK1 could be a potential therapeutic strategy in NSCLC.

Objective: Erythropoietin (EPO), as a type of the tissue-protective cytokines, is a 30.4 kDa hematopoietic glycoprotein. The purpose of this study was to explore the neuroprotective effects of EPO on the neonatal hypoxic-ischemic-induced hippocampus injury and the MMP-2 expression., Materials and Methods: Neonatal Sprague-Dawley (SD) rats were randomly divided into an untreated group (control) and two hypoxia-ischemia (HI) groups treated with saline control or EPO. Hippocampi were harvested at various times after return to normoxia (6 h, 24 h, 3 days and 7 days post-HI) for analyses of infarct areas and expression using histology, Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR)., Results: EPO injections reduced the infarction and loss of brain tissue. HI group exhibited an enhanced MMP-2 positive staining compared to controls at 24 h, 3 and 7 days post-HI by immunohistochemistry. These results were confirmed by Western blot analysis of MMP-2 expression at 7 days post-HI. Levels of MMP-2 mRNA in the injured hippocampi increased significantly at 24 h and 7 days post-HI. In particular, the EPO treatment further significantly enhanced this increase., Conclusions: EPO protected hypoxic-ischemic-induced neonatal brain damage by up-regulating the MMP-2 expression. Hence, systemic EPO may have potential utility for the treatment of HI injury in human newborns.

Objective: A previous study indicated that miR-5100 served as a tumor oncogene in lung cancer. However, whether miR-5100 may serve as a novel prognostic marker in non-small cell lung cancer (NSCLC), has not been investigated. The aim of this study was to investigate miR-5100 expression and its clinical significance in NSCLC patients., Patients and Methods: Expression of miR-5100 was detected in NSCLC tissues and matched normal lung tissues by quantitative Real-time polymerase chain reaction. The correlation between miR-5100 expression and clinical features were statistically analyzed. Survival rate was analyzed by log-rank test, and survival curves were plotted according to Kaplan-Meier. The correlation between miR-5100 expression and prognosis of NSCLC patients was further evaluated by univariate and multivariate analysis., Results: As revealed by qRT-PCR analysis, the relative level of miR-5100 expression in NSCLC tissues was significantly upregulated, compared with that in corresponding noncancerous tissues (p < 0.01). Additionally, high miR-5100 expression was statistically associated with higher clinical stage (p < 0.001), N classification (p = 0.003) and M classification (p = 0.027), but lower differentiated degree (p < 0.001). Furthermore, the results of Kaplan-Meier suggested that NSCLC patients with higher miR-5100 expression had significantly poorer overall survival (p < 0.0001) and progression-free survival (p < 0.0001). Multivariate survival analysis verified that miR-5100 expression level was an independent predictor of both overall survival and progression-free survival for NSCLC patients., Conclusions: Our data suggested that up-regulation of miR-5100 was correlated with NSCLC progression, which provided a potential prognostic biomarker and therapeutic target.

Objective: This paper researches on the protective effects of antioxidants on metabolic syndrome induced by thyroid dysfunction. While the role of Lipoic acid (LA), Resveratrol (R) and Quercetin (Q) are recognized, the mechanisms for their ameliorative effects are partially understood. Therefore, the objective of this study was to determine the prevalence of MS among university workers and to examine the relationship with thyroid function and mechanisms for protective effects of LA, Resveratrol and Quercetin on the heart, kidneys and lungs., Subjects and Methods: In the cross-sectional study, a total of 2273 university workers (1198 males and 1075 females) aged 22-60 participated. Anthropometric measurements (weight and height), blood pressure, fasting plasma glucose (FPG), lipids, liver and kidney function tests were carried out, thyroid stimulating hormone (TSH), free thyroxine (FT4), free triiodothyronine (FT3), total antioxidant capacity (T-AOC), lipid peroxidation products, malondialdehyde (MDA), advanced oxidation protein products (AOPP) and dityrosine levels were measured., Results: A further evaluation of oxidative stress markers in subclinical hypothyroidism (SCH) compared with normal thyroid function showed the differences. Among middle-aged men with SCH (n = 467), MDA concentrations (8.11 ± 1.39 nmol/ml) were significantly higher euthyroid controls (7.34 ± 1.31 nmol/ml; n = 190) while AOPP, dityrosine and T-AOC levels were not different., Conclusions: It was demonstrated that prevalence of MS components was high. Targeting thyroid hormone restoration, inhibition of ACE and GSK3β via PI3K/AKT signaling pathway using LA, Resveratrol and Quercetin are potential novel therapeutic approaches for developing pharmaceuticals that could make significance in MS treatment.

Objective: The purpose of this paper is to investigate the fluid status of patients in the early stages of continuous ambulatory peritoneal dialysis (CAPD)., Patients and Methods: A total of 36 patients (13 males and 23 females), hospitalized in the Nephrology CAPD Center, Peking University Third Hospital, and undergoing intubation and CAPD treatment, were recruited in this study. By utilize a bioelectrical impedance analyzer, changes in extracellular fluid and intracellular fluid within the patients' cells, and overall fluid changes were monitored throughout six months following CAPD treatment. Blood pressure was taken before dialysis and during six months following dialysis. Dietary assessment was also performed by recording and analyzing the patients' dietary protein and caloric intake during this six months period., Results: Over a six-month period, following CAPD treatment, the fluid status of the patients displayed a rising trend, indicated by weight gain, increasing extracellular fluid (ECW), intracellular fluid (ICW), overall water (TBW) and standardized extracellular fluid (NECW). Peritoneal ultrafiltration volume, and residual urine volume, showed no significant difference before or after treatment. During the six-month period, the dietary caloric intake of patients increased. Prior to CAPD, the patients' systolic blood pressure level was higher than normal. Following treatment, it returned to normal, and, due to the patients' rising fluid status, no change occurred during the six-month monitoring period., Conclusions: During the early stages of CAPD treatment, patients' fluid status increased, as a result of dietary improvement and the increased intake of water and salt. However, weight gain, in the early stages of the CAPD, is more likely due to rising fluid status than nutritional improvement. Early control of water and salt intake is of crucial importance for CAPD patients.

Objective: To investigate the difference in fractional amplitude of low-frequency fluctuation (fALFF) of localized brain activities in the resting-state between bipolar depression and unipolar depression patients and to find biological markers that differentiate the two groups of patients., Patients and Methods: Thirteen patients with bipolar depression, 15 patients with unipolar depression, and 16 healthy control subjects that were matched in age and years of education were subjected to 3.0 T resting-state functional magnetic resonance scans. The values of whole brain fALFF were calculated and statistical analysis was performed., Results: The fALFF-values of the right inferior temporal gyrus, left cerebellar posterior lobe, right middle temporal gyrus, left inferior frontal gyrus/insula, right inferior frontal gyrus/insula, left lingual gyrus and right middle temporal gyrus of the three groups showed significant differences (p < 0.05). Compared with the healthy control (HC) group, the fALFF-values of the unipolar depression (UD) patient group significantly increased in the right superior temporal gyrus, left insula, left inferior frontal gyrus, right inferior frontal gyrus, right supramarginal gyrus and right medial frontal gyrus but significantly decreased in the right medial occipital gyrus, left frontal lobe, right superior parietal lobule; the fALFF-values of the bipolar depression (BD) patient group significantly decreased in the left cerebellum posterior lobe, right lingual gyrus, left lingual gyrus, right middle temporal gyrus, left middle temporal gyrus, and left superior frontal gyrus and significantly increased in the right inferior frontal gyrus and left insula compared to those of the HC group; compared with those of the UD group, the fALFF-values of the BD group significantly decreased in the left middle occipital gyrus, right middle temporal gyrus, left middle frontal gyrus, and left medial frontal gyrus., Conclusions: The brain activities of BD and UD patients in the resting-state exhibit abnormalities, which differ between the two groups of patients.

Objective: To study the expression profile and role of microRNA miR-34a in Leukemia stem cells (LSC) and during its metastasis. We examined upon the enforced expression of miR-34a in TIM3 positive leukemia stem cells and study the impact of leukemia stem cells and its metastasis., Patients and Methods: Samples were collected from acute myeloid leukemia (AML) children along with controls. Immunohistochemistry analysis was performed with TIM3 antibody followed by Sorting of TIM3 positive cells by flow cytometry and the expression level of miR-34a was quantified by qRT-PCR assay., Results: Immunohistochemistry in accordance with Sorting of TIM3 positive cells by flow cytometry concludes that the leukemia stem cells (LSC) were present in the samples. Induced expression of miR-34a in TIM3 positive leukemia stem cells (LSC), inhibits the clonogenic expansion, tumor progression and metastasis of leukemia., Conclusions: The enforced expression of miR-34a in TIM3 positive leukemia stem cells inhibits the leukemia stem cells and its metastasis. Our study illustrates that miR-34a is a key regulator and which will be developed as a novel therapeutic agent against leukemia stem cells (LSC).

Objective: MiR-18a is a miRNA that is aberrantly overexpressed in triple-negative breast cancer (TNBC). However, its biophysical function in TNBC is still not clear. In this study, we investigated the association among miR-18a dysregulation, Dicer dysregulation and paclitaxel (PTX) resistance in TNBC cells., Patients and Methods: 20 TNBC patients who received neoadjuvant chemotherapy before surgery were recruited. MiR-18a expression was quantified using QRT-PCR. The effects of miR-18a overexpression or knockdown on cell viability and apoptosis of PTX sensitive MDA-MB-231 cells and PTX resistant MDA-MB-231 cells after PTX treatment were studied. The influence of miR-18a overexpression on Dicer expression was measured by qRT-PCR and Western blot analysis., Results: Tissues from patients with stable disease (SD, n = 5) and progressive disease (PD, n = 2) to paclitaxel (PTX) containing neoadjuvant chemotherapy had significantly higher miR-18a expression than that from patients with partial response (PR, n = 13). MDA-MB-231/PTX cells had higher miR-18a expression than MDA-MB-231 cells. MiR-18a overexpression directly led to Dicer repression at mRNA and protein level. MiR-18a overexpression significantly increased PTX IC50 and reduced PTX induced cell apoptosis, while miR-18a suppression substantially decreased PTX IC50 and increased PTX induced cell apoptosis., Conclusions: This study found that miR-18a is an important miRNA that suppresses Dicer expression and increases PTX resistance in TNBC cells.

Objective: Chronic obstructive pulmonary disease (COPD) is both a pulmonary and systematic disease, which will cause abnormal expression of some circulating factors. Angiopoietin-like protein 4 (ANGPTL4) has been reported to play important role in inflammatory responses and several diseases. However, whether it contributes to COPD is an open question. The aim of this study is to explore the potential relationship between ANGPTL4 and COPD., Patients and Methods: In this study, circulating levels of ANGPTL4, C-reactive protein (CRP), adiponectin, tumor necrosis factor (TNF)-α, matrix metalloproteinase (MMP)-9 and monocyte chemotactic protein (MCP)-1 in 73 COPD patients and 40 healthy volunteers were investigated using multiplex enzyme-linked immunosorbent assay Kits. Then, we analyzed the correlations between ANGPTL4 with other inflammatory mediators and pulmonary function., Results: Serum ANGPTL4 levels were significantly elevated in COPD patients compared with healthy controls (122.86 ± 38.59 ng/mL versus 99.03 ± 31.84 ng/mL, p = 0.001). Besides, serum ANGTPL4 levels were much higher in ever-smokers with COPD than in never-smokers with COPD (131.71 ± 32.92 ng/mL versus 113.25 ± 42.34 ng/mL, p = 0.03). More importantly, the concentrations of circulating ANGPLT4 correlated inversely with forced expiratory volume in 1 second (FEV1) % predicted, an index of lung function in COPD (r = -0.450, p < 0.001) and in all participants (r = -0.369, p < 0.001), while correlated positively with CRP (r = 0.312, p = 0.007 for COPD; r = 0.404, p < 0.001 for total subjects), adiponectin (r = 0.266, p = 0.004 for total subjects), and MMP-9 (r = 0.254, p = 0.03 for COPD)., Conclusions: Our results suggest that circulating ANGPTL4 levels are up-regulated in COPD patients, and have correlations with pulmonary function and systematic inflammation in COPD, which provides a novel idea to further dig the pathogenic mechanisms of COPD, and justifies more studies to determine how ANGPTL4 contributes to COPD.

Objective: Hypoxia is an important risk factor for pulmonary arterial remodeling in pulmonary arterial hypertension (PAH). Pulmonary artery smooth muscle cell (PASMC) proliferation is a major contributor to pulmonary vascular remodeling. The intermediate-conductance Ca2+-activated K+ channel (Kca3.1) has been implicated in disease states characterized by excessive cell proliferation, but its role in hypoxia-induced PASMC proliferation is unknown. In the present study, we sought to investigate the effect of TRAM-34 (triarylmethane-34), a selective blocker of Kca3.1, on hypoxia-induced PASMC proliferation and underlying mechanisms., Methods: PASMC was exposed to hypoxia (2% O2) for 24 hours, cell proliferation and cell cycle analysis were measured by cell counting kit (CCK-8) and flow cytometry. Cell signaling were examined using Quantitative real-time PCR and Western blotting., Results: CCK8 results showed that TRAM-34 reduced PASMC proliferation under hypoxia. Flow cytometry revealed that TRAM-34 inhibited PASMC proliferation by G0/G1 arrest. Quantitative real-time PCR and western blotting results showed that Kca3.1 mRNA and protein levels were greater in PASMC after hypoxia exposure for 24 hours. Elevated BMP2 (bone morphogenetic protein 2) levels and decreased BMPR2/Smad1 signaling activation were also observed under hypoxia, which were significantly attenuated by TRAM-34 intervention., Conclusions: These results suggest that Kca3.1 inhibition with TRAM-34 inhibited hypoxia-induced PASMC proliferation in the G0/G1 phase. The capability of TRAM-34 to increase BMPR2/p-Smad1 signaling may be part of the mechanisms for hypoxia-induced cell proliferation. Thus, our study implies that blockade of kca3.1 might provide benefits to attenuating PAH vascular remodeling.

Objective: Kt/V urea has been used to assess adequacy of peritoneal dialysis. However, Kt/V urea only reflects the clearance of solute without taking into consideration the effects of dietary protein intake (DPI). The objective of this study is to evaluate the value of Kt/V based on nitrogen balance and to observe if it is the best adequacy index., Methods: On the premise that nitrogen balance is obtained, we calculated the minimal adequate dialysate volume and dialysis index (DI), Kt/V and solute removal index (SRI). We compared the values of DI, Kt/V and SRI to evaluate the adequacy of peritoneal dialysis., Results: Kt/V was changed with DPI and body weight of continuous ambulatory peritoneal dialysis (CAPD) patients. We cannot define adequate dialysis with a single value while DPI and body weight are different since CAPD, SRI and Kt/V are numerically equal. However, dialysis index (DI) can reflect the minimal adequate dialysate volume when DPI and body weight are different and, thus, reflects the adequacy of dialysis., Conclusions: DI reflects the balance between DPI and solute clearance; thus, it is more useful to evaluate dialysis adequacy than Kt/V and SRI in clinically stable peritoneal dialysis patients.

Objective: To evaluate the relationship between gantry rotation time, heart rate and image quality during multislice spiral CT coronary angiography (MSCTCA)., Patients and Methods: Data of 83 patients who underwent MSCTCA were reviewed. Based on the ratio between cardiac cycle and gantry rotation time, the patients were divided into two groups. Patients whose heart rates fell in the resonance frequency (the cardiac cycle / gantry rotational time ratio of 1.5, 2 or 2.5) ± 2 bpm were classified as synchronous (25 cases), while the remaining 58 patients (included a subgroup of 34 cases in whom heart rates were the same as in synchronous group but who had a different gantry rotation time). comprised the asynchronous group. Image qualities were compared between both groups., Results: In the synchronous group, most (199/287; 69.33%) images were poor. When gantry rotation time was changed in the subgroup of the asynchronous group, the majority (423/442 or 95.70%) of images improved. There was a significant difference (p < 0.001) in the image quality among these patients. In 58 patients from asynchronous group, 757 segments of coronary arteries were evaluated, and 716 segments were of best quality (716/757; 94.58%)., Conclusions: When heart rate and gantry rotation time correlate and synchronous, the so-called frequency harmonics, coronary artery image quality is poor. However, by changing gantry rotation time to avoid the harmonic helps to improve the image quality on MSCTCA. Based on the patient's heart rate, appropriate gantry rotation time can be selected in order to avoid resonance and obtain high quality images.

Background and Objectives: Recent studies suggest that hydrogen has great therapeutic and prophylactic potential against organ injury caused by oxidative stress and inflammation. Here we investigated the effect of hydrogen-rich saline on airway inflammation and remodeling in a murine model of asthma., Materials and Methods: Asthma was induced by ovalbumin (OVA) sensitization and challenge. Then mice were treated with normal saline or hydrogen-rich saline at low and high doses. Cell counts and cytokine levels in bronchoalveolar lavage fluid (BALF) were determined, bronchial tissue was analyzed for pathology, and expression of MUC5AC, collagen III, VEGF, and total and phosphorylated NF-κB p65 was measured. Immunohistochemistry was used to identify levels and localization of VEGF expression in lung., Results: The results showed that hydrogen-rich saline reduced cell counts and levels of cytokines IL-4, IL-5, IL-13 and TNF-α in BALF. Hydrogen-rich saline treatment also significantly decreased mucus index, collagen deposition, and expression of MUC5AC, collagen III and VEGF. The ratio of phospho-NF-κB p65 to total NF-κB p65 was much lower in mice treated with hydrogen-rich saline than in untreated mice. These effects of hydrogen-rich saline on airway inflammation and remodeling were dose-dependent., Conclusions: These findings suggest that hydrogen-rich saline reduces airway inflammation and remodeling in OVA-exposed mice by inhibiting NF-κB.

Background and Objectives: Tuberculous pleural effusion (TPE) is associated with enhanced local fibrinolysis; however, its role in TPE has not been studied. The present study aims to investigate whether pleural D-dimer, a fibrinolysis marker, plays a diagnostic role for TPE., Patients and Methods: Patients with pleural effusion were recruited prospectively. All subjects underwent a standard thoracocentesis and pleural effusion samples were collected. The diagnosis of pleural effusion was based on clinical, radiological, bacteriological, and histopathological examinations. Pleural D-dimer levels were measured by immunonephelometry assay. The capacity of pleural D-dimer to differentiate TPE from non-TPE was assessed with receiver operating characteristic curve analyses., Results: A total of 87 patients with pleural effusion were included in the study (32 TPE cases and 55 non-TPE controls). Subjects with TPE showed a marked elevation of pleural D-dimer than those with other etiologies (1082.66±453.83 vs. 319.98±266.78 mg/L FEU, p < 0.05). The area under curve when pleural D-dimer was used to differentiate TPE from non-TPE was 0.928 (95% confidence interval: 0.878-979). With a cut-off value of 622.5 mg/L FEU, the sensitivity and specificity were 84.38% and 85.45%, respectively., Conclusions: Pleural D-dimer levels are higher in TPE than other causes of pleural effusions. D-dimer might be useful as a simple, surrogate marker for TPE. Further studies are needed to confirm our findings.