Notes

Human population seroprevalence involving SARS-CoV-2 antibodies throughout Anambra Point out, South-East, Africa.
Local and systemic inflammatory markers and pro-inflammatory cytokines are increased in children with obstructive sleep apnea syndrome (OSAS). Therefore, systemic or topical anti-inflammatory agents are used to treat this syndrome. We evaluated the treatment with systemic corticosteroids in children with severe OSAS and adenotonsillar hypertrophy before surgery.

This was an unblinded open label study. selleck chemicals Children with severe OSAS (diagnosed through polysomnography, obstructive apnea-hypopnea index [AHI] > 10eV/h) were recruited. Exclusion criteria included age < 3years, history of acute or chronic cardiorespiratory or neuromuscular or metabolic disease; major craniofacial abnormalities; and chromosomal syndromes and epilepsy. Computer-generated random numbers were used for simple randomization of subjects. All children were treated with intranasal beclomethasone spray, and 15 children additionally received oral betamethasone and 0.1mg/kg per day for 7days. Sleep clinical record (SCR) and pulsoximetry were performed before and after 7days in all children.

Among 28 children with severe OSAS mean age was4.5 ± 1.8years, AHI 20.4 ± 1.8eV/h). In children treated with intranasal and oral corticosteroids, mean (95.3 ± 1.1 vs 97.0 ± 0.8%, p = 0.0001) and minimum oxygen saturation (78.8 ± 6.3 vs 89.2 ± 4.2, p = 0.001) improved, and the SCR score (12.6 ± 1.2 vs 8.3 ± 1.1, p = 0.0001) was reduced. Children treated onlywith intranasal beclomethasone spray showed no differences in outcome measures before and after treatments. When we considered the oximetry measures, after corticosteroid treatment, we obtained statistical differences between the 2 groups (p < 0.01).

These results seem to suggest that a short course of oral betamethasone could be useful to treat children with severe OSAS and adenotonsillar hypertrophy waiting for surgery.
These results seem to suggest that a short course of oral betamethasone could be useful to treat children with severe OSAS and adenotonsillar hypertrophy waiting for surgery.
Insomnia is a common sleep disorder which has high comorbidity with a number of cardiovascular diseases (CVD). As a possible risk factor for the CVDs, arterial stiffness may be assessed non-invasively by pulse wave velocity (PWV) and augmentation index (AI). The aim of this study was to evaluate any relation between insomnia and arterial stiffness.

Patients with insomnia were included in the study after the exclusion of other sleep disorders by polysomnography. Sleep quality and the degree of insomnia symptoms were evaluated by the Pittsburgh sleep quality index (PSQI) and insomnia severity index (ISI), respectively. PWV and AI were assessed by Mobil-O-Graph arteriograph system.

Consecutive patients with insomnia (n = 72, 56 women, meanage 55.8 ± 9.1years) were included. Patients were grouped as those with severe ISI scores (22-28) and those with mild to moderate ISI scores (8-21). Despite no significant difference in characteristics and clinical data, patients with severe ISI scores had significantly higher total PSQI scores and NREM-2 with significantly lower REM duration. They also had significantly higher systolic blood pressure, mean blood pressure, pulse pressure, PWV, and AI compared to patients with mild and moderate ISI scores. Correlation analysis revealed that PWV and AI were significantly correlated with the ISI score and PSQI score.

There is a close relation between arterial stiffness and insomnia suggesting a risk for CVD in patients with insomnia.
There is a close relation between arterial stiffness and insomnia suggesting a risk for CVD in patients with insomnia.To reveal genetic risks of early-onset sporadic dilated cardiomyopathy (DCM) patients in the Chinese Han population, we enlisted 363 DCM cases and 414 healthy controls. Whole-exome sequencing and phenotypic characterization were conducted. In total, we identified 26 loss-of-function (LOF) candidates and 66 pathogenic variants from 33 genes, most of which were novel. The deleterious variants can account for 25.07% (91/363) of all patients. Furthermore, rare missense variants in 21 genes were found to be significantly associated with DCM in burden tests. Other than rare variants, twelve common SNPs were significantly associated with an increased risk of DCM in allele-based genetic model association analysis. Of note, in the cumulative risk model, high-risk subjects had a 3.113-fold higher risk of developing DCM than low-risk subjects. Also, DCM in the high-risk group had a younger age of onset than that in the low-risk group. In terms of cardiac function, the mean left ventricular ejection fraction of patients with the deleterious variants was lower than those without (27.73%±10.02% vs. 30.61%±10.85%, P=0.026). To conclude, we mapped a comprehensive atlas of genetic risks in Chinese patients with DCM that might lead to new insights into the mechanisms and risk stratification for DCM.Early human embryogenesis is a very sophisticated process due to its unique gene regulatory network. Autophagy has been suggested to play an important role in mediating the development of early embryonic cells in mammals. However, evidence showing how autophagy regulates early human embryogenesis remains to be further explored. In this study, we systematically investigated the human transcriptome and methylome patterns of autophagy-related (ATG) genes in early embryonic cells at single-cell resolution. We analyzed the transcriptomic data of 365 cells and methylome data of 265 cells. The results showed that most ATG genes remained epigenetically active and were expressed stably throughout early embryogenesis, whereas the dynamics varied among different developmental stages. This evidence indicated that the autophagy pathway was constitutively activated and exerted a fundamental role in early human embryo development. Our work, for the first time, comprehensively reveals the features of autophagy during early human embryo development.
TP53 status based on TP53 signature, a gene expression profile to determine the presence or absence of TP53 mutation, is an independent prognostic factor of breast cancer. The purpose of this study was to develop a simple diagnostic system for TP53 signature status.

We developed a multiplex reverse transcription-polymerase chain reaction system to determine TP53 status. Based on this system, prospectively collected 189 patients with stage I and II breast cancer were determined to have TP53 mutant signature or TP53 wild-type signature. The prognostic significance of the TP53 signature by the diagnostic system was analyzed.

The diagnostic accuracy of TP53 status and reproducibility of this diagnosis system was confirmed. Using the diagnostic system, 89 patients were classified as TP53 mutant signature and the remaining 100 cases were classified as TP53 wild-type signature. Recurrence-free survival (RFS) among patients with TP53 mutant signature was significantly shorter than that among those with TP53 wild-type signature.
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