Postpartum quality of life and mental health in women with heart disease: Integrated clinical communication and treatment.

BACKGROUND: Postpartum quality of life (QoL) in women with heart disease has been neglected. AIM: To improve clinical communication and treatment, we integrated medical data and subjective characteristics to study postpartum QoL concerns. METHODS: The study assessed QoL 6 wk after birth using the 12-Item Short-Form Health Survey. The Edinburgh Postnatal Depression Scale, Cardiac Anxiety Questionnaire, European Heart Failure Self-Care Behavior Scale, and a self-designed questionnaire based on earlier research were also used to assess patient characteristics. Patient data were collected. Prediction models were created using multiple linear regression. RESULTS: This retrospective study examined postpartum QoL in 105 cardiac patients. Postpartum QoL scores were lower (90.69 ± 13.82) than those of women without heart disease, with physical component scores (41.09 ± 9.91) lower than mental component scores (49.60 ± 14.87). Postpartum depression (33.3%), moderate anxiety (37.14%), pregnancy concerns (57.14%), offspring heart problems (57.14%), and life expectancy worries (48.6%) were all prevalent. No previous cardiac surgery, multiparity, higher sadness and cardiac anxiety, and fear of unfavorable pregnancy outcomes were strongly related to lower QoL (R2 = 0.525). CONCLUSION: Postpartum QoL is linked to physical and mental health in women with heart disease. Our study emphasizes the need for healthcare workers to recognize the unique characteristics of these women while developing and implementing comprehensive management approaches during their maternity care.

Preliminary findings on diagnostic performance of computed tomography perfusion images for intracranial arterial stenosis: a retrospective study.

OBJECTIVES: Computed tomographic perfusion (CTP) can play an auxiliary role in the selection of patients with acute ischemic stroke for endovascular treatment. However, data on CTP in non-stroke patients with intracranial arterial stenosis are scarce. We aimed to investigate images in patients with asymptomatic intracranial arterial stenosis to determine the detection accuracy and interpretation time of large/medium-artery stenosis or occlusion when combining computed tomographic angiography (CTA) and CTP images. METHODS: We retrospectively reviewed 39 patients with asymptomatic intracranial arterial stenosis from our hospital database from January 2021 to August 2023 who underwent head CTP, head CTA, and digital subtraction angiography (DSA). Head CTA images were generated from the CTP data, and the diagnostic performance for each artery was assessed. Two readers independently interpreted the CTA images before and after CTP, and the results were analyzed. RESULTS: After adding CTP maps, the accuracy (area under the curve) of diagnosing internal carotid artery (R1: 0.847 vs. 0.907, R2: 0.776 vs. 0.887), middle cerebral artery (R1: 0.934 vs. 0.933, R2: 0.927 vs. 0.981), anterior cerebral artery (R1: 0.625 vs. 0.750, R2: 0.609 vs. 0.750), vertebral artery (R1: 0.743 vs. 0.764, R2: 0.748 vs. 0.846), and posterior cerebral artery (R1: 0.390 vs. 0.575, R2: 0.390 vs. 0.585) occlusions increased for both readers (p < 0.05). Mean interpretation time (R1: 72.4 ± 6.1 s vs. 67.7 ± 6.4 s, R2: 77.7 ± 3.8 s vs. 72.6 ± 4.7 s) decreased when using a combination of both images both readers (p < 0.001). CONCLUSIONS: The addition of CTP images improved the accuracy of interpreting CTA images and reduced the interpretation time in asymptomatic intracranial arterial stenosis. These findings support the use of CTP imaging in patients with asymptomatic intracranial arterial stenosis.

Solvent-Free Ultrafast Construction of Se-Deficient Heterojunctions of Bimetallic Selenides toward Flexible Sodium-Ion Full Batteries.

Flexible quasi-solid-state sodium ion batteries featuring their low-cost, high safety and excellent mechanical strength have attracted widespread interest in the field of wearable electronic devices. However, the development of such batteries faces great challenges including the construction of interfacial compatible flexible electrode materials and addressing the high safety demands of electrolyte. Here selenium-vacancies regulated bimetallic selenide heterojunctions anchored on waste cotton cloth-derived flexible carbon cloth (FCC) with robust interfacial C-Se-Co/Fe chemical bonds as a flexible anode material (CCFSF) is proposed by ultrafast microwave pyrolysis method. Rich selenium vacancies and CoSe2 /FeSe2-x heterostructures are synchronously formed that can significantly improve ionic and electronic diffusion kinetics. Additionally, a uniform carbon layer coating on the surface of Se-deficient heterostructures endows it with outstanding structural stability. The flexible cathode (PB@FCC) is also fabricated by directly growing Prussian blue nanoparticles on the FCC. Furthermore, an advanced flexible quasi-solid-state Na-ion pouch cell is assembled by coupling CCFSF anode, PB@FCC cathode with P(VDF-HFP)-based gel polymer electrolyte. The full cell not only demonstrates excellent energy storage performance but also robust mechanical flexibility and safety. The present work offers an effective avenue to achieve high safety flexible energy storage device, promoting the development of flexible wearable electronic devices.

Revisiting the association of sudden infant death syndrome (SIDS) with polymorphisms of NHE3 and IL13.

OBJECTIVES: Disturbances of the central nervous system and immune system are thought to play a role in sudden infant death syndrome (SIDS). Dysregulated expression of sodium (Na+)/hydrogen (H+) exchanger 3 (NHE3) in the brainstem and of interleukin 13 (IL13) in the lungs has been observed in SIDS. An association of single-nucleotide polymorphisms (SNPs) in NHE3 and IL13 with SIDS has been proposed, but controversial results were reported. Therefore, there is a need to revisit the association of SNPs in NHE3 and IL13 with SIDS. METHODS: Genotyping of rs71597645 (G1131A) and rs2247114 (C2405T) in NHE3 and rs20541 (+ 4464A/G) in IL13 was performed in 201 SIDS cases and 338 controls. A meta-analysis was performed after merging our data with previously published data (all from European populations). RESULTS: Polymorphisms rs2247114 (NHE3) and rs20541 (IL13) were significantly associated with SIDS overall and in multiple subgroups, but no association was found for rs71597645 (NHE3). After combining our data with previously published data, a fixed-effect meta-analysis showed that rs2247114 in NHE3 retained a significant association with SIDS under a recessive model (OR 2.78, 95%CI 1.53 to 5.06; p = 0.0008). CONCLUSION: Our findings suggest an association of NHE3 variant rs2247114 (C2405T), though not rs71597645 (NHE3), with SIDS. A potential role of rs20541 (IL13) still has to be elucidated. Especially NHE3 seems to be an interesting topic for future SIDS research.

A 4D Proteome Investigation of the Potential Mechanisms of SA in Triggering Resistance in Kiwifruit to Pseudomonas syringae pv. actinidiae.

Kiwifruit bacterial cankers caused by Pseudomonas syringae pv. actinidiae (Psa) are a serious threat to the kiwifruit industry. Salicylic acid (SA) regulates plant defense responses and was previously found to enhance kiwifruit's resistance to Psa. However, the underlying mechanisms of this process remain unclear. In this study, we used 4D proteomics to investigate how SA enhances kiwifruit's resistance to Psa and found that both SA treatment and Psa infection induced dramatic changes in the proteomic pattern of kiwifruit. Psa infection triggered the activation of numerous resistance events, including the MAPK cascade, phenylpropanoid biosynthesis, and hormone signaling transduction. In most cases, the differential expression of a number of genes involved in the SA signaling pathway played a significant role in kiwifruit's responses to Psa. Moreover, SA treatment upregulated numerous resistance-related proteins, which functioned in defense responses to Psa, including phenylpropanoid biosynthesis, the MAPK cascade, and the upregulation of pathogenesis-related proteins. We also found that SA treatment could facilitate timely defense responses to Psa infection and enhance the activation of defense responses that were downregulated in kiwifruit during infection with Psa. Thus, our research deciphered the potential mechanisms of SA in promoting Psa resistance in kiwifruit and can provide a basis for the use of SA to enhance kiwifruit resistance and effectively control the occurrence of kiwifruit bacterial cankers.

A systematic review of tea pigments: Prevention of major diseases, protection of organs, and potential mechanisms and applications.

With the growing awareness of a healthy life, tea pigments (TPGs) are in focus for their health benefits. TPGs not only provide specific color to tea liquor but also possess health benefits such as anti-obesity, anti-tumor, anti-inflammatory, anti-viral, anti-oxidative, and bacteriostatic properties. Also, TPGs can benefit bone, liver, kidney, cardiovascular, gut microbiome, and sleep health. Based on previous reports, this review provides a brief introduction to the health benefits of TPGs, focusing on the prevention of human diseases and the protection of organs. Also, the latest research on the functional mechanism(s), practical application, and development strategies of TPGs is discussed.

Single-cell transcriptomic analysis reveals a systemic immune dysregulation in COVID-19-associated pediatric encephalopathy.

Unraveling the molecular mechanisms for COVID-19-associated encephalopathy and its immunopathology is crucial for developing effective treatments. Here, we utilized single-cell transcriptomic analysis and integrated clinical observations and laboratory examination to dissect the host immune responses and reveal pathological mechanisms in COVID-19-associated pediatric encephalopathy. We found that lymphopenia was a prominent characteristic of immune perturbation in COVID-19 patients with encephalopathy, especially those with acute necrotizing encephalopathy (AE). This was characterized a marked reduction of various lymphocytes (e.g., CD8+ T and CD4+ T cells) and significant increases in other inflammatory cells (e.g., monocytes). Further analysis revealed activation of multiple cell apoptosis pathways (e.g., granzyme/perforin-, FAS- and TNF-induced apoptosis) may be responsible for lymphopenia. A systemic S100A12 upregulation, primarily from classical monocytes, may have contributed to cytokine storms in patients with AE. A dysregulated type I interferon (IFN) response was observed which may have further exacerbated the S100A12-driven inflammation in patients with AE. In COVID-19 patients with AE, myeloid cells (e.g., monocytic myeloid-derived suppressor cells) were the likely contributors to immune paralysis. Finally, the immune landscape in COVID-19 patients with encephalopathy, especially for AE, were also characterized by NK and T cells with widespread exhaustion, higher cytotoxic scores and inflammatory response as well as a dysregulated B cell-mediated humoral immune response. Taken together, this comprehensive data provides a detailed resource for elucidating immunopathogenesis and will aid development of effective COVID-19-associated pediatric encephalopathy treatments, especially for those with AE.

Age-related cytokine imbalance in the thymus in sudden infant death syndrome (SIDS).

BACKGROUND: Sudden infant death syndrome (SIDS) has been considered to be triggered by a combination of underlying immune dysregulation and infections. The thymus is a crucial lymphatic organ responsible for T cell development in infancy. We hypothesized that an altered thymic immune status may be detectable by intrathymic cytokine profiling in SIDS. METHODS: 27 cytokines in protein lysates of thymus tissue and thymus weights were assessed in 26 SIDS cases and 16 infants who died of other reasons. RESULTS: Seventeen out of 27 cytokines were increased in thymic tissue of SIDS compared to controls without infections, and the most significant discrepancy was in infants younger than 20 weeks. The thymic cytokine profiles in SIDS cases were similar to those in controls with severe infection; however, the magnitude of the cytokine concentration elevation in SIDS was less pronounced, indicating sub-clinical infections in SIDS. In contrast to SIDS, intrathymic cytokine concentrations and thymus weight were increased with age in control children. CONCLUSIONS: Elevated thymic cytokine expression and thymus weight, as well as impaired age-related alterations in SIDS, may be influenced by subclinical infection, which may play a role in initiating SIDS in infants with a compromised immune response. IMPACT STATEMENT: Increased thymic weight and cytokine concentration may suggest possible subclinical infection in SIDS. Elevated thymic weight and cytokine concentration mainly in SIDS cases aged <20 weeks. Age-related impairment in the thymic weight and cytokine expression may be impaired by subclinical infection in SIDS.

Rapid, ultrasensitive and highly specific diagnosis of Mycoplasma pneumoniae by a CRISPR-based detection platform.

Mycoplasma pneumoniae (MP) is an important causative agent of morbidity and mortality among all age groups, especially among patients of extreme ages. Improved and readily available tests for accurate, sensitive and rapid diagnosis of MP infection is sorely needed. Here, we developed a CRISPR-Cas12b-based detection platform on the basis of recombinase polymerase amplification (RPA) for rapid, simple, and accurate diagnosis of MP infection, named MP-RPA-CRISPR. The RPA was employed for amplifying the community-acquired respiratory distress syndrome (CARDS) toxin gene of MP strains at the optimal reaction temperature 37°C. The resulting amplicons were decoded by the CRISPR-Cas12b-based detection platform, which was interpreted by real-time PCR system and by naked eye under blue light. The MP-RPA-CRISPR can detected down to 5 fg of genomic DNA templates of MP strains and accurately distinguish MP strains from non-MP strains without any cross-reactivity. A total of 96 bronchoalveolar lavage fluid (BALF)samples collected from patients suspected of respiratory infection were used to evaluate the clinical performance of the MP-RPA-CRISPR assay. As a result, our assay accurately diagnosed 45 MP-infected samples and 51 non-MP infected sample, and the results obtained from MP-RPA-CRISPR were consistent with microfluidic chip technology. In conclusion, our MP-RPA-CRISPR assay is a simple, rapid, portable and highly sensitive method to diagnose MP infection, which can be used as a promising tool in a variety of settings including clinical, field, and resource-limited aeras.

Rapid detection of Pseudomonas aeruginosa by recombinase polymerase amplification combined with CRISPR-Cas12a biosensing system.

Pseudomonas aeruginosa (P. aeruginosa) is an important bacterial pathogen involved in a wide range of infections and antimicrobial resistance. Rapid and reliable diagnostic methods are of vital important for early identification, treatment, and stop of P. aeruginosa infections. In this study, we developed a simple, rapid, sensitive, and specific detection platform for P. aeruginosa infection diagnosis. The method integrated recombinase polymerase amplification (RPA) technique with clustered regularly interspaced short palindromic repeat (CRISPR)-CRISPR-associated protein 12a (Cas12a) biosensing system and was termed P. aeruginosa-CRISPR-RPA assay. The P. aeruginosa-CRISPR-RPA assay was subject to optimization of reaction conditions and evaluation of sensitivity, specificity, and clinical feasibility with the serial dilutions of P. aeruginosa genomic DNA, the non-P. aeruginosa strains, and the clinical samples. As a result, the P. aeruginosa-CRISPR-RPA assay was able to complete P. aeruginosa detection within half an hour, including RPA reaction at 42°C for 20 min and CRISPR-Cas12a detection at 37°C for 10 min. The diagnostic method exhibited high sensitivity (60 fg per reaction, ~8 copies) and specificity (100%). The results of the clinical samples by P. aeruginosa-CRISPR-RPA assay were consistent to that of the initial result by microfluidic chip method. These data demonstrated that the newly developed P. aeruginosa-CRISPR-RPA assay was reliable for P. aeruginosa detection. In summary, the P. aeruginosa-CRISPR-RPA assay is a promising tool to early and rapid diagnose P. aeruginosa infection and stop its wide spread especially in the hospital settings.

Post-mortem genetic analysis of sudden unexplained death in a young cohort: a whole-exome sequencing study.

Sudden unexplained death (SUD) constitutes a considerable portion of unexpected sudden death in the young. Molecular autopsy has proved to be an efficient diagnostic tool in the multidisciplinary management of SUD. Yet, many cases remain undiagnosed using the widely adopted targeted genetic screening strategies. Here, we investigated the genetic substrates of a young SUD cohort (18-40 years old) from China using whole-exome sequencing (WES), with the primary aim to identify novel SUD susceptibility genes. Within 255 previously acknowledged SUD-associated genes, 21 variants with likely functional effects (pathogenic/likely pathogenic) were identified in 51.9% of the SUD cases. More importantly, a set of 33 candidate genes associated with myopathy were identified to be novel susceptibility genes for SUD. Comparative analysis of the cumulative PHRED-scaled CADD score and polygenetic burden score showed that the amount and deleteriousness of variants in the 255 SUD-associated genes and the 33 candidate genes identified by this study were significantly higher compared with 289 randomly selected genes. A significantly higher genetic burden of rare variants (MAF < 0.1%) in the 33 candidate genes also highlighted putative roles of these genes in SUD. After incorporating these novel genes, the genetic testing yields of the current SUD cohort elevated from 51.9 to 66.7%. Our study expands understanding of the genetic variants underlying SUD and presents insights that improve the utility of genetic screenings.

Gut Microbiota Participates in Polystyrene Microplastics-Induced Hepatic Injuries by Modulating the Gut-Liver Axis.

Dietary pollution by polystyrene microplastics (MPs) can cause hepatic injuries and microbial dysbiosis. Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, exerts beneficial effects on the liver by modulating the gut microbiota. However, the role of microbiota in MPs-induced hepatic injuries and the protective effect of EGCG have not been clarified. Here, 5 µm MPs were orally administered to mice to induce hepatic injuries. Subsequently, antibiotic cocktail (ABX) and fecal microbial transplant (FMT) experiments were performed to investigate the underlying microbial mechanisms. Additionally, EGCG was orally administered to mice to explore its protection against MPs-induced hepatic injuries. Our results showed that MPs activated systemic and hepatic inflammation, promoted fibrosis, and altered the liver metabolome; meanwhile, MPs damaged the gut homeostasis by disturbing the gut microbiome, promoting colonic inflammation, and impairing the intestinal barrier. Notably, MPs reduced the abundance of the probiotics Akkermansia, Mucispirillum, and Faecalibaculum while increasing the pathogenic Tuzzerella. Interestingly, the elimination of gut microbiota mitigated MPs-induced colonic inflammation and intestinal barrier impairment. Moreover, ABX ameliorated MPs-induced systemic and hepatic inflammation but not fibrosis. Correspondingly, microbiota from MPs-administered mice induced colonic, systemic, and hepatic inflammation, while their profibrosis effect on the liver was not observed. Finally, EGCG elevated the abundance of probiotics and effectively repressed MPs-induced colonic inflammation. MPs-induced systemic and hepatic inflammation, fibrosis, and remodeling of the liver metabolome were also attenuated by EGCG. These findings illustrated that gut microbiota contributed to MPs-induced colonic and hepatic injuries, while EGCG could serve as a potential prevention strategy for these adverse consequences.

The clinical significance of renal resistance index (RRI) and renal oxygen saturation (RrSO2) in critically ill children with AKI: a prospective cohort study.

OBJECTIVE: The purpose of this study was to look into the clinical significance of the renal resistance index (RRI) and renal oxygen saturation (RrSO2) in predicting the development of acute kidney injury (AKI) in critically ill children. A new non-invasive method for the early detection and prediction of AKI needs to develop. METHODS: Patients admitted to the pediatric intensive care unit (PICU) affiliated with the capital institute of pediatrics from December 2020 to March 2021 were enrolled consecutively. Data of clinical information, renal Doppler ultrasound, RrSO2, and hemodynamic index within 24 h of admission were prospectively collected. Patients were divided into two groups: the study group was AKI occurred within 72 h, while the control group did not. SPSS (version 25.0) was used to analyze the data, and P < 0.05 was considered a statistical difference. RESULTS: 1) A total of 66 patients were included in this study, and the incidence of AKI was 19.70% (13/66). The presence of risk factors (shock, tumor, severe infection) increased the incidence of AKI by three times. 2) Univariate analysis showed significant differences in length of hospitalization, white blood cells (WBC), C-reactive protein (CRP), renal resistance index (RRI), and ejection fraction (EF) between the study and control groups (P < 0.05). There were no significant differences in renal perfusion semi-quantitative score (P = 0.053), pulsatility index (P = 0.051), pediatric critical illness score (PCIS), and peripheral vascular resistance index (P > 0.05). 3) Receiver operating characteristic (ROC) curve showed that if RRI > 0.635, the sensitivity, specificity, and AUC for predicting AKI were 0.889, 0.552, and 0.751, respectively; if RrSO2 < 43.95%, the values were 0.615, 0.719 and 0.609, respectively; if RRI and RrSO2 were united, they were 0.889, 0.552, and 0.766, respectively. CONCLUSIONS: The incidence of AKI is high in PICU patients. And infection, RRI, and EF are risk factors for AKI in PICU patients. RRI and RrSO2 have certain clinical significance in the early prediction of AKI and may provide a new non-invasive method for early diagnosis and prediction of AKI.

Loop-mediated isothermal amplification combined with lateral flow biosensor for rapid and sensitive detection of monkeypox virus.

The ongoing outbreak of the monkeypox, caused by monkeypox virus (MPXV), has been a public health emergency of international concern, indicating an urgent need for rapid and sensitive MPXV detection. Here, we designed a diagnostic test based on loop-mediated isothermal amplification (LAMP) and nanoparticle-based lateral flow biosensor(LFB)for diagnosis of MPXV infection, termed MPX-LAMP-LFB. A set of six LAMP primers was designed based the ATI gene of MPXV, and LAMP amplification of MPXV templates was performed at 63°C for only 40 min. The results were rapidly and visually decided using the LFB test within 2 min. The MPX-LAMP-LFB assay can specifically detect MPXV strains without cross-reaction with non-MPXV pathogens. The sensitivity of the MPX-LAMP-LFB assay is as low as 5 copies/µl of plasmid template and 12.5 copies/µl of pseudovirus in human blood samples. The whole process of the MPX-LAMP-LFB assay could be completed ~1 h, including rapid template preparation (15 min), LAMP reaction (40 min)and result reporting (<2 min). Collectively, MPX-LAMP-LFB assay developed here is a useful tool for rapid and reliable diagnosis of MPXV infection.

Multi-omics analysis reveals underlying host responses in pediatric respiratory syncytial virus pneumonia.

Respiratory syncytial virus (RSV) is an important pathogen causing pneumonia in children. Few studies have used multi-omics data to investigate the pathogenies of RSV pneumonia. Here, metabolomics was first used to identify potential biomarkers for RSV diagnosis. In the training cohort, serum from 36 healthy controls (HCs), 45 RSV pneumonia children, and 32 infectious disease controls (IDCs) were recruited. After analyses, six metabolites had potential diagnostic value. Using an independent cohort of 49 subjects, two biomarkers (neuromedin N and histidyl-proline diketopiperazine) were validated. Next, multi-omics analysis were applied to analyze the pathogenies of RSV pneumonia. Accumulation of collagen in the serum of RSVs indicated that RSV infection could lead to increased levels of soluble collage. Activation of the complement system and imbalance in lipid metabolism were also observed in RSV patients. The multi-omics analysis presented here revealed the signature protein and metabolite changes in serum caused by RSV infection.

Serum-integrated omics reveal the host response landscape for severe pediatric community-acquired pneumonia.

OBJECTIVE: Community-acquired pneumonia (CAP) is the primary cause of death for children under five years of age globally. Hence, it is essential to investigate new early biomarkers and potential mechanisms involved in disease severity. METHODS: Proteomics combined with metabolomics was performed to identify biomarkers suitable for early diagnosis of severe CAP. In the training cohort, proteomics and metabolomics were performed on serum samples obtained from 20 severe CAPs (S-CAPs), 15 non-severe CAPs (NS-CAPs) and 15 healthy controls (CONs). In the verification cohort, selected biomarkers and their combinations were validated using ELISA and metabolomics in an independent cohort of 129 subjects. Finally, a combined proteomics and metabolomics analysis was performed to understand the major pathological features and reasons for severity of CAP. RESULTS: The proteomic and metabolic signature was markedly different between S-CAPs, NS-CAPs and CONs. A new serum biomarker panel including 2 proteins [C-reactive protein (CRP), lipopolysaccharide (LBP)] and 3 metabolites [Fasciculol C, PE (14:0/16:1(19Z)), PS (20:0/22:6(4Z, 7Z, 10Z, 13Z, 16Z, 19Z))] was developed to identify CAP and to distinguish severe pneumonia. Pathway analysis of changes revealed activation of the cell death pathway, a dysregulated complement system, coagulation cascade and platelet function, and the inflammatory responses as contributors to tissue damage in children with CAP. Additionally, activation of glycolysis and higher levels of nucleotides led to imbalanced deoxyribonucleotide pools contributing to the development of severe CAP. Finally, dysregulated lipid metabolism was also identified as a potential pathological mechanism for severe progression of CAP. CONCLUSION: The integrated analysis of the proteome and metabolome might open up new ways in diagnosing and uncovering the complexity of severity of CAP.

The changed endemic pattern of human adenovirus from species B to C among pediatric patients under the pressure of non-pharmaceutical interventions against COVID-19 in Beijing, China.

BACKGROUND: Under the pressure of non-pharmaceutical interventions (NPIs) targeting severe acute respiratory syndrome coronavirus 2, the prevalence of human adenovirus (HAdV) was monitored before and after NPIs launched on Jan 24, 2020 in pediatric patients in Beijing, China. METHODS: Respiratory samples collected from children hospitalized with acute respiratory infections from Jan 2015 to Dec 2021 were screened by direct immunofluorescence test or capillary electrophoresis-based multiplex PCR assay. The hexon, penton base, and fiber genes were amplified from HAdV positive specimens, then sequenced. For HAdV typing, phylogenetic trees were built by MEGA X. Then clinical data of HAdV positive cases were collected. All data were evaluated using SPSS Statistics 22.0 software. RESULTS: A total of 16,097 children were enrolled and 466 (2.89%, 466/16,097) were HAdV-positive. The positive rates of HAdV varied, ranging from 4.39% (151/3,438) in 2018 to1.25% (26/2,081) in 2021, dropped from 3.19% (428/13,408) to 1.41% (38/2,689) from before to after NPIs launched (P < 0.001). There were 350 cases typed into nine types of species B, C, or E and 34 recorded as undetermined. Among them, HAdV-B3 (51.56%, 198/384) was the most prevalent types from 2015 to 2017, and HAdV-B7 (29.17%, 112/384) co-circulated with HAdV-B3 from 2018 to 2019. After NPIs launched, HAdV-B3 and B7 decreased sharply with HAdV-B7 undetected in 2021, while HAdV-C1 became the dominant one and the undetermined were more. CONCLUSIONS: The endemic pattern of HAdV changed in Beijing because of the NPIs launched for COVID-19. Especially, the dominant types changed from HAdV-B to HAdV-C.

Clinical characteristics and outcomes of children with prolonged mechanical ventilation in PICUs in mainland China: A national survey.

OBJECTIVE: The number of children on prolonged mechanical ventilation (PMV) in pediatric intensive care units (PICU) has increased markedly, but little is known about the situation in mainland China. We carried out a multicenter retrospective investigation to describe the clinical characteristics and prognosis of Chinese children receiving long-term ventilation in the PICU. METHODS: A retrospective study was performed in 11 PICUs. All participating patients with prolonged mechanical ventilation in the study were retrospectively identified and included from cases admitted to PICUs between January 1, 2017 and December 31, 2019. RESULTS: A total of 346 children diagnosed with prolonged mechanical ventilation were included in the study. Overall, 240 survived and were discharged from PICU, 55 died in hospital, and 51 withdrew from mechanical ventilation support with 41 died after discharge. Lower airway diseases were the most common underlying causes (41.6%), followed by central nervous system diseases (29.5%), and neuromuscular diseases (13.3%). Most children (327, 94.5%) received invasive mechanical ventilation (IMV) and only 19 (5.5%) children received noninvasive ventilation (NIV). The median time of tracheostomy after ventilation was 21 days (15-35). Children with tracheostomy had lower mortality with longer PICU stay compared with patients without tracheostomy. Children who underwent tracheostomy were more likely to have central nervous system diseases and neuromuscular diseases. CONCLUSION: This study showed a steady increase in the number of children receiving prolonged mechanical ventilation during the study period in Chinese PICUs with distinct clinical characteristics and outcomes. A better community-based care for PMV children is needed in mainland China.

Pulmonary immune profiling of SIDS: impaired immune maturation and age-related cytokine imbalance.

BACKGROUND: For sudden infant death syndrome (SIDS), an impaired immunocompetence has been discussed for a long time. Cytokines and chemokines are soluble immune mediators (SIM) whose balance is essential for the immune status. We hypothesized that an imbalanced immune response might contribute to the etiology of SIDS. METHODS: We investigated 27 cytokines, chemokines, and growth factors in protein lysates of lungs derived from 29 SIDS cases and 15 control children deceased for other reasons. RESULTS: Except for the CCL5, no significant differences were detected in the lungs between SIDS cases with and without mild upper respiratory tract infections. In contrast, IL-1RA, IL-7, IL-13, and G-CSF were decreased in the merged SIDS cases compared to control cases without evidence of infection. Plotting SIM concentrations against infant age resulted in increasing concentrations in control but not in SIDS lungs, indicating a disturbed immune maturation. Moreover, an age-dependent shift towards a Th2-related pattern was observed in SIDS. CONCLUSIONS: Our findings suggest that an impaired maturation of the immune system, an insufficient response to respiratory pathogens, and an immune response modulated by Th1/Th2 imbalance might play a possible role in triggering SIDS. These findings might in part be explained by chronic stress. IMPACT: Maturation of the cytokine and chemokine network may be impaired in SIDS. An imbalance between Th1- and Th2-related cytokines, which may reflect a state of chronic stress causing a more Th2 shift. An impaired immune maturation, an insufficient response to respiratory pathogens, and an immune response modulated by Th1/Th2 imbalance might play a possible role in SIDS.

Real-time multiple cross displacement amplification assay for rapid and sensitive detection of Haemophilus influenzae.

Haemophilus influenzae is an opportunistic pathogen usually causing bacteremia, meningitis, and pneumonia in children. Here, we developed a method based on multiple cross displacement amplification (MCDA) method and real-tme fluorescence technique for rapid detection of H. influenzae. A set of 10 primers was designed for the H. influenzae real-time MCDA reaction, and a core primer was modified with a restriction endonuclease recognition sequence, a fluorescent, and a quencher according to the principle of the real-time MCDA assay. The H. influenzae real-time MCDA reactions were performed using a fluorescence instrument at 63°C for 40 min. The H. influenzae real-time MCDA assay can specifically detect H. influenzae without any cross-reaction with other bacteria as our results confirmed. The sensitivity of our assay is as low as 10 CFU per reaction. To validate its feasibility, our assay was applied to 40 DNA extracted from sputum samples. The results obtained from H. influenzae real-time MCDA were compared with that of H. influenzae-loop-mediated isothermal amplification (H. influenzae-LAMP) and MCDA-based lateral flow biosensor (MCDA-LFB). The positive rate of the real-time MCDA assay was 62.5%, which was consistent with the H. influenzae-MCDA-LFB assay, but was more sensitive than H. influenzae-LAMP (57.5%). Furthermore, the H. influenzae real-time MCDA assay takes only 40 min, which was less than that of a traditional PCR test. Taken together, the H. influenzae real-time MCDA assay reported here offers a new and valuable diagnostic tool for the reliable and rapid detection of H. influenzae.