The oncolytic bacteria-mediated delivery system of CCDC25 nucleic acid drug inhibits neutrophil extracellular traps induced tumor metastasis.

BACKGROUND: Neutrophil extracellular traps (NETs), antibacterial weapons of neutrophils (NEs), have been found to play a crucial role in cancer metastasis in recent years. More and more cancer research is focusing on anti-NETs. However, almost all anti-NETs treatments have limitations such as large side effects and limited efficacy. Therefore, exploring new anti-NETs therapeutic strategies is a long-term goal. RESULTS: The transmembrane protein coiled-coil domain containing 25 (CCDC25) on tumor cell membranes can bind NETs-DNA with high specificity and affinity, enabling tumor cells to sense NETs and thus promote distant metastasis. We transformed shCCDC25 into VNP20009 (VNP), an oncolytic bacterium, to generate VNP-shCCDC25 and performed preclinical evaluation of the inhibitory effect of shCCDC25 on cancer metastasis in B16F10 lung metastasis and 4T1 orthotopic lung metastasis models. VNP-shCCDC25 effectively blocked the downstream prometastatic signaling pathway of CCDC25 at tumor sites and reduced the formation of NETs while recruiting more neutrophils and macrophages to the tumor core, ultimately leading to excellent metastasis inhibition in the two lung metastasis models. CONCLUSION: This study is a pioneer in focusing on the effect of anti-NET treatment on CCDC25. shCCDC25 is effectively delivered to tumor sites via the help of oncolytic bacteria and has broad application in the inhibition of cancer metastasis via anti-NETs.

TRAF3/STAT6 axis regulates macrophage polarization and tumor progression.

Converting tumor-associated macrophages (TAMs) from the M2 to the M1 phenotype is considered an effective strategy for cancer therapy. TRAF3 is known to regulate NF-κB signaling. However, the role of TRAF3 in TAM polarization has not yet been completely elucidated. Here, we found that ablation of TRAF3 increased M1 markers, iNOS, FGR and SLC4A7, while down-regulated M2 markers, CD206, CD36 and ABCC3, expression levels in macrophages. Moreover, TRAF3 deficiency enhanced LPS-induced M1 and abolished IL-4-induced macrophage polarization. Next, quantitative ubiquitomics assays demonstrated that among the quantitative 7618 ubiquitination modification sites on 2598 proteins, ubiquitination modification of IL-4 responding proteins was the most prominently reduced according to enrichment analysis. STAT6, a key factor of IL-4 responding protein, K450 and K129 residue ubiquitination levels were dramatically decreased in TRAF3-deficient macrophages. Ubiquitination assay and luciferase assay demonstrated that TRAF3 promotes STAT6 ubiquitination and transcriptional activity. Site mutation analysis revealed STAT6 K450 site ubiquitination played a vital role in TRAF3-mediated STAT6 activation. Finally, B16 melanoma mouse model demonstrated that myeloid TRAF3 deficiency suppressed tumor growth and lung metastasis in vivo. Taken together, TRAF3 plays a vital role in M2 polarization via regulating STAT6 K450 ubiquitination in macrophages.

Regulatory Effect and Mechanism of Erythroblastic Island Macrophages on Anemia in Patients with Newly Diagnosed Multiple Myeloma.

Objective: To examine the clinical characteristics and anemia-related factors in patients with newly diagnosed multiple myeloma (NDMM), as well as the effect and mechanism of erythroblastic islands (EBIs) and EBI macrophages in NDMM patients with anemia. Methods: We collected and analyzed clinical data to find anemia-related factors. Using flow cytometry, the numbers and ratios of erythroblasts and EBI macrophages were determined. RNA sequencing (RNA-seq) was used to determine the differences of EBI macrophages in NDMM patients with or without anemia. Results: Based on the clinical characteristics of NDMM patients with anemia, MCV, abnormal levels of albumin, osteolytic lesions, and Durie-Salmon (DS) stage are risk factors for anemia. Patients with anemia have fewer erythroblasts, erythroblastic islands (EBIs), and EBI macrophages in their bone marrow than patients without anemia. RNA-seq analysis of EBI macrophages from the bone marrow of patients with and without anemia revealed that macrophages from patients with anemia are impaired and tend to promote the production of interleukin-6, which has been demonstrated to be an essential survival factor of myeloma cells and protects them from apoptosis. Conclusion: In NDMM patients with anemia, EBI macrophages are impaired, which causes anemia in those patients. Our finding highlights the significance of EBI macrophages in anemia in NDMM patients and provides a new strategy for recovery from anemia in these patients.

Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aß1-42.

Voltage-gated sodium channel beta 2 (Nav2.2 or Navß2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Navß2 in amyloid-ß 1-42- (Aß1-42-) induced neural injury model and the potential underlying molecular mechanism. The results showed that Navß2 knockdown restored neuronal viability of Aß1-42-induced injury in neurons; increased the contents of brain-derived neurotrophic factor (BDNF), enzyme neprilysin (NEP) protein, and NEP enzyme activity; and effectively altered the proportions of the amyloid precursor protein (APP) metabolites including Aß42, sAPPα, and sAPPß, thus ameliorating cognitive dysfunction. This may be achieved through regulating NEP transcription and APP metabolism, accelerating Aß degradation, alleviating neuronal impairment, and regulating BDNF-related signal pathways to repair neuronal synaptic efficiency. This study provides novel evidence indicating that Navß2 plays crucial roles in the repair of neuronal injury induced by Aß1-42 both in vivo and in vitro.

[Genetic screening and prenatal diagnosis in high-risk families with tuberous sclerosis complex syndrome].

OBJECTIVE: To carry out genetic testing and prenatal diagnosis for 29 Chinese pedigrees affected with tuberous sclerosis complex (TSC) and assess efficacy of combined next generation sequencing (NGS) and multiple ligation-dependent probe amplification (MLPA) for the diagnosis. METHODS: NGS and MLPA were used in conjunct to detect variants of TSC1 and TSC2 genes among the probands of the pedigrees. Paternity test was carried out to exclude maternal DNA contamination. Prenatal diagnosis was provided to 14 couples based on the discoveries in the probands. RESULTS: Twenty-seven variants were identified in the TSC1 and TSC2 genes among the 29 pedigrees, which yielded a detection rate of 93.1%. Respectively, 5 (18.5%) and 22 (81.5%) variants were identified in the TSC1 and TSC2 genes. Twelve variants were unreported previously. Prenatal diagnosis showed that five fetuses were affected with TSC, whilst the remaining nine were unaffected. CONCLUSION: Above finding has expanded the spectrum of TSC1 and TSC2 gene variants. Combined NGS and MLPA has enabled diagnosis of TSC with efficiency and accuracy.

Liquid biopsy for ALK-positive early non-small-cell lung cancer predicts disease relapse.

Background: We aimed to determine whether circulating tumor cells (CTCs) and cell-free DNA (cfDNA) aids in prognosis of relapse-free survival (RFS). Methods: Non-small cell lung cancer patients with ALK mutations were recruited prospectively. CTCs and cfDNA were quantified at different time points. RFS was estimated and correlated. Results: Baseline median CTCs and cfDNA were 16 cells and 57 ng/mL and declined to nine cells and 30 ng/mL, respectively, postsurgery in 150 patients. Interestingly, patients without detectable CTCs postsurgery fared better for RFS. cfDNA monitoring showed deviations within 7 months of surgery that were significant predictors for RFS. Conclusion: Short-term monitoring of CTCs and cfDNA variations shows promise for early risk detection and may aid in better disease control.

Simulation stress model of the undersea environment activates the central nervous, neuroendocrine and immune systems and anxiety in rats.

The present study was designed to assess the stress responses to a simulation model of the undersea environment that is similar to some undersea working conditions such as submarine rescue, underwater salvage and underwater construction. Restraint, hyperbaric air and immersion were chosen to produce the simulation stress model in rats for four hours. Rats were randomized into five groups: control group, restraint (R) group, hyperbaric air (H) group, restraint plus hyperbaric air (RH) group, and restraint plus hyperbaric air plus immersion (RHI) group. The results showed that the responses to the simulation stress model of the undersea environment induced by R, H, RH and RHI involved the upregulated norepinephrine (NE), dopamine (DA) and 5-hydroxytryptamine (5-HT) of the central nervous system (CNS), upregulated adrenocorticotropic hormone (ACTH), corticosterone (CORT) and blood glucose of the neuroendocrine system, upregulated interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) of the immune system, and increased anxiety in rats. Compared with hyperbaric air, restraint tended to activate stronger stress responses. Conclusively, this work established a simulation stress model of the undersea environment induced by restraint, hyperbaric air and immersion. It further provided experimental data of such a model that showed significant activation of the CNS, neuroendocrine and immune systems and anxiety in rats. In this experiment we provided an experimental basis for undersea work such as working aboard a submarine.

RP11­284F21.9 promotes lung carcinoma proliferation and invasion via the regulation of miR­627­3p/CCAR1.

Lung carcinoma is a prominent cause of mortality among patients with cancer. Previous studies have reported the vital role of long non­coding RNAs (lncRNAs) in the malignant progression of lung cancer. lncRNA RP11­284F21.9 was originally identified to be expressed in lung carcinoma, but its specific function remains unknown. Therefore, the present study aimed to elucidate the role of lncRNA RP11­284F21.9 in lung carcinoma progression. The expression of RP11­284F21.9 in lung cell lines and tissues was measured using reverse transcription­quantitative PCR. The endogenous expression of RP11­284F21.9 was silenced using RNA interference, and cell viabilities were measured with a Cell Counting Kit­8 assay. The invasion and apoptosis of cells were determined via Transwell assays and flow cytometry, respectively. The protein expression levels were measured by western blotting. An increased expression of RP11­284F21.9 was identified in both lung carcinoma tissues and cells. Knockdown of RP11­284F21.9 in lung carcinoma cells inhibited cell proliferation and invasion, but promoted cell apoptosis. The present study identified the existence of a direct interaction between RP11­284F21.9 and microRNA (miRNA/miR)­627­3p. Mechanistically, it was demonstrated that RP11­284F21.9 promoted the proliferation and invasiveness of lung carcinoma cells, in part, via the regulation of miR­627­3p. Furthermore, cell division cycle and apoptosis regulator 1 (CCAR1) was identified as a target gene of miR­627­3p. The in vivo tumor growth assay also demonstrated that the knockdown of RP11­284F21.9 suppressed tumor growth, upregulated miR­627­3p and downregulated CCAR1 in the xenograft model of nude mice. Thus, the present findings indicated the tumor promoting functions of RP11­284F21.9 in the progression of lung carcinoma, and provided a novel lncRNA/miRNA axis as a target for the management of lung cancer.

MYB-QKI rearrangement in angiocentric glioma.

AIMS: To evaluate the occurrence and diagnostic value of MYB-QKI rearrangement status in angiocentric glioma (AG) in Chinese patients. MATERIALS AND METHODS: 27 cases were collected from six hospitals, followed by a retrospective analysis of clinical, radiological, and morphological data. MYB protein expression was assessed by immunohistochemical staining (IHC), and the MYB-QKI rearrangement was detected by fluorescence in situ hybridization (FISH). RESULTS: Among the 27 cases (16 males), the median age at surgery was 17 years (range 3 - 43 years); 24 (88.9%) cases had a history of refractory epilepsy, and the mean history of pre-surgical epilepsy was 13 years (range 1.5 - 27 years); 26 (96.3%) cases had lesions located in the superficial cerebrocortical regions, and 1 (3.7%) case had a lesion in the brainstem. Except for the classic histological features, the involvement of superficial cortex extending to the leptomeninges, microcalcification, and cystic pattern with microcystic formations was observed in 11 (40.7%), 3 (11.1%), and 4 (14.8%) cases, respectively. IHC showed that all 27 cases were positive for glial fibrillary acidic protein (GFAP) and vimentin, and negative for neuronal nuclear antigen (NeuN). The positive rates of epithelial membrane antigen (EMA) and D2-40 were 81.5% (22/27) and 74.1% (20/27), respectively. A total of 14 (51.9%) cases were positive for MYB. The rate of Ki-67 proliferation was 1 - 5% in 25 cases, and in 2 cases with anaplastic features it was 10 and 20%. MYB-QKI rearrangement was revealed by FISH examination in 95.8% (23/24) of the AGs, including 3 cases with atypical histological appearance. CONCLUSION: Compared to IHC, FISH was more appropriate for detecting MYB-QKI rearrangement. MYB-QKI rearrangement was detected in the majority of Chinese AG cases, and therefore represents a potential diagnostic biomarker for AG.

[Pathogen Diagnosis of a Febrile HIV Case by the Metagenomic Next-generation Sequencing].

This study is aimed to explore the value of metagenomic next-generation sequencing (mNGS) in diagnosing pathogen in fever patients. It is often a challenge to identify the pathogen that caused the infection in the HIV patients with fever. How could the mNGS be helpful for pathogen diagnosis is unclear. Here we reported a case of human immunodeficiency virus (HIV) patient with 2-month period of fever. After routine clinical laboratory tests including the conventional smear, culture, serological tests and pathological examinations, the causal pathogen still remained undiagnosed. Then the lymph node biopsy tissue was subjected to broad-range polymerase chain reaction (PCR) and the peripheral blood was subjected to mNGS. At the same time, peripheral blood culture was carried out with an extension of culture time to acquire the pathogen. Results from both broad-range PCR and mNGS revealed the pathogen was Talaromyces marneffei. The isolate recovered from the peripheral blood culture was subjected to the whole-genome sequencing. Whole genome sequencing revealed that the antimicrobial resistance gene FLU1 existed in this pathogen's genome, but mNGS did not detect the FLU1 gene. Phylogenetic analysis based on whole genome sequence revealed that this isolate was far from other clones published in NCBI database. Here we reported a case of Talaromyces marneffei infection diagnosed by mNGS, showing that mNGS is helpful in etiological diagnosis for HIV patients with unexplained fever. However, application of mNGS in antimicrobial resistant genes detection and pathogen tracing need to be well-studied in the future.

Analysis of the efficacy and safety of bortezomib for treating newly diagnosed multiple myeloma through different administration methods.

BACKGROUND: This study aims to compare the efficacy and adverse reactions of bortezomib for treating newly diagnosed multiple myeloma (MM) through two different administration methods: intravenous (IV) injection and subcutaneous (SC) injection. METHODS: A retrospective analysis was performed in 205 patients with newly diagnosed MM, who were treated by the Department of Hematopathology, Henan Cancer Hospital, from June 2009 to December 2017. These patients were divided into two groups according to the treatment methods: IV injection group, IV injection of bortezomib; SC injection group, SC injection of bortezomib. RESULTS: After the first course of treatment, the effect of very good partial remission (VGPR) or above (≥VGPR) in the IV injection group (IV group) and SC injection group (SC group) was 31.0% and 14.3%, respectively (P=0.004), while the overall response rate (ORR) was 72.0% and 49.5%, respectively (P=0.001). From the 2nd course to the 6th course of treatment, the ORR was not statistically different between these two groups. No significant difference was found in median progression-free survival (37 vs 45 months) and overall survival (63 vs 59 months). A lower frequency of adverse events, especially Grade 3 peripheral neuropathy, was observed in SC group compared with the IV group. CONCLUSION: Compared with IV administration, SC bortezomib can provide a better balance between efficacy and toxicity.

Silencing interleukin 1α underlies a novel inhibitory role of miR-181c-5p in alleviating low-grade inflammation of rats with irritable bowel syndrome.

Irritable bowel syndrome (IBS) is a common disorder of unknown etiology. Studies have found a close relation between IBS and microRNAs (miRNAs), but the study concerning the relationship between IBS and miR-181c-5p in IBS is still blank. Thus, this study aims to explore the role of miR-181c-5p in IBS via interleukin 1α (IL1A). Initially, microarray analysis was used to retrieve the genes related to IBS and to predict miRNAs regulating IL1A gene. IBS model was then established with abdominal withdraw reflection (AWR) and Bristol stool grading in mice measured. Afterwards, the functional role of miR-181c-5p in IBS was determined using the ectopic expression, depletion and reporter assay experiments, as well as miR-181c-5p and IL1A expression detected. Subsequently, expression of tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2), and IL-6 were detected to further determine the effects of miR-181c-5p and IL1A on inflammation in IBS. miR-181c-5p and IL1A might be involved in IBS. miR-181c-5p was found to be decreased while IL1A was increased in IBS rats. In addition, miR-181c-5p could target and inhibit expression of IL1A, and IBS mice exhibited elevated AWR and Bristol stool grading, namely 6 to 7 points (70.4 [38 of 54]). Moreover, with the overexpression of miR-181c-5p or silencing of IL1A, the expression of TNF-α, IL-2, and IL-6 was decreased. Collectively, this study suggested that overexpressed miR-181c-5p could silence IL1A, thus inhibiting low-grade inflammation in IBS rats. miR-181c-5p/IL1A is expected to serve as a novel target for the treatment of IBS.

[Study on application of salvianolic acids reference extract in quality control of Salvia miltiorrhiza and salvianolic acids for injection].

The purpose of this study was to investigate the feasibility of the salvianolic acids reference extract for quality control for Salvia miltiorrhiza and salvianolic acids for injection. An Agilent ZORBAX SB-C18( 4. 6 mm×250 mm,5 µm) column was used with mobile phase consisting of 0. 1% formic acid-water and 0. 1% formic acid-acetonitrile in gradient elution procedure. The column temperature was 30 ℃; the flow rate was 1 m L·min-1; and the detection wavelength was 288 nm. The content of rosmarinic acid,lithospermic acid and salvianolic acid B in S. miltiorrhiza was determined by using the salvianolic acids reference extract as control substance. The content of caffeic acid,salvianolic acid E,rosmarinic acid,lithospermic acid,salvianolic acid B,and salvianolic acid Y in the salvianolic acids for injection was also determined. The linear relationship between chemicals was good( r>0. 998 9),and the injection precision RSD was 0. 30%-0. 90%. The sexual RSD is between 1. 4% and 3. 0%,and the RSD of the reproducibility of the extract is between 2. 1% and 5. 2%. The recovery rate of the three components in S. miltiorrhiza was 96. 80%-99. 20%,and the recovery rate of the six components in salvianolic acids for injection was 88. 90%-107. 5%. The solution of S. miltiorrhiza and salvianolic acids for injection were stable within 48 h. A total of 8 batches of S. miltiorrhiza and injection were determined by the reference extract,and the difference was smaller than that measured by the monomer control. This study preliminarily verified that the salvianolic acids reference extract can be used as a substitute for the monomer control for the quality control of S. miltiorrhiza and salvianolic acids for injection.

Circulating Levels of Osteoprotegerin, Osteocalcin and Osteopontin in Patients with Rheumatoid Arthritis: A Systematic Review and Meta-Analysis.

OBJECTIVE: Currently published data regarding the potential role of osteoprotegerin (OPG), osteocalcin (OCN) and osteopontin (OPN) for the discrimination between rheumatoid arthritis (RA) and osteoarthritis (OA) are contradictory. To derive a more precise evaluation, a meta-analysis was performed. METHODS: Published literatures comparing plasma/serum OPG, OCN and OPN levels between RA group and OA controls were searched in PubMed, Embase and the Cochrane Library. The Newcastle-Ottawa Scale was used to assess the study quality. Pooled standard mean difference (SMD) with 95% confidence interval (CI) was calculated by random-effect model analysis. Heterogeneity test was performed by the Q statistic and quantified using I2. RESULTS: Nine studies including 438 RA patients and 255 OA patients were finally incorporated in the meta-analysis after examining title, type, abstracts and full text. The results showed that RA patients had higher plasma/serum OPN (pooled SMD = -2.57, 95% CI = -4.72 to -0.41) levels when compared to OA patients. No significant difference in plasma/serum OPG (pooled SMD = -0.29, 95% CI = -1.07‒0.49) and OCN (pooled SMD = -0.09, 95% CI = -0.48‒0.31) levels were found between RA patients and OA patients. Subgroup analysis indicated that plasma/serum OPG levels had no significant differences between RA patients and OA patients in Europe and Asian. CONCLUSIONS: Overall, there is no significant difference in circulating OPG and OCN levels between RA patients and OA patients. However, plasma/serum OPN level is significantly higher in RA patients compared with OA patients.

Induction chronomodulated chemotherapy plus radiotherapy for nasopharyngeal carcinoma: A Phase II prospective randomized study.

PURPOSE: The aim of this study was to evaluate the efficacy and toxicities of induction chronomodulated chemotherapy in comparison with conventional induction chemotherapy for nasopharyngeal carcinoma (NPC). PATIENTS AND METHODS: Between 2003 and 2004, 60 patients with pathologically confirmed NPC were included and randomly assigned to two groups. Patients in the chronomodulated chemotherapy group (n = 30, CC group) received cisplatin at 80 mg/m2 through intravenous infusion from 10:00 to 22:00 and 5-fluorouracil (5-FU) at 1000 mg/m2 plus citrovorum factor at 200 mg/m2 from 22:00 to 10:00 each day for 3 days. Patients in the routine chemotherapy group (n = 30, RC group) received cisplatin infusion within 1 h and 5-FU infusion for about 24 h. The dose in the RC group was the same as that in the CC group. The total irradiation dose in each group was 70 Gy for the whole nasopharynx. RESULTS: One month after induction chemotherapy, the overall response rate was 96.7% in the CC group versus 73.3% in the RC group (P = 0.011). By the end of the 10-year follow-up, 11 patients (36.7%) in the CC group had experienced local recurrence versus 11 patients (36.7%) in the RC group (P > 0.999). The overall survival rates at 1, 5, and 10 years were 96.7%, 53.3%, and 43.3%, respectively, in the CC group, and 96.7%, 43.3%, and 33.3%, respectively, in the RC group (P = 0.346). During induction chemotherapy, the incidence rates of leukocytopenia (43.3% vs. 80%, P = 0.003), thrombocytopenia (26.7% vs. 56.7%, P = 0.018), and nausea/vomiting (40% vs. 66.7%, P = 0.038) were significantly lower in the CC group than in the RC group. The incidence of radiation-induced complications was similar in these two groups. CONCLUSION: Compared with conventional chemotherapy, induction chrono-chemotherapy seemed to reduce chemotherapy-related toxicities and improve average local relapse time in patients treated with combined chemoradiotherapy for NPC.

Clinical observation of recombinant human endostatin in treating relapsed refractory multiple myeloma.

Recombinant human endostatin (rhES) can inhibit multiple myeloma, while its clinical efficacy in treating relapsed refractory multiple myeloma (RRMM) has not been assessed. One hundred and eleven RRMM patients were treated with four different regimens: combination of VD (velcade+dexamethasone) and rhES (n = 25), Thalidomide (Tha) and VD (VTD, n = 22) combination, rhES and conventional chemotherapy combination (n = 32), and combination of conventional chemotherapy and Tha (n = 32). Significant differences were found in progression-free survival (PFS) between rhES combination groups and conventional chemotherapy combination groups. No statistical difference was found in overall response rate, overall survival or incidences of adverse effects. The combination of rhES with VD or conventional chemotherapy is active in patients with RRMM and prolongs the PFS to improve the quality of life.

Multimodality Image Post-processing in Detection of Extratemporal MRI-Negative Cortical Dysplasia.

Purpose: To determine the diagnostic value of individual image post-processing techniques in a series of patients who underwent extratemporal operations for histologically proven, MRI-negative focal cortical dysplasia (FCD). Methods: The morphometric analysis program (MAP), PET/MRI co-registration and statistical parametric mapping (SPM) analysis of PET (SPM-PET) techniques were analyzed in 33 consecutive patients. The epileptogenic zone (EZ) assumed by MAP, PET/MRI, and SPM-PET was compared with the location of the FCD lesions determined by stereoelectroencephalography (SEEG) and histopathological study. The detection rate of each modality was statistically compared. Results: Three lesions were simultaneously detected by the three post-processing methods, while two lesions were only MAP positive, and 8 were only PET/MRI positive. The detection rate of MAP, PET/MRI, SPM-PET and the combination of the three modalities was 24.2, 90.9, 57.6, and 97.0%, respectively. Taking the pathological subtype into account, no type I lesions were detected by MAP, and PET/MRI was the most sensitive method for detecting FCD types II and IIA. During a mean follow-up period of 22.94 months, seizure freedom was attained in 26/33 patients (78.8%) after focal corticectomy. Conclusions: MAP, PET/MRI, and SPM-PET provide complementary information for FCD detection, intracranial electrode design, and lesion resection. PET/MRI was particularly useful, with the highest detection rate of extratemporal MRI-negative FCD.

Biological effects of trans fatty acids and their possible roles in the lipid rafts in apoptosis regulation.

A large number of recent studies are focused on evaluating the mechanism of action of trans fatty acids (TFAs) on the progression of apoptosis. A strong positive association has been reported between TFA and coronary heart disease (CHD), obesity and nonalcoholic steatohepatitis and so on. The present study reviewed the biological effects of trans fatty acids (TFA) and their possible roles in lipid rafts in regulating apoptosis. The following aspects of TFA were included: the research about TFA and diseases affecting serum lipid levels, inducing system inflammation and immune response, and the correlation between TFA and apoptosis. The primary purpose of the review article was to comprehensively evaluate the potential correlation between lipid rafts and apoptosis induced by different structures of TFA and provide some new research progress and future directions about it.