Cost-benefit analysis of hepatic resection, radiofrequency ablation and liver transplantation in small hepatocellular carcinoma.

OBJECTIVE: The aim of the present study was to evaluate the cost-effectiveness ratio of surgical treatment options for small hepatocellular carcinoma (SHC) by using the decision tree model and providing a reference for the clinical therapeutic decisions for SHC. METHODS: The data of 719 cases with SHC in the BCLC 0-A who were treated in the past were collected. The survival duration and treatment cost of patients in each experimental group after hepatic resection (HR), radiofrequency ablation (RFA), and orthotopic liver transplantation (OLT) were statistically analyzed. RESULTS: For SHC with a diameter of less than 3.0 cm, HR, RFA, and OLT had similar cost-effectiveness ratios. OLT could achieve a longer life expectancy, but it was greatly affected by the dropout rate while waiting for the liver donor. RFA was preferred when the willingness to pay (WTP) < 2,5000 RMB/QALY, OLT was preferred when WTP > 75,000 RMB/QALY, and HR was preferred when WTP was between the two. EXPERT OPINION: HR in SHC with OLT had the longest life expectancy, but due to the limitations of organ sources, OLT was the preferred treatment option when the WTP was large enough.

Long Non-coding RNAs in Traumatic Brain Injury Accelerated Fracture Healing.

It is commonly observed that patients with bone fracture concomitant with traumatic brain injury (TBI) had significantly increased fracture healing, but the underlying mechanisms were not fully revealed. Long non-coding RNAs (lncRNAs) are known to play complicated roles in bone homeostasis, but their role in TBI accelerated fracture was rarely reported. The present study was designed to determine the role of lncRNAs in TBI accelerated fracture via transcriptome sequencing and further bioinformatics analyses. Blood samples from three fracture-only patients, three fracture concomitant with TBI patients, and three healthy controls were harvested and were subsequently subjected to transcriptome lncRNA sequencing. Differentially expressed genes were identified, and pathway enrichment was performed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. High-dimensional data visualization by self-organizing map (SOM) machine learning was applied to further interpret the data. An xCell method was then used to predict cellular behavior in all samples based on gene expression profiles, and an lncRNA-cell interaction network was generated. A total of 874 differentially expressed genes were identified, of which about 26% were lncRNAs. Those identified lncRNAs were mainly enriched on TBI-related and damage repair-related pathways. SOM analyses revealed that those differentially expressed lncRNAs could be divided into three major module implications and were mainly enriched on transcriptional regulation and immune-related signal pathways, which promote us to further explore cellular behaviors based on differentially expressed lncRNAs. We have predicted that basophils, CD8+ T effector memory cells, B cells, and naïve B cells were significantly downregulated, while microvascular endothelial cells were predicted to be significantly upregulated in the Fr/TBI group, was the lowest and highest, respectively. ENSG00000278905, ENSG00000240980, ENSG00000255670, and ENSG00000196634 were the most differentially expressed lncRNAs related to all changes of cellular behavior. The present study has revealed for the first time that several critical lncRNAs may participate in TBI accelerated fracture potentially via regulating cellular behaviors of basophils, cytotoxic T cells, B cells, and endothelial cells.

Effect of upper gastrointestinal bleeding on prognosis of middle-aged patients with acute ischemic stroke: a retrospective study.

BACKGROUND: Upper gastrointestinal bleeding (UGIB) is a common complication of acute ischemic stroke (AIS), but the effect of UGIB on the prognosis of middle-aged AIS patients is not clear. METHODS: Patients with AIS admitted to our hospital from January 2011 to December 2015 were eligible to be included in this study. All included patients were divided into UGIB and non-UGIB groups. Some clinical characteristics were retrospectively collected. Primary outcomes were all-cause mortality within 1, 3, and 5 years, as well as the incidence of stroke recurrence. Cox proportional hazards regression analyses were used to determine the effect of UGIB on 5-year mortality and the incidence of stroke recurrence. Logistic regression was also used to identify the predictors of UGIB in AIS patients. RESULTS: A total of 405 AIS patients were included in this study and then divided into UGIB and non-UGIB groups. The mean age of the UGIB group and non-UGIB group was 61.5±9.6 and 53.1±14.0 years, respectively (P<0.001). The baseline score of the National Institute of Health Stroke Scale (NIHSS) was significantly higher in the UGIB group than in the non-UGIB group (P<0.001). AIS patients in the UGIB group had a higher 1-, 3-, and 5-year mortality and a higher incidence of stroke recurrence (all P<0.001). Kaplan-Meier curves showed that AIS patients with UGIB had a higher 5-year mortality and a higher incidence of stroke recurrence (both P<0.001). Cox proportional hazards regression models indicated that the occurrence of UGIB, older age, a high NIHSS score, and stroke recurrence were related to a higher 5-year mortality. Similarly, the occurrence of UGIB, older age, a high NIHSS score, and hypertension increased the incidence of stroke recurrence. According to the multivariate logistic regression analysis, older age, a high NIHSS score, and previous anticoagulant use were identified as predictors of UGIB. CONCLUSIONS: UGIB has important effects on the prognosis of AIS patients. The incidence of UGIB increases with older age, a high NIHSS score, and previous anticoagulant use, which provides important evidence for the treatment and nursing of AIS patients.

TGF-ß1-Mediated Activation of SERPINE1 is Involved in Hemin-Induced Apoptotic and Inflammatory Injury in HT22 Cells.

BACKGROUND: Intracerebral hemorrhage (ICH) is a severe subtype of stroke with high mortality and morbidity. Serpin Family E Member 1 (SERPINE1) has been documented to be upregulated following ICH, however, the participation of SERPINE1 in the development of ICH has never been studied. METHODS: Hemin was utilized to develop an in vitro model of ICH. Gene levels were evaluated by the use of quantitative reverse transcription polymerase chain reaction, Western blot, as well as enzyme-linked immunoassay assay. The activity of caspase-3 was determined using a commercial kit. Cell viability and apoptosis were assessed using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and Terminal deoxynucleotidyl transferase (TdT) d UTP Nick-End Labeling assay. RESULTS: SERPINE1 was upregulated in hemin-treated HT22 cells. Silencing of SERPINE1 attenuated hemin-induced inhibition of cell viability. Moreover, knockdown of SERPINE1 repressed hemin-induced apoptosis in HT22 cells, as evidenced by the decrease in the number of TUNEL positive cells, caspase-3 activity, and Bax expression, and the increase in Bcl-2 expression. Meanwhile, knockdown of SERPINE1 repressed hemin-induced inflammation in HT22 cells, as indicated by reduced levels of tumor necrosis factor-α, interleukin-6 (IL-6), IL-1ß, and inducible nitric oxide synthase. We also found that transforming growth factor-beta 1 (TGF-ß1) induced SERPINE1 expression in a dose-dependent manner. Besides, SERPINE1 knockdown attenuated the effects of TGF-ß1 on hemin-induced neuronal damage. CONCLUSION: TGF-ß1-induced SERPINE1 activation exacerbated hemin-induced apoptosis and inflammation in HT22 cells, manifesting a novel mechanism for ICH progression.

miR-130a alleviates neuronal apoptosis and changes in expression of Bcl-2/Bax and caspase-3 in cerebral infarction rats through PTEN/PI3K/Akt signaling pathway.

Effect of micro ribonucleic acid (miR)-130a on neuronal apoptosis in rats with cerebral infarction (CI) was studied to explore whether phosphatase and tensin homolog deleted on chromosome ten (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (Akt) is involved in the regulation of neuronal apoptosis. Thirty-six Sprague-Dawley (SD) rats were randomly divided into blank control group, model group and miR-130a low-expression group. miR-130a was determined by quantitative polymerase chain reaction (qPCR), the content of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 was detected using the enzyme-linked immunosorbent assay (ELISA) kits, and the neuronal apoptosis level in each group was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The neurobehavioral score was significantly lower in model group than that in blank control group (P<0.01), while it was significantly higher in miR-130a low-expression group than that in model group (P<0.01). Compared with blank control group, the model group had obviously increased content of TNF-α and IL-6 (P<0.01), decreased content of IL-10 (P<0.01), more apoptotic neurons (P<0.01), higher expression of caspase-3 (P<0.01), and obviously lower Bcl-2/Bax (P<0.01). Moreover, expression of phosphorylated (p)-PTEN, PI3K and p-Akt in brain tissues was remarkably lower in the model group than those in the blank control group (P<0.01). The expression level of miR-130a in brain tissues of CI rats is significantly increased. miR-130a promotes the release of inflammatory factors and facilitates neuronal apoptosis through suppressing the PTEN/PI3K/Akt signaling pathway.

Human amniotic epithelial cells combined with silk fibroin scaffold in the repair of spinal cord injury.

Treatment and functional reconstruction after central nervous system injury is a major medical and social challenge. An increasing number of researchers are attempting to use neural stem cells combined with artificial scaffold materials, such as fibroin, for nerve repair. However, such approaches are challenged by ethical and practical issues. Amniotic tissue, a clinical waste product, is abundant, and amniotic epithelial cells are pluripotent, have low immunogenicity, and are not the subject of ethical debate. We hypothesized that amniotic epithelial cells combined with silk fibroin scaffolds would be conducive to the repair of spinal cord injury. To test this, we isolated and cultured amniotic epithelial cells, and constructed complexes of these cells and silk fibroin scaffolds. Implantation of the cell-scaffold complex into a rat model of spinal cord injury resulted in a smaller glial scar in the damaged cord tissue than in model rats that received a blank scaffold, or amniotic epithelial cells alone. In addition to a milder local immunological reaction, the rats showed less inflammatory cell infiltration at the transplant site, milder host-versus-graft reaction, and a marked improvement in motor function. These findings confirm that the transplantation of amniotic epithelial cells combined with silk fibroin scaffold can promote the repair of spinal cord injury. Silk fibroin scaffold can provide a good nerve regeneration microenvironment for amniotic epithelial cells.

Interleukin-21 expression in hippocampal astrocytes is enhanced following kainic acid-induced seizures.

OBJECTIVE: Interleukin-21 (IL-21) is a cytokine that is an important modulator of immune responses. However, its roles in epilepsy are not completely clear. Here, we investigated the expression and distribution of IL-21 in a kainic acid (KA)-induced acute seizure mouse model. MATERIALS AND METHODS: Mice (n = 146) were randomly divided into an age-matched group, PBS injection group, and a KA injection group. The KA-injected mice were evaluated at 1, 3, and 24 h post-injection. IL-21 mRNA and protein expression levels were measured using RT-PCR and western blotting. Immunohistochemistry and immunofluorescence staining were performed to further characterize the pattern and distribution of IL-21 expression. RESULTS: The IL-21 mRNA and protein expression levels in the hippocampal tissues of the KA-treated mice were significantly increased as early as 1 h compared with the age-matched mice and PBS-treated mice. After this time point, the expression was reduced, but it remained higher than the level in the PBS-treated mice (p < 0.01). Immunohistochemical staining showed that IL-21 expression was distributed throughout the hippocampus, including areas CA1 and CA3, the dentate gyrus and the hilus. Moreover, immunofluorescence further showed that in the hippocampi of the KA-treated mice, IL-21 was mainly expressed in GFAP-positive astrocytes rather than in NeuN-positive neurons or CD11b-positive microglia. SIGNIFICANCE: Our data suggest that an increase in astrocyte-derived IL-21 expression in hippocampal subregions following KA-induced seizures may have potent regulatory effects on epileptogenesis.

Metabolomic Analysis of Plasma From Patients With Acute Mountain Sickness Using Chromatography-Mass Spectrometry.

Although acute mountain sickness (AMS) has long been recognized, little is known about this condition to date. The current study was conducted to explore changes in the metabolomic profiles of AMS patients and to further assess the potential of using these changes for the diagnosis of AMS. Plasma samples from 12 patients with AMS and 12 individuals without AMS were collected and used for further bioinformatics analysis by gas chromatography-mass spectrometry (GC-MS). The following analytical methods were used: gas chromatography-mass spectrometry data preprocessing, principal components analysis, partial least squares-discriminant analysis, model validation, orthogonal partial least squares-discriminant analysis, and the screening and identification of differences in metabolites. The results revealed a significantly difference between the subjects with AMS and those in the control group. Compared with plasma from the controls, plasma from the AMS patients contained significantly increased hypoxanthine, cysteinylglycine, D-arabitol, L-allothreonine, 2-ketobutyric acid, and succinate semialdehyde. The identification of metabolomic changes may be useful for the diagnosis of AMS in the future and may lay the foundation for further study of AMS pathogenesis.

Association of arterial oxygen saturation and acute mountain sickness susceptibility: a meta-analysis.

Acute mountain sickness (AMS) is the most common high altitude illnesses experienced during rapid ascent to a higher altitude without prior acclimation. It is mainly characterized by a headache which may be accompanied with nausea, vomiting, anorexia, dizziness, lethargy, fatigue, and sleep disturbance. If not diagnosed and treated in a timely manner, AMS can develop into deadly high altitude pulmonary edema or high altitude cerebral edema. In the previous studies of individual variation in susceptibility to AMS, arterial oxygen saturation (SO2) was identified as being associated with AMS. However, other studies have reported no association between AMS and arterial oxygen saturation. In this study, the association between SO2 and AMS was assessed through a meta-analysis of published data. The literature databases PubMed, Web of Science, LWW, Science Direct, and Embase were queried for papers published before 15 April 2014. A fixed-effects model and a random-effects model were applied (Revman 5.0) on the basis of heterogeneity, and the study quality was assessed in duplicate. Twelve studies with 614 AMS patients and 1,025 control subjects were analyzed. There was a significant association with differences in SO2 and the risk of developing AMS. SO2 values are associated with AMS incidence.

[Prevalence and causes of blindness and moderate and severe visual impairment among adults aged 50 years or above in Yongchuan District of Chongqing City: the China Nine-Province survey].

OBJECTIVE: To investigate the prevalence and causes of blindness and moderate and severe visual impairment among adults aged 50 years or above in Yongchuan of Chongqing City, China. METHODS: It was a population-based cross-section study.Geographically defined cluster sampling was used in randomly selecting 5663 individuals aged ≥ 50 years in Yongchuan District. The survey was preceded by a pilot study where operational methods were refined and quality assurance evaluation was carried out. All participants were enumerated through village registers followed door-to-door visits.Eligible individuals were invited to receive visual acuity measurement and eye examination. Prevalence of blindness and moderate and severe visual impairment was calculated according to different age, gender or education. And the reasons of blindness were analyzed.Statistical analyses were performed using Stata/SE Statistical Software, release 9.0. Chi-square test was used to investigate the association of age, gender and education with presenting and best corrected visual acuity. RESULTS: Five thousands six hundreds and sixty-three individuals were enumerated and 5390 persons were examined, the response rate was 95.18%. Based on the criteria of World Health Organization visual impairment classification in 1973, the prevalence of blindness and moderate and severe visual impairment defined as best corrected visual acuity was 2.12% (114/5390) and 5.40% (291/5390) respectively. The prevalence of blindness and moderate and severe visual impairment defined as presenting visual acuity was 2.49% (134/5390) and 10.71% (577/5390) respectively. The prevalence of blindness and moderate and severe visual impairment was higher in aged (trend χ(2) = 951.32, P = 0.000) , female (χ(2) = 33.35, P = 0.000) and illiterate (trend χ(2) equals; 141.32, P = 0.000) persons. Cataract was still the first leading cause of blindness and visual impairment.Un-corrected refractive error also was the main cause of visual impairment. CONCLUSIONS: The prevalence of blindness and moderate and severe visual impairment is relatively higher among older adults aged 50 years or above in Yongchuan District. The first leading cause of blindness and visual impairment is still cataract.