Initial clinical experience with Xpert-Pro peripheral self-expanding stent system for internal carotid artery dissection:Two case reports

Background:The standard treatment for internal carotid artery(ICA)dissection is obscure.Current therapeutic strategies include the use of antiplatelet drugs,anticoagulant drugs,intravenous thrombolysis,and endovascular treatment.Endovascular treatment is important in acute internal carotid artery dissection.This study reports two acute internal carotid artery dissection cases that were treated successfully using the Xpert-Pro peripheral selfexpanding stent system.Case summary:The first case was of a 38-year-old male patient with transient speechlessness and paralysis of the right limb in July 2021.Cervical computed tomographic angiography(CTA)showed ICA occlusion on the left side.Digital subtraction angiography(DSA)showed severe stenosis of the C1 segment of the left internal carotid artery with intermural hematoma.The patient subsequently underwent Xpert-Pro peripheral self-expanding stent implantation,and his condition stabilized.The second case was of a 56-year-old male patient with speechlessness and paralysis of the right limb.Cervical CTA showed a dissected left ICA,and DSA showed an occluded left ICA and middle cerebral artery.The patient subsequently underwent stent implantation,and his condition stabilized.

Systemic air embolism in a fungal pneumonia patient with lung cavities formation and review of literature

Systemic air embolism is a rare but potentially fatal complication related to many factors.The purpose of this article is to alert clinicians once patients occurs an abnormal neurological and cardiovascular status,following minor traumatic treatment,air embolism should be considered.A 20-year-old man who presented with fungal pneumonia with lung cavities formation was adm让ted to an intensive care unit(ICU)and received positive airway pressure ventilation.Four days later,the fun gal pneumonia was improved,but the patient's blood pressure and arterial oxygen saturation deteriorated,so computed tomography(CT)scans were preformed to reevaluate him.The scans detected air embolism in the left atrium and ventricle,ascending aorta,aortic arch and its branches(right brachiocephalic,bilateral common carotid and right subclavian arteries),descending aorta and right coronary artery.A CT scan of the abdomen revealed air in the spleen,cauda pancreatic,superior mesenteric artery and right external iliac artery.The patient died two days later from multiple organ dysfunction.We suggest that vascular air embolism should be considered under mechanical ventilation when patients'neurologic and cardiovascular status deteriorates,and hyperbaric oxygen therapy should be conducted immediately.

HPDL deficiency causes a neuromuscular disease by impairing the mitochondrial respiration

Mitochondrial diseases are caused by variants in both mitochondrial and nuclear genomes.A nuclear gene HPDL(4-hydroxyphenylpyruvate dioxygenase-like),which encodes an intermembrane mitochondrial protein,has been recently implicated in causing a neurodegenerative disease characterized by pediatric-onset spastic movement phenotypes.Here,we report six Chinese patients with bi-allelic HPDL pathogenic variants from four unrelated families showing neuropathic symptoms of variable severity,including developmental delay/intellectual disability,spasm,and hypertonia.Seven different pathogenic variants are identified,of which five are novel.Both fibroblasts and immortalized lymphocytes derived from patients show impaired mitochondrial respiratory function,which is also observed in HPDL-knockdown(KD)He La cells.In these He La cells,overexpression of a wild-type HPDL gene can rescue the respiratory phenotype of oxygen consumption rate.In addition,a decreased activity of the oxidative phosphorylation(OXPHOS)complex II is observed in patient-derived lymphocytes and HPDL-KD He La cells,further supporting an essential role of HPDL in the mitochondrial respiratory chain.Collectively,our data expand the clinical and mutational spectra of this mitochondrial neuropathy and further delineate the possible disease mechanism involving the impairment of the OXPHOS complex II activity due to the bi-allelic inactivations of HPDL.