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Background: Due to limited therapeutic options and potential for spread, carbapenem-resistant Enterobacteriaceae (CRE)-producing New Delhi metallo-β-lactamases (NDMs) are a public health priority. We investigated the epidemiology of NDM-producing CRE reported to the CDC to clarify its distribution and relative prevalence. Methods: The CDC’s Antibiotic Resistance Laboratory Network supports molecular testing of CRE for 5 carbapenemases nationally. Although KPC is the most common carbapenemase in the United States, non-KPC carbapenemases are a growing concern. We analyzed CRE with any of 4 non-KPC plasmid-mediated carbapenemases (NDM, VIM, IMP, or OXA-48 type) isolated from specimens collected from January 1, 2017, through June 30, 2019; only a patient’s first isolate per organism–carbapenemase combination was included. We excluded isolates from specimen sources associated with colonization screening (eg, perirectal). We compared the proportion of NDM-producing CRE to all non-KPC–producing CP-CRE between period A (January to June 2018) and period B (January to June 2019). Health departments and the CDC collected additional exposure and molecular information in selected states to better describe current NDM-producing CRE epidemiology. Results: Overall, 47 states reported 1,013 non–KPC-producing CP-CRE (range/state, 1–109 isolates; median, 11 isolates); 46 states reported 631 NDM-producing CRE (range/state, 1–84; median, 6). NDM-producing CRE increased quarterly from the third quarter of 2018 through the second quarter of 2019; CP-CRE isolates with other non-KPC carbapenemases remained stable (Fig. 1). In period A, 124 of 216 emerging CP-CRE had NDM (57.1%), compared with 255 of 359 emerging CP-CRE (71.0%) during period B (P = .1179). Among NDM-producing CRE, the proportion of Enterobacter spp increased from 10.5% in 2018 to 18.4% in 2019 (P = .0467) (Fig. 2). In total, 18 states reported more NDM-producing CRE in the first 6 months of 2019 than in all of 2018. Connecticut, Ohio, and Oregon were among states that conducted detailed investigations; these 3 states identified 24 NDM-producing CRE isolates from 23 patients in period B. Overall, 5 (21.7%) of 22 patients with history available traveled internationally ≤12 months prior to culture; 17 (73.9%) acquired NDM-producing CRE domestically. Among 15 isolates sequenced, 8 (53.3%) carried NDM-5 (6 E. coli, 1 Enterobacter spp and 1 Klebsiella spp) and 7 (46.7%) carried NDM-1 (6 Enterobacter spp and 1 Klebsiella spp). Species were diverse; no single strain type was shared by >2 isolates. Conclusions: Detection of NDM-producing CRE has increased across the AR Lab Network. Among states with detailed information available, domestic acquisition was common, and no single variant or strain predominated. Aggressive public health response and further understanding of current US NDM-CRE epidemiology are needed to prevent further spread.
Background: Methicillin-resistant Staphylococcus aureus (MRSA) is responsible for the largest number of invasive infections due to a multidrug-resistant pathogen. Approximately 10% of hospitalized carriers will experience invasive MRSA disease in the year following discharge incurring antibiotic therapy beyond focused treatment of MRSA. Objective: We aimed to quantify the extent of non-MRSA empiric antibiotics incurred by MRSA infections and further assess the risk of Clostridioides difficile Infection (CDI) as a result of treatment of MRSA infection. Methods: The CLEAR Trial was a postdischarge randomized controlled trial of 2,121 MRSA carriers comparing MRSA education alone to education plus repeated decolonization that demonstrated a 30% reduction in MRSA infection and a 17% reduction in all-cause infection attributable to decolonization in the year following hospital discharge (Huang SS, NEJM 2019). We included all hospitalization outcomes due to MRSA infection in the CLEAR Trial with detailed medication administration records to quantify unintended consequences of MRSA infection related to empiric non-MRSA antibiotic use and resultant CDI. Full-text medical records were reviewed with a standardized abstraction form to collect inpatient administered antibiotics and hospital-associated CDI. Results: In total,154 hospitalizations due to MRSA infection with a mean length-of-stay of 10.6 days were identified. During 25 hospitalizations (16.2%), patients received only anti-MRSA antibiotics. During the remaining 129 (83.8%) hospitalizations, patients received a mean of 1.6 distinct non-MRSA antibiotics totaling a mean of 6.6 days of therapy (DOT). Empiric non-MRSA therapy was given for 3.2 DOT before MRSA culture results became available and was continued for an additional 3.4 DOT afterward. Among all 849 non-MRSA DOT, the most common were due to piperacillin-tazobactam (293 DOT, 34.5%), levofloxacin (105 DOT, 12.4%), and metronidazole (93 DOT, 11.0%). Across all 154 hospitalizations, a mean of 5.5 non-MRSA DOT was calculated per MRSA hospitalization, with 6 CDI cases (3.9%) as a direct sequelae of empiric non-MRSA antibiotics provided for MRSA infection. Conclusions: Hospitalization for MRSA infection results in extensive non-MRSA empiric antibiotic therapy both before and after MRSA culture results are known. This antibiotic use is associated with a 3.9% risk of CDI that exceeds the national risk of acquiring CDI (3.2 per 1,000 admissions) by 12-fold during any hospital stay (Barrett ML, AHRQ 2018). The CLEAR Trial findings that postdischarge decolonization reduces MRSA infection and hospitalization by 30% suggests that decolonization may also reduce non-MRSA antibiotic use and CDI in this population.
Severe fever with thrombocytopenia syndrome (SFTS) is a disease with a high case-fatality rate that is caused by infection with the SFTS virus (SFTSV). Five electronic databases were systematically searched to identify relevant articles published from 1 January 2011 to 1 December 2019. The pooled rates with 95% confidence interval (CI) were calculated by a fixed-effect or random-effect model analysis. The results showed that 92 articles were included in this meta-analysis. For the confirmed SFTS cases, the case-fatality rate was 0.15 (95% CI 0.11, 0.18). Two hundred and ninety-six of 1384 SFTS patients indicated that they had been bitten by ticks and the biting rate was 0.21 (95% CI 0.16, 0.26). The overall pooled seroprevalence of SFTSV antibodies among the healthy population was 0.04 (95% CI 0.03, 0.05). For the overall seroprevalence of SFTSV in animals, the seroprevalence of SFTSV was 0.25 (95% CI 0.20, 0.29). The infection rate of SFTSV in ticks was 0.08 (95% CI 0.05, 0.11). In conclusion, ticks can serve as transmitting vectors of SFTSVs and reservoir hosts. Animals can be infected by tick bites, and as a reservoir host, SFTSV circulates continuously between animals and ticks in nature. Humans are infected by tick bites and direct contact with patient secretions.
Fat metabolism is an important and complex biochemical reaction in vivo and is regulated by many factors. Recently, the findings on high expression of fibroblast growth factor-16 (FGF16) in brown adipose tissue have led to an interest in exploring its role in lipogenesis and lipid metabolism. The study cloned the goat’s FGF16 gene 624 bp long, including the complete open reading frame that encodes 207 amino acids. We found that FGF16 expression is highest in goat kidneys and hearts, followed by subcutaneous fat and triceps. Moreover, the expression of FGF16 reached its peak on the 2nd day of adipocyte differentiation (P < 0.01) and then decreased significantly. We used overexpression and interference to study the function of FGF16 gene in goat intramuscular preadipocytes. Silencing of FGF16 decreased adipocytes lipid droplet aggregation and triglyceride synthesis. This is in contrast to the situation where FGF16 is overexpressed. Furthermore, knockdown of FGF16 also caused down-regulated expression of genes associated with adipocyte differentiation including CCAAT enhancer-binding protein beta (P < 0.01), fatty acid-binding protein-2 (P < 0.01) and sterol regulatory element binding protein-1 (P < 0.05), but the preadipocyte factor-1 was up-regulated. At the same time, the genes adipose triglyceride lipase (P < 0.01) and hormone-sensitive lipase (P < 0.05) associated with triglyceride breakdown were highly expressed. Next, we locked the fibroblast growth factor receptor-4 (FGFR4) through the protein interaction network and interfering with FGF16 to significantly reduce FGFR4 expression. It was found that the expression profile of FGFR4 in adipocyte differentiation was highly similar to that of FGF16. Overexpression and interference methods confirmed that FGFR4 and FGF16 have the same promoting function in adipocyte differentiation. Finally, using co-transfection technology, pc-FGF16 and siRNA-FGFR4, siRNA2-FGF16 and siRNA-FGFR4 were combined to treat adipocytes separately. It was found that in the case of overexpression of FGF16, cell lipid secretion and triglyceride synthesis showed a trend of first increase and then decrease with increasing interference concentration. In the case of interference with FGF16, lipid secretion and triglyceride synthesis showed a downward trend with the increase of interference concentration. These findings illustrated that FGF16 mediates adipocyte differentiation via receptor FGFR4 expression and contributed to further study of the functional role of FGF16 in goat fat formation.
Surface waves called meniscus waves often appear in systems that are close to the capillary length scale. Since the meniscus shape determines the form of the meniscus waves, the resulting streaming circulation has features distinct from those caused by other capillary–gravity waves recently reported in the literature. In the present study, we produce symmetric and antisymmetric meniscus shapes by controlling boundary wettability and excite meniscus waves by oscillating the meniscus vertically. The symmetric and antisymmetric configurations produce different surface capillary–gravity wave modes and streaming flow structures. The root-mean-square speed of the streaming circulation increases with the second power of the forcing amplitude in both configurations. The flow symmetry of streaming circulation is retained under the symmetric meniscus, while it is lost under the antisymmetric meniscus. The streaming circulation pattern beneath the meniscus observed in our experiments is qualitatively explained using the method introduced by Nicolás & Vega (Fluid Dyn. Res., vol. 32 (4), 2003, pp. 119–139) and Gordillo & Mujica (J. Fluid Mech., vol. 754, 2014, pp. 590–604).
To assess healthy-related quality of life and psychosocial adjustment in children with newly diagnosed cancer and their parents immediately and 6 months after diagnosis and treatment of cancer.
A prospective, case control study was conducted on eighty-nine children with newly diagnosed cancer, aged between 6 months to 16.7 years (mean, 8.2 years), and ninety healthy children of matched age group and social background. The children were assessed with the Child Behavior Checklist (CBCL), and the Parenting Stress Index (PSI) and the SF-36 questionnaire were administered to their parents immediately after diagnosis of cancer, 3 months after chemotherapy, and 6 months after chemotherapy.
No matter at the period immediately after diagnosis of cancer, 3 months or 6 months after starting chemotherapy, the parents of children with cancer scored significantly worse on every domains of SF-36 except body pain and every subscales of PSI except distractibility/hyperactivity and attachment when compared with the control group. The cancer group scored consistently lower on all CBCL syndrome scales than the control group, with anxiety, depression and body pain being significantly different. After starting chemotherapy, the parents reported improved scores on quality of life and decreasing parenting stress in both parent and child domains since 3 months or 6 months after starting chemotherapy.
Considerable distress was experienced by both children with newly diagnosed cancer and their parents during the period immediately after diagnosis. However, parents can adjust gradually since 3 months after starting chemotherapy and experience improved quality of life.
The purpose of this study was to predict quality of life (QoL) and associated factors in patients with chronic mental illness (CMI) in Kaohsiung, Taiwan.
Patients (N = 2,023; 52.9% male, 47.1% female) were recruited using cross-sectional and convenience sampling. Structured questionnaires, including a living conditions questionnaire, a psychotic symptom assessment scale, the Caregiver Burden Scale, the 5-item Brief Symptom Rating Scale (BSRS-5), and the Medical Outcomes Study Short Form-12 (MOS SF-12) were used to collect data.
Single-factor analyses showed that those who were single, employed, and younger had better QoL. Additionally, patients who had fewer psychological problems and lower levels of psychological distress reported better QoL. Current psychotic symptoms, especially positive symptoms, were negatively correlated with QoL. For disease factors, schizophrenic patients and hospitalized patients reported better QoL than both bipolar patients and community patients. For family factors, caregiver's attitude and caregiver's burden were negatively correlated with QoL. For social factors, unstable housing and community social dysfunction were negatively correlated with QoL. The results showed that all four dimensions (social, family, disease and personal factors) were significant predictors of the mental component summary (MCS) and physical component summary (PCS) dimensions of QoL.
Personal factors and disease factors were the most important predictors of QoL in CMI patients of this sample. Family factors were more important than social factors in the MCS dimension, but social factors were more important than family factors in the PCS dimension.
Efficacy of conventional repetitive transcranial magnetic stimulation (rTMS) in major depressive disorder (MDD) is limited. The authors report here on an alternative treatment using low energy synchronized TMS (sTMS) at the intrinsic frequency of subjects’ alpha electroencephalogram (EEG).
Establish efficacy and safety profile of sTMS in MDD.
(1) Examine the clinical effectiveness of sTMS.
(2) Identify adverse effects associated with sTMS.
Fifty-two MDD subjects with 17-item Hamilton Depression Rating Scale (HAMD17) scores >17 were enrolled into a randomized, sham controlled, double-blind trial. Current medication remained unchanged during the trial. Depressive symptoms were evaluated by HAMD17 administered weekly.
EEGs were recorded at baseline to determine the stimulus frequency and at week 4 to evaluate the physiological effect. sTMS was delivered through three 6000-G cylindrical neodymium magnets synchronously rotating at a rate equal to the subject's intrinsic alpha frequency.
Forty-five subjects completed at least 1 week of treatment and were evaluable. Those who received active treatment had superior clinical response to sham (t = 2.54, P = 0.01), where 55.2% in the active treatment group were clinical responders versus 12.5% in sham (X2 = 7.82, P = 0.005). No significant side effects were reported. The clinical improvement was correlated with the degree of EEG improvement (r = .46, P = 0.009).
A therapeutic effect in MDD subjects can be achieved through administration of sTMS at the subject's alpha EEG frequency. Because of minimal side effects, this appears to be a safe and effective treatment option.
The presence of comorbid anxiety disorders (AD) and bipolar II disorders (BP-II) compounds disability complicates treatment, worsens prognosis, and has been understudied. The genes involved in metabolizing dopamine and encoding dopamine receptors, such as aldehyde dehydrogenase 2 (ALDH2) and dopamine D2 receptor (DRD2) genes, may be important to the pathogenesis of BP-II comorbid with AD. We aimed to clarify ALDH2 and DRD2 genes for predisposition to BP-II comorbid with and without AD. The sample consisted of 335 subjects BP-II without AD, 127 subjects BP-II with AD and 348 healthy subjects as normal control. The genotypes of the ALDH2 and DRD2 Taq-IA polymorphisms were determined using polymerase chain reactions plus restriction fragment length polymorphism analysis. Logistic regression analysis showed a statistically significant association between DRD2 Taq-I A1/A2 genotype and BP-II with AD (OR = 2.231, P = 0.021). Moreover, a significant interaction of the DRD2 Taq-I A1/A1 and the ALDH2*1*1 genotypes in BP-II without AD was revealed (OR = 5.623, P = 0.001) compared with normal control. Our findings support the hypothesis that a unique genetic distinction between BP-II with and without AD, and suggest a novel association between DRD2 Taq-I A1/A2 genotype and BP-II with AD. Our study also provides further evidence that the ALDH2 and DRD2 genes interact in BP-II, particularly BP-II without AD.
To demonstrate whether the communication between two SD rats base on the similar genetic basis or the same living environment, who separated (including visual, auditory, tactile, olfactory and tasting inputs)from each other, occurs.
One SD rat (RECEIVER) was examined by EEG spectral analysis and ECG analysis under anesthesia while the other SD rat (SENDER) received optimal stimuli or malignant stimuli. The course was conducted in the shielded and the unshielded. Compare the EEG and ECG of RECEIVER between the stimulation state and resting state of SENDER.
This study show no significant difference in EEG (index: percentile weight and average weight of EEG on frontal lobe, temporal lobe, hippocampus of each frequency band) and ECG (index: R, PR segment, ST segment, QRS segment, QT segment) of RECEIVER during the time that the SENDER suffered from malignant stimulation, experienced optimal stimulation and of resting state.
The communication of SD rats, not through common five sense organ may not exist, even though the same genetic basis or the common living surrounding.The optimal stimuli and the malignant stimuli of SENDER cannot influence the EEG of Frontal lobe, temporal lobe, hippocampus and ECG on RECEIVER. There is no sufficient evidence for the existence of this communication of animal.
Patients with chronic kidney disease (CKD) have more cognitive impairments. However, the etiologies are not fully clear. Plasma homocysteine levels and vascular burden rise in CKD; meanwhile, high homocysteine levels and vascular factors are known risk factors of dementia in non-CKD patients. Thus, we aimed to investigate the association between homocysteine, vascular burden and cognitive impairment in CKD and to see if the effect of elevated homocysteine on cognitive impairment mediated by vascular factor.
146 patients with CKD and 69 normal comparisons were recruited. Cognitive function was evaluated by comprehensive neuropsychological tests assessing processing speed, executive function, language, visuospatial function, memory, and attention domains. Vascular burden was assessed by Framinghan cardiovascular risk scale (FCRS) which indicates risk of atherosclerotic diseases including stroke.
In controlled analysis, patients with CKD had lower scores in all cognitive domains, and had higher homocysteine levels (18.5±6.4 vs. 9.8±2.9, p< 0.0001) and FCRS(17.0±4.7 vs. 14.0±4.7, p< 0.0001). Among patients with CKD, higher homocysteine levels (p=0.026) were associated with lower score on digit symbol task which is related to processing speed and executive function with controlling for age, sex, education and stage of CKD. The association persisted (p=0.047) after controlling for vascular risks.
Patients with CKD had extensive cognitive impairments. Elevated homocysteine levels may be an risk factor, which is independent of vascular burden, of cognitive impairment on processing speed and executive function. Further studies to investigate if normalization of homocysteine can improve cognitive function will be suggested.
Increasing evidence supports that 5HTTLPR polymorphism of the serotonin transporter gene(5HTTLPR) might associate to bipolar disorder and affective temperaments as measured by TEMPS-A. But the results are discrepant, furthermore, there are no data from Chinese population.
The present study was designed to investigate association between 5HTTLPR and bipolar disorder and affective temperaments of patients with bipolar disorder in the specific Chinese population and add new evidence to the field.
There hundred and five patients with bipolar disorder and 272 normal controls were included in the present case-control study⌧Temperament Evaluation of Memphis, Pisa, Paris and San Diego -autoquestionnaire version (TEMPS-A) in Chinese was used to assess affective temperament. Chi-square test, T test, Nonparametric test and ANOVA were employed to explore association between 5HTTLPR polymorphism and bipolar disorder and affective temperament of patients with bipolar disorder.
5-HTTLPR L/S polymorphism was associated with bipolar disorder in female (genotype χ2 = 6.769⌧P = 0.034⌧allele χ2 = 6.028⌧P = 0.014) and the S allele was associated with anxious temperament (t = 8.248⌧P = 0.005) in patients with bipolar disorder. the LA allele of 5-HTTLPR rs25531 A/G polymorphism was associated with hyperthymic temperament in patients with bipolar disorder (Z = −2.205⌧P = 0.027).
5-HTTLPR might have an effect on the prevalence of bipolar disorder in female and regulate affective temperaments of patients with bipolar disorder in some degree in Chinese population.
Bioinformatic investigations indicate that has-mir-206 (microRNA-206, miRNA-206) could regulate BDNF protein synthesis by interfering with BDNF mRNA translation, which is disrupted in bipolar disorder (BPD).
This study is to investigate whether miRNA-206 gene variants were associated with BPD susceptibility in a Han Chinese population.
342 patients who met DSM-IV criteria for bipolar disorder type I (BPD-I) or type II (BPD-II) and 386 matched health controls were enrolled into this study. the miRNA-206 gene and +/-500bp were selected for gene sequencing. for the case-control genetic comparisons, differences in the genotype and allele distributions between patients and controls were examined using Pearson's χ2 test.
Gene sequencing showed that there are two polymorphisms rs16882131(C/T) and rs62408583 (A/C) located at the upstream of miRNA-206 gene, which are complete linkage disequilibrium. the association analysis showed that there was no significant difference for genotype frequencies (χ2 = 2.075, df = 2, P = 0.354) or for allele frequencies (χ2 = 0.041, df = 1, P = 0.839) between BPD patients and controls. Similarly, no significant difference was found between BPD-I patients and controls (genotype χ2 = 1.411, df = 2, P = 0.494; allele χ2 = 0.380, df = 1, P = 0.538). However, there was significant difference between BPD-II patients and controls (genotype χ2 = 7.933, df = 2, P = 0.019; allele χ2 = 5.403, df = 1, P = 0.020).
Our findings do not support that BPD susceptibility was associated with miRNA-206 gene polymorphisms in the studied Han Chinese population. the association between miRNA-206 gene polymorphisms and bipolar disorder type II is needed to be carefully interpreted. Further studies are necessary to elucidate the involvement miRNA-206 in the pathophysiology of BPD.
Increasing evidence indicates that major depressive disorder (MDD) is associated with cognitive as well as mood disturbances.
To evaluate cognitive function and white matter structure, resting-state brain function in first-episode, treatmentnaive patients with MDD.
To explore brain structure and function mechanisms of cognitive impairment in MDD.
46 Han Chinese MDD patients aged 18–45 year and 46 controls were assessed by a series of validated test procedures.Then, 30 patients and 30 controls were obtained by MRI scan.White matter abnormalities evaluated using diffusion tensor imaging (DTI) were analyzed using tract based spatial statistics (TBSS) and resting-state brain function was evaluated using regional homogeneity (ReHo) analysis.
Cognitive impairment in patients with MDD was demonstrated by reduced accuracy in the Wisconsin Card Sorting test (WSCT) and to a lesser extent the Continuous Performance test (CPT) and Trail Making tests (TMT). White matter abnormalities found in the left cerebellum, and resting-state abnormalities present in the left inferior parietal gyrus, left anterior cingulate nucleus and left hippocampal gyrus were associated with impaired performance in the WSCT and CPT tests. We also showed that poor WSCT performance was associated with increased interconnectivity between the left ventral anterior cingulate nucleus and the medial frontal lobe areas.
The present study indicates cognitive disturbances in patients with MDD are associated with white matter and resting-state changes and altered interconnections in specific brain areas.
The association between gray matter and cognitive dysfunction in young major depression remains unclear.
To investigate the brain gray matter and the correlation with cognitive function in first-episode, treatment-naive patients with major depressive disorder (MDD).
To explore brain structural pathological mechanisms of cognitive impairment in MDD.
46 MDD aged 18-45 year and 46 controls were assessed by Wisconsin Card Sorting Test (WCST) and Trail making test (TMT). Then, 30 patients and 30 controls were obtained by MRI scan.
The total number of errors, number of preservative errors, random errors of WSCT in MDD were significantly more than that in controls, and the completion time in the TMT-A and TMT-B was longer than that in controls. MDD showed significant less gray matter volumns than controls in frontal lobe (right precentral gyrus, bilateral superior frontal gyrus and right middle frontal gyrus), parietal lobe (left postcentral gyrus, left paracentral lobule, and bilateral precuneus), temporal lobe (right superior temporal gyrus), and occipital lobe (left superior occipital gyrus). There was a significant negative correlation between left postcentral gyrus and left superior occipital gyrus gray matter density and the TMT-B completion time (r=-0.462, P=0.017; r=-0.448, P=0.022).
The first-episode MDD patient exhibiteded cognitive impairment and showed significant lower gray matter density than controls in frontal lobe, parietal lobe, temporal lobe, occipital lobe. Decreased gray matter density in left postcentral gyrus and left superior occipital gyrus may be involved in the executive dysfunction.
Antipsychotic drugs (APDs) are the first-line pharmacological treatments for schizophrenia. Recent human studies have found that myelin integrity could be improved by APD treatment in schizophrenia patients. Previous studies indicated that regulation of oligodendrocyte development and function may be a novel target for APDs.
The aim of this current study was to examine the possible effects of the antipsychotic drugs (APDs) haloperidol (HAL), olanzapine (OLA), and quetiapine (QUE) on the development of oligodendroglial lineage cells.
CG4 cells, an oligodendrocyte progenitor cell line, were treated with various concentrations of HAL, OLA, or QUE for specific periods. The proliferation and differentiation of the CG4 cells were measured. The regulation of CG4 cell differentiation by oligodendrocyte lineage transcription factors 1 and 2 (Olig1 and Olig2) was examined.
The APDs used in this study had no effect on the proliferation of CG4 cells. The APDs elevated the expression of 2’,3’-cyclic nucleotide 3’-phosphodiesterase (CNP), a specific marker of oligodendrocytes, and promoted the CG4 cells to differentiate into CNP positive oligodendrocytes. QUE and OLA increased the expression of Olig1 and Olig2 whereas HAL only increased the expression of Olig2.
Our findings suggest that oligodendrocyte development is a target of HAL, OLA, and QUE and provide further evidence of the important role of oligodendrocytes in the pathophysiology and treatment of schizophrenia. They also indicate that the expression level of oligodendrocyte/myelinrelated genes could be profoundly affected by APDs.
To explore the feature of functional connectivity of default mode network (DMN), central-executive network(CEN), and salience network (SN) in patients with schizophrenia during a resting state by functional magnetic resonance imaging (fMRI).
The SPM8, DPARSFA, conn, REST softwares combined with data-driven region of interest analysis were used to compare the functional connectivity (FC) of the DMN, CEN, and SN in 74 patients with schizophrenia(SZ) and 79 age- and gender-matched normal controls(NC). Medial prefrontal cortex(MPFC)was selected as seed region for identifying DMN and CEN; right anterior insula(rAI) for SN.
Compared with NC, SZ showed increased FC with bilateral dorsolateral prefrontal cortex(DLPFC) and bilateral putamen of the MPFC, and increased FC with left middle frontal cortex and precuneus/ posterior cingulate cortex(Pcu/PCC) of the rAI. SZ also showed enhanced interconnectivity strengths of CEN-DMN, CEN-SN, and DMN-SN(p>0.05). Correlation analyses showed that the increased FC between MPFC and left DLPFC significantly negatively correlated with PANSS-negative symptoms(r=-0.224,p=0.030) and increased FC between rAI and Pcu/PCC significantly correlated with PANSS-positve symptoms (r=0.243,p=0.020).
This study provides evidence for resting state functional abnormalities of DMN, CEN, and SN in schizophrenia patients. These aberrant functional connectivities in some key brain regions of the three network could be responsible for the schizophrenic symptoms.
In this study, we aimed to identify protein molecules in the hypothalamus in the female rats injected exogenous androgen before sexual differentiation.
Neonatal female SD rats were randomly divided into two groups: experimental group and control female group. Four neonatal male SD rats were control male group. All animals were subjected to intraperitoneal injection of testosterone propionate as experimental group or aseptic oil as control. The rats were sacrificed 90 days after the injection and the brains were collected. 2-DE were performed in order to establish profiles of proteome from rat hypothalamus and followed by MALDITOF- TOF mass spectrometry was used to identify proteins differentially expressed in rat hypothalamus from experimental group as compared to normal control group.
11 differential spots were cut off from the Silver stained gel, and 9 of the spots were identified, which were Dihydropyrimidinase-like 3 (DPYSL3), heterogeneous nuclear ribonucleoprotein K(hnRNP K), Profilin2, Triosephosphate isomerase 1(Tpi 1), Carbonic anhydrase II(CA II), Annexin A3, Protein disulfide isomerase associated 3 (PDIA3), Creatine kinase-B and Secernin 1.
The results of the present study indicate that the development of sexual differentiation may be associated with the alteration in the expression of a large number of cytosolic proteins in the hypothalamus.