OBJECTIVE: We aimed to describe the clinical features and outcome of human parechovirus (HPeV) encephalitis cases identified by the Australian Childhood Encephalitis (ACE) study. METHODS: Infants with suspected encephalitis were prospectively identified in 5 hospitals through the (ACE) study. Cases of confirmed HPeV infection had comprehensive demographic, clinical, laboratory, imaging, and outcome at discharge data reviewed by an expert panel and were categorized by using predetermined case definitions. Twelve months after discharge, neurodevelopment was assessed by using the Ages and Stages Questionnaire (ASQ). RESULTS: We identified thirteen cases of suspected encephalitis with HPeV infection between May 2013 and December 2014. Nine infants had confirmed encephalitis; median age was 13 days, including a twin pair. All had HPeV detected in cerebrospinal fluid with absent pleocytosis. Most were girls (7), admitted to ICU (8), and had seizures (8). Many were born preterm (5). Seven patients had white matter diffusion restriction on MRI; 3 with normal cranial ultrasounds. At discharge, 3 of 9 were assessed to have sequelae; however, at 12 months’ follow-up, by using the ASQ, 5 of 8 infants showed neurodevelopmental sequelae: 3 severe (2 cerebral palsy, 1 central visual impairment). A further 2 showed concern in gross motor development. CONCLUSIONS: Children with HPeV encephalitis were predominantly young, female infants with seizures and diffusion restriction on MRI. Cranial ultrasound is inadequately sensitive. HPeV encephalitis is associated with neurodevelopmental sequelae despite reassuring short-term outcomes. Given the absent cerebrospinal fluid pleocytosis and need for specific testing, HPeV could be missed as a cause of neonatal encephalopathy and subsequent cerebral palsy.

https://pediatrics.aappublications.org/content/pediatrics/early/2016/01/19/peds.2015-2848.full.pdf

Parechovirus Encephalitis and Neurodevelopmental Outcomes.

Bronchopulmonary dysplasia (BPD) is the most common cause of morbidity and mortality in preterm infants. A key histopathological feature of BPD is stunted late lung development, where the process o...

/pdf/recent-advances-in-our-understanding-of-the-mechanisms-of-3lk66wlk8b.pdf

Recent advances in our understanding of the mechanisms of lung alveolarization and bronchopulmonary dysplasia.

Enterovirus (EV) is a common cause of infection in neonates. Neonates are at high risk of enterovirus infection with serious clinical manifestations and high lethality. This review systematically summarized the clinical characteristics of neonates with severe enteroviral infection to provide evidence for the identification and treatment of severe neonatal EV infection. PubMed, Embase, and Web of Science were searched for original studies on neonates with severe EV infections from January 1, 2000, to November 27, 2020. Two reviewers independently screened the literature, extracted the data, and performed a descriptive analysis. In total, 66 articles with 237 cases of severe neonatal enterovirus infection were included. All neonates developed severe complications. Among them, 46.0% neonates had hepatitis or coagulopathy, 37.1% had myocarditis, 11.0% had meningoencephalitis, and 5.9% had other complications such as hemophagocytic lymphohistiocytosis and pulmonary hemorrhage. The lethality rate of neonates with severe infection was 30.4%. The highest lethality rate was 38.6%, which was observed in neonates with myocarditis. In 70.5% neonates, the age at the onset of symptoms was less than 7 days. Coxsackievirus B infection was seen in 52.3% neonates. The most common symptoms included temperature abnormalities (127, 53.6%), rash (88, 37.1%), poor feeding (58, 24.5%), and respiratory symptoms (52, 21.9%). The main treatment included transfusion of empirical antibiotics (127, 53.6%), blood components (100, 42.2%), intravenous immunoglobulin (IVIG; 97, 40.9%), mechanical ventilation (51, 21.5%), and extracorporeal membrane oxygenation (ECMO; 43, 18.1%). Additionally, antiviral medications pleconaril (14, 5.9%) and pocapavir (3, 1.3%) were administered. Lethality was high in neonates with severe enterovirus infection, especially in those complicated with myocarditis. The most common symptoms included temperature abnormalities, rash, and poor feeding. The chief supportive treatment consisted of transfusion of blood components, mechanical ventilation, and ECMO. Empirical antibiotics and IVIG were widely used. Antiviral medications included pocapavir and pleconaril; however, more clinical evidence regarding their efficacy is needed.

/pdf/clinical-characteristics-of-severe-neonatal-enterovirus-2z0dp7ehdd.pdf

Clinical characteristics of severe neonatal enterovirus infection: a systematic review

Pyroptosis is a relatively newly discovered programmed cell death accompanied by an inflammatory response. In the classical view, pyroptosis is mediated by caspases-1,-4,-5,-11 and executed by GSDMD, however, recently it was demonstrated that caspase-3 and-8 also participate in the process of pyroptosis, by cleaving GSDMD/E and GSDMD respectively. Different from autophagy and apoptosis, many pores are formed on the cell membrane during pyroptosis, which makes the cell membrane lose its integrity, eventually leading to the release of cytokines interleukin(IL)-1β and IL-18. When the body is infected with pathogens or exposed to some stimulations, pyroptosis could play an immune defense role. It is found that pyroptosis exists widely in infectious and inflammatory respiratory diseases such as acute lung injury, bronchial dysplasia, chronic obstructive pulmonary disease, and asthma. Excessive pyroptosis may accompany airway inflammation, tissue injury, and airway damage, and induce an inflammatory reaction, leading to more serious damage and poor prognosis of respiratory diseases. This review summarizes the relationship between pyroptosis and related respiratory diseases.

/pdf/pyroptosis-and-respiratory-diseases-a-review-of-current-1kgtkx3g.pdf

Pyroptosis and respiratory diseases: A review of current knowledge

Hyperinsulinaemic hypoglycaemia (HH) is a biochemical finding of low blood glucose levels due to the dysregulation of insulin secretion from pancreatic β-cells. Under normal physiological condition...

https://journals.sagepub.com/doi/pdf/10.1177/2042018820965068

Somatostatin analogues for the treatment of hyperinsulinaemic hypoglycaemia

Intrauterine infection/inflammation plays an important role in the development of lung injury and bronchopulmonary dysplasia (BPD) in preterm infants, While a multifactorial genesis is likely, mechanisms involved in BPD after intrauterine infection/inflammation are largely unknown. Recent studies have suggested microRNAs (miRNAs) are likely to play a role. Therefore, this study aimed to study the effects and mechanisms of intrauterine infection/inflammation on lung development, and to identify miRNAs related to lung injury and BPD. An animal model of intrauterine infection/inflammation was established with pregnant SD rats endocervically inoculated with E.coli. The fetal and neonatal rats were observed at embryonic day (E) 17, 19, 21 and postnatal day (P) 1, 3, 7, 14, respectively. Body weight, lung weight, the expression levels of NLRP3, TNF-α, IL-lβ, IL-6, VEGF, Collagen I, SP-A, SP-B and SP-C in the lung tissues of fetal and neonatal rats were measured. Expression profiles of 1218 kinds of miRNAs in the lungs of neonatal rats were detected by miRNA microarray technique. Target genes of the identified miRNAs were predicted through online software. Intrauterine infection/inflammation compromised not only weight development but also lung development of the fetal and neonatal rats. The results showed significantly increased expression of NLRP3, TNF-α, IL-1β, IL-6, Collagen I, and significantly decreased expression of VEGF, SP-A, SP-B and SP-C in the fetal and neonatal rat lung tissues in intrauterine infection group compared to the control group at different observation time point (P < 0.05). Forty-three miRNAs with significant differential expression were identified. Possible target genes regulated by the identified miRNAs are very rich. Intrauterine infection/inflammation results in lung histological changes which are very similar to those observed in BPD. Possible mechanisms may include NLRP3 inflammasome activation followed by inflammatory cytokines expression up-regulated, inhibiting the expression of pulmonary surfactant proteins, interfering with lung interstitial development. There are many identified miRNAs which target a wide range of genes and may play an important role in the processes of lung injury and BPD.

/pdf/effects-and-molecular-mechanisms-of-intrauterine-infection-3wfrrtdgkl.pdf

Effects and molecular mechanisms of intrauterine infection/inflammation on lung development

Aim Congenital glucose-galactose malabsorption (CGGM) is a rare disease characterised by severe diarrhoea, dehydration and weight loss. To better understand CGGM, we investigated all the case reports and series of CGGM from 2001 to 2019. Methods A review of reports of CGGM published from 2001 to 2019 was undertaken, using PubMed, Ovid Medline, Springer, Wanfang Database, CBMD database and CKNI database. The clinical features, diagnosis, treatment and prognosis of CGGM in these reports were obtained and analysed. Results We reviewed 107 cases for this study. Out of 55 cases from Saudi Arabia and Turkey, 43 cases (78.2%) were from consanguineous marriage. Forty-nine cases (73.1%) were infants. Dehydration, diarrhoea and weight loss occurred in almost all cases. Half of the cases presented hypernatremia and abdominal distension. Vomiting, polyuria/haematuria and fever were reported in 11, 7 and 3 cases, respectively. Twenty cases (18.7%) showed hypercalcaemia or nephrolithiasis. Stool pH was tested in 43 cases (40.2%). Fifty-five cases (51.4%) were diagnosed for more than 1 month after the onset of symptoms. Two cases (1.9%) died, one needed amputation, and the other 104 cases (97.2%) recovered with fructose formula. Seventy-three cases (68.2%) underwent gene testing, 30 SLC5A1 gene mutations were detected, with 23 cases homozygous, and seven heterozygous mutation. Conclusion The clinical characteristics of CGGM are nonspecific, and the diagnosis method is not conventionally applied. Fasting and gene testing are the two most important diagnostic methods. The best treatment of CGGM is supplementation with fructose-based formula.

Literature review on congenital glucose–galactose malabsorption from 2001 to 2019

Fluorescence imaging with advanced multi-channel observation, high sensitivity, and high spatio-temporal resolution holds great promise for biomedical applications. However, the different absorption and scattering spectra of complex tissue structures present significant challenges for real-time investigations of live biological and physiological processes. Herein, we present Yb/Er/Ho-engineered rare earth fluoride nanoparticles with integrated multimodal imaging functions that can provide synergistic effects over any modality alone. The engineered nanoparticles can realize efficient and accurate diagnoses in clinical research. Employing Yb3+ sensitizers and both Er3+ and Ho3+ emitters, NaGdF4:15%Yb,15%Er,x%Ho nanoparticles absorb an excitation wavelength of 980 nm and emit luminescence centered at 1525 nm and 1155 nm in the second near-infrared (NIR-II) window. In addition, upconversion emission in the visible region is also observed for multiplex signals. T1- and T2-weighted magnetic resonance (MR) imaging is achieved owing to the presence of paramagnetic Gd3+ and Ho3+ species. The high X-ray attenuation ability of the elemental constituents permits the use of the prepared nanoparticles as high-contrast X-ray computed tomography (CT) imaging agents. Taken together, this study shows the construction of an alternative multimodal nanoprobe with synergistic T1- and T2-MR/CT/downconversion luminescence (DCL) imaging abilities, which can provide an alternative approach for in vivo disease diagnosis and supervision.

Yb/Er/Ho-engineered rare earth fluoride nanoparticles to unlock multimodal in vivo medical imaging.

Aim
To explore the imaging findings of neonatal infants infected with enteroviruses.

Methods
A retrospective study was conducted on 12 patients who were diagnosed with encephalitis caused by enterovirus. Clinical presentation, cranial ultrasonography (cUS), magnetic resonance imaging (MRI) findings and neurodevelopment outcome of 12 cases were analysed.

Results
Twelve infants, with a gestational age of 35 to 39 weeks, presented at 36 to 41 weeks postmenstrual age with clinical symptoms of enterovirus infections. Ten of 12 neonatal infants had a fever and 4 of 12 presented with a sepsis-like illness. cUS in one preterm infant showed periventricular echogenicity. Neonatal MRI confirmed white matter changes in 12 infants. Follow-up of infants were 18 months. Outcome was variable with cerebral palsy in 2 infants and normal neurodevelopment outcome in 10 infants.

Conclusions
Enterovirus may cause severe central nervous system infection in the neonatal period. The neuroimaging studies are informative and should be a part of care for infants with enteroviruses.

Enterovirus infections are associated with white matter damage in neonates.

Objective Congenital hyperinsulinism (CHI) is a rare but severe cause of hypoglycemia. The present study investigates the clinical presentation, therapeutic outcomes and genetic mutations of CHI in Chinese individuals over the past 15 years. Methods The authors retrospectively reviewed one case in their department and 206 cases reported from January 2002 to October 2016 in China. PubMed, Ovid Medline, Springer and Wanfang Database, CBMD database, and CKNI database were the sources used to collect the data. Results In total, 207 cases were recruited. Of these, the ages of 100 (48.3%) were within the 4th week after birth. Seventy-seven cases (37.2%) were born large for gestational age (LGA). Seizures occurred in 140 cases (67.6%). Among 140 cases (67.6%) who were administered diazoxide treatment, 90 (64.3%) were responsive. Seven cases (3.4%) received octreotide treatment and 19 cases (9.2%) underwent surgery. 63/129 cases (48.8%) were detected to have gene mutations, including ABCC8 (69.8%), KCNJ11 (12.7%), GLUD1, GCK, HADH, and HNF4A. Among the diazoxide-unresponsive cases, gene mutations were detected in 20/36 (55.6%) cases with ABCC8 and in 2 (5.6%) cases with KCNJ11. Among the diazoxide-responsive cases, gene mutations were detected in 8 patients with ABCC8, 4 with KCNJ11, 5 with GLUD1, and 1 with GCK. Conclusion The present study indicates that most CHI cases occurred in neonates and that 1/3 of the cases were born LGA. ABCC8 and KCNJ11 are the most common gene mutations. More than half of the diazoxide-unresponsive CHI detected mutations are in ABCC8 and KCNJ11 genes. The GLUD1 gene mutations cause diazoxide-responsive CHI. Identifying the gene mutations can assist in the diagnosis and treatment of CHI.

/pdf/congenital-hyperinsulinism-in-china-a-review-of-chinese-5cs7fp1vnt.pdf

Congenital Hyperinsulinism in China: A Review of Chinese Literature Over the Past 15 Years.

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