Search Results (40)

Post-hemorrhagic hydrocephalus (PHH) is a serious neurological sequela of severe intraventricular hemorrhage (IVH) in premature infants and remains one of the leading indications for ventriculoperitoneal (VP) shunt placement. Evaluating possible VP shunt-related complications can be challenging because clinical manifestations are often nonspecific, neuroimaging may initially appear unchanged, and microbiological cultures may remain negative. We report the case of a 19-month-old male born at 28 weeks’ gestation who developed Grade IV germinal matrix/intraventricular hemorrhage with bilateral intraparenchymal extension, early periventricular cystic leukomalacia, and post-hemorrhagic communicating hydrocephalus requiring multiple cerebrospinal fluid diversion procedures culminating in long-term VP shunt dependence. His medical history was notable for recurrent neonatal meningitis, secondary epilepsy with previous episodes of status epilepticus, secondary adrenal insufficiency, and severe global developmental delay. He presented with fever, recurrent coffee-ground vomiting, abdominal distension, progressive lethargy, reduced responsiveness, and localized erythematous swelling over the cranial VP shunt reservoir, raising concern for possible shunt-related pathology. During hospitalization, he deteriorated with status epilepticus and respiratory failure, with clinical concern for increased intracranial pressure, requiring admission to the Pediatric Intensive Care Unit (PICU). Laboratory investigations demonstrated leukocytosis, elevated C-reactive protein, cerebrospinal fluid pleocytosis, markedly elevated CSF protein, and CSF glucose of 2.0 mmol/L, for which a paired serum glucose value was unavailable, while repeated blood, urine, wound, and CSF cultures remained negative. Initial computed tomography (CT) demonstrated no significant interval change in the chronic hydrocephalus despite progressive neurological deterioration; however, serial neuroimaging later revealed progressive bilateral extra-axial fluid collections with radiological features suggestive of an evolving subacute subdural hemorrhage. The patient was managed with empirical broad-spectrum intravenous antibiotics, aggressive seizure control, stress-dose corticosteroids, respiratory support, and continuous multidisciplinary monitoring. His neurological and respiratory status subsequently improved, and he returned to his pre-admission neurological baseline before discharge with planned further evaluation at a tertiary pediatric neurosurgical center. This case highlights the diagnostic uncertainty surrounding acute neurological deterioration in a child with shunt-dependent PHH. VP shunt-related infection or malfunction remained important but unconfirmed diagnostic considerations, alongside competing or potentially overlapping contributors including status epilepticus, evolving extra-axial collections, respiratory infection, and endocrine or metabolic decompensation. No single etiology was definitively established. The case emphasizes the importance of serial neurological assessment, consideration of alternative diagnoses, repeat neuroimaging, and multidisciplinary evaluation when initial investigations do not establish the cause of deterioration. Full article

Doxorubicin (DOX) remains an effective chemotherapeutic agent, but its clinical use is limited by dose-dependent cardiotoxicity. Mitochondrial dysfunction and metabolic remodeling are central features of DOX-induced cardiac injury. ATP synthase inhibitory factor-1 (IF1) is an endogenous inhibitor of the hydrolytic activity of mitochondrial ATP synthase and has emerged as an important regulator of cellular bioenergetics. Cardiac IF1 expression is increased in multiple pathological conditions; however, its role in chemotherapy-induced cardiotoxicity remains unclear. Here, we investigated the contribution of IF1 to DOX-induced cardiotoxicity using male C57BL/6J wild-type (WT) and IF1 knockout (IF1KO) mice, isolated cardiac mitochondria, cultured neonatal cardiomyocytes, and AC16 human cardiomyocytes. Cardiac function was assessed by echocardiography, mitochondrial function by high-resolution respirometry and Seahorse metabolic flux analysis, and myocardial injury by histological and ultrastructural analyses. DOX treatment markedly increased cardiac IF1 protein levels despite reduced IF1 mRNA expression. IF1 deficiency enhanced mitochondrial respiration in isolated cardiac mitochondria and cultured cardiomyocytes under both basal and DOX-stressed conditions. IF1KO mice exhibited attenuated cardiac dysfunction and improved myocardial ultrastructure following DOX treatment compared with WT mice. In AC16 cardiomyocytes exposed to DOX, overexpression of WT IF1 improved cellular metabolic activity but provided only limited preservation of mitochondrial respiratory capacity. In contrast, overexpression of the dominant-negative IF1 mutant (IF1E30A) not only improved metabolic activity but also preserved mitochondrial respiration. These findings identify IF1 as a key regulator of metabolic adaptation during DOX stress. Upregulation of functional IF1 may represent an adaptive response that promotes glycolytic ATP production during mitochondrial stress, whereas inhibition of IF1 activity preserves metabolic activity primarily through maintenance of mitochondrial function. Collectively, these findings provide new insights into the role of IF1 in DOX-induced cardiomyopathy and highlight IF1 as a potential therapeutic target in cardio-oncology. Full article

Background and Objectives: Lung ultrasound (LUS) has fundamentally transformed neonatal respiratory diagnostics, offering a radiation-free, bedside-applicable modality capable of guiding surfactant therapy, characterizing pulmonary pathology, and monitoring treatment response in real time. While surfactant replacement therapy is firmly established for neonatal respiratory distress syndrome (RDS), its role in acute complications—specifically pulmonary hemorrhage (PH) and pneumothorax (PTX)—remains uncertain and heterogeneous in clinical practice. This review examines how LUS-based phenotyping can improve the diagnostic precision and therapeutic sequencing of surfactant administration in these high-risk scenarios, and how comorbidities such as hemodynamically significant patent ductus arteriosus, persistent pulmonary hypertension, sepsis, and coagulopathy modulate clinical outcomes. Materials and Methods: We conducted a structured narrative review of studies published from 2020 onward, sourced from PubMed, Web of Science, Semantic Scholar, and Mendeley, using PRISMA-inspired selection principles. The search combined terms including “lung ultrasound,” “neonatal POCUS,” “surfactant therapy,” “pulmonary hemorrhage,” “neonatal pneumothorax,” and “LUS score.” Studies focusing on neonatal populations, clinical LUS applications, and surfactant use in PH and PTX were prioritized. Results: Quantitative LUS scoring systems (range 0–18) predict surfactant need and re-dosing with AUC values of 0.85–0.87, outperforming clinical estimates alone. In PH, LUS reveals dense consolidation with alveolar flooding patterns, guiding the timing of rescue surfactant after hemodynamic stabilization; response monitoring via serial LUS is feasible and informative. In PTX, hallmark signs—absent lung sliding, loss of B-lines, and the pathognomonic lung point—allow diagnosis within seconds, guiding immediate thoracentesis and subsequent surfactant administration if underlying RDS is confirmed. Nationally implemented LUS protocols in neonatal intensive care units have demonstrated significant reductions in radiation exposure without compromising diagnostic accuracy. Conclusions: LUS-guided decision algorithms—integrating ultrasonographic phenotyping, quantitative scoring, and hemodynamic assessment—represent the current best framework for individualizing surfactant therapy in neonatal PH and PTX. Standardization of POCUS training and protocol implementation in neonatal units is essential. Prospective multicenter trials are urgently needed to define optimal indications, timing, and dosing in these vulnerable populations. Full article

Background: Pneumonia of viral and polymicrobial origin predominates the pathological profile of clinical childhood pneumonia, with high admissions rates in recent times. Identifying factors associated with prolonged hospital stay may aid in developing risk reduction strategies for improved admission outcomes. Methods: A facility-based historical cross-sectional study was conducted with a random selection of 186 medical records from January 2020 to December 2024 of children aged 0 to 5 with clinical pneumonia at a tertiary Hospital in Mthatha. Results: Over the five-year study period, clinical pneumonia accounted for 10.4% (95% CI: 9.8–11.1%, n = 950/9098) of the total under-five admissions. The median age was 108.5 (interquartile range (IQR) = 48.0–345.5) days, mainly comprising males (51.1%) and infants (65.2%), with viral (91.6%) and mild (88.0%) forms of pneumonia. The median length of hospital stay was 5 (IQR = 3.3–8) days, and 91 (49.5%) of the children had a prolonged hospital stay. In modified Poisson regression, infants [(relative risk (RR) = 2.7, 95% confidence interval (CI): 1.6–4.3), p < 0.001]; neonates (RR = 2.3, 95% CI: 1.2–4.6, p = 0.013); bacterial pneumonia (RR = 1.7, 95% CI: 1.2–2.6, p = 0.007); being hypoxic (RR = 2.2, 95% CI: 1.3–3.6, p = 0.003); absence of other respiratory tract infections (RR = 1.6, 95% CI: 1.2–2.1, p = 0.003), incomplete vaccination (RR = 1.5, 95% CI: 1.0–2.2, p = 0.038), non-usage of herbal medications (RR = 1.7, 95% CI: 1.3–2.2, p < 0.001), difficult breathing (RR = 1.7, 95% CI: 1.1–2.6, p = 0.028), current breastfeeding (RR = 0.6, 95% CI: 0.4–1.0, p = 0.048), other morbidities (RR = 0.7, 95% CI: 0.5–0.9, p = 0.002) were associated with prolonged length of hospital stay. Conclusion: Stratification of under-five children at admission according to age, type of pneumonia, vaccination status, and presence of other morbidities are needed to enhance monitoring and timely medical interventions. Full article

Objective: This study aims to investigate the protective effect of Shengmai San (SMS) against high-glucose (HG)-induced injury in neonatal rat ventricular myocytes (NRVMs) and to elucidate the underlying pharmacological molecular mechanisms. We hypothesize that SMS ameliorates HG-induced calcium homeostasis imbalance in NRVMs by improving mitochondrial energy metabolism disorder, and this protective effect is associated with the downregulation of oxidized and phosphorylated CaMKII expression to inhibit CaMKII signaling pathway overactivation. Herein, we verify this hypothesis by assessing mitochondrial function, calcium transients, sarcoplasmic reticulum (SR) calcium handling and CaMKII phosphorylation levels in NRVMs. Methods: First, ultra-high performance liquid chromatography–high resolution mass spectrometry was used to identify the chemical components of SMS to clarify its material basis. Primary NRVMs were then cultured under low-glucose (LG) or HG conditions, with 2% SMS-medicated serum (SMS-MS) as the experimental intervention, and NAC (ROS scavenger) and KN93 (CaMKII inhibitor) as positive controls. Following intervention, we sequentially detected key indicators corresponding to the proposed pathological pathway: intracellular reactive oxygen species (ROS) levels (oxidative stress), mitochondrial ROS, mitochondrial function indices including oxygen consumption rate (OCR) (energy metabolism), calcium transients and diastolic intracellular free calcium concentration (global calcium homeostasis), sarcoplasmic reticulum (SR) calcium leak (calcium handling disorder), and, finally, the phosphorylation, oxidation levels of CaMKII and RyR2 phosphorylation (Ser2814) (p-RyR2) (key regulatory pathway) via Western blot to systematically elucidate the mechanistic link between SMS intervention and HG-induced NRVM injury. Results: Quantitative analysis revealed that high-glucose (HG) induction significantly reduced calcium transient amplitude and prolonged the decay time constant (tau) in NRVMs at 72 h (p < 0.01 vs. LG), with these parameters normalizing by 120 h—an effect indicative of a compensatory adaptive response. The 2%SMS-MS markedly ameliorated HG-induced calcium transient abnormalities at 72 h (p < 0.01 vs. HG). Additionally, 2%SMS-MS significantly enhanced mitochondrial basal oxygen consumption rate, spare respiratory capacity, ATP production, and maximal respiration in HG-exposed NRVMs (p < 0.01 vs. HG). SMS also significantly reduced intracellular reactive oxygen species (ROS) levels (p < 0.01 vs. HG), mitochondrial ROS levels (p < 0.01 vs. HG), diastolic intracellular free calcium concentration (p < 0.01 vs. HG), and SR calcium leak (p < 0.05 vs. HG). Western blot analysis revealed that 2%SMS-MS intervention effectively downregulated the expression of oxidized CaMKII (Ox-CaMKII) (p < 0.01 vs. HG), phosphorylated CaMKII (p-CaMKII) (p < 0.01 vs. HG), and RyR2 phosphorylation (Ser2814) (p < 0.05 vs. HG), which may be the potential mechanism in maintaining calcium homeostasis in HG-induced NRVMs. Conclusions: This study suggests that SMS enhances mitochondrial energy metabolism and exerts a protective effect against high-glucose-induced calcium homeostasis imbalance in NRVMs, which supports our proposed hypothesis. Its potential mechanism indicates that the protective effects of SMS are associated with its ability to downregulate the expression of oxidized and phosphorylated CaMKII. These findings highlight SMS as a potential therapeutic candidate for alleviating HG-related myocardial injury and provide evidence for its application in the prevention of early diabetic cardiomyopathy. Full article

The thymus is important for neonatal immune development; however, information on its ultrasonographic appearance in newborn puppies is limited. Because the thymus occupies a substantial portion of the cranial mediastinum in neonates, it may be confused with pathological mediastinal masses during thoracic imaging. Defining its normal ultrasonographic appearance is therefore crucial for accurate clinical interpretation. This study aimed to describe the topographic anatomy and ultrasonographic features of the thymus in neonatal dogs. Ten puppy cadavers were examined. Under ultrasound guidance, the thymus was injected with methylene blue, and its location confirmed by dissection. Subsequently, transcutaneous ultrasonographic examinations were performed in 40 clinically normal puppies aged 1–5 days. In all puppies, the thymus was consistently visualized from the left side of the thorax within the precardiac mediastinum. In the transverse imaging plane, the thoracic portion of the thymus typically appeared triangular, with variations related to respiratory movements and cardiac and vascular pulsations. The thymic parenchyma was predominantly homogeneous and hypoechoic with scattered hyperechoic areas and fine lines. In some cases, the echotexture was more heterogenous, showing fusiform hypo- and hyperechoic linear structures. The thymus was easily differentiated from adjacent thoracic structures due to its distinctive echotexture. The thymus in newborn puppies demonstrates a consistent and recognizable ultrasonographic pattern, allowing reliable identification using transcutaneous ultrasonography. These findings provide a useful reference for clinical and diagnostic evaluation of the neonatal canine thymus. Full article

Lung ultrasound (LUS) has emerged as a valuable diagnostic modality for the evaluation of respiratory disorders in neonates, infants and children. LUS has high diagnostic accuracy for identification of lung lesions in neonates, infants and children, where most lung lesions abut the pleura. Furthermore, LUS has the advantage of rapid execution and ease of use, and does not require ionizing radiation. Its sensitivity, cost-effectiveness, and clinical efficiency make it an important tool for supporting clinical decision-making and improving patient management. Moreover, LUS may represent a reliable alternative to chest radiography for the assessment of pediatric lung conditions and, in selected cases, could potentially replace routine chest X-rays (CXRs). Because LUS is a user-friendly technique that enables real-time imaging without radiation, it has increasingly been used in clinical practice in recent years. Here, we discuss the diagnostic role of LUS for the accurate identification of pulmonary lesions in pediatric patients. In addition, we present LUS sonographic findings associated with common pediatric lung diseases, including signs and artifacts that can be used during diagnosis and evaluation of pediatric patients. Full article

Calreticulin is a highly conserved and multifunctional molecular chaperone ubiquitously expressed in humans and animals. Beyond its well-established roles in calcium homeostasis, protein folding, and immune regulation, recent studies in aquatic species have suggested a previously unrecognized antimicrobial function of calreticulin. These findings raise the question of whether calreticulin also exerts antibacterial activity in terrestrial mammals, which has not been systematically investigated to date. To address this knowledge gap, we successfully constructed and expressed recombinant goat calreticulin using the Pichia pastoris expression system, yielding a protein of over 99% purity that predominantly exists in dimeric form. Functional assays demonstrated that both recombinant goat and human calreticulin exhibited preliminary inhibitory activity against Escherichia coli, Salmonella typhimurium, and Pasteurella multocida. Calreticulin was capable of binding to these three bacterial species as well as bacterial lipopolysaccharides (LPS). Notably, in the presence of Ca²⁺, calreticulin induced bacterial aggregation, indicating a potential mechanism for limiting bacterial dissemination and proliferation. Given the high anatomical, genetic, and physiological similarity between goats and humans—particularly in respiratory tract structure and mucosal immune function—neonatal goats were selected as a relevant model for evaluating the in vivo antimicrobial efficacy of calreticulin. Accordingly, we established an intranasal infection model using Pasteurella multocida to assess the protective role of calreticulin against respiratory bacterial challenge. Following infection, calreticulin expression was markedly upregulated in the nasal mucosa, trachea, and lung tissues. Moreover, intranasal administration of exogenous calreticulin significantly alleviated infection-induced pathological injury to the respiratory system and effectively decreased bacterial loads in infected tissues. Collectively, this study systematically elucidates the antimicrobial activity of calreticulin in a mammalian model and highlights its potential as a natural immune effector, providing novel insights for the development of host-targeted antimicrobial strategies. Full article

Background: Among patients with congenital heart disease, particularly those with a history of undergoing the Fontan operation, pregnancy presents a significant maternal–fetal risk, especially when complicated by severe valvular dysfunction. Lung reperfusion syndrome (LRS) is a rare but life-threatening complication occurring following valve intervention. Multidisciplinary management, including by Cardio-Obstetrics teams, is essential for optimizing outcomes in such high-risk cases. Methods: We present the case of a 37-year-old pregnant patient with previously repaired tetralogy of Fallot (via the Fontan procedure) who presented at 24 weeks gestation with worsening severe pulmonary stenosis and right-ventricular dysfunction. The patient had been lost to cardiac follow-up for over a decade. She experienced recurrent arrhythmias, including supraventricular and non-sustained ventricular tachycardia, prompting hospital admission. A multidisciplinary team recommended transcatheter pulmonic valve replacement (TPVR), performed at 28 weeks’ gestation. Results: Post-TPVR, the patient developed acute hypoxia and hypotension, consistent with Lung Reperfusion Syndrome, necessitating intensive cardiopulmonary support. Despite initial stabilization, progressive maternal respiratory failure and fetal compromise led to an emergent cesarean delivery. The neonate’s neonatal intensive care unit (NICU) course was complicated by spontaneous intestinal perforation, while the mother required intensive care unit (ICU)-level care and a bronchoscopy due to new pulmonary findings. She was extubated and discharged in stable condition on postoperative day five. Conclusions: This case underscores the complexity of managing severe congenital heart disease and valve pathology during pregnancy. Lung reperfusion syndrome should be recognized as a potential complication following TPVR, particularly in pregnant patients with Fontan physiology. Early involvement of a multidisciplinary Cardio-Obstetrics team and structured peripartum planning are critical to improving both maternal and neonatal outcomes. Full article

Neonatal mammals must rapidly adapt to significant physiological changes during the transition from the intrauterine to extrauterine environments. This adaptation, particularly in the metabolic and respiratory systems, is essential for survival. MicroRNAs (miRNAs) are small noncoding RNAs that regulate various physiological and pathological processes by binding to the 3′ untranslated regions of mRNAs. This study aimed to identify miRNAs involved in the early extrauterine adaptation of neonatal piglets and explore their functions. We performed small RNA sequencing on six tissues (heart, liver, spleen, lung, multifidus muscle, and duodenum) from piglets 24 h before birth (day 113 of gestation) and 6 h after birth. A total of 971 miRNA precursors and 1511 mature miRNAs were identified. Tissue-specific expression analysis revealed 881 tissue-specific miRNAs and 164 differentially expressed miRNAs (DE miRNAs) across the tissues. Functional enrichment analysis showed that these DE miRNAs are significantly enriched in pathways related to early extrauterine adaptation, such as the NFκB, PI3K/AKT, and Hippo pathways. Specifically, miR-22-3p was significantly upregulated in the liver post-birth and may regulate the PI3K/AKT pathway by targeting AKT3, promoting gluconeogenesis, and maintaining glucose homeostasis. Dual-luciferase reporter assays and HepG2 cell experiments confirmed AKT3 as a target of miR-22-3p, which activates the AKT/FoxO1 pathway, enhancing gluconeogenesis and glucose production. Furthermore, changes in blood glucose and liver glycogen levels in newborn piglets further support the role of miR-22-3p in glucose homeostasis. This study highlights the importance of miRNAs, particularly miR-22-3p, in the early extrauterine adaptation of neonatal piglets, offering new insights into the physiological adaptation of neonatal mammals. Full article

Congenital titinopathies reported to date show autosomal recessive inheritance and are caused by a variety of genomic variants, most of them located in metatranscript (MTT)-only exons. The aim of this study was to describe additional patients and establish robust genotype–phenotype associations in titinopathies. This study involved analyzing molecular, clinical, pathological, and muscle imaging features in 20 patients who had at least one pathogenic or likely pathogenic TTN variant in MTT-only exons, with onset occurring antenatally or in the early postnatal stages. The 20 patients with recessive inheritance exhibited a heterogeneous range of phenotypes. These included fetal lethality, progressive weakness, cardiac or respiratory complications, hyper-CKemia, or dystrophic muscle biopsies. MRI revealed variable abnormalities in different muscles. All patients presented severe congenital myopathy at birth, characterized by arthrogryposis (either multiplex or axial–distal) or neonatal hypotonia in most cases. This study provides detailed genotype–phenotype correlations in congenital titinopathies caused by mutations in MTT-only exons. The findings highlight the variability in clinical presentation and the severity of phenotypes associated with these specific genetic alterations. RNA-seq analyses provided valuable insights into the molecular consequences of TTN variants, particularly in relation to splicing defects and nonsense-mediated RNA decay. In conclusion, this study reinforces the genotype–phenotype correlations between congenital myopathies and variants in TTN MTT-only exons, improves their molecular diagnosis, and provides a better understanding of their pathophysiology. Full article

Poor placental development and placental defects can lead to adverse pregnancy outcomes such as pre-eclampsia, fetal growth restriction, and stillbirth. This study introduces two sensors, which use a near-infrared spectroscopy (NIRS) technique to measure placental oxygen saturation transabdominally. The first one, an NIRS sensor, is a wearable device consisting of multiple NIRS channels. The second one, a Multimodal sensor, which is an upgraded version of the NIRS sensor, is a wireless and wearable device, integrating a motion sensor and multiple NIRS channels. A pilot clinical study was conducted to assess the feasibility of the two sensors in measuring transabdominal placental oxygenation in 36 pregnant women (n = 12 for the NIRS sensor and n = 24 for the Multimodal sensor). Among these subjects, 4 participants had an uncomplicated pregnancy, and 32 patients had either maternal pre-existing conditions/complications, neonatal complications, and/or placental pathologic abnormalities. The study results indicate that the patients with maternal complicated conditions (69.5 ± 5.4%), placental pathologic abnormalities (69.4 ± 4.9%), and neonatal complications (68.0 ± 5.1%) had statistically significantly lower transabdominal placental oxygenation levels than those with an uncomplicated pregnancy (76.0 ± 4.4%) (F (3,104) = 6.6, p = 0.0004). Additionally, this study shows the capability of the Multimodal sensor in detecting the maternal heart rate and respiratory rate, fetal movements, and uterine contractions. These findings demonstrate the feasibility of the two sensors in the real-time continuous monitoring of transabdominal placental oxygenation to detect at-risk pregnancies and guide timely clinical interventions, thereby improving pregnancy outcomes. Full article

The objective of this study was to assess the relationship of ACS with neonatal outcomes among very preterm infants born to mothers with clinical chorioamnionitis in China. This was a multicenter retrospective cohort study. Study participants included infants born at <32 weeks’ gestation with clinical chorioamnionitis and registered in the Chinese Neonatal Network from 1 January 2019 to 31 December 2020. Infants were divided into two groups: any amount of ACS or no administration of ACS. Multivariable generalized linear models using generalized estimating equations were used to assess the association between ACS and neonatal outcomes among the study population. We identified 2193 infants eligible for this study; 1966 (89.6%) infants had received ACS therapy, and 227 (10.4%) had not received any ACS therapy. Among very preterm infants born to mothers with clinical chorioamnionitis, any ACS usage was significantly associated with decreased risks of early death (aRR 0.56, 95% CI 0.32, 0.99) and severe ROP (aRR 0.51, 95% CI 0.28, 0.93) after adjustment for maternal hypertension, gestational age at birth, Caesarean section, being inborn, and administration of systemic antibiotics to the mother within 24 h before birth. In addition, out of the 2193 infants, the placentas of 1931 infants underwent pathological examination with recorded results. Subsequently, 1490 of these cases (77.2%) were diagnosed with histological chorioamnionitis. In 1490 cases of histologic chorioamnionitis, any ACS usage was significantly related to decreased risks of overall mortality (aRR 0.52, 95% CI 0.31, 0.87), severe ROP (aRR 0.47, 95% CI 0.25, 0.97), and respiratory distress syndrome (aRR 0.52, 95% CI 0.31, 0.87). We concluded that any ACS was associated with reduced risks for neonatal early death and severe ROP among very preterm infants born to mothers with clinical chorioamnionitis. Full article

The term congenital lung malformation (CLM) is used to describe a wide range of pathological conditions with different imaging and clinical manifestations. These anomalies stem from abnormal embryological lung development, potentially occurring across various stages of prenatal life. Their natural history can be variable, presenting in a wide range of severity levels and encompassing asymptomatic individuals who remain so until adulthood, as well as those who experience respiratory distress in the neonatal period. Through the PubMed database, we performed an extensive review of the literature in the fields of congenital lung abnormalities, including their diagnostic approach and findings. From our RIS-PACS database, we have selected cases with a final diagnosis of congenital lung malformation. Different diagnostic approaches have been selected, including clinical cases studied using plain radiograph, CT scan, prenatal ultrasound, and MR images. The most encountered anomalies can be classified into three categories: bronchopulmonary anomalies (congenital pulmonary airway malformations (CPAMs), congenital lobar hyperinflation, bronchial atresia, and bronchogenic cysts), vascular anomalies (arteriovenous malformation), and combined lung and vascular anomalies (scimitar syndrome and bronchopulmonary sequestration). CLM causes significant morbidity and mortality; therefore, the recognition of these abnormalities is necessary for optimal prenatal counseling and early peri- and postnatal management. This pictorial review aims to report relevant imaging findings in order to offer some clues for differential diagnosis both for radiologists and pediatric consultants. Full article

Background: Features of cardiovascular autonomic regulation in infants are poorly studied compared with adults. However, the clinical significance of autonomic dysfunction in infants is very high. The goal of our research was to study the temporal and frequency-dependent features, as well as low-frequency synchronization in cardiovascular autonomic regulation in full-term vs. preterm newborns, based on the analysis of their heart rate variability (HRV) and photoplethysmographic waveform variability (PPGV). Methods: The study included three groups of newborns: 64 full-term newborns (with a gestational age at birth of 37–40 weeks) with a physiological course of the neonatal adaptation; 23 full-term newborns (with a gestational age at birth of 37–40 weeks) with a pathological course of the neonatal adaptation; and 17 preterm newborns (with a postconceptional age of 34 weeks or more). We conducted spectral analysis of HRV and PPGV, along with an assessment of the synchronization strength between low-frequency oscillations in HRV and in PPGV (synchronization index). We employed several options for the boundaries of the high-frequency (HF) band: 0.15–0.40 Hz, 0.2–2 Hz, 0.15–0.8 Hz, and 0.24–1.04 Hz. Results: Preterm newborns had higher heart rate, RMSSD, and PNN50 values relative to both groups of full-term newborns. Values of SDNN index and synchronization index (S index) were similar in all groups of newborns. Differences in frequency domain indices of HRV between groups of newborns depended on the considered options of HF band boundaries. Values of frequency domain indices of PPGV demonstrated similar differences between groups, regardless of the boundaries of considered options of HF bands and the location of PPG signal recording (forehead or leg). An increase in sympathetic influences on peripheral blood flow and a decrease in respiratory influences were observed along the following gradient: healthy full-term newborns → preterm newborns → full-term newborns with pathology. Conclusions: Differences in frequency domain indices of autonomic regulation between the studied groups of newborns depended on the boundaries of the considered options of the HF band. Frequency domain indices of PPGV revealed significantly more pronounced differences between groups of newborns than analogous HRV indicators. An increase in sympathetic influences on peripheral blood flow and a decrease in respiratory influences were observed along the following gradient: healthy full-term newborns → preterm newborns → full-term newborns with pathology. Full article