Associations among serum markers of inflammation, life stress and suicide risk in patients with major depressive disorder.

BACKGROUND: Patients with major depressive disorder (MDD) are at high risk for suicide. As the worst outcome of MDD and common self-concealment in patients with suicide risk, studies of biomarkers may provide useful tools for suicide prevention and treatment. METHODS: This study recruited 168 patients with MDD from the Objective Diagnostic Markers and Personalized Intervention in MDD patients (ODMPIM), including 50 patients with suicide risk. Based on previous evidence and hypothesis, 23 targeted serum biomarkers involving immune-inflammation, neurotrophins, hypothalamic-pituitary-adrenal (HPA) axis and metabolism, were measured. We used path analysis and principal components analysis (PCA) to clarify the associations among serum biomarkers, childhood adversities, adulthood life events, severity of depression and suicide risk. RESULTS: We identified that patients with suicide risk had a higher level of inflammatory markers in serum than patients without suicide risk (P < 0.001), especially chemokine (C-X-C motif) ligand 1 (CXCL-1). After using the Bonferroni correction, there were no differences in biomarkers related to neurotrophins, HPA-axis and metabolism. In addition, a higher proportion of patients with suicide risk had adulthood adversity (assessed by Life Events Scale) (P = 0.003). Intriguingly, path analysis demonstrated that the association between adulthood adversity and suicide risk mainly depended on severity of depression and inflammatory index. CONCLUSION: This study highlights the possible role of inflammation involved in suicide risk of MDD patients. Inflammatory markers have the potential for early identification and then reducing suicidal behaviors or becoming novel treatment targets in suicide risk management.

Circular RNAs in early brain development and their influence and clinical significance in neuropsychiatric disorders.

Neuropsychiatric disorders represent a set of severe and complex mental illnesses, and the exact etiologies of which are unknown. It has been well documented that impairments in the early development of the brain contribute to the pathogenesis of many neuropsychiatric disorders. Currently, the diagnosis of neuropsychiatric disorders largely relies on subjective cognitive assessment, because there are no widely accepted biochemical or genetic biomarkers for diagnosing mental illness. Circular RNAs (circRNAs) are a novel class of endogenous non-coding RNA (ncRNA) with a closed-loop structure. In recent years, there have been tremendous advances in our understanding of the expression profiles and biological roles of circRNAs. In the brain, circRNAs are particularly enriched and are expressed more abundantly in contrast to linear counterpart transcripts. They are highly active at neuronal synapses. These features make circRNAs uniquely crucial for understanding brain health, disease, and neuropsychiatric disorders. This review focuses on the role of circRNAs in early brain development and other brain-related processes that have been associated with the development of neuropsychiatric disorders. In addition, we discuss the potential for blood or cerebrospinal fluid circRNAs to be used as novel biomarkers in the early diagnosis of neuropsychiatric disorders. The findings reviewed here may provide new insight into the pathological mechanisms underlying the onset and progression of neuropsychiatric disorders.

Nonspecific Effect of Stress on Brain Gray Matter Volume in Drug-naive Female Patients with First Depressive Episode.

BACKGROUND: This study aimed to observe the differences in brain gray matter volume in drug-naive female patients after the first episode of major depression with and without stressful life events (SLEs) before the onset of depression. METHODS: Forty-three drug-naive female patients voluntarily participated in the present study after the first major depressive episode. The life event scale was used to evaluate the severity of the impact of SLEs during 6 months before the onset of the major depressive episode. High-field magnetic resonance imaging (MRI) scans were obtained, and the VBM and SPM8 software process were used to process and analyze the MRI. RESULTS: Compared to that in patients without SLEs, the volume of brain gray matter was lower in the bilateral temporal lobe, right occipital lobe, and right limbic lobe in the SLE group. However, the gray matter volume did not differ significantly between the two groups after the application of false discovery rate (FDR) correction. CONCLUSIONS: Although the results of the present study suggest the absence of significant differences in brain gray matter volume between female drug-naive patients after the first episode of major depression with and without SLEs after FDR correction, the study provides useful information for exploring the definitive role of stress in the onset of depression.

[The effect of bone marrow mesenchymal stem cell transplantation on hypoxic pulmonary hypertension in rats].

OBJECTIVE: To study the influence of bone marrow mesenchymal stem cells (MSCs) transplantation on hypoxic pulmonary hypertension (HPH) in rats. METHODS: SD rats MSCs were separated, cultivated, identified and labeled by the green fluorescence protein (GFP) gene virus and transplanted in vitro. Healthy male SD rats were randomly divided into four groups: Normal control group (NC group) and HPH group (eight rats respectively), HPH+ MSCs transplantation group and HPH+ VEGF+ MSCs transplantation group (twenty-four respectively). The test employed atmospheric intermittent low oxygen method to establish the rat model of pulmonary hypertension and stem cells were transferred and transplanted. The rats' mean pulmonary artery pressure (mPAP) was observed; right ventricular hypertrophy index (RVHI) was calculated; the morphological change of lung small artery in various groups of rats was observed under the microscope; the distribution of lung small artery and adenovirus transfection fluorescently labeled MSCs was observed under a fluorescent microscope after 7, 14 and 28 days when stem cell was transplanted. RESULTS: For NC group, the mPAP (mmHg) was 15.5 +/- 1.5 after twenty-eight days while the mPAPs for HPH , MSCs and MSCs+ VEGF were 26.1 +/- 1.9, 21.6 +/- 2.7 and 20.1 +/- 2.9 respectively which were apparently higher than that of NC group (P < 0.01) and compared with HPH group (P < 0.01), which declined clearly. There was no significant difference between MSCs and MSCs+ VEGF. After twenty-eight days, RVHI for NC group was 0.28 +/- 0.02 while the RVHI for HPH, MSCs and MSCs + VEGF were 0.43 +/- 0.07, 0.34 +/- 0.03 and 0.35 +/- 0.01 respectively which was apparently higher than that of NC group (P < 0.01) but which was clearly lower than that of MSCs and MSCs+ VEGF (P < 0.05) and there was no significant difference between MSCs and MSCs + VEGF. For HPH group, pulmonary arteriole wall became apparently thicker, the lumen became significantly narrow and nearly obstructed after twenty-eight days, the endothelial cells were incomplete; compared with HPH group, pulmonary arteriole wall of MSCs group became thin, the lumen was smooth and the completeness of endothelial cells was improved. Whereas for MSCs and MSCs + VEGF, these changes were not significantly clear. CONCLUSION: After MSCs transplantation, mPAP and RVHI decline sharply and lung small artery remodeling is improved which partially reverses HPH process; there is no significant difference between VEGF together with MSCs transplantation group and pure MSCs.

Pressure necrosis of septal cartilage associated with bilateral extended spreader grafts in rhinoplasty.

OBJECTIVE: To investigate septal cartilage compressive changes as a result of bilateral extended spreader grafts (ESGs), which are commonly used in rhinoplasty. The buckling, rupturing, or necrosis of the recipient site leads to nasal tip structural deformity. These pathologic changes associated with bilateral ESGs warrant the clinician's attention and in-depth basic and clinical research. METHODS: The basic experimental study involves New Zealand rabbits, randomly assigned to groups A, B, C, and D, with group A as a reference. The right auricular cartilage was harvested and transplanted into a corresponding anatomic location of the left ear. The compressive effect was studied by gross observation and microscopic examination with hematoxylin-eosin staining after 3 months. In a clinical experiment, revision rhinoplasty surgical procedures were performed in 10 human patients 6 months to 1 year after placement of bilateral ESGs. The compressive changes of septal cartilages between the ESGs were observed intraoperatively. RESULTS: In group A of the rabbits, no pathologic change was noted, but 2 cases of attenuation were observed in group B (33.3%), 6 cases of central fracture (100%) with 1 case of perforation (16.7%) in group C, and 6 cases of different degrees of defects in group D (100%). Clinical intraoperative observations revealed 1 case of defects and necrosis (10%), 4 cases of attenuations and cracks (40%), and 5 cases of attenuations (50%). CONCLUSIONS: Septal cartilage compressive necrosis leading to structural damage by bilateral septal ESGs is a clinically significant complication of rhinoplasty. Owing to its affect on the viability of the original septal cartilages, we believe the unilateral ESG with columellar strut is preferred, especially in Asian patients.

[Genome-wide search for linkage to attention deficit hyperactivity disorder (ADHD) on the X chromosome].

Attention deficit hyperactivity disorder (ADHD) is the most common childhood-onset behavioral. Boys are more often affected than girls. Family, twin and adoption studies have supported a strong genetic basis. The etiology of this disorder is not clear. Molecular genetic and pharmacological studies suggest the involvement of dopaminergic and noradrenergic neurotransmitter systems in ADHD, e.g , Several reports have found association between ADHD and the dopamine receptor gene DRD-4.the dopamine transporter gene DAT1, and the catechol-o-methyltransferase. Our previous studies showed an association between ADHD and the DXS7 locus, which is located in closely linked to the MAO gene, and MAOA gene on chromosome X. To test this hypothesis, we used the genome scan for a predisposing locus on chromosome X to ADHD. We used the tramsmission/disequilibrium test (TDT) to test for linkage between a VNTR polymorphism at the 48 markers of chromosome X and DSM-III-R oliagnosed ADHD in 84 nuclear families of the Chinese population. The TDT analysis revealed linkage between ADHD and the DXS1214(TDT: Chi2=18.1, df=7, P<0.01), DXS8102(TDT: Chi2=7.9, df=3, P<0.05), DXS1068(TDT: Chi2=21.9, df=9, P<0.01), DXS8015(TDT: Chi2=14.6, df=7, P<0.05), DXS1059(TDT: Chi2=27.8, df=10, P<0.01) and DXS8088(TDT: Chi2=20.4, df=3, P<0.01).The data showed that susceptibility loci might reside in chromosome Xp11.4-Xp21 and Xq23 for ADHD.