Promethazine inhibits neuronal apoptosis via PI3K/Akt signaling pathway in rats with cerebral infarction.

The article "Promethazine inhibits neuronal apoptosis via PI3K/Akt signaling pathway in rats with cerebral infarction, by X.-D. Pan, X.-L. Chen, S.-F. Ding, D. Kou, H.-L. Hu, L. Li, published in Eur Rev Med Pharmacol Sci 2019; 23 (3 Suppl): 126-134-DOI: 10.26355/eurrev_201908_18639-PMID: 31389591" has been withdrawn from the authors stating that they "have not yet studied their work completely and have some difficulties answering questions and quickly providing solutions in the paper". The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18639.

MiR-126 facilitates apoptosis of retinal ganglion cells in glaucoma rats via VEGF-Notch signaling pathway.

OBJECTIVE: The aim of this study was to explore the effect of micro ribonucleic acid (miR)-126 on the apoptosis of retinal ganglion cells in glaucoma rats via the vascular endothelial growth factor (VEGF)-Notch signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley (SD) rats were randomly divided into three groups, including normal group (n=12), model group (n=12) and miR-126 antagomir group (n=12). Rats in normal group did not receive any treatment. In model group and miR-126 antagomir group, the rats were used to establish glaucoma models and intervened with normal saline and miR-126 antagomir, respectively. Intraocular pressure was detected at the completion of modeling and the last intervention, at 7 days after which samples were taken. Western blotting was adopted to detect the relative protein expressions of Notch1 and Notch2. The content of VEGF was examined via enzyme-linked immunosorbent assay (ELISA). Quantitative polymerase chain reaction (qPCR) was carried out to detect the messenger RNA (mRNA) expressions of VEGF, Notch1 and Notch2. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay was performed to detect cell apoptosis. RESULTS: After modeling, intraocular pressure in model group and miR-126 antagomir group was significantly higher than that in normal group (p<0.05). At the end of the intervention, intraocular pressure in miR-126 antagomir group was notably lower than that in model group (p<0.05). VEGF content in model group and miR-126 antagomir group was notably higher than that in normal group (p<0.05). However, it was markedly lower in miR-126 antagomir group than model group (p<0.05). Model group exhibited remarkably higher protein expressions of Notch1 and Notch2 than normal group (p<0.05). However, the protein expressions of Notch1 and Notch2 in miR-126 antagomir group were evidently reduced (p<0.05). Besides, the mRNA expressions of VEGF, Notch1 and Notch2 in model group were significantly higher than those in normal group (p<0.05). However, they were significantly lower in miR-126 antagomir group than those in model group (p<0.05). Furthermore, the apoptosis rate in model group was distinctly higher than that in normal group (p<0.05). However, it was notably lower in miR-126 antagomir group than model group (p<0.05). CONCLUSIONS: MiR-126 facilitates the apoptosis of retinal ganglion cells in glaucoma rats by promoting the VEGF-Notch signaling pathway.

Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6.

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, "Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6, by Y. Zhao, X.-P. Qin, Y.-P. Lang, D. Kou, Z.-W. Shao, published in Eur Rev Med Pharmacol Sci 2019; 23 (13): 5603-5610-DOI: 10.26355/eurrev_201907_18294-PMID: 31298312" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18294.

MiR-200c inhibits proliferation and promotes apoptosis of Wilms tumor cells by regulating akt signaling pathway.

OBJECTIVE: The aim of this study was to explore the effect of micro ribonucleic acid (miR)-200c on the proliferation and apoptosis of Wilms tumor cells, and to further elucidate its potential mechanisms. PATIENTS AND METHODS: Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was used to detect the expression level of miR-200c in cancer tissues and adjacent normal tissues of 20 patients with Wilms tumor. Human primary Wilms tumor cells were taken as research objects, and were divided into Control group and miR-200c mimic group. In miR-200c mimic group, miR-200c was overexpressed in Wilms tumor cells using liposome transfection technology. Subsequently, the proliferation and apoptosis of cells in each group were observed by functional assays. The expression levels of phosphorylated protein kinase B (p-Akt), total Akt (T-Akt) and glucose transporter protein type 1 (GLUT1) in each group of cells were finally detected by Western blotting. RESULTS: In Wilms tumor patients, the expression level of miR-200c in cancer tissues was notably lower than that in adjacent normal tissues (p<0.05). Wilms tumor cells were cultured in vitro, and were transfected with miR-200c mimic. Subsequent cell counting kit-8 (CCK-8) assay results showed that the proliferation ability of cells in miR-200c mimic group was remarkably weakened (p<0.05). Colony formation assay indicated the number of formed colonies in miR-200c mimic group was remarkably less than that in Control group (p<0.05). Western blotting results manifested that overexpression of miR-200c markedly increased the ratio of B-cell lymphoma protein 2 (Bcl-2) to Bcl-2-associated X protein (Bax) (p<0.05). Flow cytometry results revealed that miR-200c overexpression significantly elevated the apoptosis rate of Wilms tumor cells (p<0.05). In addition, it was discovered that the overexpression of miR-200c could prominently reduce the phosphorylation level of intracellular Akt and the expression of its downstream protein GLUT1. Finally, immunohistochemical staining results verified that the expression levels of p-Akt and GLUT1 in cancer tissues of Wilms tumor patients were significantly higher than those in adjacent normal tissues (p<0.05). CONCLUSIONS: MiR-200c was lowly expressed in cancer tissues of Wilms tumor patients. Besides, overexpression of miR-200c inhibited the proliferation and promoted the apoptosis of cells through targeted inhibition of the Akt/GLUT1 signaling pathway.

TGIF2 promotes cervical cancer metastasis by negatively regulating FCMR.

OBJECTIVE: We aimed at studying the correlation between TGIF2 expression and clinicopathological features of cervical cancer (CCa). The relationship between TGIF2 and FCMR and its influence on the proliferation and metastasis of tumor cells were investigated using molecular biology techniques, so as to reveal the pathogenesis of CCa and provide a new target for clinical treatment. PATIENTS AND METHODS: TGIF2 expression in 60 pairs of cervical tumors and paracancerous tissues samples collected from CCa patients of our hospital was studied by quantitative real-time polymerase chain reaction (qPCR) analysis, and the association between TGIF2 expression and the clinical indicators or prognosis of CCa patients were analyzed. CCa cells with TGIF2 knockdown were constructed using transfection technology. Changes in the biological phenotypes (proliferation, migration, invasion) of CCa cells C33-A and HeLa after TGIF2 knockdown were determined by Cell Counting Kit-8 (CCK-8) and transwell assays. In addition, the effects of TGIF2/FCMR axis on CCa metastasis were further explored in nude mice in vivo. RESULTS: Our data revealed a significant increase in TGIF2 mRNA expression in CCa tissue specimens compared to adjacent ones, and the increasing degree was positively correlated with the incidence of lymph node or distant metastasis of CCa patients. The results of CCK-8 and transwell suggested that knocking down TGIF2 effectively attenuated the proliferative ability and invasiveness of CCa cells. Luciferase assay confirmed that TGIF2 can directly bind to the DNA promoter of its target gene FCMR. Simultaneous transfection of sh-TGIF2 and sh-FCMR partially reversed the inhibitory effect of single transfection of TGIF2 knockdown on the malignant progression of CCa. Experiments in nude mice also suggested that TGIF2 could promote CCa tumorigenesis through the modulation of FCMR expression. CONCLUSIONS: In summary, TGIF2 can promote the migration and proliferation ability of cervical cancer cells via down-regulating FCMR. Our study provides a new therapeutic target for the clinical treatment of cervical cancer.

LncRNA NEAT1/miR-1224/KLF3 contributes to cell proliferation, apoptosis and invasion in lung cancer.

OBJECTIVE: The aim of this study was to detect the relationship between long-chain non-coding RNA (lncRNA) NEAT1 and microRNA-1224 (miR-1224) in lung cancer and to explore its underlying mechanism. MATERIALS AND METHODS: The expression levels of lncRNA NEAT1 and miR-1224 in lung cancer tissues and cells were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The interaction between lncRNA NEAT1 with miR-1224, miR-1224, and KLF3 was detected by Dual-Luciferase Reporter Gene Assay. MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and flow cytometry were used to detect the changes in the proliferative and apoptosis abilities of lung cancer cells after silencing lncRNA NEAT1 or up-regulating miR-1224, respectively. RESULTS: Compared with adjacent normal tissues, lncRNA NEAT1 was significantly up-regulated, while miR-1224 was significantly down-regulated in lung cancer tissues. LncRNA NEAT1 could specifically bind to the 3'UTR of miR-1224 and regulate its expression. The inhibition of lncRNA NEAT1 remarkably reduced the proliferation and enhanced the apoptosis of lung cancer cells. However, the upregulation of the expression of miR-1224 level could significantly inhibit proliferation and promote the apoptosis rate of lung cancer cells. Furthermore, miR-1224 could downregulate KLF3 expression by directly binding to its 3'UTR. CONCLUSIONS: LncRNA NEAT1 can sponge the expression of miR-1224, thereby affecting the proliferation and apoptosis of lung cancer.

Promethazine inhibits neuronal apoptosis via PI3K/Akt signaling pathway in rats with cerebral infarction.

OBJECTIVE: To study the effect of promethazine on neuronal apoptosis in rats with cerebral infarction (CI) through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into the sham group (n=12), model group (n=12), and promethazine group (n=12). The external carotid artery was only exposed in the model group, and the ischemia-reperfusion model after CI was established using the suture method in the other two groups. After modeling, the normal saline was intraperitoneally injected in the sham group and model group, while promethazine was intraperitoneally injected in the promethazine group. The rats were sampled after 1 week of intervention. The neurological deficits of rats were evaluated using the Zea-Longa score, and the cognitive function, the spatial learning, and memory of rats were detected via the water maze test. Moreover, the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in brain tissues were detected via immunohistochemistry, and the relative protein expressions of PI3K p85, PI3K p110, and p-Akt were detected via Western blotting. The mRNA expressions of Bax and Bcl-2 were detected via quantitative Polymerase Chain Reaction (qPCR), and the apoptosis was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS: The Zea-Longa score was significantly increased in the model group and promethazine group compared with that in the sham group (p<0.05), while it significantly declined in the promethazine group compared with that in the model group (p<0.05). The escape latency was significantly prolonged and the times of crossing platform were significantly reduced in the model group and promethazine group compared with those in the sham group (p<0.05), while the escape latency was significantly shortened and the times of crossing platform were significantly increased in the promethazine group compared with those in the model group (p<0.05). Compared with those in the sham group, the positive expression of Bax was significantly increased, while the positive expression of Bcl-2 was remarkably decreased in the model group and promethazine group (p<0.05). Compared with those in the model group, the positive expression of Bax was significantly decreased, while the positive expression of Bcl-2 was remarkably increased in the promethazine group (p<0.05). Besides, the model group and promethazine group had evidently higher relative protein expressions of PI3K p85, PI3K p110, and p-Akt than the sham group (p<0.05), while the promethazine group also had evidently higher relative protein expressions of PI3K p85, PI3K p110, and p-Akt than the model group (p<0.05). Compared with the sham group, model group, and promethazine group had remarkably increased relative mRNA expression of Bax, and remarkably decreased relative mRNA expression of Bcl-2 (p<0.05). Compared with those in the model group, the relative mRNA expression of Bax was remarkably decreased, while the relative mRNA expression of Bcl-2 was remarkably increased in the promethazine group (p<0.05). Finally, the apoptosis rate was significantly higher in the model group and promethazine group than that in the sham group (p<0.05), while it was significantly lower in the promethazine group than that in the model group (p<0.05). CONCLUSIONS: Promethazine inhibits neuronal apoptosis in CI rats by upregulating the PI3K/Akt signaling pathway, thereby exerting a protective effect.

Observation of efficacy of TACE combined with HIFU on patients with middle-advanced liver cancer.

OBJECTIVE: To study the efficacy of transarterial chemoembolization (TACE) combined with high-intensity focused ultrasound (HIFU) in patients with middle-advanced liver cancer. PATIENTS AND METHODS: A total of 100 patients with middle-advanced liver cancer treated in our hospital from January 2015 to January 2018 were selected and randomly divided into TACE group (control group, n=50) and TACE combined with HIFU group (experimental group, n=50) according to different therapeutic regimens. The efficacy was observed after the operation, the blood was collected to detect the postoperative liver function indexes aspartate aminotransferase (AST) and alanine aminotransferase (ALT), the postoperative complications were observed. Also, the immune indexes cluster of differentiation 3+ (CD3+), CD4+, and CD8+ were determined. Moreover, the quality of life (QOL) score was compared between the two groups, the 1-, 2-, 3-, and 5-year survival rates were observed after the operation. Also, the changes in the levels of tumor markers α-L-fucosidase (AFU), alpha-fetoprotein (AFP), carbohydrate antigen 19-9 (CA19-9), and carcinoembryonic antigen (CEA) were observed. RESULTS: In experimental group, the levels of AST, ALT, and blood urea nitrogen (BUN) after the operation were significantly decreased (p<0.05), while the postoperative efficacy was significantly superior to that in control group (p<0.05). The incidence of postoperative complications was significantly reduced (p<0.05), the levels of CD3+, CD4+, CD8+, and natural killer (NK) cells were markedly increased (p<0.05). Also, the QOL score was evidently better than that in control group (p<0.05) and the 1-, 2-, 3-, and 5- year survival rates after the operation were evidently higher than those in control group (p<0.05). After treatment, the levels of AFU, AFP, CA19-9, and CEA were remarkably lower than those before treatment in both groups, while they were remarkably lower in experimental group than those in control group (p<0.05). CONCLUSIONS: TACE combined with HIFU in the treatment of patients with middle-advanced liver cancer can restore the hepatic metabolism, enhance the immunity, improve the QOL, prolong the survival time of patients, and significantly reduce the tumor markers. Also, it has fewer adverse reactions and definite overall efficacy, which is worthy of popularization and application.

Circular RNA circ-SMAD7 promoted ovarian cancer cell proliferation and metastasis by suppressing KLF6.

OBJECTIVE: Recently, the roles of circular RNAs (circRNAs) in tumor progression have attracted much attention. Currently, circ-SMAD7 has been identified as an oncogene in cancers. The aim of this study was to investigate the function of circ-SMAD7 in the progression of ovarian cancer. PATIENTS AND METHODS: Circ-SMAD7 expression in both ovarian cancer cells and tissue samples was detected by quantitative Real Time-Polymerase Chain reaction (qRT-PCR). Circ-SMAD7 shRNA was constructed and transfected into the ovarian cancer cells. To identify the function of circ-SMAD7 in ovarian cancer, cell proliferation assay, colony formation assay, transwell assay, and Matrigel assay were conducted, respectively. In addition, qRT-PCR and Western blot assays were performed to elucidate the underlying mechanism and, then, it was analyzed. RESULTS: Circ-SMAD7 expression was remarkably higher in ovarian cancer tissue samples than in corresponding normal tissues. The proliferation of the ovarian cancer cells was significantly inhibited after circ-SMAD7 downregulation. Meanwhile, the migration and invasion of ovarian cancer cells were significantly inhibited after circ-SMAD7 downregulation in vitro. Both the mRNA and the protein expressions of the Krüppel-like factor 6 (KLF6) were remarkably promoted after circ-SMAD7 was knocked down in ovarian cancer cells. Furthermore, the KLF6 expression level was negatively correlated with circ-SMAD7 expression level in ovarian cancer samples. CONCLUSIONS: Our study suggests that circ-SMAD7 promotes the progression of ovarian cancer and enhances cell metastasis and proliferation via suppressing KLF6. In addition, circ-SMAD7 may be a novel therapeutic strategy in ovarian cancer.

Correlation between acute myocardial infarction complicated with cerebral infarction and expression levels of MMP-2 and MMP-9.

OBJECTIVE: To investigate the correlation between the acute myocardial infarction (AMI) complicated with cerebral infarction (CI) and expression levels of matrix metalloproteinase-2 (MMP-2) and MMP-9. PATIENTS AND METHODS: A total of 50 AMI patients treated in our hospital were enrolled, including 23 AMI patients complicated with CI in the AMI-CI group, and 27 patients with AMI alone in the AMI group. Venous blood was collected from each patient after admission. The serum levels of MMP-2 and MMP-9 were detected via enzyme-linked immunosorbent assay (ELISA), and their mRNA expressions were measured via quantitative Polymerase Chain Reaction (qPCR). The cerebral computed tomography (CT) scan was performed for calculating the CI size. The neurological function was evaluated using the neurological deficit score. The correlations between the levels of MMP-2 and MMP-9 with CI size and neurological deficit score were investigated using Pearson correlation analysis. RESULTS: The expression levels of MMP-2 and MMP-9 in the AMI-CI group were significantly higher than those in the AMI group with significant differences (p<0.05). The mRNA expressions of MMP-2 and MMP-9 in AMI-CI group were also significantly higher than those in the AMI group, and the differences between the two groups were statistically significant (p<0.05). Larger CI size was observed in the AMI-CI group than that in the AMI group, showing a statistically significant difference between the two groups (p<0.05). The neurological deficit score in the AMI-CI group was significantly higher than that in the AMI group, with a statistically significant difference between the two groups (p<0.05). The expression levels of MMP-2 and MMP-9 were positively correlated with the CI size and neurological deficit score in AMI patients complicated with CI. CONCLUSIONS: Disease severity of AMI complicated with CI is positively correlated with the expression levels of MMP-2 and MMP-9. Higher expression levels of MMP-2 and MMP-9 are expected to indicate a higher risk of AMI complicated with CI.

Mucosal T-cell immunoregulation varies in early and late inflammatory bowel disease.

BACKGROUND AND AIMS: Crohn's disease is a life-long form of inflammatory bowel disease (IBD) mediated by mucosal immune abnormalities. Understanding of the pathogenesis is limited because it is based on data from adults with chronic Crohn's disease. We investigated mucosal T-cell immunoregulatory events in children with early Crohn's disease. METHODS: Mucosal biopsies and T-cell clones were derived from children experiencing the first attack of Crohn's disease, children with long-standing Crohn's disease, infectious colitis, and children without gut inflammation. RESULTS: As in acute infectious colitis, interleukin (IL) 12 induced T cells from early Crohn's disease to acquire a strongly polarised T helper (Th) type 1 response characterised by high IFN-gamma production and IL12Rbeta2 chain expression. Th1 polarisation was not induced in clones from late Crohn's disease. Mucosal levels of IL12p40 and IL12Rbeta2 messenger RNA were significantly higher in children with early than late Crohn's disease. These results demonstrate that susceptibility to IL12-mediated modulation is strongly dependent on the stage of Crohn's disease. CONCLUSIONS: At the onset of Crohn's disease mucosal T cells appear to mount a typical Th1 response that resembles an acute infectious process, and is lost with progression to late Crohn's disease. This suggests that mucosal T-cell immunoregulation varies with the course of human IBD. Patients with the initial manifestations of IBD may represent an ideal population in which immunomodulation may have optimal therapeutic efficacy.

[Preparation and evaluation of in-situ synthesis zeolite gas-liquid modified columns].

A new kind of NaA zeolite column has been prepared by in-situ synthesis technique. In comparing with traditional coating method, the in-situ NaA zeolite carrier is much more uniform and rigid. Several kinds of zeolite gas-liquid modified columns have been prepared with this in-situ technology, which showed satisfactory features in separation property and thermal stability. The successful utilization of mini-length and wide-bore columns showed good practical prospect of this new kind of zeolite column.

Gas injection membrane extraction for fast on-line analysis using GC detection.

Membrane extraction has been interfaced with gas chromatography and mass spectroscopy for the analysis of volatile organics in water. The vacuum in a mass spectrometer provides fast mass transport. The time required to complete permeation in a GC interface can be fairly long, because the positive pressure of the carrier gas on the permeate side slows down the analyte permeation. The aqueous boundary layer formed on the membrane is considered to be the biggest contributor to the resistance to mass transfer. Another issue is the dispersion of analyte in the aqueous stream, which broadens the input pulse to the membrane. The overall effect of these two factors is to increase the analysis time. Gas injection of aqueous samples is presented in this paper to address these issues. Gas injection reduces the formation of boundary layer, and increases the overall diffusion coefficient seven times. Axial mixing of the sample with a gaseous eluent is minimal, and this eliminates the tailing in permeation profiles. The overall membrane extraction is found to be significantly faster when a gas is used to inject an aqueous sample. This method is also simpler in terms of instrumentation and operational procedures.

Stimulatory effect of trans-cinnamaldehyde on noradrenaline secretion in guinea-pig ileum myenteric nerve terminals.

The effect of trans-cinnamaldehyde (CNMA) on the release of noradrenaline (NA) from nerve terminal was investigated using isolated ileal synaptosomes of guinea-pig. Release was determined as the amount of NA, quantified by h.p.l.c.-electrochemical detection, from samples incubated with CNMA minus that in parallel blanks treated with same volume of vehicle. CNMA stimulated the secretion of NA in a concentration-dependent manner from 5 microM to 50 microM, while the value of lactate dehydrogenase in the incubated medium was not influenced by CNMA. However, trans-cinnamic acid, cinnamoyl chloride and cinnamamide failed to produce similar effect. Specific action of CNMA can thus be considered. Guanethidine inhibited the release of NA by CNMA in a concentration- dependent manner. Saxitoxin attenuated the action of CNMA at concentrations sufficient to block sodium channels. The depolarizing effect of CNMA on the membrane potential was also illustrated by a concentration-dependent increase in the fluorescence of bisoxonol, a potential sensitive dye. The NA releasing action of CNMA was deleted by removal of calcium chloride from the bathing medium. This action of CNMA was also attenuated by Rp-cAMP at concentrations sufficient to inhibit the action of cyclic AMP. These findings suggest that CNMA can depolarize the membrane to result in a calcium-dependent and cyclic AMP-related release of NA from noradrenergic terminals.

[Molten organic salt--a new class of stationary phases for GC].

Molten organic salts are a new class of polar, selective stationary phases for gas chromatography. Their types and characters are reported in detail and compared with some common stationary phases.

[Determination of carboxylic acid on a new capillary column prepared by ourselves].

In this paper, use of tri-n-butylammonium dodecylsulfonate as liquid phase to prepare a capillary column suitable to separate carboxylic acids in a direct injection mode, by the method of dynamic coating with mercury plug, is reported. The results showed that the column has good gas chromatographic properties and high selectivity, especially to strong polar compounds, such as carboxylic acids. The preparation of the capillary column, separation and quantitative analysis of carboxylic acids were investigated. Several examples are given.

Pediatric hepatic trauma: does clinical course support intensive care unit stay?

PURPOSE: The objective of this study is to determine if grade of liver injury predicts outcome after blunt hepatic trauma in children and to initiate analysis of current management practices to optimize resource utilization without compromising patient care. METHODS: A retrospective review of 36 children who had blunt hepatic trauma treated at a pediatric trauma center from 1989 to present was performed. Hepatic injuries graded (AAST Organ Injury Scaling) ranged from grade I to IV. Injury Severity Score (ISS), Glasgow Coma Score (GCS), transfusion requirements, liver transaminase levels, associated injuries, intensive care unit (ICU) length of stay, and survival were analyzed. RESULTS: Mean (+/-SEM) age was 6.6+/-0.8 years, mean grade of hepatic injury was 2.4+/-0.2, mean ISS was 17+/-2.6, mean GCS was 13+/-1, and mean transfusion was 15.4 mL/kg of packed red blood cells (PRBC). There were three deaths with a mean ISS of 59+/-9 and a mean GCS of 3+/-0. Death was not associated with a high-grade liver injury, survivors versus nonsurvivors, 2.3+/-0.2 versus 2.7+/-0.3, but was associated with ISS, 13+/-1.4 versus 59+/-9 (P = .005) and GCS, 14+/-1 versus 3+/-0 (P = .005). Only one patient (grade III, ISS = 43) underwent surgery. There were no differences in mean ISS or GCS between grades I to IV patients. The hepatic injury grades of patients requiring transfusion versus no transfusion were significantly different, 3.4+/-0.2 versus 2.2+/-0.2 (P = 0.04). Abused patients had high-grade hepatic injuries and significant laboratory and clinical findings. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly higher in grade III and IV injuries than in grades I and II, 1,157+/-320 versus 333+/-61 (P= .02) and 1,176+/-299 versus 516+/-86 (P= .04), respectively. No children with grade I or II injury had a transfusion requirement or surgical intervention. There were no liver-related complications. CONCLUSIONS: Mortality and morbidity rates in pediatric liver injuries, grades I to IV, correlate with associated injuries not the degree of hepatic damage. ALT, AST, and transfusion requirements are significantly related to degree of liver injury. Low-grade and isolated high-grade liver injuries seldom require transfusion. Blunt liver trauma rarely requires surgical intervention. In retrospect, the need for expensive ICU observation for low-grade and isolated high-grade hepatic injuries is questionably warranted.