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As the second common diagnosed cancer among gynecological tumors, endometrial cancer (EC) has heterogeneous pathogenesis and clinical manifestations. Therefore, prognosis prediction that considers gene expression value and clinical characteristics, is helpful to patients with EC. We downloaded RNA expression and clinical data from the TCGA database. We achieved 4 DEPRGs and constructed the PRG panel by univariate, lasso and multivariate Cox analysis. Based on the median value of the risk score, patients were divided into two groups. The Kaplan–Meier curve suggested that the patients with lower risk scores had better clinical outcomes of EC. AUC of ROC curves suggested the panel can be used as an independent predictor. Future analysis indicated the positive correlations between risk score and clinical characteristics. What’s more, we performed GO and KEGG functional analysis and immune environment exploration to get an understanding of the potential molecular mechanism and immunotherapeutic target. To future validate the panel, we found that the relapse-free and overall survival probability of 4 prognostic DEPRGs between high-expression group and low-expression group were different through the Kaplan–Meier plotter in UCEC. In addition, GEPIA database and RT-PCR experiment indicated GPX4 and GSDMD were highly expressed in UCEC compared to normal endometrial tissue, and TIRAP and ELANE were downregulated. This study identified a PRG panel to predict the prognosis immune microenvironment in human EC. Then, Kaplan–Meier analysis and AUC below the ROC curves was used to validate the panel. In addition, Chi-square was used to show the clinical significance. GO, KEGG and GSEA were used to show the functional differences. Different immune-related databases were used to analyze the immune characteristics. The Kaplan–Meier plotter website was used to assess the effect of genes on survival. GEPIA and RT-PCR were used to analyze the expression level. In summary, we identified 4 prognosis-associated pyroptosis-related genes (ELANE, GPX4, GSDMD, and TIRAP). The panel can also predict prognosis prediction and immune microenvironment in human endometrial cancer.

Accumulating evidence suggests that neural abnormalities in conduct disorder (CD) may be subject to genetic influences, but few imaging studies have taken genetic variants into consideration. The Val66Met polymorphism of brain-derived neurotrophic factor (BDNF) has emerged as a high-interest genetic variant due to its importance in cortical maturation, and several studies have implicated its involvement in neurodevelopmental disorders. Thus, it is unclear how this polymorphism may influence brain anatomy and aberrant behaviors in CD. A total of 65 male adolescents with CD and 69 gender-, IQ- and socioeconomic status-matched healthy controls (HCs) (age range 13-17 years) were enrolled in this study. Analyses of variance (ANOVAs) were used to assess the main effects of CD diagnosis, BDNF genotype, and diagnosis-genotype interactions on brain anatomy and behaviors. We detected a significant main effect of BDNF genotype on temporal gyrification and antisocial behaviors, but not on CD symptoms. Diagnosis-genotype interactive effects were found for cortical thickness of the superior temporal and adjacent areas. These results suggest that the BDNF Val66Met polymorphism may exert its influence both on neural alterations and delinquent behaviors in CD patients. This initial evidence highlights the importance of elucidating potentially different pathways between BDNF genotype and cortical alterations or delinquent behaviors in CD patients.

Objective Identification of state-independent and -dependent neural biomarkers may provide insight into the pathophysiology and effective treatment of major depressive disorder (MDD), therefore we aimed to investigate the state-independent and -dependent topological alterations of MDD. Method Brain resting-state functional magnetic resonance imaging (fMRI) data were acquired from 59 patients with unmedicated first episode current MDD (cMDD), 48 patients with remitted MDD (rMDD) and 60 demographically matched healthy controls (HCs). Using graph theory, we systematically studied the topological organization of their whole-brain functional networks at the global and nodal level. Results At a global level, both patient groups showed decreased normalized clustering coefficient in relative to HCs. On a nodal level, both patient groups showed decreased nodal centrality, predominantly in cortex-mood-regulation brain regions including the dorsolateral prefrontal cortex, posterior parietal cortex and posterior cingulate cortex. By comparison to cMDD patients, rMDD group had a higher nodal centrality in right parahippocampal gyrus. Limitations The present study, an exploratory analysis, may require further confirmation with task-based and experimental studies. Conclusions Deficits in the topological organization of the whole brain and cortex-mood-regulation brain regions in both rMDD and cMDD represent state-independent biomarkers.

Background It has been proposed that state-independent, or trait, neurobiological alterations across illness phases may contribute to the high recurrence of major depressive disorder (MDD). Although intrinsic brain network abnormalities have been implicated consistently in MDD neuropathology, MDD state-independent and -dependent resting-state network alterations have not been clearly studied. Methods Resting-state functional magnetic resonance imaging (fMRI) data were collected from 57 medication-naive first-episode current MDD patients, 35 remitted MDD patients, and 66 healthy controls (HCs). Independent component analysis (ICA) was used to extract subnetworks of the default mode network (DMN), central executive network (CEN), and salience network (SN). Results Relative to HCs, the current MDD and remitted MDD groups had decreased intra-intrinsic functional connectivity (iFC) in the dorsal lateral prefrontal cortex (dlPFC) of the left CEN, increased inter-FC between the SN and right CEN (rCEN), and decreased inter-FC between the anterior DMN (aDMN) and rCEN. The altered intra-iFC in the left CEN were correlated negatively with the depressive level in the remitted MDD. Conclusions Hypoactivity of the dlPFC in the left CEN, increased inter-FC between the SN and rCEN, and decreased inter-FC between the aDMN and rCEN may reflect state-independent biomarkers of MDD.

Background: There were 313959 cases of newly diagnosed ovarian cancer (OC) and 207252 new deaths for OC in 2020 and OC lacks effective treatment options. Therefore, identifying novel therapeutic targets is imminent. Here, we use an integrated bioinformatics analysis to key genes involved in ovarian cancer and reveal potential therapeutic targets.Methods: GSE105437, GSE14407 and GSE18520 downloaded from Gene Expression Omnibus (GEO) were used to screen differentially expressed genes (DEGs). Gene ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to predict the potential functions of the DEGs. Protein-protein interaction network (PPI) was drawn through STRING database and select CDC20 having the highest degrees of connectivity as the potential therapeutic target. Oncomine database and quantitative Real-time RT-PCR (RT-qPCR) of the ovarian tissues were used to validate the mRNA expression of CDC20. We use Gene Set Enrichment Analysis (GSEA) software to explore the potential biological function of CDC20 in OC. Results: A total of 821 DEGs were obtained, including 497 upregulated genes and 324 downregulated genes. Functional and pathway enrichment analyses indicated the DEGs were mainly involved in DNA-binding transcription activator activity, tubulin binding, microtubule binding, cell cycle, Wnt signaling pathway, p53 signaling pathway, and metabolism changes. Oncomine database analysis and RT-qPCR showed that CDC20 is significantly upregulated in OC tissues. GSEA analysis showed that CDC20 may regulate OC via cell cycle, citrate and TCA cycle, Oxidative phosphorylation and ubiquitin mediated proteolysis pathways. Conclusion: The results of the present study deduced that CDC20 is overexpressed in OC and may be a promising therapeutic target for the treatment of OC.

B cell acute lymphoid leukemia uses the mitochondrial respiration as the main energy source that enhances drug resistance., How metabolic status controls the fates of different types of leukemia cells remains elusive. Using a SoNar-transgenic mouse line, we demonstrated that B cell acute lymphoblastic leukemia (B-ALL) cells had a preference in using oxidative phosphorylation. B-ALL cells with a low SoNar ratio (SoNar-low) had enhanced mitochondrial respiration capacity, mainly resided in the vascular niche, and were enriched with more functional leukemia-initiating cells than that of SoNar-high cells in a murine B-ALL model. The SoNar-low cells were more resistant to cytosine arabinoside (Ara-C) treatment. cyclic adenosine 3′,5′-monophosphate response element–binding protein transactivated pyruvate dehydrogenase complex component X and cytidine deaminase to maintain the oxidative phosphorylation level and Ara-C–induced resistance. SoNar-low human primary B-ALL cells also had a preference for oxidative phosphorylation. Suppressing oxidative phosphorylation with several drugs sufficiently attenuated Ara-C–induced resistance. Our study provides a unique angle for understanding the potential connections between metabolism and B-ALL cell fates.

Background: Obsessive-compulsive personality disorder (OCPD) is one of the most prevalent personality disorders in general population. However, neural mechanisms underlying OCPD remain elusive. The aim of this study is to use functional magnetic resonance imaging (fMRI) to examine whether OCPD patients will exhibit altered spontaneous brain activity as compared to healthy controls (HC). Methods: Resting-state fMRI data were acquired in 37 OCPD patients and 37 matched HC. Amplitudes of low-frequency fluctuation (ALFF) were calculated and compared between the two groups. Correlation analysis was performed between regional ALFF values and OCPD severity scores. Results: Significant group differences in regional ALFF were found in multiple brain regions. Compared to HCs, OCPD subjects had increased ALFF in bilateral caudate, left precuneus, left insula, and left medial superior frontal gyrus, and decreased ALFF in the right fusiform gyrus and left lingual gyrus. The ALFF values in the left precuneus correlated with OCPD severity scores. Limitations: We excluded patients with comorbidity and did not conduct cognitive function assessments. Our findings are also limited to cross-sectional analysis. Conclusions: OCPD patients exhibit altered spontaneous neural activity as compared to healthy controls in multiple brain regions, which may reflect different characteristic symptoms of OCPD pathophysiology, including cognitive inflexibility, excessive self-control, lower empathy, and visual attention bias. Keywords: Obsessive-compulsive personality disorder, Resting-state functional MRI, Amplitude of low-frequency fluctuation, Spontaneous neuronal activity

Stress is a strong risk factor for major depressive disorder, while sensitization to stress in remitted individuals plays a key role in depression recurrence. The present study explored the state-independent (trait) and dependent (state) neural responses to psychosocial stress in major depressive disorder.Thirty-six patients with medication-naive first-episode current depression, 33 patients with remitted depression, and 36 demographically matched healthy control participants were administered the Montreal Imaging Stress Task during functional MRI. One-way analyses of variance were used to assess differences in stress responses in the three groups.Both currently depressed and remitted patients exhibited higher stress levels and cortisol responses than control subjects. Compared with control subjects, both depressed and remitted patients exhibited reduced activation in the ventromedial prefrontal cortex and increased activation in the precuneus. The stress-induced ventromedial prefrontal cortex activation changes negatively correlated with cortisol increases in all three groups. Additional increased activations were found in the dorsolateral prefrontal cortex and bilateral striatum in remitted patients compared with control subjects, and activation in these regions correlated inversely with depressive symptoms in the remitted group.These findings provide novel evidence regarding the trait and state markers of depression on neural responses to psychosocial stress. Regional activation changes in the ventromedial prefrontal cortex and precuneus may reflect the trait markers of depression. Hyperactivation in the dorsolateral prefrontal cortex and striatum may represent a state-dependent compensatory mechanism during depression remission.

Background: Irritable bowel syndrome (IBS) is a common gastrointestinal disorder without obvious structural abnormalities or consistent associated biomarkers, making its diagnosis difficult. In the present study, we used a urine-based metabolomics approach to identify IBS biomarkers. Methods: We used an ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry (UPLC-QTOF-MS) on urine samples from patients suffering from IBS and healthy controls. Data were coupled for multivariate statistical analysis methods. Results: We selected 30 differential metabolites associated with IBS and found steroid hormone biosynthesis and histidine metabolism alterations in patients with IBS that may be involved in the pathogenesis of the disease. In addition, we identified a panel of five metabolite markers composed of cortisone, citric acid, tiglylcarnitine, N6,-N6,-N6-trimethyl-L-lysine and L-histidine that could be used to discriminate between patients and healthy controls and may be appropriate as IBS diagnosis biomarkers. Conclusion: Our findings indicate that metabolomics combined with pattern recognition can be useful to identify disease diagnostic IBS markers. Clinical trial registration: ChiCTR1800020072

Background The hopelessness theory of depression posits that individuals with negative cognitive styles are at risk of developing depression following negative life events. The purpose of this work was to examine whether individuals with cognitive vulnerability to depression (CVD) exhibit similar spontaneous brain activity patterns as compared to patients with major depressive disorder (MDD). Methods Subjects with CVD (N=32), drug-naive first-episode patients with major depressive disorder (N=32), and sex-, age- and education-matched healthy controls (HCs; N=35) were subjected to resting state functional magnetic resonance imaging (RS-fMRI) and amplitudes of low-frequency fluctuation (ALFF) was compared between the groups. Pearson correlation analysis was performed between regional ALFFs and psychometric scores, namely the Cognitive Style Questionnaire (CSQ) and the Center for Epidemiologic Studies Depression (CES-D) scale scores. Results Significant group differences in ALFF values were observed bilaterally in the orbitofrontal cortex (OFC) and insular cortex (IC), and in the left fusiform gyrus (FFG). Compared to HCs, CVD subjects had reduced ALFFs in the bilateral OFC and increased ALFF in the bilateral IC and the left FFG, which were similar to the differences observed between the HCs and MDD patients. Compared to MDD patients, CVD subjects showed significant reduced ALFF values in right IC. Additionally, CSQ scores for the CVD group correlated with ALFF values in the left IC. Limitations We did not conduct a longitudinal study. Our findings were limited in cross-sectional analysis. Conclusions A hypoactive OFC and hyperactive IC in a resting-state may underlie an imbalance in the spontaneous brain activity in orbitofrontal-insular circuits, and these differences may represent a trait-related marker of vulnerability to depression.

Background there has been a recent increase in the use of connectome-based multivariate pattern analysis (MVPA) of resting-state functional magnetic resonance imaging (fMRI) data aimed at distinguishing patients with major depressive disorder (MDD) from healthy controls (HCs). However, the validity of this method needs to be confirmed in independent samples. Method we used resting-state fMRI to explore whole-brain functional connectivity (FC) patterns characteristic of MDD and to confirm the effectiveness of MVPA in distinguishing MDD versus HC groups in two independent samples. The first sample set included 29 MDD patients and 33 HCs and second sample set included 46 MDD patients and 57 HCs. Results for the first sample, we obtained a correct classification rate of 91.9% with a sensitivity of 89.6% and specificity of 93.9%. For the second sample, we observed a correct classification rate of 86.4% with a sensitivity of 84.8% and specificity of 87.7%. With both samples, we found that the majority of consensus FCs used for MDD identification were located in the salience network, default mode network, the cerebellum, visual cortical areas, and the affective network. Limitation we did not analyze potential structural differences between the groups. Conclusion results suggest that whole-brain FC patterns can be used to differentiate depressed patients from HCs and provide evidence for the potential use of connectome-based MVPA as a complementary tool in the clinical diagnosis of MDD.

Background There are limited data on neurobiological correlates of poor insight in obsessive-compulsive disorder (OCD). This study explored whether specific changes occur in small-world network (SWN) properties in the brain functional network of OCD patients with poor insight. Method Resting-state electroencephalograms (EEGs) were recorded for 12 medication-free OCD patients with poor insight, 50 medication-free OCD patients with good insight, and 36 healthy controls. Results Both of the OCD groups exhibited topological alterations in the brain functional network characterized by abnormal small-world parameters at the beta band. However, the alterations at the theta band only existed in the OCD patients with poor insight. Limitations A relatively small sample size. Subjects were naive to medications and those with Axis I comorbidity were excluded, perhaps limiting generalizability. Conclusions Disrupted functional integrity at the beta bands of the brain functional network may be related to OCD, while disrupted functional integrity at the theta band may be associated with poor insight in OCD patients, thus this study might provide novel insight into our understanding of the pathophysiology of OCD.

Regional abnormalities in brain structure and function, as well as disrupted connectivity, have been found repeatedly in adolescents with conduct disorder (CD). Yet, the large-scale brain topology associated with CD is not well characterized, and little is known about the systematic neural mechanisms of CD. We employed graphic theory to investigate systematically the structural connectivity derived from cortical thickness correlation in a group of patients with CD (N = 43) and healthy controls (HCs, N = 73). Nonparametric permutation tests were applied for between-group comparisons of graphical metrics. Compared with HCs, network measures including global/local efficiency and modularity all pointed to hypo-functioning in CD, despite of preserved small-world organization in both groups. The hubs distribution is only partially overlapped with each other. These results indicate that CD is accompanied by both impaired integration and segregation patterns of brain networks, and the distribution of highly connected neural network ‘hubs’ is also distinct between groups. Such misconfiguration extends our understanding regarding how structural neural network disruptions may underlie behavioral disturbances in adolescents with CD, and potentially, implicates an aberrant cytoarchitectonic profiles in the brain of CD patients.

Summary The metabolic properties of leukemia-initiating cells (LICs) in distinct bone marrow niches and their relationships to cell-fate determinations remain largely unknown. Using a metabolic imaging system with a highly responsive genetically encoded metabolic sensor, SoNar, we reveal that SoNar-high cells are more glycolytic, enriched for higher LIC frequency, and develop leukemia much faster than SoNar-low counterparts in an MLL-AF9-induced murine acute myeloid leukemia model. SoNar-high cells mainly home to and locate in the hypoxic endosteal niche and maintain their activities through efficient symmetric division. SoNar can indicate the dynamics of metabolic changes of LICs in the endosteal niche. SoNar-high human leukemia cells or primary samples have enhanced clonogenic capacities in vitro or leukemogenesis in vivo. PDK2 fine-tunes glycolysis, homing, and symmetric division of LICs. These findings provide a unique angle for the study of metabolisms in stem cells, and may lead to development of novel strategies for cancer treatment.

Background CD274 (programmed death ligand 1, also known as B7H1) is expressed in both solid tumors and hematologic malignancies and is of critical importance for the escape of tumor cells from immune surveillance by inhibiting T cell function via its receptor, programmed death 1 (PD-1). Increasing evidence indicates that functional monoclonal antibodies of CD274 may potently enhance the antitumor effect in many cancers. However, the role of CD274 in leukemia-initiating cells (LICs) remains largely unknown. Methods We established an MLL-AF9-induced acute myeloid leukemia (AML) model with wild-type (WT) and CD274-null mice to elucidate the role of CD274 in the cell fates of LICs, including self-renewal, differentiation, cell cycle, and apoptosis. RNA sequencing was performed to reveal the potential downstream targets, the results of which were further validated both in vitro and in vivo. Results In silico analysis indicated that CD274 level was inversely correlated with the overall survival of AML patients. In Mac-1+/c-Kit+ mouse LICs, CD274 was expressed at a much higher level than in the normal hematopoietic stem cells (HSCs). The survival of the mice with CD274-null leukemia cells was dramatically extended during the serial transplantation compared with that of their WT counterparts. CD274 deletion led to a significant decrease in LIC frequency and arrest in the G1 phase of the cell cycle. Interestingly, CD274 is not required for the maintenance of HSC pool as shown in our previous study. Mechanistically, we demonstrated that the levels of both phospho-JNK and Cyclin D2 were strikingly downregulated in CD274-null LICs. The overexpression of Cyclin D2 fully rescued the loss of function of CD274. Moreover, CD274 was directly associated with JNK and enhanced the downstream signaling to increase the Cyclin D2 level, promoting leukemia development. Conclusions The surface immune molecule CD274 plays a critical role in the proliferation of LICs. The CD274/JNK/Cyclin D2 pathway promotes the cell cycle entry of LICs, which may serve as a novel therapeutic target for the treatment of leukemia. Electronic supplementary material The online version of this article (doi:10.1186/s13045-016-0350-6) contains supplementary material, which is available to authorized users.

Functional magnetic resonance imaging (fMRI) studies have revealed abnormal neural activity in several brain regions of adolescents with conduct disorder (CD) performing various tasks. However, little is known about the spontaneous neural activity in people with CD in a resting state. The aims of this study were to investigate CD-associated regional activity abnormalities and to explore the relationship between behavioral impulsivity and regional activity abnormalities. Resting-state fMRI (rs-fMRI) scans were administered to 28 adolescents with CD and 28 age-, gender-, and IQ-matched healthy controls (HCs). The rs-fMRI data were subjected to regional homogeneity (ReHo) analysis. ReHo can demonstrate the temporal synchrony of regional blood oxygen level-dependent signals and reflect the coordination of local neuronal activity facilitating similar goals or representations. Compared to HCs, the CD group showed increased ReHo bilaterally in the insula as well as decreased ReHo in the right inferior parietal lobule, right middle temporal gyrus and right fusiform gyrus, left anterior cerebellum anterior, and right posterior cerebellum. In the CD group, mean ReHo values in the left and the right insula correlated positively with Barratt Impulsivity Scale (BIS) total scores. The results suggest that CD is associated with abnormal intrinsic brain activity, mainly in the cerebellum and temporal–parietal-limbic cortices, regions that are related to emotional and cognitive processing. BIS scores in adolescents with CD may reflect severity of abnormal neuronal synchronization in the insula.

It has been generally acknowledged that the diagnosis, treatment and prognosis evaluation of leukemia largely rely on an adequate identification of genetic abnormalities. A systemic analysis of genetic aberrations was performed in a cohort of 1346 patients with newly diagnosed acute lymphoblastic leukemia (ALL) in China. The pediatric patients had higher incidence of hyperdiploidy and t(12;21) (p13;q22)/ETV6–RUNX1 than adults (P

Background The hopelessness theory of depression posits that individuals with negative cognitive styles are at an increased risk for depression following negative life events. In neuroimaging studies, brain gray matter volume abnormalities correlate with the presence of depressive disorders. However, it is unknown whether changes in gray matter volume also appear in healthy individuals with cognitive vulnerability to depression (CVD). Methods 30 subjects diagnosed with CVD, 33 first-episode patients with major depressive disorder (MDD), and 32 healthy controls were examined using voxel-based morphometry following magnetic resonance imaging (MRI). Results We found significant volumetric differences between three groups in the left precentral gyrus, right fusiform gyrus and the right thalamus. In these regions, compared to controls, CVD subjects showed reduced gray matter volumes in the left precentral gyrus and right fusiform gyrus. MDD patients demonstrated reduced gray matter volume in the left precentral gyrus and increased gray matter volume in the right thalamus. Additionally, CVD individuals had significantly smaller right fusiform gyrus and right thalamus than MDD patients. The weakest-link scores on CSQ were negatively correlated with gray matter volumes in the left precentral gyrus. Conclusions Reductions in brain gray matter volume exist widely in individuals with CVD. In addition, there exist similar abnormalities in gray matter volume in both CVD subjects and MDD patients. Reductions of gray matter volume in the left precentral gyrus might be correlated to the negative cognitive styles, as well as an increased risk for depression.

Objective Pulse oximetry, which noninvasively detects the blood flow of peripheral tissue, has achieved widespread clinical use. We have noticed that the better the quality of cardiopulmonary resuscitation (CPR), the better the appearance of pulse oximetry plethysmographic waveform (POP). We investigated whether the area under the curve (AUC) and/or the amplitude (Amp) of POP could be used to monitor the quality of CPR. Design Prospective, randomized controlled study. Setting Animal experimental center in Peking Union Medical Collage Hospital, Beijing, China. Subjects Healthy 3-month-old male domestic swine. Interventions 34 local pigs were enrolled in this study. After 4 minutes of untreated ventricular fibrillation, animals were randomly assigned into two resuscitation groups: a “low quality” group (with a compression depth of 3cm) and a “high quality” group (with a depth of 5cm). All treatments between the two groups were identical except for the depth of chest compressions. Hemodynamic parameters [coronary perfusion pressure (CPP), partial pressure of end-tidal carbon dioxide (PETCO2)] as well as AUC and Amp of POP were all collected and analyzed. Measurements and Findings There were statistical differences between the “high quality” group and the “low quality” group in AUC, Amp, CPP and PETCO2 during CPR (P

The prevalence of extensively drug-resistant (XDR) and pre-extensively drug-resistant (pre-XDR) tuberculosis in China highlights the need for rapid diagnosis. Molecular methods based on the detection of resistance-conferring mutations provide promising solution for rapid diagnosis. Here, we evaluated the accuracy of using mutations in gyrA, rrs and tlyA to predict resistance to levofloxacin (LEV), amikacin (AMK) and capreomycin (CAP), among 208 clinical multidrug-resistant (MDR) Mycobacterium tuberculosis strains collected in a local hospital in Shandong province, China. A total of 131 (63.0%, 131/208) strains were detected resistance to at least one of the 3-s line drugs by drug susceptible tests (DSTs). By comparing the mutation data with the phenotypic results, we found all mutations in three genes could specifically (with specificities from 93.9% to 100%) predict resistances with sensitivities of 77.8% for gyrA (LEV), 71.4% for rrs (AMK), 53.6% for rrs (CAP), 14.3% for tlyA (CAP), 64.3% for rrs and tlyA (CAP). The combination of these mutations could predict 68.9% and 63.4% pre-XDR and XDR TB, respectively. However, the positive predictive value of rrs for CAP resistance (57.7%) and the negative predictive values of gyrA for LEV resistance (74.5%) were not satisfying. Our results supported the use of genetic mutations to predict resistance to AMK and fluoroquinolones. An algorithm that combines molecular methods and traditional DST would be valuable for detecting resistance to second-line drugs in our hospital.

The aim of this study was to examine cognitive emotion regulation strategies in adult outpatients with major depressive disorder (MDD). A clinical sample of 191 MDD outpatients and a non-clinical sample of 267 general adults were recruited. Nine cognitive emotion regulation strategies were assessed in all participants (aged 21–65 years). Results showed that MDD participants had significantly higher scores on the following strategies: self-blame, acceptance, rumination, catastrophizing, and blaming others, but lower scores on positive refocusing, refocus on planning, positive reappraisal, and putting in perspective strategies than general populations. In addition, self-blame, acceptance, and catastrophizing positively correlated and positive reappraisal negatively correlated with depressive symptoms in MDD populations. Further logistic regression analyses indicated that five strategies have significant and independent contributions to the prediction of MDD group membership (a higher reported use of self-blame, catastrophizing, and acceptance, and a lower reported use of positive refocusing, and putting in perspective). The results suggest that cognitive emotion regulation strategies may be a useful target for psychological assessment and treatment in patients with MDD.

Minimal residual disease (MRD) is of the most important factor for predicting prognosis and guiding treatment of acute lymphoblastic leukemia (ALL). In this study, we investigated the prognostic significance of leukemia-associated immunophenotypes (LAIPs) as assessment of index of MRD in 125 adult B-lineage ALL (B-ALL) patients by eight-color flow cytometry. The LAIPs could be identified in 96% and 81.6% of patients with the sensitivity of 10(-4) and 10(-5), respectively. MRD-negative status could clearly predict a favorable 2-year relapse-free survival (RFS) and overall survival (OS) at the end of induction of complete remission and one cycle of consolidation treatment. Moreover, we identified a group of cases with MRD of 0.001% to

Background Major depressive disorder (MDD) has been associated with abnormal structure and function of the brain's affective network, including the amygdala and orbitofrontal cortex (OFC). However, it is unclear if alterations of resting-state function in this affective network are present at the initial onset of MDD. Aims To examine resting-state function of the brain's affective network in first-episode, medication-naive patients with MDD compared to healthy controls (HCs). Methods Resting-state functional magnetic resonance imaging (rs-fMRI) was performed on 32 first-episode, medication-naive young adult patients with MDD and 35 matched HCs. The amplitude of low-frequency fluctuations (ALFF) of the blood oxygen level-dependent (BOLD) signal and amygdala-seeded functional connectivity (FC) were investigated. Results Compared to HC, MDD patients showed reduced ALFF in the bilateral OFC and increased ALFF in the bilateral temporal lobe extending to the insular and left fusiform cortices. Enhanced anti-correlation of activity between the left amygdala seed and the left OFC was found in MDD patients but not in HCs. Conclusions Reduced ALFF in the OFC suggests hypo-functioning of emotion regulation in the affective network. Enhanced anti-correlation of activity between the amygdala and OFC may reflect dysfunction of the amygdala-OFC network and additionally represent a pathological process of MDD.