Identification of volatile compounds and their bioactivities from unpolar fraction of Alpinia oxyphylla Miq. and mining key genes of nootkatone biosynthesis.

In this study, analysis of the chemical constituents and bioactivities of the unpolar fractions [petroleum ether (PE) and chloroform (C)] of fruits and leaves of Alpinia oxyphylla Miq. were carried out, as well as the bioactivities of the main compounds nootkatone and valencene. From PE and C fractions of the fruits, and PE fraction of the leaves, 95.80%, 59.30%, and 82.11% of the chemical constituents respectively were identified by GC-MS. Among these identified compounds, nootkatone was the main compound in all of three fractions, while valencene was the second main compound in the PE fractions of the fruits and leaves. The bioactivities results showed that all of the fractions and the major compound nootkatone showed tyrosinase inhibitory, as well as inhibitory effect on NO production in LPS-stimulated RAW264.7 cells. While valencene only presented inhibitory activity on NO production in RAW264.7 cells. The critical genes involved in nootkatone biosynthesis in A. oxyphylla were identified from the public transcriptome datasets, and protein sequences were preliminarily analyzed. Our studies develop the usage of the unpolar fractions of A. oxyphylla, especially its leaves as the waste during its production, and meanwhile provide the gene resources for nootkatone biosynthesis.

MicroRNA-15a promotes prostate cancer cell ferroptosis by inhibiting GPX4 expression.

Ferroptosis is a novel form of regulated cell death characterized by accumulated lipid reactive oxygen species (ROS) and inactivation of glutathione peroxidase 4 (GPX4). The present study aimed to investigate the role of microRNA (miRNA/miR)-15a in ferroptosis of prostate cancer cells. Bioinformatics analysis was performed to predict the potential interaction between miR-15a and the 3'-untranslated region (UTR) of GPX4 mRNA. The prostate cancer cell line, LNCAP was transfected with miR-15a mimics or small interfering (si)-GPX4. Reverse transcription-quantitative PCR and western blot analyses were performed to detect the mRNA and protein expression levels of GPX4, respectively. Biotin-RNA pull-down and dual-luciferase reporter assays were performed to verify the interaction between miR-15a and GPX4 mRNA. The Cell Counting Kit-8 assay was performed to assess cell proliferation, while lactate dehydrogenase (LDH) and intracellular ferrous iron levels were detected via ELISA. Lipid ROS and mitochondrial membrane potential (MMP) were assessed via flow cytometry and staining with C11-BIODIPY probes or JC-1. Furthermore, lipid peroxidation was identified by measuring malondialdehyde (MDA) levels. The results demonstrated that transfection with miR-15a mimics decreased GPX4 protein expression. Bioinformatics analysis revealed potential binding sites between miR-15a and the 3'-UTR region of GPX4, and RNA pull-down and the dual-luciferase reporter assays further confirmed the interaction between miR-15a and GPX4 mRNA. Both transfection with miR-15a mimics and si-GPX4 suppressed cell proliferation, elevated LDH release, accumulated intracellular ferrous iron and ROS, disrupted MMP and increased MDA levels. Taken together, the results of the present study suggest miR-15a induces ferroptosis by regulating GPX4 in prostate cancer cells, which provides evidence for investigating the therapeutic strategies of prostate cancer.

Genome-wide identification and expression analysis of terpene synthase gene family in Aquilaria sinensis.

Agarwood is the resinous portion of Aquilaria trees, and has been widely used as medicine and incense. Sesquiterpenes are the main chemical characteristic constituents of agarwood. Terpene synthase (TPS) is a critical enzyme responsible for biosynthesis of sesquiterpene compounds. However, limited information is available on genome-wide identification and characterization of the TPS family in Aquilaria trees. In this study, TPS gene family was identified and characterized in Aquilaria sinensis by bioinformatics methods. The expression of those genes was analyzed by RNA-seq and quantitative real-time PCR. Transcription factors regulating TPS gene expression were identified by yeast one-hybrid and dual-luciferase assay. In total, 26 AsTPS genes (AsTPS1-AsTPS26) were identified, which were classified into five subgroups. Many putative cis-elements putatively involved in stresses and phytohormones (especially jasmonic acid) were identified in the promoter regions of AsTPSs, suggesting that AsTPSs genes may be regulated by stresses and jasmonic acid. Expression analysis revealed seven TPS genes encoding sesquiterpene synthetases were induced by wounding and methyl jasmonic acid (MeJA), which may be related to sesquiterpene biosynthesis. By yeast one-hybrid screening, a ERF transcription factor AsERF1 was identified to interact with the AsTPS1 promoter. Subcellular localization analysis indicated AsERF1 was a nucleus-localized protein. Transient transfection of AsERF1 in leaves of Nicotiana benthamiana significantly enhanced the promoter activation of AsTPS1, suggesting AsERF1 may participate in sesquiterpene biosynthesis by regulating AsTPS1 expression. These data generated in this study provide a foundation for future studies on functional roles and regulation mechanisms of AsTPS in sesquiterpene biosynthesis and agarwood formation.

Shenfu injection prevents sepsis-induced myocardial injury by inhibiting mitochondrial apoptosis.

ETHNOPHARMACOLOGICAL RELEVANCE: Shenfu injection (SFI) is a well-known Chinese herbal medicine widely used in the treatment of septic shock in China. AIMS: The aims of this study are to investigate the protective effects of SFI on sepsis-induced myocardial injury in mice and to identify the underlying mechanism of action. MATERIALS AND METHODS: Seventy-two male C57/B6J mice (5-6 weeks old) were randomly divided into five groups: control (NC), sham sepsis (sham), sepsis (Lipopolysaccharide- LPS), sepsis treated with a low dose SFI, and sepsis treated with a high dose SFI. Sepsis was induced in mice by intraperitoneal injection of LPS. Myocardial tissue samples were collected from different groups at 6 h, 12 h, and 24 h post-LPS injection. Myocardial injury was examined using hematoxylin-eosin (H&E) and TUNEL staining. Western-blot analysis was performed to determine the protein expression of B-cell lymphoma 2 (Bcl-2), BH3 interacting-domain death agonist (Bid), truncated-Bid (t-Bid) and caspase-9 in all the groups. Moreover, the structural changes in the mitochondria of cardiomyocytes were also observed by transmission electron microscopy. RESULTS: H&E staining revealed structural damage, local necrosis, interstitial edema, inflammatory cell infiltration and vacuolar changes in the myocardial tissue in the sepsis (LPS) group; almost intact myocardial tissue was observed in the high dose SFI group with improvements in interstitial edema and inflammatory cell infiltration. We observed that LPS-induced cardiomyocyte apoptosis was significantly improved with high dose SFI as compared with sepsis (LPS) group (P ˂ 0.05). LPS was found to decrease the protein expression of Bcl-2 and increase the level of Bid, t-Bid and caspase-9. Treatment with SFI significantly increased the Bcl-2 protein expression (P ˂ 0.05) and decreased the protein expression of Bid, t-Bid and caspase-9 as compared with LPS group (P ˂ 0.05). Markedly swollen myocardial mitochondria with partial vacuolation were observed in LPS treated mice while SFI treatment was found to significantly improve the LPS-induced morphological damage of the mitochondria. CONCLUSION: In conclusion, we demonstrate that SFI protects against sepsis-induced myocardial injury in mice through the suppression of myocardial apoptosis. It upregulates the protein expression of Bcl-2 and downregulates the protein expression of Bid, t-Bid and caspase-9, and alleviates sepsis-induced mitochondrial damage.

E2F7, regulated by miR­30c, inhibits apoptosis and promotes cell cycle of prostate cancer cells.

Prostate cancer (PCa) remains a leading cause of mortality among men in the United States and Western Europe. The molecular mechanism of PCa pathogenesis has not been fully elucidated. In the present study, the expression profile of E2F transcription factor 7 (E2F7) in PCa was examined using immunohistochemistry and reverse transcription­quantitative PCR, whilst cell cycle progression and apoptosis were determined using fluorescent cell activated sorting techniques. Cell viability was measured using Cell Counting Kit­8 in loss­ and gain­of­function studies. Dual­luciferase reporter assay was used to verify if E2F7 was one of the potential targets of miR­30c. The staining score of E2F7 of PCa tissues was found to be notably higher compared with that of adjacent normal tissues. Suppression of E2F7 expression in PCa cell lines led to significantly reduced proliferation rates, increased proportion of cells in the G1 phase of the cell cycle and higher apoptotic rates compared with those in negative control groups. Dual­luciferase reporter assay revealed E2F7 to be one of the binding targets of microRNA (miR)­30c. In addition, transfection of miR­30c mimics into PCa cells resulted in reduced cell viability, increased proportion of cells in the G1 phase and higher apoptotic rates. By contrast, transfection with the miR­30c inhibitor led to lower apoptosis rates of PCa cells compared with negative control groups, whilst E2F7 siRNA co­transfection reversed stimulatory effects of miR­30c inhibitors on cell viability. In addition, the expression of cyclin­dependent kinase inhibitor p21 were found to be upregulated by transfection with either E2F7 siRNA or miR­30c mimics into PCa cells. In conclusion, the present study suggested that E2F7 may be positively associated with PCa cell proliferation by inhibiting p21, whereas E2F7 is in turn under regulation by miR­30c. These observations suggest the miR­30c/E2F7/p21 axis to be a viable therapeutic target for PCa.

New tricyclic prezizaane sesquiterpenoids from agarwood.

Ten new tricyclic prezizaane types sesquiterpenoids (1-10) were isolated from ethyl ether extract of agarwood originated from Aquilaria sp. Their structures were unambiguously elucidated on the basis of 1D and 2D NMR spectra as well as by HRESIMS data. The absolute configuration of the new prezizaenes 1, 2 and 4 was determined by single-crystal X-ray diffraction, while TDDFT-ECD method was applied for 6. Compounds 4 and 5 displayed significant inhibitory activities toward α-glucosidase with IC50 values of 0.22 and 1.99 mM, respectively.

Honokiol Attenuates the Memory Impairments, Oxidative Stress, Neuroinflammation, and GSK-3ß Activation in Vascular Dementia Rats.

Vascular dementia (VaD) is caused by chronic decreases in brain blood flow and accounts for 15-20% of dementia cases worldwide. In contrast to Alzheimer's disease (AD), no effective drug treatments are currently available for VaD. Previous studies have suggested that oxidative stress and neuroinflammation in the brain play important roles in the pathogenesis of VaD. Honokiol (HKL) is a well-known bioactive and nutraceutical compound that can act as an antioxidant and anti-inflammatory molecule. HKL can protect against memory impairments in AD mouse models. In this study, we explored whether the application of HKL was also protective against the insult of chronic cerebral hypoperfusion (CCH) in rats. We found that HKL supplementation prevented the memory impairments in the inhibitory avoidance step-down and Morris water maze tasks in CCH rats. HKL also suppressed the levels of oxidative stress and inflammation in CCH rats. Moreover, HKL prevented dendritic spines abnormalities in CCH rats. We also found that HKL inhibited the activity of GSK-3ß, which may be critical for the neuroprotective activity of HKL. Thus, our study demonstrated the protective role of HKL in VaD.

Efficacy of dexmedetomidine for treatment of patients with sepsis: A meta-analysis of randomized controlled trials.

BACKGROUND: This meta-analysis aimed to evaluate the effect of dexmedetomidine on prognosis in patients with sepsis. METHODS: Computer-related electronic databases were searched, including PubMed, Embase, Web of Science, the Cochrane Library, and the China National Knowledge Infrastructure, from the date of database construction to January 2019. Stata 12.0 was used to perform a meta-analysis of short-term mortality [intensive care unit (ICU) mortality or 28-day mortality], ICU length of stay, and mechanical ventilation. Mortality was expressed using risk ratio (RR) and 95% confidence interval (CI). ICU length of stay and mechanical ventilation were expressed as weighted mean difference (WMD) and 95% CIs. RESULTS: We finally included 8 randomized controlled trials in this meta-analysis. Compared with the control group, the dexmedetomidine group had a lower occurrence of 28-day mortality (RR, 0.49; 95% CI, 0.35 to 0.69; P = .000) and ICU mortality (RR, 0.44; 95% CI, 0.23 to 0.84; P = .013). However, there was no statistically significant difference for the length of hospital stay (WMD, -0.05; 95% CI, -0.59 to 0.48; P = .840) and mechanical ventilation time (WMD, 1.05; 95% CI, -0.27 to 2.37; P = .392) between dexmedetomidine group and control group. CONCLUSIONS: In patients with sepsis, dexmedetomidine can reduce the short-term mortality of patients, but could not shorten the ICU length of stay and mechanical ventilation time. More clinical randomized controlled trials are needed to verify the efficacy and safety of dexmedetomidine on the length of hospital stay and mechanical ventilation time.

High lncRNA HULC expression is associated with poor prognosis and promotes tumor progression by regulating epithelial-mesenchymal transition in prostate cancer.

INTRODUCTION: Recently, increasing evidence has shown that long non-coding RNAs (lncRNAs) play critical roles in tumor progression and development. However, the expression pattern and biological function of lncRNA HULC (highly upregulated in liver cancer) in prostate cancer (PCa) remain largely unclear. MATERIAL AND METHODS: The expression of lncRNA HULC in 53 paired PCa tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The χ2 test was used to explore the association of lncRNA HULC expression with clinicopathologic features. Kaplan-Meier analysis was used to detect the association between HULC expression and overall survival of PCa patients. Furthermore, the function of HULC in cell growth and metastasis was detected in PCa cells. RESULTS: Our data showed that HULC expression was upregulated in PCa tissues and cell lines compared to adjacent non-tumor tissues and the normal prostate cell line RWPE-1 (p < 0.05). High HULC expression was positively associated with advanced clinicopathologic features and poor overall survival (OS) for PCa patients (p < 0.05). HULC inhibition suppressed PCa cell growth and metastasis both in vitro and in vivo (p < 0.05). Furthermore, HULC knockdown reduced N-cadherin and vimentin expression and increased E-cadherin expression in PCa cells (p < 0.05). CONCLUSIONS: Our data suggested that lncRNA HULC might play oncogenic roles in PCa progression, which provided a novel therapeutic strategy for PCa patients.

MicroRNA-183 functions as the tumor suppressor via inhibiting cellular invasion and metastasis by targeting MMP-9 in cervical cancer.

OBJECTIVE: MicroRNAs have been reported to play an important role in the invasion and metastasis of cervical cancer. miR-183 was found to inhibit or promote the invasion and metastasis of multiple solid tumors. However, the roles of miR-183 in cervical cancer are unclear. METHODS: In this study, miR-183 expression levels were measured in 53 cervical cancer and 13 normal cervical tissues by qRT-PCR. The effects of forced expression of miR-183 on cervical cancer cells invasion and metastasis were investigated using Transwell uncoated or coated with growth factor-reduced Matrigel for migration or invasion assays, respectively. RESULTS: We found that miR-183 expression levels were significantly down-regulated in cervical cancer tissues compared with normal tissues (0.15±0.011 to 0.86±0.049). Ectopic expression of miR-183 resulted in the suppression of invasion and migration of cervical cancer cell lines, siha and Hela cells (p<0.0001). Bioinformatics analysis revealed that MMP-9 was the potential target of miR-183 and it was found that MMP-9 was remarkably up-regulated in cervical cancer. Furthermore, a dual-luciferase reporter assay showed that MMP-9 as a target of miR-183 (p<0.0001). The invasion and metastasis ability of siha and Hela was suppressed when MMP-9 was down-regulated in vitro (p<0.0001). CONCLUSIONS: In conclusion, our study revealed that miR-183 might be a tumor suppressor via inhibiting the invasion and metastasis of cervical cancer cells through targeting MMP-9, indicating that miR-183 may be a novel potential therapeutic target for cervical cancer.

MicroRNA-216b is Down-Regulated in Human Gastric Adenocarcinoma and Inhibits Proliferation and Cell Cycle Progression by Targeting Oncogene HDAC8.

PURPOSE: Accumulating evidence indicates that micro (mi)RNAs play a critical role in carcinogenesis and cancer progression; however, their role in the tumorigenesis of gastric adenocarcinoma remains unclear so the present study investigated this in gastric cancer (GC) tissues and cell lines. METHODS: Human GC specimens (n = 57) and patient-paired non-cancerous specimens were obtained from patients at the First Affiliated Hospital, Henan University of Science and Technology. The AGS and GC9811 gastric cancer cell lines were also used. Expression levels of miR-216b and HDAC8 were examined by quantitative real-time PCR and the expression of HDAC8 was also examined by Western blotting and immunohistochemistry assay. The cell cycle progression was determined by FACS. MiR-216b inhibitor, mimics, and siRNA-HDAC8 transfections were performed to study the loss and gain of function. RESULTS: We reported a significantly decreased expression of miR-216b in GC clinical specimens compared with paired non-cancerous tissues. We also observed a significant down-regulation of miR-216b expression in GC cell lines AGS and GC9811 (p < 0.0001). The introduction of miR-216b suppressed GC cell proliferation and cell cycle progression by targeting HDAC8, an oncogene shown to promote malignant tumor development with a potential miR-216b binding site in its 3' untranslated region. HDAC8 expression was shown to be significantly increased in AGS and GC9811 cell lines (p < 0.0001) and GC tissues compared with controls. Moreover, HDAC8 inhibition suppressed cell cycle progression compared with control groups (22 % ± 1.6 % vs 34 % ± 2.1), indicating that HDAC8 may function as an oncogene in the development of GC. Furthermore, HDAC8 expression was negatively correlated (p < 0.0001), while miR-216b expression was positively correlated with the clinical outcome of GC patients (p < 0.0001). DISCUSSION: Our data suggest that miR-216b functions as a tumor suppressor in human GC by, at least partially, targeting HDAC8.

The inhibition of histone deacetylase 8 suppresses proliferation and inhibits apoptosis in gastric adenocarcinoma.

Histone deacetylase 8 (HDAC8), a unique member of class I HDACs, shows remarkable correlation with advanced disease stage. The depletion of HDAC8 leads to inhibition of proliferation, apoptosis and cell cycle arrest in multiple malignant tumors. However, little is known about the contribution of HDAC8 to the tumorigenesis of gastric cancer (GC). The present study investigated expression of HDAC8 in GC cell lines and tissues, and the roles of HDAC8 inhibition in the proliferation, cell cycle and apoptosis of gastric cancer cells and explored the potential mechanisms. In the present study, quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), western blotting, and immunohistochemistry were used to examine the mRNA and protein expression of HDAC8 in GC cell lines and tissues. Then, the correlation between the clinicopathological parameters and the expression of HDAC8 was assessed. Finally, siRNA transfection and HDAC8 plasmid was performed to explore the functions of HDAC8 in GC progression in vitro. We found that the expression of HDAC8 was significantly upregulated both in GC cell lines and tumor tissues compared to human normal gastric epithelial cell, GES-1 and matched non-tumor tissues. Furthermore, depletion of HDAC8 remarkably inhibited GC cell proliferation, increased the apoptosis rate and G0/G1 phase percentage in vitro. Western blotting showed that the expression of protein promoting apoptosis such as, Bmf, activated caspase-3, caspase-6 were elevated following HDAC8 depletion. Our data exhibited an important role of HDAC8 in promoting gastric cancer tumorigenesis and identify this HDAC8 as a potential therapeutic target for the treatment of gastric cancer.

Multidrug-Resistance Related Long Non-Coding RNA Expression Profile Analysis of Gastric Cancer.

The effect of chemotherapy of gastric cancer (GC) remains very poor because of multidrug resistance (MDR). However, the mechanisms underlying MDR of GC remains far from fully understood. The aim of this study is to illustrate the potential mechanisms of the MDR of GC at mainly the long non-coding RNA (lncRNA) level. In this study, GC cell line, SGC7901, and two MDR sublines, SGC7901/VCR and SGC7901/ADR were subjected to an lncRNA microarray analysis. Bioinformatics and verification experiments were performed to investigate the potential lncRNAs involved in the development of MDR. Pathway analysis indicated that 15 pathways corresponded to down-regulated transcripts and that 20 pathways corresponded to up-regulated transcripts (p-value cut-off is 0.05). GO analysis showed that the highest enriched GOs targeted by up-regulated transcripts were "system development" and the highest esenriched GOs targeted by the down-regulated transcripts were "sterol biosynthetic process". Our study is the first to interrogate differentially expressed lncRNAs in human GC cell line and MDR sublines and indicates that lncRNAs are worthwhile for further study to be the novel candidate biomarkers for the clinical diagnosis of MDR and potential targets for further therapy.

Chondromodulin-1 functions as a tumor suppressor in gastric adenocarcinoma.

Chondromodulin-1 (ChM1) is a cartilage-specific glycoprotein that stimulates the growth of chondrocytes and inhibits the tube formation of endothelial cells. Endogenously, ChM1 is expressed in the cartilage and is an anti-angiogenic factor. ChM1 has been reported to suppress the proliferation of multiple human tumor cells in an anchorage-independent manner. However, the role of ChM1 in carcinogenesis of gastric cancer remains unknown. By quantitative RT-PCR and western blotting we examined the expression of ChM1 in gastric cancer tissue and normal gastric tissue. In vitro we investigated the functional and mechanistic roles of ChM1 in the inhibition of gastric cancer cell aggressiveness. We observed that ChM1 expression was remarkably downregulated in gastric cancer cell lines compared with the immortal normal gastric epithelial cell line GES-1. Importantly, ChM1 was frequently downregulated in gastric cancer tissue compared with normal gastric tissue. Low ChM1 mRNA expression was associated with higher clinical stages, higher lymph node metastasis, and poorer prognosis of patients. Functional assays in vitro showed that ectopic expression of ChM1 was able to inhibit gastric tumor cell proliferation by arresting the cell cycle. Overall, our findings indicate that ChM1 is a potential tumor suppressor in gastric cancer, suggesting that it may be useful as a biomarker for the treatment and prognosis of gastric cancer.

Inferior vestibular neuritis in a fighter pilot: a case report.

Spatial disorientation in airplane pilots is a leading factor in many fatal flying accidents. Spatial orientation is the product of integrative inputs from the proprioceptive, vestibular, and visual systems. One condition that can lead to sudden pilot incapacitation in flight is vestibular neuritis. Vestibular neuritis is commonly diagnosed by a finding of unilateral vestibular failure, such as a loss of caloric response. However, because caloric response testing reflects the function of only the superior part of the vestibular nerve, it cannot detect cases of neuritis in only the inferior part of the nerve. We describe the case of a Chinese naval command fighter pilot who exhibited symptoms suggestive of vestibular neuritis but whose caloric response test results were normal. Further testing showed a unilateral loss of vestibular evoked myogenic potentials (VEMPs). We believe that this pilot had pure inferior nerve vestibular neuritis. VEMP testing plays a major role in the diagnosis of inferior nerve vestibular neuritis in pilots. We also discuss this issue in terms of aeromedical concerns.

[The analysis of hepatitis delta virus infective markers in the hepatitis is B virus infective people].

OBJECTIVE: To investigate the distribution of hepatitis delta virus (HDV) marker among hepatitis B virus (HBV) infected patients and to reveal its clinical significance. METHOD: To collect the clinical data and sera samples of HBV infected patients and to detect HDAg, Anti-HDV as well as HBV infection markers by means of enzyme-linked immunosorbnent assay. These data combined with clinical diagnostic results and biochemical index were then analyzed. RESULT: 462 samples of HBV infected patients were collected including 210 HBV carriers without symptom, 175 chronic HBV infections, 35 acute HBV infections and 42 liver fibrosis. The HDV infection rate was 4.8% overall. The highest infection rate of 9.5% was found in the group of liver fibrosis whereas the lower rate of 6.9% was found in HBV chronic carriers. HDV infection rate was 7.8% among the population of 40-60 years old, obviously higher than any other age groups. CONCLUSION: HDV infection was significantly higher in the chronic HBV patients and liver fibrosis patients. Because HDV infection was highly associated with the progress of liver disease, we suggest the screen of HDV markers among hepatitis patients and discriminate whether the patient was co-infected with HDV.

[A clinical study on combined serum hepatic fibrosis-related markers and ultrasound parameters to diagnose hepatic fibrosis].

OBJECTIVE: This study attempted to explore the value of combining serum hepatic fibrosis-related markers and ultrasound parameters together on diagnosis of hepatic fibrosis. METHODS: Six serum markers and 8 ultrasound parameters were measured from 100 patients with chronic hepatitis B or cirrhosis. The results of the serum hepatic fibrosis-related markers and ultrasound in disease group were analyzed and compared with the findings of hepatic pathology. RESULTS: By filtrating,the group of platelet derived growth factor-BB (PDGF-BB) plus hyaluronic acid (HA) plus echo characteristics of liver parenchyma (LPEC) plus length of spleen (SL) had the highest Se and Spe, which were 90.7% and 85.4% respectively. CONCLUSION: The advantageous combination of serum markers and ultrasound parameters can significantly improve Se and Spe, which is superior to any single serum index or ultrasound parameter. And it was a better non-invasive method for diagnosing hepatic fibrosis.

The presence of anti-mitochondrial antibodies in Chinese patients with liver involvement in systemic lupus erythematosus.

Sixty-six hospitalized patients with systemic lupus erythematosus (SLE) were enrolled into this study. The test for anti-mitochondrial antibodies (AMAs) was performed and biochemical parameters were determined. AMAs were detected in 15 of the 66 patients with SLE. Meanwhile, we compared enzymatic levels in AMA-positive and -negative patients and found that serum aminotransferase levels were significantly higher in AMA-positive patients than in AMA-negative individuals. Furthermore, we found a positive correlation between serum AMA titration and serum aminotransferase levels. This study suggests that AMAs might contribute to the elevation of aminotransferases. Although much remains to be learned about the pathogenesis of autoimmune liver disease associated with AMAs, this report might provide greater insight into the metabolic mechanisms of AMAs in AMA-positive patients.

Increased serum aminotransferases associated with anti-mitochondrial antibodies in systemic lupus erythematosus patients with autoimmune liver disease.

BACKGROUND: Serum aminotransferase activities are increased in many liver diseases, but the causes for the elevation might be difficult to determine. Whether the elevation of aminotransferases correlates with anti-mitochondrial antibodies (AMA) in systemic lupus erythematosus (SLE) patients with autoimmune liver disease deserves further consideration. METHODS: A meticulous review was done in a large SLE cohort searching for laboratory features of the presence of AMA. Forty-eight hospitalized SLE patients with AMA and 60 randomly selected SLE patients without AMA as a matched case control were enrolled into the retrospective study. Laboratory data were collected, analyzed and compared in SLE patients with and without AMA. RESULTS: Serum activities of aminotransferases were significantly increased in the 48 SLE patients with AMA compared with the 60 subjects without AMA. Meanwhile, we found a positive correlation between serum AMA titers and serum aminotransferase activities. CONCLUSION: Although much remains to be learned about the pathogenesis of autoimmune liver disease associated with AMA, it is possible to suggest that AMA might contribute to the elevation of aminotransferases in SLE patients with the progressive disease.