Auditory training remodels hippocampus-related memory in adult rats.

Consequences of perceptual training, such as improvements in discriminative ability, are highly stimulus and task specific. Therefore, most studies on auditory training-induced plasticity in adult brain have focused on the sensory aspects, particularly on functional and structural effects in the auditory cortex. Auditory training often involves, other than auditory demands, significant cognitive components. Yet, how auditory training affects cognition-related brain regions, such as the hippocampus, remains unclear. Here, we found in female rats that auditory cue-based go/no-go training significantly improved the memory-guided behaviors associated with hippocampus. The long-term potentiations of the trained rats recorded in vivo in the hippocampus were also enhanced compared with the naïve rats. In parallel, the phosphorylation level of calcium/calmodulin-dependent protein kinase II and the expression of parvalbumin-positive interneurons in the hippocampus were both upregulated. These findings demonstrate that auditory training substantially remodels the processing and function of brain regions beyond the auditory system, which are associated with task demands.

Hypothermic rescue by veno-arterial extracorporeal membrane oxygenation: A case report.

INTRODUCTION: Severe hypothermia is a life-threatening condition that often causes hemodynamic instability or cardiac arrest and carries a high risk of mortality. The use of VA-ECMO in this indication has greatly improved the prognosis of patients. CASE REPORT: We describe an incredible case involving the complete recovery of a 47-year-old man placed on VA-ECMO for cardiogenic shock and protracted ventricular fibrillation caused by hypothermia. The patient was discharged home in 20 days with no neurologic sequelae. CLINICAL DISCUSSION: Extracorporeal life support (ECLS) with cardiopulmonary bypass (CPB) or extracorporeal membrane oxygenation (ECMO) has been recommended as the gold standard for the treatment of severe hypothermia due to its rapid availability and the possibility of prolonged support. Our case demonstrates the effectiveness of ECMO in treating patients with hypothermic cardiogenic shock. At the same time, nutritional support and rehabilitation therapy play an integral role in the whole treatment process. Therefore, it is recommended that such patients be managed by an experienced cardiac team that can evaluate the patient's condition in multiple aspects. CONCLUSION: ECMO may be an effective treatment for hypothermia-induced cardiogenic shock, but further research is needed on the effectiveness of this method of treatment.

Leveraging senescence-oxidative stress co-relation to predict prognosis and drug sensitivity in breast invasive carcinoma.

Introduction: Female breast cancer has risen to be the most common malignancy worldwide, causing a huge disease burden for both patients and society. Both senescence and oxidative stress attach importance to cancer development and progression. However, the prognostic roles of senescence and oxidative stress remain obscure in breast cancer. In this present study, we attempted to establish a predictive model based on senescence-oxidative stress co-relation genes (SOSCRGs) and evaluate its clinical utility in multiple dimensions. Methods: SOSCRGs were identified via correlation analysis. Transcriptome data and clinical information of patients with breast invasive carcinoma (BRCA) were accessed from The Cancer Genome Atlas (TCGA) and GSE96058. SVM algorithm was employed to process subtype classification of patients with BRCA based on SOSCRGs. LASSO regression analysis was utilized to establish the predictive model based on SOSCRGs. Analyses of the predictive model with regards to efficacy evaluation, subgroup analysis, clinical association, immune infiltration, functional strength, mutation feature, and drug sensitivity were organized. Single-cell analysis was applied to decipher the expression pattern of key SOSCRGs in the tumor microenvironment. Additionally, qPCR was conducted to check the expression levels of key SOSCRGs in five different breast cancer cell lines. Results: A total of 246 SOSCRGs were identified. Two breast cancer subtypes were determined based on SOSCRGs and subtype 1 showed an active immune landscape. A SOSCRGs-based predictive model was subsequently developed and the risk score was clarified as independent prognostic predictors in breast cancer. A novel nomogram was constructed and exhibited favorable predictive capability. We further ascertained that the infiltration levels of immune cells and expressions of immune checkpoints were significantly influenced by the risk score. The two risk groups were characterized by distinct functional strengths. Sugar metabolism and glycolysis were significantly upregulated in the high risk group. The low risk group was deciphered to harbor PIK3CA mutation-driven tumorigenesis, while TP53 mutation was dominant in the high risk group. The analysis further revealed a significantly positive correlation between risk score and TMB. Patients in the low risk group may also sensitively respond to several drug agents. Single-cell analysis dissected that ERRFI1, ETS1, NDRG1, and ZMAT3 were expressed in the tumor microenvironment. Moreover, the expression levels of the seven SOSCRGs in five different breast cancer cell lines were quantified and compared by qPCR respectively. Conclusion: Multidimensional evaluations verified the clinical utility of the SOSCRGs-based predictive model to predict prognosis, aid clinical decision, and risk stratification for patients with breast cancer.

Prognosis stratification of patients with breast invasive carcinoma based on cysteine metabolism-disulfidptosis affinity.

PURPOSE: The rise of female breast cancer has created a significant global public health issue that requires effective solutions. Disulfidptosis, a recently identified form of cell death characterized by an excessive accumulation of disulfides, has unique initiatory and regulatory mechanisms. The formation of disulfide bonds is a metabolic event typically associated with cysteines. This study aims to explore the potential of the affinity between cysteine metabolism and disulfidptosis in risk stratification for breast invasive carcinoma (BRCA). METHODS: We used correlation analysis to decipher co-relation genes between cysteine metabolism and disulfidptosis (CMDCRGs). Both LASSO regression analysis and multivariate Cox regression analysis were employed to construct the prognostic signature. Additionally, we conducted investigations concerning subtype identification, functional enhancement, mutation landscape, immune infiltration, drug prioritization, and single-cell analysis. RESULTS: We developed and validated a six-gene prognostic signature as an independent prognostic predictor for BRCA. The prognostic nomogram, based on risk score, demonstrated a favorable capability in predicting survival outcomes. We identified distinct gene mutations, functional enhancements, and immune infiltration patterns between the two risk groups. Four clusters of drugs were predicted as potentially effective for patients in the low-risk group. We identified seven cell clusters within the tumor microenvironment of breast cancer, and RPL27A was found to be widely expressed in this environment. CONCLUSION: Multidimensional analyses confirmed the clinical utility of the cysteine metabolism-disulfidptosis affinity-based signature in risk stratification and guiding personalized treatment for patients with BRCA.

Pairing with Enriched Sound Exposure Restores Auditory Processing Degraded by an Antidepressant.

Antidepressants, while effective in treating depression and anxiety disorders, also induce deficits in sensory (particularly auditory) processing, which in turn may exacerbate psychiatric symptoms. How antidepressants cause auditory signature deficits remains largely unknown. Here, we found that fluoxetine-treated adult female rats were significantly less accurate when performing a tone-frequency discrimination task compared with age-matched control rats. Their cortical neurons also responded less selectively to sound frequencies. The degraded behavioral and cortical processing was accompanied by decreased cortical perineuronal nets, particularly those wrapped around parvalbumin-expressing inhibitory interneurons. Furthermore, fluoxetine induced critical period-like plasticity in their already mature auditory cortices; therefore, a brief rearing of these drug-treated rats under an enriched acoustic environment renormalized auditory processing degraded by fluoxetine. The altered cortical expression of perineuronal nets was also reversed as a result of enriched sound exposure. These findings suggest that the adverse effects of antidepressants on auditory processing, possibly because of a reduction in intracortical inhibition, can be substantially alleviated by simply pairing drug treatment with passive, enriched sound exposure. They have important implications for understanding the neurobiological basis of antidepressant effects on hearing and for designing novel pharmacological treatment strategies for psychiatric disorders.SIGNIFICANCE STATEMENT Clinical experience suggests that antidepressants adversely affect sensory (particularly auditory) processing, which can exacerbate patients' psychiatric symptoms. Here, we show that the antidepressant fluoxetine reduces cortical inhibition in adult rats, leading to degraded behavioral and cortical spectral processing of sound. Importantly, fluoxetine induces a critical period-like state of plasticity in the mature cortex; therefore, a brief rearing under an enriched acoustic environment is sufficient to reverse the changes in auditory processing caused by the administration of fluoxetine. These results provide a putative neurobiological basis for the effects of antidepressants on hearing and indicate that antidepressant treatment combined with enriched sensory experiences could optimize clinical outcomes.

A degradome-based prognostic signature that correlates with immune infiltration and tumor mutation burden in breast cancer.

Introduction: Female breast cancer is the most common malignancy worldwide, with a high disease burden. The degradome is the most abundant class of cellular enzymes that play an essential role in regulating cellular activity. Dysregulation of the degradome may disrupt cellular homeostasis and trigger carcinogenesis. Thus we attempted to understand the prognostic role of degradome in breast cancer by means of establishing a prognostic signature based on degradome-related genes (DRGs) and assessed its clinical utility in multiple dimensions. Methods: A total of 625 DRGs were obtained for analysis. Transcriptome data and clinical information of patients with breast cancer from TCGA-BRCA, METABRIC and GSE96058 were collected. NetworkAnalyst and cBioPortal were also utilized for analysis. LASSO regression analysis was employed to construct the degradome signature. Investigations of the degradome signature concerning clinical association, functional characterization, mutation landscape, immune infiltration, immune checkpoint expression and drug priority were orchestrated. Cell phenotype assays including colony formation, CCK8, transwell and wound healing were conducted in MCF-7 and MDA-MB-435S breast cancer cell lines, respectively. Results: A 10-gene signature was developed and verified as an independent prognostic predictor combined with other clinicopathological parameters in breast cancer. The prognostic nomogram based on risk score (calculated based on the degradome signature) showed favourable capability in survival prediction and advantage in clinical benefit. High risk scores were associated with a higher degree of clinicopathological events (T4 stage and HER2-positive) and mutation frequency. Regulation of toll-like receptors and several cell cycle promoting activities were upregulated in the high-risk group. PIK3CA and TP53 mutations were dominant in the low- and high-risk groups, respectively. A significantly positive correlation was observed between the risk score and tumor mutation burden. The infiltration levels of immune cells and the expressions of immune checkpoints were significantly influenced by the risk score. Additionally, the degradome signature adequately predicted the survival of patients undergoing endocrinotherapy or radiotherapy. Patients in the low-risk group may achieve complete response after the first round of chemotherapy with cyclophosphamide and docetaxel, whereas patients in the high-risk group may benefit from 5-flfluorouracil. Several regulators of the PI3K/AKT/mTOR signaling pathway and the CDK family/PARP family were identified as potential molecular targets in the low- and high-risk groups, respectively. In vitro experiments further revealed that the knockdown of ABHD12 and USP41 significantly inhibit the proliferation, invasion and migration of breast cancer cells. Conclusion: Multidimensional evaluation verified the clinical utility of the degradome signature in predicting prognosis, risk stratification and guiding treatment for patients with breast cancer.

Identification and validation of hub genes in CD5-positive diffuse large B-cell lymphoma.

CD5+ diffuse large B-cell lymphoma (DLBCL), as a significant heterogeneity category of DLBCL, is reflected in both the molecular biological and genetic levels, which in turn induces ever-changing clinical manifestations, and what mediates tumor survival mechanisms are still unclear. This study aimed to predict the potential hub genes in CD5+ DLBCL. A total of 622 patients with DLBCL diagnosed between 2005 and 2019 were included. High expression of CD5 was correlated with IPI, LDH, and Ann Arbor stage, patients with CD5-DLBCL have longer overall survival. We identified 976 DEGs between CD5-negative and positive DLBCL patients in the GEO database and performed GO and KEGG enrichment analysis. After intersecting the genes obtained through the Cytohubba and MCODE, further external verification was performed in the TCGA database. Three hub genes were screened: VSTM2B, GRIA3, and CCND2, of which CCND2 were mainly involved in cell cycle regulation and JAK-STAT signaling pathways. Analysis of clinical samples showed that the expression of CCND2 was found to be correlated with CD5 (p = 0.001), and patients with overexpression of CCND2 in CD5+ DLBCL had poor prognosis (p = 0.0455). Cox risk regression analysis showed that, for DLBCL, CD5, and CCND2 double positive was an independent poor prognostic factor (HR: 2.545; 95% CI: 1.072-6.043; p = 0.034). These findings demonstrate that CD5 and CCND2 double-positive tumors should be stratified into specific subgroups of DLBCL with poor prognosis. CD5 may regulate CCND2 through JAK-STAT signaling pathways, mediating tumor survival. This study provides independent adverse prognostic factors for risk assessment and treatment strategies for newly diagnosed DLBCL.

Expression of glucose transporter-1 in follicular lymphoma affected tumor-infiltrating immunocytes and was related to progression of disease within 24 months.

OBJECTIVE: Follicular lymphoma (FL) occurring progression within 24 months (POD24) after initial immunochemotherapy has poor prognosis. GLUT1 affects glycolysis within tumor microenvironment (TME) and promotes tumor progression. However, its specific mediated mechanism remains unclear in FL. METHODS: Baseline GLUT1 expression, infiltrations of M2 macrophage, and CD8+ T-cells were assessed by immunohistochemistry in FL with POD24 and long-term remission respectively. The spatial features of TME were assessed by MIBI-TOF and proteomics. Predictive immunophenotypes for POD24 occurrence was analyzed by random forest algorithm. The lactate production and the induction of M2 macrophages were detected when GLUT1 was transfected or knocked down in DOHH2. The activation of PI3K/Akt/mTOR signaling in DOHH2 and WSU-FSCCL cells co-cultured with induced inhibitory immunocytes was tracked by western blotting. RESULTS: The FL with POD24 exhibited higher baseline GLUT1 expression and increased infiltration of various inhibitory immunocytes. Spatial signatures of 69 immunophenotypes could predict POD24 occurrence. The activation of PI3K/ Akt /mTOR signaling pathway was not significant in both groups. The supernatant of DOHH2-GLUT1 cells which had more lactate content could induce more M2-type macrophages than that of DOHH2/siRNA GLUT1 cells. When co-cultured with exhausted CD8+ T cells, M2-type macrophages and Tregs, compared with WSU-FSCCL cells, DOHH2 cells with high GLUT1 expression induced more M2-type macrophages and was triggered activation of PI3K/ Akt /mTOR signaling pathway. CONCLUSION: Tumor cells overexpressing GLUT1 could domesticate immunocytes to form an immunosuppressive TME, which promotes occurrence of POD24 and gradually activates PI3K/ Akt /mTOR pathway of tumor cells in FL. SIGNIFICANCE: Tumor cells overexpressing GLUT1 could domesticate immunocytes to form an immunosuppressive microenvironment, which in turn promoted the growth of tumor cells and was related to the progression of disease within 24 months in FL. Suppressive immunocytes gradually activated PI3K/ Akt /mTOR pathway of tumor cells in later stage. Distinguishing spatial features of immunocytes could well predict POD24 occurrence, hoping to benefit these patients from early anti-metabolism therapy based on GLUT1 in the future.

Developmental Exposure to Bisphenol a Degrades Auditory Cortical Processing in Rats.

Developmental exposure to bisphenol A (BPA), an endocrine-disrupting contaminant, impairs cognitive function in both animals and humans. However, whether BPA affects the development of primary sensory systems, which are the first to mature in the cortex, remains largely unclear. Using the rat as a model, we aimed to record the physiological and structural changes in the primary auditory cortex (A1) following lactational BPA exposure and their possible effects on behavioral outcomes. We found that BPA-exposed rats showed significant behavioral impairments when performing a sound temporal rate discrimination test. A significant alteration in spectral and temporal processing was also recorded in their A1, manifested as degraded frequency selectivity and diminished stimulus rate-following by neurons. These post-exposure effects were accompanied by changes in the density and maturity of dendritic spines in A1. Our findings demonstrated developmental impacts of BPA on auditory cortical processing and auditory-related discrimination, particularly in the temporal domain. Thus, the health implications for humans associated with early exposure to endocrine disruptors such as BPA merit more careful examination.

Serum amyloid A 1 induces suppressive neutrophils through the Toll-like receptor 2-mediated signaling pathway to promote progression of breast cancer.

Immune inflammation plays a key role in breast cancer development, progression, and therapeutic efficacy. Neutrophils are crucial for the regulation of the suppressive tumor microenvironment and are associated with poor clinical survival. However, the mechanisms underlying the activation of suppressive neutrophils in breast cancer are poorly understood. Here, we report that breast cancer cells secrete abundant serum amyloid A 1 (SAA1), which is associated with the accumulation of suppressive neutrophils. High expression of SAA1 in breast cancer induces neutrophil immunosuppressive cytokine production through the activation of Toll-like receptor 2 (TLR2)-mediated signaling pathways. These include the TLR2/myeloid differentiation primary response 88 (MYD88)-mediated PI3K/nuclear factor-κB signaling pathway and p38 MAPK-associated apoptosis resistance pathway, which eventually promote the progression of breast cancer. Our study shows a mechanistic link between breast cancer cell secretion of SAA1 and suppressive neutrophils that potentiate tumor progression. These findings provide potential therapeutic targets for breast cancer.

Degraded cortical temporal processing in the valproic acid-induced rat model of autism.

Hearing disorders, such as abnormal speech perception, are frequently reported in individuals with autism. However, the mechanisms underlying these auditory-associated signature deficits in autism remain largely unknown. In this study, we documented significant behavioral impairments in the sound temporal rate discrimination task for rats prenatally exposed to valproic acid (VPA), a well-validated animal model for studying the pathology of autism. In parallel, there was a large-scale degradation in temporal information-processing in their primary auditory cortices (A1) at both levels of spiking outputs and synaptic inputs. Substantially increased spine density of excitatory neurons and decreased numbers of parvalbumin- and somatostatin-labeled inhibitory inter-neurons were also recorded in the A1 after VPA exposure. Given the fact that cortical temporal processing of sound is associated with speech perception in humans, these results in the animal model of VPA exposure provide insight into a possible neurological mechanism underlying auditory and language-related deficits in individuals with autism.

Analysis of C-X-C motif chemokine receptors in breast cancer: potential value in immunotherapy and prognostic prediction.

Background: The concept of individualized therapy has advanced the development of prognostic biomarkers to manage patients with breast cancer (BRCA). Immunotherapy has shown great potential in treating BRCA, and the C-X-C motif chemokine receptor (CXCR) has generated interest in regulating tumor progression through the immune microenvironment. Although CXCRs were utilized for prognosis prediction in glioma with favourable capability, the prognostic and therapeutic role of CXCR in BRCA is unclear. Methods: We used The Cancer Genome Atlas (TCGA) database to analyze 1,095 BRCA patients' transcription, mutation, survival time and survival status. Estimation of STromal and Immune cells in MAlignant Tumor tissues using Expression data (ESTIMATE), Cell-type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT), quanTIseq, and Estimating the Proportion of Immune and Cancer cells (EPIC) algorithms were performed to infer the association of CXCR genes with immune cells. We randomly divided the TCGA dataset into a training set and a validation set according to 1:1, constructed a LASSO Cox regression model based on CXCR family genes using the glmnet R package in the training set, assembled clinical variables to draw a visual Nomogram using the R package rms, and validated the model by receiver operating characteristic (ROC) curves, calibration curves with clinical decision curves in the validation set efficacy. Results: Compared to normal samples, CXCR3/4/5 messenger RNA (mRNA) expression levels were upregulated in BRCA samples, whereas CXCR1/2 mRNA expression levels were downregulated. High CXCR3/5/6 expression was associated with a good prognosis. Subsequently, we divided the CXCRs into 2 molecular subgroups based on their expression patterns and explored prognosis, immune infiltration, functional enrichment, hallmarks, and immune response differentiation between the two subgroups. After LASSO Cox regression modeling, a CXCR score predicting overall survival (OS) was constructed, and the predictive accuracy was assessed. By pooling clinical variables, a nomogram individual risk assessment method was established to measure the identification of genuinely high-risk patients who should receive interventions. Conclusions: In summary, CXCR genes were associated with immune infiltration and survival in BRCA patients, and our CXCR-based prognostic model could better predict the prognosis of BRCA patients and provide potential immunotherapy targets for clinical purposes.

Identification and validation of endocrine resistance-related and immune-related long non-coding RNA (lncRNA) signatures for predicting endocrinotherapy response and prognosis in breast cancer.

Background: Endocrine resistance remains a major challenge in breast cancer (BRCA). Increasing evidence has revealed that long non-coding RNA (lncRNA) are closely implicated in tumorigenesis, drug resistance, and the immune-related pathways of cancer. However, the immune-related lncRNA remains to be thoroughly investigated in predicting the endocrine therapeutic response and prognosis of BRCA. Methods: Based on the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases, and calculating the correlation of lncRNAs with immune-related genes obtained from ImmPort and InnateDB databases, we finally obtained endocrine resistance-related and immune-related long non-coding RNAs (ERIR-lncRNAs). Univariate Cox and least absolute shrinkage and selection operator (LASSO) Cox regression were performed to screen prognosis-associated ERIR-lncRNAs and establish signatures, using 2 separate datasets from GEO for external validation. Principal component analysis (PCA), Kaplan-Meier analysis, receiver operating characteristic (ROC) curves, and multivariate Cox regression were performed to demonstrate the robustness and predictability of the signature. We investigated tumor immune infiltration and tumor mutation burden (TMB) between high- and low-risk groups, and the role of key lncRNAs in endocrine resistant breast cancer was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR), Cell Counting Kit 8 (CCK 8) and transwell assays. Results: A total of 781 endocrine resistance related lncRNAs were identified, of which 12 lncRNAs were associated with immunity. Then, three ERIR-lncRNAs with prognostic relevance were screened to successfully construct the risk signature. Compared to sensitive patients, the endocrine resistant patients had higher risk scores in both the training and validation sets (P<0.05). The high-risk group had significantly shorter survival times (P<0.001) with area under the curve (AUC) values of 0.710, 0.649, and 0.672 at 1, 3, and 5 years. Univariate and multivariate Cox regression indicated that our signature was an independent prognostic factor (P<0.001). Through immune infiltration analysis, it was revealed that the high-risk scores were associated with T follicular helper (Tfh) differentiation and exhibited a pro-tumor phenomenon with the Th1/Th2 balance shifting toward Th2. The key lncRNAs promote cell proliferation and migration as confirmed by qRT-PCR, CCK-8 and transwell assays. Conclusions: The ERIR-lncRNA signature is valuable in predicting endocrine therapeutic response and prognosis of BRCA, revealing a potential relationship between endocrine resistance and TME.

Environmental noise degrades hippocampus-related learning and memory.

The neural mechanisms underlying the impacts of noise on nonauditory function, particularly learning and memory, remain largely unknown. Here, we demonstrate that rats exposed postnatally (between postnatal days 9 and 56) to structured noise delivered at a sound pressure level of ∼65 dB displayed significantly degraded hippocampus-related learning and memory abilities. Noise exposure also suppressed the induction of hippocampal long-term potentiation (LTP). In parallel, the total or phosphorylated levels of certain LTP-related key signaling molecules in the synapses of the hippocampus were down-regulated. However, no significant changes in stress-related processes were found for the noise-exposed rats. These results in a rodent model indicate that even moderate-level noise with little effect on stress status can substantially impair hippocampus-related learning and memory by altering the plasticity of synaptic transmission. They support the importance of more thoroughly defining the unappreciated hazards of moderately loud noise in modern human environments.

Characterization of Selenoprotein P cDNA of the Antarctic toothfish Dissostichus mawsoni and its role under cold pressure.

Our previous study using comparative genome analysis revealed a significant gene copy number gain of Dissostichus mawsoni selenoprotein P (Dm-SEPP) during the evolutionary radiation of Antarctic notothenioids, suggesting that Dm-SEPP contribute to this process, but the detailed structure and function of this gene product remain unclear. In the present study, the Dm-SEPP cDNA was cloned and characterized. The Dm-SEPP cDNA contains 17 selenocysteines (Sec) encoded by TGA codons and 2 typical SECIS elements located in the 3'-UTR. Evolutionary analysis of the Dm-SEPP gene revealed that it's closely related to the SEPP gene of zebrafish (Danio rerio), showing 51% amino acid similarity. Over-expression of Dm-SEPP could protect mammalian cells under cold pressure, probably via eliminating ROS. Further study showed an increase of endogenous SEPP in zebrafish ZF4 cells under cold pressure, and knockdown of SEPP decreased cell viability, accompanied with increased ROS. Our results suggested a protective role of Dm-SEPP in cold adaptation in Antarctic notothenioids.

Spontaneous Hematoma of Posterior Mediastinum with an Uncommon Cause: A Case Report and Review of the Literature.

Spontaneous mediastinal hematoma is exceedingly rare. We described such a case of a 61-year-old male with a posterior mediastinal hematoma from ruptured small aneurysm, which was ascertained via contrast-enhanced computed tomography examination. Subsequent super-selective angiography of left gastric artery revealed a ruptured aneurysm with contrast medium leakage, feeding vessels respectively from caudal and cranial artery. The left gastric artery branch caudally feeding aneurysm was successfully occluded, while cranially feeding artery from the branch of left bronchial artery failed to embolize due to complex anatomic factor. Our management still yields to a satisfactory outcome.

Dynamic change of intestinal duplication in an adult patient: a case report and literature review.

Intestinal duplication in an adult is an uncommon congenital abnormality because only minority of cases present in adulthood. More than 80% of cases occur before the age of two years as an acute abdomen, bowel obstruction or other complications associated with it. Duplication has two types, either cystic or tubular. Here, we report a case of an adult who was diagnosed preoperatively on CT scan as tubular intestinal duplication. CT images showed change in the morphology of the cystic mass after one week of antibiotics administration. On histopathological analysis, the resected duplicated segment had esophageal epithelium in addition to the intestinal gland. So far, we found no report describing CT findings of dynamic change of ileal duplication in the English literatures.

Endobronchial lipoma: an unusual cause of bronchial obstruction.

Endobronchial lipoma is a rare benign tumor. It is difficult to differentiate benign endobronchial lipoma from their malignant counterparts, as their symptoms and complications are almost alike. Here, we describe the clinical and radiological features of EL in two cases. Multislice CT (MSCT) may play an important role in the diagnosis for EL.