Common and Specific Alterations of Amygdala Subregions in Major Depressive Disorder With and Without Anxiety: A Combined Structural and Resting-State Functional MRI Study.

Anxious major depressive disorder is a common subtype of major depressive disorder; however, its unique neural mechanism is not well-understood currently. Using multimodal MRI data, this study examined common and specific alterations of amygdala subregions between patients with and without anxiety. No alterations were observed in the gray matter volume or intra-region functional integration in either patient group. Compared with the controls, both patient groups showed decreased functional connectivity between the left superficial amygdala and the left putamen, and between the right superficial amygdala and the bilateral anterior cingulate cortex and medial orbitofrontal cortex, while only patients with anxiety exhibited decreased activity in the bilateral laterobasal and superficial amygdala. Moreover, the decreased activity correlated negatively with the Hamilton depression scale scores in the patients with anxiety. These findings provided insights into the pathophysiologic processes of anxious major depressive disorder and may help to develop new and effective treatment programs.

Imaging features of the initial chest thin-section CT scans from 110 patients after admission with suspected or confirmed diagnosis of COVID-19.

BACKGROUND: In December 2019, an outbreak of a novel coronavirus pneumonia, now called COVID-19, occurred in Wuhan, Hubei Province, China. COVID-19, which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has spread quickly across China and the rest of the world. This study aims to evaluate initial chest thin-section CT findings of COVID-19 patients after their admission at our hospital. METHODS: Retrospective study in a tertiary referral hospital in Anhui, China. From January 22, 2020 to February 16, 2020, 110 suspected or confirmed COVID-19 patients were examined using chest thin-section CT. Patients in group 1 (n = 51) presented with symptoms of COVID-19 according to the diagnostic criteria. Group 2 (n = 29) patients were identified as a high degree of clinical suspicion. Patients in group 3 (n = 30) presented with mild symptoms and normal chest radiographs. The characteristics, positions, and distribution of intrapulmonary lesions were analyzed. Moreover, interstitial lesions, pleural thickening and effusion, lymph node enlargement, and other CT abnormalities were reviewed. RESULTS: CT abnormalities were found only in groups 1 and 2. The segments involved were mainly distributed in the lower lobes (58.3%) and the peripheral zone (73.8%). The peripheral lesions, adjacent subpleural lesions, accounted for 51.8%. Commonly observed CT patterns were ground-glass opacification (GGO) (with or without consolidation), interlobular septal thickening, and intralobular interstitial thickening. Compared with group 1, patients in group 2 presented with smaller lesions, and all lesions were distributed in fewer lung segments. Localized pleural thickening was observed in 51.0% of group 1 patients and 48.2% of group 2 patients. The prevalence of lymph node enlargement in groups 1 and 2 combined was extremely low (1 of 80 patients), and no significant pleural effusion or pneumothorax was observed (0 of 80 patients). CONCLUSION: The common features of chest thin-section CT of COVID-19 are multiple areas of GGO, sometimes accompanied by consolidation. The lesions are mainly distributed in the lower lobes and peripheral zone, and a large proportion of peripheral lesions are accompanied by localized pleural thickening adjacent to the subpleural region.

TRB3 is elevated in psoriasis vulgaris lesions and mediates HaCaT cells proliferation in vitro.

Psoriasis is a chronic skin disease characterized by abnormal keratinocyte proliferation and differentiation, inflammation, and angiogenesis. Overexpression of tribbles homolog3 (TRB3), which belongs to the tribbles family of pseudokinases, has been found in several human tumors and metabolic diseases, but its role in psoriasis has not been fully clarified. The aim of this study is to investigate the expression of TRB3 in psoriasis and explore its roles in the proliferation of keratinocytes. Twenty-four patients with psoriasis vulgaris were recruited for the study. Diagnosis of psoriasis was based on clinical and histologic examinations. Immunohistochemistry and real-time reverse transcription PCR (RT-PCR) were performed to determine protein and messenger RNA (mRNA) expression of TRB3 in psoriasis lesions. 5-Bromo-2-deoxyUridine (BrdU) incorporation assay were performed for cell proliferation. Cell cycle distribution was assessed by flow cytometry analysis. The levels of TRB3 is elevated in psoriatic lesions compared with psoriatic non-lesions. The HaCat cells expressed the TRB3 gene. We found TRB3 silencing to significantly inhibit HaCat cell proliferation. Furthermore, the specific knockdown of TRB3 slowed down the cell cycle at the gap 0/first gap phase. In conclusion, our data suggest that TRB3 is overexpressed in lesions of patients with psoriasis and may be involved in the abnormal proliferation of keratinocytes. Therefore, TRB3 may be a potential therapeutic target for psoriasis.

Genomic comparisons between paired bacterial strains with strong and weak GC skews.

A majority of known eubacterial genomes are characteristic of GC skew, i.e., the leading strand has exceeding number of G over C. The cause of this compositional bias is still not very clear. In this study, we chose five pairs of genomes from distantly related bacterial genera, i.e., Buchnera, Haemophilus, Mycoplasma, Mycobacterium, and Synechococcus, each containing one with strong GC skew and the other with weak GC skew. Through comparison of the orthologous genes in these genera, we found that neither chromosomal rearrangement nor CDS skew has direct relationship with GC skew.

[Identification and analysis of a putative pathogenicity island Uu146-Uu170 in Ureaplasma urealyticum collected from sterile patients].

OBJECTIVE: To identify and analyze a putative pathogenicity island (PAI) Uu146-Uu170 of Ureaplasma urealyticum (Uu) and explore the relationship between PAI and infertility. METHODS: Fifty-one Uu isolates were collected from healthy females, 57 isolates from sterile females with fallopian tube disease, 42 isolates from healthy males and 38 isolates from sterile males. Biovar-typing was performed based on the gene of multiple-banded antigen (MBA). The distribution of PAI was analyzed by PCR. The association of clinical phenotype with biovar type and PAI distribution was calculated by Fisher's exact test. RESULTS: In female healthy group and female disease group, biovar type 1 account for 68.6% (35/51) and 73.7% (42/57), whereas the positive rate of PAI were 15.7% (8/51) and 12.3% (7/57) in the two groups, both difference were not statistically significant. In male healthy group and male disease group, biovar type 1 account for 71.4% (30/42) and 65.8% (25/38), whereas the positive rate of PAI were 21.4% (9/42) and 18.4% (7/38) in the two groups, both difference were not statistically significant. The positive rate of PAI in biovar type 2 was significantly higher than that in biovar type 1 in the fallopian tube disease and male infertility groups (5/15 vs 2/42, 5/13 vs 2/25, both P < 0.05) whereas no significant difference was found between two biovar types in normal groups (both P > 0.05). CONCLUSIONS: There is insufficient evidence that Uu with presence of PAI is more pathogenic to cause infertility. The Uu strain of biovar type 2 with PAI Uu146-Uu170 may be associated with infertility.