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The current paper presents the results of numerical and experimental clocking investigations performed in a high-pressure transonic turbine with a downstream vane row. The objective was a detailed analysis of shock and wake interactions in such a 1.5-stage machine while clocking the vanes. Therefore, a transient 3D Navier-Stokes calculation was done for two clocking positions, and the three-dimensional results are compared with laser-Doppler-velocimetry measurements at midspan. Additionally, the second vane was equipped with fast response pressure transducers to record the instantaneous surface pressure for 20 different clocking positions at midspan.

This paper presents an experimental investigation of the flow field in a high-pressure transonic turbine with a downstream vane row (1.5 stage machine) concerning the airfoil indexing. The objective is a detailed analysis of the three-dimensional aerodynamics of the second vane for different clocking positions. To give an overview of the time-averaged flow field, five-hole probe measurements were performed upstream and downstream of the second stator. Furthermore in these planes additional unsteady measurements were carried out with laser Doppler velocimetry in order to record rotor phase-resolved velocity, flow angle, and turbulence distributions at two different clocking positions. In the planes upstream of the second vane, the time-resolved pressure field has been measured by means of a fast response aerodynamic pressure probe. This paper shows that the secondary flows of the second vane are significantly modified by the different clocking positions, in connection with the first vane modulation of the rotor secondary flows. An analysis of the performance of the second vane is also carried out, and a 0.6% variation in the second vane loss coefficient has been recorded among the different clocking positions. [DOI: 10.1115/1.3072715]

The demand of further increased bypass ratios for turbofan engines will lead to low pressure turbines with larger diameter and lower rotational speed in conventional highbypass aeroengine architectures. Due to that, it is necessary to guide the flow leaving the high pressure turbine to the low pressure turbine at a larger diameter without any severe loss generating separation or flow disturbances. To reduce costs and weight this turbine duct has to be as short as possible. This results in superaggressive (very high diffusion) S-shaped geometries where the boundary layers are not able to withstand the strong adverse pressure gradient, which results inflow separation. This paper describes the flow through a fully separated duct as a baseline configuratiOn. In a next step the influence of passive flow control devices onto this separation has been investigated. Therefore, lowprofile vortex generators were applied within the first bend of this S-shaped intermediate turbine diffuser in order to energize the boundary layer and further reduce or even suppress the occurring separation. This configuration was investigated downstream a transonic turbine stage. Measurements were performed by means of five-hole-probes, static wall pressure taps, and oil flow visualization at the duct endwalls. For a better understanding of the flow behavior the vortex generators were also investigated in a two-dimensional rectangular S-shaped duct using the same Mach number level. Results showed that the vortex generators reduce the separation in the 2D-duct but have no distinct influence on the separation within the turbine duct due to wakes as well as strong secondary flow effects. [ABSTRACT FROM AUTHOR]

An abstract of the article "Congenital cytomegalovirus infection: an interesting case of clinical, molecular and pathologic correlations," S. Visentin and colleagues is presented.

Abstract Under certain experimental conditions, neurotrophic factors may reduce epileptogenesis. We have previously reported that local, intrahippocampal supplementation of fibroblast growth factor-2 (FGF-2) and brain-derived neurotrophic factor (BDNF) increases neurogenesis, reduces neuronal loss, and reduces the occurrence of spontaneous seizures in a model of damage-associated epilepsy. Here, we asked if these possibly anti-epileptogenic effects might involve anti-inflammatory mechanisms. Thus, we used a Herpes-based vector to supplement FGF-2 and BDNF in rat hippocampus after pilocarpine-induced status epilepticus that established an epileptogenic lesion. This model causes intense neuroinflammation, especially in the phase that precedes the occurrence of spontaneous seizures. The supplementation of FGF-2 and BDNF attenuated various parameters of inflammation, including astrocytosis, microcytosis and IL-1β expression. The effect appeared to be most prominent on IL-1β, whose expression was almost completely prevented. Further studies will be needed to elucidate the molecular mechanism(s) for these effects, and for that on IL-1β in particular. Nonetheless, the concept that neurotrophic factors affect neuroinflammation in vivo may be highly relevant for the understanding of the epileptogenic process.

Sudden infant death syndrome (SIDS) "gray zone" or borderline cases are those in which it is challenging to define whether the pathological findings are sufficiently severe to lead to death. We report a case of a 17-day old male newborn who came to our attention for unexplained death. A complete autopsy was performed, including close examination of the cardiac conduction system. Lungs presented diffuse alveolar damage and interstitial inflammation, the cardiac conduction system showed fetal dispersion, resorptive degeneration, junctional tissue islands and cartilaginous hypermetaplasia of the central fibrous body. The final cause of death was a "gray zone" SIDS. This case report will highlight the intersection of SIDS and pneumonia in newborns, exploring the challenges and controversies surrounding the diagnosis and management of this complex condition., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Inc. All rights reserved.)

This review explores the historical development of cardiology knowledge, from ancient Egyptian psychostasis to the modern comprehension of cardiac neuromodulation. In ancient Egyptian religion, psychostasis was the ceremony in which the deceased was judged before gaining access to the afterlife. This ritual was also known as the "weighing of the heart" or "weighing of the soul". The Egyptians believed that the heart, not the brain, was the seat of human wisdom, emotions, and memory. They were the first to recognize the cardiocentric nature of the body, identifying the heart as the center of the circulatory system. Aristotle (fourth century BC) considered the importance of the heart in human physiology in his philosophical analyses. For Galen (third century AD), the heart muscle was the site of the vital spirit, which regulated body temperature. Cardiology knowledge advanced significantly in the 15th century, coinciding with Leonardo da Vinci and Vesalius's pioneering anatomical and physiological studies. It was William Harvey, in the 17th century, who introduced the concept of cardiac circulation. Servet's research and Marcello Malpighi's discovery of arterioles and capillaries provided a more detailed understanding of circulation. Richard Lower emerged as the foremost pioneer of experimental cardiology in the late 17th century. He demonstrated the heart's neural control by tying off the vagus nerve. In 1753, Albrecht von Haller, a professor at Göttingen, was the first to discover the heart's automaticity and the excitation of muscle fibers. Towards the end of the 18th century, Antonio Scarpa challenged the theories of Albrecht von Haller and Johann Bernhard Jacob Behrends, who maintained that the myocardium possessed its own "irritability", on which the heartbeat depended, and was independent of neuronal sensitivity. Instead, Scarpa argued that the heart required innervation to maintain life, refuting Galenic notions. In contemporary times, the study of cardiac innervation has regained prominence, particularly in understanding the post-acute sequelae of SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection (PASC), which frequently involves cardiorespiratory symptoms and dysregulation of the intrinsic cardiac innervation. Recently, it has been recognized that post-acute sequelae of acute respiratory infections (ARIs) due to other pathogens can also be a cause of long-term vegetative and somatic symptoms. Understanding cardiac innervation and modulation can help to recognize and treat long COVID and long non-COVID-19 (coronavirus disease 2019) ARIs. This analysis explores the historical foundations of cardiac neuromodulation and its contemporary relevance. By focusing on this concept, we aim to bridge the gap between historical understanding and modern applications. This will illuminate the complex interplay between cardiac function, neural modulation, cardiovascular health, and disease management in the context of long-term cardiorespiratory symptoms and dysregulation of intrinsic cardiac innervations.

Cerebellum is devoted to motor coordination and cognitive functions. Endoplasmic reticulum is the largest intracellular calcium store involved in all neuronal functions. Intralumenal calcium binding proteins play a pivotal role in calcium storage and contribute to both calcium release and uptake. Calsequestrin, a key calcium binding protein of sarco-endoplasmic reticulum in skeletal and cardiac muscles, was identified in chicken and fish cerebellum Purkinje cells, but its expression in mammals and human counterpart has not been studied in depth. Aim of the present paper was to investigate expression and localization of Calsequestrin in mammalian cerebellum. Calsequestrin was found to be expressed at low level in cerebellum, but specifically concentrated in Calbindin D28- and zebrin- immunopositive-Purkinje cells. Two additional fundamental calcium store markers, sarco-endoplasmic calcium pump isoform 2, SERCA2, and Inositol-trisphosphate receptor isoform 1, IP3R1, were found to be co-expressed in the region, with some localization peculiarities. In conclusion, a new marker was identified for Purkinje cells in adult mammals, including humans. Such a marker might help in staminal neuronal cells specification and in dissection of still unknown neurodegeneration and physio-pathological effects of dysregulated calcium homeostasis., Competing Interests: Conflict of interest The authors have no conflicts of interest to declare., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

Several lines of evidence link deficient serotonin function and SUDEP. Chronic treatment with serotonin reuptake inhibitors (SRIs) reduces ictal central apnoea, a risk factor for SUDEP. Reduced medullary serotonergic neurones, modulators of respiration in response to hypercapnia, were reported in a SUDEP post-mortem series. The amygdala and hippocampus have high serotonergic innervation and are functionally implicated in seizure-related respiratory dysregulation. We explored serotonergic networks in mesial temporal lobe structures in a surgical and post-mortem epilepsy series in relation to SUDEP risk. We stratified 75 temporal lobe epilepsy patients with hippocampal sclerosis (TLE/HS) into high (N = 16), medium (N = 11) and low risk (N = 48) groups for SUDEP based on generalised seizure frequency. We also included the amygdala in 35 post-mortem cases, including SUDEP (N = 17), epilepsy controls (N = 10) and non-epilepsy controls (N = 8). The immunohistochemistry labelling index (LI) and axonal length (AL) of serotonin transporter (SERT)-positive axons were quantified in 13 regions of interest with image analysis. SERT LI was highest in amygdala and subiculum regions. In the surgical series, higher SERT LI was observed in high risk than low risk cases in the dentate gyrus, CA1 and subiculum (p < 0.05). In the post-mortem cases higher SERT LI and AL was observed in the basal and accessory basal nuclei of the amygdala and peri-amygdala cortex in SUDEP compared to epilepsy controls (p < 0.05). Patients on SRI showed higher SERT in the dentate gyrus (p < 0.005) and CA4 (p < 0.05) but there was no difference in patients with or without a psychiatric history. Higher SERT in hippocampal subfields in TLE/HS cases with SUDEP risk factors and higher amygdala SERT in post-mortem SUDEP cases than epilepsy controls supports a role for altered serotonergic networks involving limbic regions in SUDEP. This may be of functional relevance through reduced 5-HT availability., (© 2022 The Authors. Brain Pathology published by John Wiley & Sons Ltd on behalf of International Society of Neuropathology.)

This article is aimed to contribute to the current knowledge on the role of toxic substances such as nicotine on sudden intrauterine unexplained deaths' (SIUDS') pathogenetic mechanisms. The in-depth histopathological examination of the autonomic nervous system in wide groups of victims of SIUDS (47 cases) and controls (20 cases), with both smoking and no-smoking mothers, highlighted the frequent presence of the hypodevelopment of brainstem structures checking the vital functions. In particular, the hypoplasia of the pontine parafacial nucleus together with hypoplastic lungs for gestational age were observed in SIUDS cases with mothers who smoked cigarettes, including electronic ones. The results allow us to assume that the products of cigarette smoke during pregnancy can easily cross the placental barrier, thus entering the fetal circulation and damaging the most sensitive organs, such as lungs and brain. In a non-negligible percentage of SIUDS, the mothers did not smoke. Furthermore, based on previous and ongoing studies conducted through analytical procedures and the use of scanning electron microscopy, the authors envisage the involvement of toxic nanoparticles (such as agricultural pesticides and nanomaterials increasingly used in biomedicine, bioscience and biotechnology) in the death pathogenesis, with similar mechanisms to those of nicotine.

Sudden unexpected infant death (SUID) is a major cause of death in infants < 1 year of age. Sudden infant death syndrome (SIDS) is a SUID still unexplained after post-mortem examination. In 2014, a protocol of post-mortem investigation was introduced to assess both the prevalence and the etiopathogenesis of SUID. Our aim was to compare SUID data before and after the application of a standardized autopsy protocol of investigation. In the time interval 2004-2018, SUID cases occurring in the Veneto Region, North-East Italy, were referred to our Core Lab. Since 2014, a complete autopsy was performed, including gross and histological study with toxicologic and molecular analysis carried out at the referral center. A total of 36 SUIDs (22 M, mean age 95.5 ± 80 days), 17 before (group A) and 19 after (group B) 2014, were collected. In group A, only 1 (6%) resulted as explained SUID, due to lymphocytic myocarditis and 16 (94%) were SIDS. In group B, 8 were SIDS (42%) and 11 (58%) explained SUID cases (p < 0.01), consisting of interstitial pneumonia and bronchiolitis in 9 and lymphocytic myocarditis in 2 cases. Molecular analysis was positive for viruses in 8 of them (73%). In conclusion, since the application of a standardized protocol of post-mortem investigation, inflammatory, mostly infective, cardio-pulmonary diseases have been identified as the most common cause of SUID, with SIDS falling from 94 to 42% of SUID. Efforts must be made to implement a uniform autopsy protocol to provide reliable epidemiological data on SIDS.

Objective: The "adenosine hypothesis of SUDEP" (sudden unexpected death in epilepsy) predicts that a seizure-induced adenosine surge combined with impaired metabolic clearance can foster lethal apnea or cardiac arrest. Changes in adenosine receptor density and adenosine kinase (ADK) occur in surgical epilepsy patients. Our aim was to correlate the distribution of ADK and adenosine A 2A and A 1 receptors (A 2A R and A 1 R) in surgical tissue from patients with temporal lobe epilepsy and hippocampal sclerosis (TLE/HS) with SUDEP risk factors., Methods: In 75 cases, patients were stratified into high-risk (n = 16), medium-risk (n = 11) and low-risk (n = 48) categories according to the frequency of generalized seizures before surgery. Using whole-slide scanning Definiens image analysis we quantified the labeling index (LI) for ADK, A 2A R, and A 1 R in seven regions of interest: temporal cortex, temporal lobe white matter, CA1, CA4, dentate gyrus, subiculum, and amygdala and relative to glial and neuronal densities with glial fibrillary acidic protein (GFAP) and neuronal nuclear antigen (NeuN)., Results: A 1 R showed predominant neuronal, A 2A R astroglial, and ADK nuclear labeling in all regions but with significant variation. Compared with the low-risk group, the high-risk group had significantly lower A 2A R LI in the temporal cortex. In HS cases with severe neuronal cell loss and gliosis predominantly in the CA1 and CA4 regions, significantly higher A 1 R was present in the amygdala in high-risk than in low-risk cases. There was no significant difference in neuronal loss or gliosis between the risk groups or differences for ADK labeling., Significance: Reduced cortical A 2A R suggests glial dysfunction and impaired adenosine modulation in response to seizures in patients at higher risk for SUDEP. Increased neuronal A 1 R in the high-risk group could contribute to periictal amygdala dysfunction in SUDEP., (© 2020 The Authors. Epilepsia published by Wiley Periodicals, Inc. on behalf of International League Against Epilepsy.)

Central failure of respiration during a seizure is one possible mechanism for sudden unexpected death in epilepsy (SUDEP). Neuroimaging studies indicate volume loss in the medulla in SUDEP and a post mortem study has shown reduction in neuromodulatory neuropeptidergic and monoaminergic neurones in medullary respiratory nuclear groups. Specialised glial cells identified in the medulla are considered essential for normal respiratory regulation including astrocytes with pacemaker properties in the pre-Botzinger complex and populations of subpial and perivascular astrocytes, sensitive to increased pCO 2, that excite respiratory neurones. Our aim was to explore niches of medullary astrocytes in SUDEP cases compared to controls. In 48 brainstems from three groups, SUDEP (20), epilepsy controls (10) and non-epilepsy controls (18), sections through the medulla were labelled for GFAP, vimentin and functional markers, astrocytic gap junction protein connexin43 (Cx43) and adenosine A1 receptor (A1R). Regions including the ventro-lateral medulla (VLM; for the pre-Bötzinger complex), Median Raphe (MR) and lateral medullary subpial layer (MSPL) were quantified using image analysis for glial cell populations and compared between groups. Findings included morphologically and regionally distinct vimentin/Cx34-positive glial cells in the VLM and MR in close proximity to neurones. We noted a reduction of vimentin-positive glia in the VLM and MSPL and Cx43 glia in the MR in SUDEP cases compared to control groups (p < 0.05-0.005). In addition, we identified vimentin, Cx43 and A1R positive glial cells in the MSPL region which likely correspond to chemosensory glia identified experimentally. In conclusion, altered medullary glial cell populations could contribute to impaired respiratory regulatory capacity and vulnerability to SUDEP and warrant further investigation., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: Radiofrequency (RF) catheter ablation is one of the most common strategies for the current management of cavotricuspid isthmus (CTI)-dependent atrial flutter (AFL). The interindividual anatomic variability can influence the duration and outcome of ablation procedure., Objective: The purpose of this study was to establish complication rates in patients undergoing RF catheter ablation for CTI-dependent AFL, assess the role of CTI morphology in procedural success, and determine the anatomic variability of CTI ex vivo., Methods: RF catheter ablation for CTI-dependent AFL was performed in 337 consecutive patients. Angiographically determined CTI morphology was classified as either simple or complex due to pouchlike recesses. Macroscopic and histologic examination of the CTI was performed in 104 heart specimens from consecutive autopsies., Results: Complex CTI anatomy was present in 10.9% of AFL patients. RF application time to achieve bidirectional isthmus block was longer in patients showing pouchlike recesses than in those without (10.7 vs 8.3 min; P= .025). Acute procedure failure or major complications occurred in 3 cases, all with complex CTI anatomy. A pouchlike recess of the CTI was present in 9.6% of autopsy hearts. Histomorphometric analysis of the CTI atrial wall demonstrated that the central level was the thinnest in the 3 sectors and the paraseptal level was the thickest., Conclusion: Although RF catheter ablation is a safe and effective procedure for AFL treatment, CTI anatomic complexity can affect ablation parameters and outcome. Standard definition of CTI morphologic variants is recommended. Preprocedural assessment of CTI anatomy might lead to personalized ablation preventing potential difficulties and complications., (Copyright © 2019 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.)

Objective: To find a possible pathogenetic mechanism of the early sudden infant death occurring in newborns during the skin-to-skin care (SSC), through the examination of neuronal centers regulating the vital activities., Study Design: This is an in-depth examination of the brain stem in 22 healthy term newborns, suddenly died in the first hour of life without the identification of a cause at autopsy (early sudden infant death syndrome [eSIDS]), 12 of them concomitantly with SSC, and 10 with age-matched controls died of known pathology., Results: Developmental alterations of neuronal structures of the brain stem were highlighted in 19 of the 22 eSIDS, but not in control. The hypoplasia of the pontine Kölliker-Fuse nucleus (KFN), an important respiratory center, was diagnosed at the histological examination, validated by morphometric quantifications, in 11 of the 12 eSIDS while they were placed on the mother's chest and in 2 of the 10 SSC unrelated neonatal deaths., Conclusion: The delayed development of the KFN could represent a specific finding of eSIDS occurring during SSC. Therefore, it is necessary to point out that the SSC represents a further risk factor that must be added to others already known for sudden infant death syndrome. Then this practice needs appropriate monitoring strategies of the infant's conditions., Competing Interests: None., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)