National Natural Science Foundation of China.

Previous studies have demonstrated that patients with traumatic brain injury (TBI) who also have progressive hemorrhagic injury (PHI), have a higher risk of clinical deterioration and worse outcomes than do TBI patients without PHI. Therefore, the early prediction of PHI occurrence is useful to evaluate the status of patients with TBI and to improve outcomes. The objective of this study was to develop and validate a prognostic model that uses information available at admission to determine the likelihood of PHI after TBI. Retrospectively collected data were used to develop a PHI prognostic model with a logistic regression analysis. The prediction model was validated in 114 patients from a separate hospital. Eight independent prognostic factors were identified: age ‡ 57 years (5 points), intra-axial bleeding/brain contusion (4 points), midline shift ‡ 5 mm (6 points), platelet (PLT) count < 100 · 10 9 /L (10 points), PLT count ‡ 100 but < 150 · 10 9 /L (4 points), prothrombin time > 14 sec (7 points), D-dimer ‡ 5 mg/L (12 points), and glucose ‡ 10 mmol/L (10 points). Each patient was assigned a number of points proportional to the regression coefficient. We calculated risk scores for each patient and defined three risk groups: low risk (0-13 points), intermediate risk (14-22 points), and high risk (23-54 points). In the development cohort, the PHI rates after TBI for these three groups were 10.3%, 47.3%, and 85.2%, respectively. In the validation cohort, the corresponding PHI rates were 10.9%, 47.3%, and 86.9%. The C-statistic for the point system was 0.864 ( p = 0.509 by the Hosmer-Lemeshow test) in the development cohort, and 0.862 ( p = 0.589 by the Hosmer-Lemeshow test) in the validation cohort. In conclusion, a relatively simple risk score using admission predictors accurately predicted the risk for PHI after TBI.

We examined the incidence and timing of posttraumatic cerebral infarction (PTCI) and provide predictive factors for the development of PTCI in patients with moderate or severe traumatic brain injury. Three hundred and fifty-three consecutive patients with moderate or severe head trauma were retrospectively reviewed to determine the incidence and timing of PTCI and to evaluate the effects of age, gender, admission Glasgow Coma Scores (GCS), decompressive craniectomy, brain herniation, and low systolic blood pressure (BP) on the development of cerebral infarction. Risk factors for posttraumatic cerebral infarction were evaluated using logistic regression analysis. PTCI was observed in 36 (11.96%) of the 353 patients, and in a majority of cases, cerebral infarction developed within 2 weeks after injury. Poor admission GCS (P<0.01), low systolic BP (P<0.01), brain herniation (P<0.05), and decompression craniotomy (P<0.05) were significantly associated with the development of PTCI. No relationship was found between PTCI and gender or increased age. Posttraumatic cerebral infarction is a relatively common complication in patients with head trauma that develops early in the clinical course. Low GCS, low systolic BP, brain herniation, and decompression craniotomy may be risk factors for PTCI in patients with moderate or severe traumatic brain injury.

Purpose: We hypothesize that changes in the transcription of up-regulated genes are biologically meaningful and may be linked to variations in tumor behavior and clinical features. This study aimed to find individual up-regulated genes responsible for clinicopathologic variations in human colorectal cancer. Experimental Design: Genes up-regulated concurrently in four microarray experiments were taken as candidate genes; 20 candidate genes were verified using real-time reverse transcription-PCR in these four experiments, along with 27 new samples. The presence or absence of up-regulation of these genes was correlated with 10 clinicopathologic variables from 31 patients. The mRNA transcript levels of these 20 candidate genes in the 31 paired samples were also correlated with each other to disclose any expression relationship. Results: Forty percent (8/20) of the candidate genes were verified by real-time reverse transcription-PCR to have a tumor/normal expression ratio > 2. Up-regulation of THY1 and PHLAD1 was associated with the presence of anemia in colon cancer patients (P = 0.036 and 0.009, respectively). Upregulation of HNRPA1 was more significant in cancer growing in the right-sided colon than the left side (P = 0.027). Up-regulated GPX2 was related to a higher degree of tumor differentiation (P = 0.019). c-MYC was significantly over-expressed in specimens from male compared with female colon cancer patients (P = 0.012). GRO1 was significantly up-regulated in patients younger than 65 years old (P = 0.010) and was found to be frequently overexpressed when cancers were less invasive. In addition, we found that normalized transcript levels of HNRPA1 were tightly associated with that of c-MYC (r = 0.948).

BackgroundMesenchymal stem cells (MSCs) at maternal-fetal interface are considered to play an important role in the pathogenesis of pre-eclampsia (PE). microRNAs (miRNAs) also have an important influence on differentiation, maturation, and functions of MSCs. Our aim in this study was to determine the differential expression of miRNAs in decidua-derived MSCs (dMSCs) from severe PE and normal pregnancies.ResultsmiRNA expression profiles in dMSCs from five patients with severe PE and five healthy pregnant women were screened using microarray. Then, bioinformatic analysis of the microarray results was performed. Out of 179 differentially expressed miRNAs, 49 miRNAs had significant (p < 0.05) differential expression of ≥ 2.0-fold changes, including 21 up-regulated and 28 down-regulated. miRNA-Gene-network and miRNA-Gene ontology (GO) -network analyses were performed. Overall, 21 up-regulated and 15 down-regulated miRNAs showed high degrees in these analyses. Moreover, the significantly enriched signaling pathways and GOs were identified. The analyses revealed that pathways associated with cell proliferation, angiogenesis, and immune functions were highly regulated by the differentially expressed miRNAs, including Wnt signaling pathway, mitogen-activated protein kinase signaling pathway, transforming growth factor beta signaling pathway, T-cell receptor signaling pathway, and B cell receptor signaling pathway. Four miRNA predicted target genes, vascular endothelial growth factor A (VEGFA), indoleamine 2,3-dioxygenase, suppression of cytokine signaling 3, and serine/threonine protein phosphatase 2A 55 kDa regulatory subunit B α isoform (PPP2R2A) were all decreased in dMSCs from patients with PE. Furthermore, the physiological roles of miR-16 and miR-136 in the down-regulation of VEGFA and PPP2R2A, respectively, were confirmed through reporter assays.ConclusionsThese findings suggest that miRNAs in dMSCs may be important regulatory molecules in the development of PE.

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Progressive epidural hematoma (PEDH) after head injury is often observed on serial computerized tomography (CT) scans. Recent advances in imaging modalities and treatment might affect its incidence and outcome. In this study, PEDH was observed in 9.2% of 412 head trauma patients in whom two CT scans were obtained within 24 hours of injury, and in a majority of cases, it developed within 3 days after injury. In multivariate logistic regression, patient gender, age, Glasgow Coma Scale (GCS) score at admission, and skull fracture were not associated with PEDH, whereas hypotension (odds ratio (OR) 0.38, 95% confidence interval (CI) 0.17–0.84), time interval of the first CT scanning (OR 0.42, 95% CI 0.19–0.83), coagulopathy (OR 0.36, 95% CI 0.15–0.85), or decompressive craniectomy (DC) (OR 0.46, 95% CI 0.21–0.97) was independently associated with an increased risk of PEDH. The 3-month postinjury outcome was similar in patients with PEDH and patients without PEDH (χ 2 = 0.07, P = 0.86). In conclusion, epidural hematoma has a greater tendency to progress early after injury, often in dramatic and rapid fashion. Recognition of this important treatable cause of secondary brain injury and the associated risk factors may help identify the group at risk and tailor management of patients with TBI.

Edited by Tamas DalmayKeywords: Preeclampsia Mesenchymal stem cell microRNA-494-3p Vascular endothelial growth factor Angiogenesis a b s t r a c t Mesenchymal stem cells (MSCs) play an important role in the pathology of preeclampsia (PE). Our previous microarray analysis found that microRNA-494 (miR-494) is highly expressed in deciduaderived MSCs (dMSCs) from PE. We hypothesized that aberrant expression of miR-494 in dMSCs is involved in PE development. In the present study, we found that miR-494 arrests G1/S transition in dMSCs by targeting CDK6 and CCND1. We also found that supernatant from miR-494-overexpressing dMSCs reduces HTR-8/SVneo migration and impairs HUVEC capillary formation by suppressing VEGF. Taken together, we report an unrecognized mechanism of miR-494 affecting dMSC proliferation and function in the pathology of PE.