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Background: Pulmonary vein stenosis is a progressive disease associated with a high rate of mortality in children. If left untreated, myofibroblastic proliferation can lead to pulmonary vein atresia (PVA). In our experience, transcatheter recanalization has emerged as a favorable interventional option. We sought to determine the acute success rate of recanalization of atretic pulmonary veins and mid-term outcomes of individual veins after recanalization. Methods: We reviewed all patients with PVA at our institution between 2008 and 2020 diagnosed by either catheterization or cardiac computed tomography. All veins with successful recanalization were reviewed and procedural success rate and patency rate were noted. Competing risk analysis was performed to demonstrate outcomes of individual atretic veins longitudinally. Results: Between 2008 and 2020, our institution diagnosed and treated 131 patients with pulmonary vein stenosis. Of these, 61 patients developed atresia of at least one pulmonary vein. In total, there were 97 atretic pulmonary veins within this group. Successful recanalization was accomplished in 47/97 (48.5%) atretic veins. No atretic pulmonary veins were successfully recanalized before 2012. The majority of veins were recanalized between 2017 and 2020—39/56 (70%). The most common intervention after recanalization was drug-eluting stent placement. At 2-year follow-up 42.6% of recanalized veins (20.6% of all atretic veins) remained patent with a median of 4 reinterventions per person. Conclusions: Transcatheter recanalization of PVA can result in successful reestablishment of flow to affected pulmonary veins in many cases. Drug-eluting stent implantation was the most common intervention performed immediately post-recanalization. Vein patency was maintained in 42.6% of patients at 2-year follow-up from recanalization with appropriate surveillance and reintervention. Overall, only a small portion of atretic pulmonary veins underwent successful recanalization with maintained vessel patency at follow-up. Irrespective of successful recanalization, there was no detectable survival difference between the more recently treated PVA cohort and non-PVA cohort.

Background Anatomic interventions for pulmonary vein stenosis (PVS) in infants and children have been met with limited success. Sirolimus, a mammalian target of rapamycin inhibitor, has demonstrated promise as a primary medical therapy for PVS, but the impact on patient survival is unknown. Objectives The authors sought to investigate whether mTOR inhibition with sirolimus as a primary medical therapy would improve outcomes in high-risk infants and children with PVS. Methods In this single-center study, patients with severe PVS were considered for systemic sirolimus therapy (SST) following a strict protocol while receiving standardized surveillance and anatomic therapies. The SST cohort was compared with a contemporary control group. The primary endpoint for this study was survival. The primary safety endpoint was adverse events (AEs) related to SST. Results Between 2015 and 2020, our PVS program diagnosed and treated 67 patients with ≥moderate PVS. Of these, 15 patients were treated with sirolimus, whereas the remaining patients represent the control group. There was 100% survival in the SST group compared with 45% survival in the control group (log-rank p = 0.004). A sensitivity analysis was completed to address survival bias using median time from diagnosis of PVS to SST. A survival advantage persisted (log-rank p = 0.027). Two patients on sirolimus developed treatable AEs. Patients in the SST group underwent frequent transcatheter interventions with 3.7 catheterizations per person-year (25th to 75th percentile: 2.7 to 4.4 person-years). Median follow up time was 2.2 years (25th to 75th percentile: 1.2 to 2.9 years) in the SST group versus 0.9 years (25th to 75th percentile: 0.5 to 2.7 years) in the control group. Conclusions The authors found a survival benefit associated with SST in infants and children with moderate-to-severe PVS. This survival benefit persisted after adjusting the analysis for survival bias. There were 2 mild AEs associated with SST during the study period; both patients were able to resume therapy without recurrence.

Due to high efficiency, cycling life, and specific energy, the Lithium-ion battery has been the best-favored selection for the Electric Vehicles (EV’s) despite high cost. The performance of the battery pack is strongly dependent on the operation condition of the EV’s and the environment. Under the extreme operation and environmental conditions of the battery, the rate of heat generation is very high which adversely affects the dissipation rate, decreases the battery life, and sometimes leads to the explosion and fire (i.e. thermal runaway). In electric vehicles, the battery thermal management technology plays a crucial role when the temperature of the cell rises exponentially during the operating environment. The temperature, therefore, between (15 to 35 °C) should be controlled. Our work presents the modeling of heat generation in the battery pack under various operation conditions. The parametric studies have been conducted to study the effect of battery operation conditions on heat generation rate and battery pack temperature. This study would be very useful in the selection of battery thermal management technology to control the battery temperature to retain the optimum condition.

Summary Background To investigate the incidence of death and of new cardiovascular events at long-term follow-up of patients with and without PAD seen in a vascular surgery clinic. Material/Methods We investigated the incidence of death, new stroke/transient ischemic attack, new myocardial infarction, new coronary revascularization, new carotid endarterectomy, new peripheral arterial disease (PAD) revascularization, or at least one of the above outcomes at long-term follow-up of patients with and without PAD followed in a vascular surgery clinic. Results At least one of the above outcomes occurred in 259 of 414 patients (63%) with PAD at 33-month follow-up and in 21 of 89 patients (24%) without PAD at 48-month follow-up (p

Apicomplexan parasites undergo cell division using an evolutionarily conserved mechanism first described in the positioning and assembly of flagella in algae., Apicomplexa are intracellular parasites that cause important human diseases including malaria and toxoplasmosis. During host cell infection new parasites are formed through a budding process that parcels out nuclei and organelles into multiple daughters. Budding is remarkably flexible in output and can produce two to thousands of progeny cells. How genomes and daughters are counted and coordinated is unknown. Apicomplexa evolved from single celled flagellated algae, but with the exception of the gametes, lack flagella. Here we demonstrate that a structure that in the algal ancestor served as the rootlet of the flagellar basal bodies is required for parasite cell division. Parasite striated fiber assemblins (SFA) polymerize into a dynamic fiber that emerges from the centrosomes immediately after their duplication. The fiber grows in a polarized fashion and daughter cells form at its distal tip. As the daughter cell is further elaborated it remains physically tethered at its apical end, the conoid and polar ring. Genetic experiments in Toxoplasma gondii demonstrate two essential components of the fiber, TgSFA2 and 3. In the absence of either of these proteins cytokinesis is blocked at its earliest point, the initiation of the daughter microtubule organizing center (MTOC). Mitosis remains unimpeded and mutant cells accumulate numerous nuclei but fail to form daughter cells. The SFA fiber provides a robust spatial and temporal organizer of parasite cell division, a process that appears hard-wired to the centrosome by multiple tethers. Our findings have broader evolutionary implications. We propose that Apicomplexa abandoned flagella for most stages yet retained the organizing principle of the flagellar MTOC. Instead of ensuring appropriate numbers of flagella, the system now positions the apical invasion complexes. This suggests that elements of the invasion apparatus may be derived from flagella or flagellum associated structures., Author Summary Malaria, toxoplasmosis, and related diseases are caused by infection with unicellular parasites called Apicomplexa. Their name refers to the elaborate invasion machinery that occupies the apical end of the parasite cell. This apparatus allows the parasite to force its way into the cells of its host, and to deliver factors that will manipulate host cell structure, gene expression, and metabolism. Once in the host cell the parasite will begin to grow. The parasite replicates its genome and organelles numerous times and then loads these various elements into numerous daughter cells that will further spread the infection. Here we report a fiber that coordinates the daughter cell budding process. The fiber links the centrosome, which controls the mitotic spindle, and the genome with the microtubule organizing center of the budding daughter. Parasite mutants lacking the proteins that build the fiber fail to form daughter cells at the earliest step. The fiber and its components are remarkably similar to fibers that coordinate flagella in algae. While Apicomplexa are not flagellated (with the exception of certain gamete stages) they evolved from flagellated algae. We propose that elements of the invasion apparatus evolved from the flagellum or flagellum associated structures.