Pre-admission virus detection during the COVID-19 pandemic in children with and without symptoms of infection.

Aim: Pre-admission viral screening is used only in exceptional situations such as pandemics. We therefore evaluated pre-admission screening for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), respiratory syncytial virus (RSV) and influenza during the COVID-19 pandemic, comparing epidemiology and clinical features of admitted children.

Methods: Children were screened at a paediatric emergency department from 1 March 2020 to 30 June 2022 by nasopharyngeal sampling and polymerase chain reaction kit.

The Incidence of Carpal Tunnel Syndrome Diagnosis Increases after Arthroscopic Shoulder Surgery.

Purpose: Arthroscopic shoulder surgery has been identified as a potential risk factor for carpal tunnel syndrome (CTS). The purposes of this study were as follows: to (1) examine the percentage of patients who underwent arthroscopic shoulder procedures and later developed ipsilateral CTS within 1 year of the procedure, (2) determine the percentage of those patients with CTS who subsequently underwent an injection or release, and (3) examine comorbidities associated with developing CTS after surgery.

Methods: Patients who underwent arthroscopic rotator cuff repair (RCR), labral repair, or biceps tenodesis were retrospectively identified in a national database.

Animal Models of Preeclampsia: Mechanistic Insights and Promising Therapeutics.

Preeclampsia (PE) is a common pregnancy-specific disorder that is a major cause of both maternal and fetal morbidity and mortality. Central to the pathogenesis of PE is the production of antiangiogenic and inflammatory factors by the hypoxic placenta, leading to the downstream manifestations of the disease, including hypertension and end-organ damage. Currently, effective treatments are limited for PE; however, the development of preclinical animal models has helped in the development and evaluation of new therapeutics.

Elastin-Like Polypeptide: VEGF-B Fusion Protein for Treatment of Preeclampsia.

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Syncytialization alters the extracellular matrix and barrier function of placental trophoblasts.

The human placenta is of vital importance for proper nutrient and waste exchange, immune regulation, and overall fetal health and growth. Specifically, the extracellular matrix (ECM) of placental syncytiotrophoblasts, which extends outward from the placental chorionic villi into maternal blood, acts on a molecular level to regulate and maintain this barrier. Importantly, placental barrier dysfunction has been linked to diseases of pregnancy such as preeclampsia and intrauterine growth restriction.

Animal models of preeclampsia: investigating pathophysiology and therapeutic targets.

Animal models have been critical in investigating the pathogenesis, mediators, and even therapeutic options for a number of diseases, including preeclampsia. Preeclampsia is the leading cause of maternal and fetal morbidity and mortality worldwide. The placenta is thought to play a central role in the pathogenesis of this disease because it releases antiangiogenic and proinflammatory factors into the maternal circulation, resulting in the maternal syndrome.

The glycocalyx: a central regulator of vascular function.

The endothelial glycocalyx is a specialized extracellular matrix that covers the apical side of vascular endothelial cells, projecting into the lumen of blood vessels. The composition of the glycocalyx has been studied in great detail, and it is known to be composed of a mixture of proteoglycans, glycosaminoglycans, and glycoproteins. Although this structure was once believed to be a passive physical barrier, it is now recognized as a multifunctional and dynamic structure that participates in many vascular processes, including but not limited to vascular permeability, inflammation, thrombosis, mechanotransduction, and cytokine signaling.

Unfractionated heparin displaces sFlt-1 from the placental extracellular matrix.

Soluble vascular endothelial growth factor receptor-1 (sFlt-1) is an anti-angiogenic protein which is secreted by numerous cell types and acts as a decoy receptor for the angiogenic protein vascular endothelial growth factor (VEGF). Despite its physiologic importance in maintaining angiogenic balance, excess sFlt-1 levels are associated with the pathogenesis of many diseases, especially those with angiogenic imbalance, endothelial dysfunction, and hypertension. Although sFlt-1 is a soluble protein, it contains a binding site for the extracellular matrix component heparan sulfate.

Differential regulation of sFlt-1 splicing by U2AF65 and JMJD6 in placental-derived and endothelial cells.

Despite years of study, the gestational disorder preeclampsia (PE) remains poorly understood. One proposed mechanism of PE development is increased soluble VEGF receptor-1 (sFlt-1), ultimately causing angiogenic imbalance and endothelial dysfunction. The soluble protein is an alternative splice variant of FLT1, which also encodes for the full-length receptor Flt-1.

Biopolymer-Delivered, Maternally Sequestered NF-κB (Nuclear Factor-κB) Inhibitory Peptide for Treatment of Preeclampsia.

Preeclampsia is a hypertensive disorder of pregnancy that causes significant acute and long-term risk to the mother and the baby. The multifaceted maternal syndrome is driven by overproduction of circulating anti-angiogenic factors, widespread inflammation, and endothelial dysfunction. Nuclear factor-κB (NF-κB) is a transcription factor that plays a central role in the inflammatory response.

Heparanase regulation of sFLT-1 release in trophoblasts in vitro.

Introduction: Preeclampsia is a common pregnancy disorder which is characterized by new onset hypertension and endothelial dysfunction. Despite efforts to determine the causal factors of this disease, little progress has been made in discerning the etiology. The hypoxic and ischemic placenta, however, is generally accepted as the source for secreted factors in the maternal circulation, such as sFLT-1, which drive the maternal syndrome.

Acute Hypoxia and Chronic Ischemia Induce Differential Total Changes in Placental Epigenetic Modifications.

Preeclampsia is a common obstetrical complication, hallmarked by new-onset hypertension. Believed to result from placental insufficiency and chronic placental ischemia, the symptoms of preeclampsia are caused by release of pathogenic factors from the placenta itself, although the mechanisms of their regulation are in many cases unknown. One potential mechanism is through changes in placental epigenetic chromatin modifications, particularly histone acetylation and DNA methylation.

Pro-angiogenic therapeutics for preeclampsia.

Preeclampsia is a pregnancy-induced hypertensive disorder resulting from abnormal placentation, which causes factors such as sFlt-1 to be released into the maternal circulation. Though anti-hypertensive drugs and magnesium sulfate can be given in an effort to moderate symptoms, the syndrome is not well controlled. A hallmark characteristic of preeclampsia, especially early-onset preeclampsia, is angiogenic imbalance resulting from an inappropriately upregulated sFlt-1 acting as a decoy receptor binding vascular endothelial growth factor (VEGF) and placental growth factor (PlGF), reducing their bioavailability.

A Maternally Sequestered, Biopolymer-Stabilized Vascular Endothelial Growth Factor (VEGF) Chimera for Treatment of Preeclampsia.

Background: Preeclampsia is a hypertensive syndrome that complicates 3% to 5% of pregnancies in the United States. Preeclampsia originates from an improperly vascularized and ischemic placenta that releases factors that drive systemic pathophysiology. One of these factors, soluble fms-like tyrosine kinase-1, is believed to sequester vascular endothelial growth factor (VEGF), leading to systemic endothelial dysfunction and hypertension.

Triple-Layered Closure of an Oroantral Fistula: A Case Report.

Oroantral fistulae (OAF) are surgical sequelae that require complete resection and often leave large defects for the surgeon to repair. Closing these lesions is often technique sensitive and requires a detailed protocol, which, if not adhered to, can lead to recurrence. This case report presents a combined approach to closing an OAF by first excising the fistula and then resecting to retrieve the buccal fat pad to form a pedicle graft over the wound site.

Carbon Monoxide Releasing Molecules Blunt Placental Ischemia-Induced Hypertension.

Background: Preeclampsia is a pregnancy complication which manifests as new-onset hypertension, proteinuria, and a spectrum of other symptoms. While the underlying causes are still a subject of much debate, it is commonly believed that placental ischemia is a central cause. The ischemic placenta secretes factors which are believed to be responsible for the maternal syndrome; most notably the anti-angiogenic protein soluble fms-like tyrosine kinase 1 (sFlt-1).

Preeclampsia and the brain: neural control of cardiovascular changes during pregnancy and neurological outcomes of preeclampsia.

Preeclampsia (PE) is a form of gestational hypertension that complicates ∼5% of pregnancies worldwide. Over 70% of the fatal cases of PE are attributed to cerebral oedema, intracranial haemorrhage and eclampsia. The aetiology of PE originates from abnormal remodelling of the maternal spiral arteries, creating an ischaemic placenta that releases factors that drive the pathophysiology.

Therapeutic angiogenesis by vascular endothelial growth factor supplementation for treatment of renal disease.

Purpose Of Review: Vascular endothelial growth factors (VEGFs) influence renal function through angiogenesis, with VEGF-A being the most potent inducer of vascular formation. In the normal glomerulus, tight homeostatic balance is maintained between the levels of VEGF-A isoforms produced by podocyte cells, and the VEGF receptors (VEGFRs) expressed by glomerular endothelial, mesangial, and podocyte cells. Renal disease occurs when this homeostatic balance is lost, manifesting in the abnormal autocrine and paracrine VEGF-A/VEGFR signaling, ultrastructural glomerular and tubular damage, and impaired filtration.

Photobleaching studies reveal that a single amino acid polymorphism is responsible for the differential binding affinities of linker histone subtypes H1.1 and H1.5.

Mammals express six major somatic linker histone subtypes, all of which display dynamic binding to chromatin, characterized by transient binding at a given location followed by rapid translocation to a new site. Using photobleaching techniques, we systematically measured the exchange rate of all six mouse H1 subtypes to determine their relative chromatin-binding affinity. Two subtypes, H1.

Corneal Penetrating Elastin-Like Polypeptide Carriers.

Purpose: Elastin-like polypeptide (ELP) is a bioengineered protein widely applied as a drug carrier due to its biocompatibility and amenability to modification with cell-penetrating peptides (CPPs) and therapeutic agents. The purpose of this study was to determine whether topically applied ELP or CPP-fused ELPs penetrate the corneal barrier.

Methods: In vitro binding and cytotoxicity to human corneal epithelial (HCE) cells were determined for ELP or CPP-ELPs.

Heme oxygenase induction attenuates TNF-α-induced hypertension in pregnant rodents.

Pre-eclampsia is a hypertensive disorder of pregnancy initiated by placental insufficiency and chronic ischemia. In response, several pathways activated in the placenta are responsible for the maternal syndrome, including increased production of the anti-angiogenic protein, sFlt-1, and inflammatory cytokines, especially tumor necrosis factor-alpha (TNF-α). Previous studies have demonstrated that heme oxygenase (HO) induction can block TNF-α pathways in vitro and attenuate placental ischemia-induced sFlt-1 in vivo.