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Objetivo: analisar as características e os desfechos obstétricos adversos em gestantes/puérperas infectadas pelo SARS-CoV-2 em serviço de referência. Método: série de casos retrospectiva entre gestantes com Covid-19 em um hospital universitário em Minas Gerais, Brasil, atendidas no serviço de 2020 a 2021, coletados em abril de 2022, empregando-se estatística descritiva para análise dos dados através do Statistical Package for the Social Science. Resultados: incluídas 26 gestantes, em sua maioria brancas, que tiveram como principais desfechos obstétricos adversos a internação em UTI (43,5%), parto prematuro (34,6%), dado reestratificado de semanas para dias para investigar o encurtamento da gestação, onde constatou-se média de 38,6 dias potenciais de gravidez perdidos dos 280 dias ideais, e ainda 15,4% evoluíram para óbito materno. Conclusão: o estudo proporcionou evidenciar a necessidade de vigilância e atenção às gestantes com foco nos principais desfechos adversos, podendo-se intervir em tempo oportuno para diminuir adversidades.
Objective: to analyze the characteristics and adverse obstetric outcomes in pregnant/puerperal women infected by SARS-CoV-2 at a reference service. Method: a retrospective case series conducted among pregnant women with Covid-19 in a university hospital from Minas Gerais, Brazil, treated at the service from 2020 to 2021. The cases were collected in April 2022 employing descriptive statistics for data analysis in the Statistical Package for the Social Science. Results: a total of 26 pregnant women were included, mostly white-skinned, whose main adverse obstetric outcomes were admission to the ICU (43.5%), premature birth (34.6%) and data restratified from weeks to days to investigate shortening of pregnancy, where a mean of 38.6 potential days of pregnancy were lost out of the ideal 280 days, and 15.4% resulted in maternal death. Conclusion: the study provided evidence of the need for surveillance and care for pregnant women with a focus on the main adverse outcomes, enabling timely intervention to reduce adversities.
Objetivo: analizar las características y resultados obstétricos adversos en gestantes/puérperas infectadas por SARS-CoV-2 en un servicio de referencia. Método: serie de casos retrospectiva entre gestantes con Covid-19 en un hospital universitario de Minas Gerais, Brasil, atendidas en el servicio de 2020 a 2021. Los datos se recolectaron en abril de 2022, se utilizó estadística descriptiva para analizar los datos mediante el Statistical Package for the Social Science. Resultados: se incluyeron 26 gestantes, la mayoría de raza blanca, cuyos principales resultados obstétricos adversos fueron ingreso a UCI (43,5%), parto prematuro (34,6%), dato reestratificado de semanas a días para investigar el acortamiento de la gestación, que arrojó como resultado un promedio de 38,6. Se comprobó que se perdieron en promedio 38,6 días potenciales de embarazo de los 280 días ideales, y muerte materna (15,4%). Conclusión: la evidencia que proporcionó el estudio indica que es necesario vigilar y atender a las gestantes enfocándose en los principales resultados adversos, lo que permite intervenir de forma oportuna para reducir adversidades.
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BACKGROUND: This study compared the mortality risk of long-lived siblings with the U.S. population average and their spouse controls, and investigated the leading causes of death and the familial effect in death pattern. METHODS: In the Long Life Family Study (LLFS), 1,264 proband siblings (Mean age 90.1, SD 6.4) and 172 spouses (83.8, 7.2) from 511 U.S.-based families were recruited and followed over 12 years. Their survival function was compared with a birth cohort-, baseline age-, sex-, and race-matched pseudo sample from U.S. census data. To examine underlying and contributing causes, we examined in detail 338 deaths with complete death adjudication at the University of Pittsburgh Field Center through the year 2018. A familial effect on survival and death pattern was examined using mixed effect models. RESULTS: The LLFS siblings had better survival than the matched U.S. population average. They also had slightly but not significantly better survival than their spouses' (HR=1.18 [95%CI 0.94-1.49]) after adjusting for age and sex. Age at death ranged from 75-104 years, mean 91.4. The leading causes of death were cardiovascular disease (33.1%), dementia (22.2%), and cancer (10.7%). Mixed effect model shows a significant random effect of family in survival, with adjustment of baseline age and sex. There was no significant familial effect in the underlying cause of death or conditions directly contributing to death among siblings recruited by the University of Pittsburgh Field Center. CONCLUSION: Our findings demonstrate a higher survival in the LLFS siblings than the U.S. census data, with a familial component of survival. We did not find significant correspondence in causes of death between siblings within families.
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BACKGROUND: Dyslipidemia increases cardiovascular disease risk, the leading cause of death worldwide. Under time-restricted feeding (TRF), wherein food intake is restricted to a consistent window of <12 hours, weight gain, glucose intolerance, inflammation, dyslipidemia, and hypercholesterolemia are all reduced in mice fed an obesogenic diet. LDLR (low-density lipoprotein receptor) mutations are a major cause of familial hypercholesterolemia and early-onset cardiovascular disease. METHODS: We subjected benchmark preclinical models, mice lacking LDLR-knockout or ApoE knockout to ad libitum feeding of an isocaloric atherogenic diet either ad libitum or 9 hours TRF for up to 13 weeks and assessed disease development, mechanism, and global changes in hepatic gene expression and plasma lipids. In a regression model, a subset of LDLR-knockout mice were ad libitum fed and then subject to TRF. RESULTS: TRF could significantly attenuate weight gain, hypercholesterolemia, and atherosclerosis in mice lacking the LDLR-knockout mice under experimental conditions of both prevention and regression. In LDLR-knockout mice, increased hepatic expression of genes mediating ß-oxidation during fasting is associated with reduced VLDL (very-low-density lipoprotein) secretion and lipid accumulation. Additionally, increased sterol catabolism coupled with fecal loss of cholesterol and bile acids contributes to the atheroprotective effect of TRF. Finally, TRF alone or combined with a cholesterol-free diet can reduce atherosclerosis in LDLR-knockout mice. However, mice lacking ApoE, which is an important protein for hepatic lipoprotein reuptake do not respond to TRF. CONCLUSIONS: In a preclinical animal model, TRF is effective in both the prevention and regression of atherosclerosis in LDLR knockout mice. The results suggest TRF alone or in combination with a low-cholesterol diet can be a lifestyle intervention for reducing cardiovascular disease risk in humans.
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OBJECTIVE: Understanding the local characteristics and statistics related to stillbirths may be the first step in a series of strategies associated with a reduction in stillbirth ratio. The aim of this study was to estimate the fetal mortality ratio and evaluate the investigation processes related to the causes of death, comparing the investigation according to the specific cause of death. METHODS: A cross-sectional study was retrospectively conducted in 10 tertiary obstetric care centers. Medical records of women with stillbirth managed between January 1, 2009 and December 31, 2018 were analyzed and classified, according to sociodemographic characteristics, and gestational and childbirth data, culminating in stillbirth. The stillbirth ratio and its causes were presented in proportions for the study period and individually for each health facility. RESULTS: Cases of 3390 stillbirths were analyzed. The stillbirth ratio varied from 10.74/1000 live births (LBs) in 2009 to 9.31/1000 in 2018. "Intrauterine hypoxia and asphyxia" (ICD-10 P20) and "unspecific causes of death" (ICD-10 P95) represented 40.8% of the causes of death. Investigation for TORCHS and diabetes occurred in 90.8% and 61.4% of deaths, respectively. Placental and necroscopic tests were performed in 36.6% of the cases. CONCLUSION: The adoption of a rational and standardized investigation of stillbirth remains an unmet need; the use of additional tests and examinations are lacking, especially when unspecific causes are attributed.
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Serine protease inhibitors (serpins) constitute the largest family of protease inhibitors expressed in humans, but their role in infection remains largely unexplored. In infected macrophages, the mycobacterial ESX-1 type VII secretion system permeabilizes internal host membranes and causes leakage into the cytosol of host DNA, which induces type I interferon (IFN) production via the cyclic GMP-AMP synthase (cGAS) and stimulator of IFN genes (STING) surveillance pathway, and promotes infection in vivo. Using the Mycobacterium marinum infection model, we show that ESX-1-mediated type I IFN signaling in macrophages selectively induces the expression of serpina3f and serpina3g, two cytosolic serpins of the clade A3. The membranolytic activity of ESX-1 also caused leakage of cathepsin B into the cytosol where it promoted cell death, suggesting that the induction of type I IFN comes at the cost of lysosomal rupture and toxicity. However, the production of cytosolic serpins suppressed the protease activity of cathepsin B in this compartment and thus limited cell death, a function that was associated with increased bacterial growth in infected mice. These results suggest that cytosolic serpins act in a type I IFN-dependent cytoprotective feedback loop to counteract the inevitable toxic effect of ESX-1-mediated host membrane rupture. IMPORTANCE: The ESX-1 type VII secretion system is a key virulence determinant of pathogenic mycobacteria. The ability to permeabilize host cell membranes is critical for several ESX-1-dependent virulence traits, including phagosomal escape and induction of the type I interferon (IFN) response. We find that it comes at the cost of lysosomal leakage and subsequent host cell death. However, our results suggest that ESX-1-mediated type I IFN signaling selectively upregulates serpina3f and serpina3g and that these cytosolic serpins limit cell death caused by cathepsin B that has leaked into the cytosol, a function that is associated with increased bacterial growth in vivo. The ability to rupture host membranes is widespread among bacterial pathogens, and it will be of interest to evaluate the role of cytosolic serpins and this type I IFN-dependent cytoprotective feedback loop in the context of human infection.
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BACKGROUND: Non-small-cell lung cancer (NSCLC) often presents at later stages, typically associated with poor prognosis. Autophagy genes play a role in the progression of tumors. This study investigated the clinical relevance, prognostic value, and biological significance of RBBP4 in NSCLC. METHODS: We assessed RBBP4 expression using the GSE30219 and TCGA NSCLC datasets and NSCLC cells, exploring its links with clinical outcomes, tumor immunity, and autophagy genes through bioinformatics analysis after transcriptome sequencing of RBBP4-knockdown and control PC9 cells. We identified differentially expressed genes (DEGs) and conducted Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway enrichment, and protein-protein interaction network analyses. The significance of autophagy-related DEGs was evaluated for diagnosis and prognosis using the GSE30219 dataset. Experiments both in vivo and in vitro explored the biological mechanisms behind RBBP4-mediated autophagic cell death in NSCLC. RESULTS: RBBP4 overexpression in NSCLC correlates with a poorer prognosis. Eighteen types of immune cell were significantly enriched in cultures that had low RBBP4 expression compared high expression. DEGs associated with RBBP4 are enriched in autophagy pathways. Transcriptomic profiling of the PC9 cell line identified autophagy-related DEGs associated with RBBP4 that exhibited differential expression in NSCLC, suggesting prognostic applications. In vitro experiments demonstrated that RBBP4 knockdown induced autophagy and apoptosis in PC9 cells, promoting cell death, which was inhibited by 3-MA. In vivo, targeted siRNA against RBBP4 significantly reduced tumor development in PC9 cell-injected nude mice, elevating autophagy-related protein levels and inducing apoptosis and necrosis in tumor tissues. CONCLUSION: In NSCLC, RBBP4 upregulation correlates with poor prognosis and altered immunity. Its knockdown induces autophagic cell death in NSCLC cells. These results indicate RBBP4 as a potential NSCLC diagnostic marker and its autophagy modulation as a prospective therapeutic target.
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Autophagie , Marqueurs biologiques tumoraux , Carcinome pulmonaire non à petites cellules , Régulation de l'expression des gènes tumoraux , Tumeurs du poumon , Protéine-4 de liaison à la protéine du rétinoblastome , Carcinome pulmonaire non à petites cellules/génétique , Carcinome pulmonaire non à petites cellules/anatomopathologie , Carcinome pulmonaire non à petites cellules/métabolisme , Carcinome pulmonaire non à petites cellules/mortalité , Humains , Tumeurs du poumon/génétique , Tumeurs du poumon/anatomopathologie , Tumeurs du poumon/métabolisme , Tumeurs du poumon/mortalité , Autophagie/génétique , Animaux , Marqueurs biologiques tumoraux/génétique , Marqueurs biologiques tumoraux/métabolisme , Pronostic , Souris , Protéine-4 de liaison à la protéine du rétinoblastome/génétique , Protéine-4 de liaison à la protéine du rétinoblastome/métabolisme , Lignée cellulaire tumorale , Souris nude , Mâle , Analyse de profil d'expression de gènes , Femelle , Biologie informatique/méthodes , Cartes d'interactions protéiques , Tests d'activité antitumorale sur modèle de xénogreffeRÉSUMÉ
The first symptoms of catecholaminergic polymorphic ventricular tachycardia (CPVT) usually occur in childhood and adolescence. 60% of patients experience syncope before the age of 40. Sudden cardiac death (SCD) is the first symptom of the disease in 30-50% of patients with CPVT. Early diagnosis is therefore crucial for the patient's prognosis. The diagnosis of CPVT is confirmed by a normal resting ECG, exclusion of structural heart disease, detection of bidirectional or polymorphic ventricular tachycardia (VT) in the stress ECG and/or detection of a pathogenic mutant in a gene associated with CPVT. Up to 60% of CPVT patients carry changes in the RYR2 gene. This gene encodes the cardiac ryanodine receptor, the most important Ca2+-releasing channel of the sarcoplasmic reticulum, which plays a central role in the contraction and relaxation of the heart muscle. If the function of the ryanodine receptor is impaired, too much calcium enters the cells, which triggers life-threatening arrhythmias. The overactive ryanodine receptor is therefore the main target for gene therapy methods. Even though the development of gene therapy is progressing, there is still no causal therapy available and it is all the more important to make a diagnosis as early as possible, which enables appropriate behavior and adequate symptomatic therapy. The decisive factor here is the evaluation of the genetic analysis in the context of the clinical findings. Based on this, recommendations can be made for preventive measures and the avoidance of specific triggers that could lead to life-threatening arrhythmias.
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Mort subite cardiaque , Canal de libération du calcium du récepteur à la ryanodine , Tachycardie ventriculaire , Humains , Tachycardie ventriculaire/génétique , Tachycardie ventriculaire/diagnostic , Tachycardie ventriculaire/thérapie , Mort subite cardiaque/étiologie , Mort subite cardiaque/prévention et contrôle , Canal de libération du calcium du récepteur à la ryanodine/génétique , Adolescent , Enfant , Électrocardiographie , Adulte , Pronostic , Jeune adulteRÉSUMÉ
Pulmonary arterial hypertension (PAH) is a severe pulmonary vascular disease characterized by increased pulmonary vascular resistance because of vascular remodeling and vasoconstriction. Subsequently, PAH leads to right ventricular hypertrophy and heart failure. Cell death mechanisms play a significant role in development and tissue homeostasis, and regulate the balance between cell proliferation and differentiation. Several basic and clinical studies have demonstrated that multiple mechanisms of cell death, including pyroptosis, apoptosis, autophagy, ferroptosis, anoikis, parthanatos, and senescence, are closely linked with the pathogenesis of PAH. This review summarizes different cell death mechanisms involved in the death of pulmonary artery smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs), the primary target cells in PAH. This review summarizes the role of these cell death mechanisms, associated signaling pathways, unique effector molecules, and various pro-survival or reprogramming mechanisms. The aim of this review is to summarize the currently known molecular mechanisms underlying PAH. Further investigations of the cell death mechanisms may unravel new avenues for the prevention and treatment of PAH.
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Cellules endothéliales , Myocytes du muscle lisse , Hypertension artérielle pulmonaire , Artère pulmonaire , Transduction du signal , Humains , Cellules endothéliales/anatomopathologie , Myocytes du muscle lisse/anatomopathologie , Hypertension artérielle pulmonaire/physiopathologie , Hypertension artérielle pulmonaire/anatomopathologie , Artère pulmonaire/anatomopathologie , Artère pulmonaire/physiopathologie , Mort cellulaire , Animaux , Apoptose , Autophagie/physiologie , Hypertension pulmonaire/anatomopathologie , Hypertension pulmonaire/physiopathologieRÉSUMÉ
Aim: The aim of the study is to quantify the main ways in which the sex of the driver/occupant of a passenger car affects the severity of road crashes. Methods: All 171 230 cars occupied by the driver and one or more passengers included in the Spanish Register of Victims of Road Crashes from 2014 to 2020 were included. We designed two cohort studies: In the first one, we estimated the Incidence Rate Ratios (IRR) between the sex of the drivers and the occurrence of any death and/or severe injuries among their passengers. In the second one we estimated the conditioned IRR between the sex of the occupants of the same car and their risk of death and/or severe injuries. We used fixed Poisson models to obtain IRR estimates, crude and adjusted by individual- environment- and vehicle-related variables. Results: A consistent inverse relationship between driver's female sex and passenger's severity was found, (IRR 0.72, 95 % CI 0.68-0.77), stronger for single crashes (IRR 0.67, 95 % CI 0.60-0.65). The magnitude decreased after adjusting for vehicle- and environment-related variables (IRR 0.82, 95 % CI 0.73-0.92). In the second study, the risk of death or hospitalization was higher for occupants of female sex (IRR 1.23, 95 % CI 1.17-1.30). Conclusions: The risk of death or severe injuries among passengers of cars involved in single crashes is lower for female drivers, probably due to safer driving. On the contrary, in similar crashes, the risk of injuries leading to hospitalization is higher for females.
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Harmful cyanobacterial blooms (HCBs) pose a global ecological threat. Ultraviolet C (UVC) irradiation at 254 nm is a promising method for controlling cyanobacterial proliferation, but the growth suppression is temporary. Resuscitation remains a challenge with UVC application, necessitating alternative strategies for lethal effects. Here, we show synergistic inhibition of Microcystis aeruginosa using ultraviolet A (UVA) pre-irradiation before UVC. We find that low-dosage UVA pre-irradiation (1.5 J cm-2) combined with UVC (0.085 J cm-2) reduces 85% more cell densities compared to UVC alone (0.085 J cm-2) and triggers mazEF-mediated regulated cell death (RCD), which led to cell lysis, while high-dosage UVA pre-irradiations (7.5 and 14.7 J cm-2) increase cell densities by 75-155%. Our oxygen evolution tests and transcriptomic analysis indicate that UVA pre-irradiation damages photosystem I (PSI) and, when combined with UVC-induced PSII damage, synergistically inhibits photosynthesis. However, higher UVA dosages activate the SOS response, facilitating the repair of UVC-induced DNA damage. This study highlights the impact of UVA pre-irradiation on UVC suppression of cyanobacteria and proposes a practical strategy for improved HCBs control.
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Objective: This study aimed to develop and validate a survival prediction model and nomogram to predict survival in patients with advanced gastric or gastroesophageal junction (G/GEJ) adenocarcinoma undergoing treatment with anti-programmed cell death 1 receptor (PD-1). This model incorporates immune-related adverse events (irAEs) alongside common clinical characteristics as predictive factors. Method: A dataset comprising 255 adult patients diagnosed with advanced G/GEJ adenocarcinoma was assembled. The irAEs affecting overall survival (OS) to a significant degree were identified and integrated as a candidate variable, together with 12 other candidate variables. These included gender, age, Eastern cooperative oncology group performance status (ECOG PS) score, tumor stage, human epidermal growth factor receptor 2 (HER2) expression status, presence of peritoneal and liver metastases, year and line of anti-PD-1 treatment, neutrophil-to-lymphocyte ratio (NLR), controlling nutritional status (CONUT) score, and Charlson comorbidity index (CCI). To mitigate timing bias related to irAEs, landmark analysis was employed. Variable selection was performed using the least absolute shrinkage and selection operator (LASSO) regression to pinpoint significant predictors, and the variance inflation factor was applied to address multicollinearity. Subsequently, a Cox regression analysis utilizing the forward likelihood ratio method was conducted to develop a survival prediction model, excluding variables that failed to satisfy the proportional hazards (PH) assumption. The model was developed using the entire dataset, then internally validated through bootstrap resampling and externally validated with a cohort from another Hospital. Furthermore, a nomogram was created to delineate the predictive model. Results: After consolidating irAEs from the skin and endocrine systems into a single protective irAE category and applying landmark analysis, variable selection was conducted for the prognostic prediction model along with other candidate variables. The finalized model comprised seven variables: ECOG PS score, tumor stage, HER2 expression status in tumor tissue, first-line anti-PD-1 treatment, peritoneal metastasis, CONUT score, and protective irAE. The overall concordance index for the model was 0.66. Calibration analysis verified the model's accuracy in aligning predicted outcomes with actual results. Clinical decision curve analysis indicated that utilizing this model for treatment decisions could enhance the net benefit regarding 1- and 2-year survival rates for patients. Conclusion: This study developed a prognostic prediction model by integrating common clinical characteristics of irAEs and G/GEJ adenocarcinoma. This model exhibits good clinical practicality and possesses accurate predictive ability for overall survival OS in patients with advanced G/GEJ adenocarcinoma.
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Adénocarcinome , Inhibiteurs de points de contrôle immunitaires , Nomogrammes , Tumeurs de l'estomac , Humains , Mâle , Femelle , Adulte d'âge moyen , Sujet âgé , Adénocarcinome/traitement médicamenteux , Adénocarcinome/mortalité , Adénocarcinome/immunologie , Inhibiteurs de points de contrôle immunitaires/usage thérapeutique , Inhibiteurs de points de contrôle immunitaires/effets indésirables , Tumeurs de l'estomac/traitement médicamenteux , Tumeurs de l'estomac/mortalité , Tumeurs de l'estomac/immunologie , Adulte , Récepteur-1 de mort cellulaire programmée/antagonistes et inhibiteurs , Tumeurs de l'oesophage/traitement médicamenteux , Tumeurs de l'oesophage/mortalité , Tumeurs de l'oesophage/immunologie , Pronostic , Sujet âgé de 80 ans ou plusRÉSUMÉ
Normothermic regional perfusion (NRP) is a relatively new approach to procuring organs for transplantation. After circulatory death is declared, perfusion is restored to either the thoracoabdominal organs (in TA-NRP) or abdominal organs alone (in A-NRP) using extracorporeal membrane oxygenation. Simultaneously, surgeons clamp the cerebral arteries, causing a fatal brain injury. Critics claim that clamping the arteries is the proximate cause of death in violation of the dead donor rule and that the procedure is therefore unethical. We disagree. This account does not consider the myriad other factors that contribute to the death of the donor, including the presence of a fatal medical condition, the decision to withdraw life support, and the physician's actions in withdrawing life support and administering medication that may hasten death. Instead, we claim that physicians play a causative role in many of the events that lead to a patient's death and that these actions are often ethically and legally justified. We advance an "all things considered" view according to which TA-NRP may be considered ethically acceptable insofar as it avoids suffering and respects the wishes of the patient to improve the lives of others through organ donation. We conclude with a series of critical questions related to the practice of NRP and call for the development of national consensus on this issue in the United States.
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Perfusion , Humains , Perfusion/méthodes , Acquisition d'organes et de tissus/éthique , Conservation d'organe/méthodes , Conservation d'organe/éthique , Oxygénation extracorporelle sur oxygénateur à membrane/éthique , Oxygénation extracorporelle sur oxygénateur à membrane/méthodesRÉSUMÉ
Primary amoebic meningoencephalitis is caused by the free-living amoeba Naegleria fowleri. The lack of standardized treatment has significantly contributed to the high fatality rates observed in reported cases. Therefore, this study aims to explore the anti-Naegleria activity of eight synthesized cyanoacrylamides and 5-iminopyrrol-2-ones. Notably, QOET-109, QOET-111, QOET-112, and QOET-114 exhibited a higher selectivity index against Naegleria compared to those of the rest of the compounds. Subsequently, these chemicals were assessed against the resistant stage of N. fowleri, demonstrating activity similar to that observed in the vegetative stage. Moreover, characteristic events of programmed cell death were evidenced, including chromatin condensation, increased plasma membrane permeability, mitochondrial damage, and heightened oxidative stress, among others. Finally, this research demonstrated the in vitro activity of the cyanoacrylamide and 5-iminopyrrol-2-one molecules, as well as the induction of metabolic event characteristics of regulated cell death in Naegleria fowleri.
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BACKGROUND: It is widely acknowledged that midwives are essential in providing care for mothers experiencing perinatal death. However, midwifery students lack the knowledge and skills needed to deal with perinatal death, and. There is limited research on perinatal bereavement care training for midwifery students. AIM: To investigate undergraduate midwifery students' experiential learning of perinatal bereavement care and serve as a reference for future perinatal bereavement care teaching and training. DESIGN: Qualitative descriptive design. SETTING: University in Guangzhou, China. PARTICIPANTS: Undergraduate midwifery students at a university in Guangzhou, China. METHOD: This research was conducted at a university in Guangzhou, China. The participants were recruited using purposeful sampling. Semi-structured, in-depth interviews were conducted with 11 midwifery students who participated in perinatal bereavement care training from May to June 2023. The Colalizzi 7-step data analysis method was used for data analysis. RESULTS: From the data, five themes emerged: 1) immersive experience of perinatal bereavement care, 2) formation of perspectives on perinatal bereavement care, 3) clarification of the service boundaries and internalization of the professional service spirit, 4) emotional impact and coping strategies, and 5)) factors influencing practice optimization. CONCLUSIONS: Experiential learning is an effective teaching strategy. However, participants continued to feel unprepared to provide perinatal bereavement care. Implementing relevant training, disseminating perinatal bereavement care knowledge and skills, and enhancing the ability of midwifery students to manage and cope with the psychological impact of perinatal death are important.
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Approximately 15 million babies are born preterm (<37 weeks of completed gestation) worldwide annually. Although neonatal and perinatal medicine have contributed to the increased survival rate of preterm newborn infants, premature infants are at increased risk of mortality in the first years of life. Infants born preterm are at four times the risk of Sudden Infant Death Syndrome (SIDS) compared to infants born at term. SIDS is believed to be multifactorial in origin. The Triple Risk hypothesis has been proposed to explain this. The model suggests that when a vulnerable infant, such as one born preterm, is at a critical but unstable developmental period in homeostatic control, death may occur if exposed to an exogenous stressor, such as being placed prone for sleep. The highest risk period is at ages 2-4 months, with 90 % of deaths occurring before 6 months. The final pathway to SIDS is widely believed to involve some combination of immature cardiorespiratory control and a failure of arousal from sleep. This review will focus on the physiological factors which increase the risk for SIDS in preterm infants and how these factors may be identified and potentially lead to effective preventative strategies.
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Canid alphaherpesvirus-1 (CaHV-1) may cause a highly fatal haemorrhagic disease in neonatal pups and is associated with reproductive, respiratory and ocular disease in older dogs. Although assumed to have a world-wide distribution, there have been few reports of CaHV-1 in Australia. The aim of this study was to investigate the seroprevalence of CaHV-1 in household dogs in a residential suburb in Townsville, as well as in dogs attending two dog shows in the region. Study participants were recruited through door-to-door non-probability sampling (Douglas dogs, n = 185) or invited to participate (Show dogs; n = 76). Dog owners completed a questionnaire that investigated possible risk factors for recent exposure to CaHV-1. A serum sample from each dog was assayed for anti-CaHV-1 antibodies using a commercially available ELISA. Associations between seropositive dogs and owner-reported risk factors were analysed using univariable analysis and multivariable logistic regression models. The seroprevalence of CaHV-1 was 11.4â¯% (95â¯% CI 6.8-15.9â¯%) and 17.1â¯% (95â¯% CI 5.5-28.8) for the Douglas and Show dogs, respectively, with a pooled seroprevalence of 13â¯% (95â¯% CI 8.3-17.7â¯%). Dogs that had suffered from conjunctivitis within the previous 3 months or were involved in breeding were more likely to be seropositive to CaHV-1. No other significant risk factors were identified. In conclusion, CaHV-1 is circulating in dogs in North Queensland and may be contributing to foetal and neonatal losses in this region.
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OBJECTIVES: To investigate whether the occurrence of ischemic stroke due to carotid stenosis is a marker of the severity of atherosclerotic disease and of an excess risk of cardiovascular morbidity and mortality, and of all-cause mortality, after carotid endarterectomy. METHODS: Patients who had undergone a carotid endarterectomy (CEA) from June 2015 to august 2016 were included. Patients were classified into two groups, namely symptomatic and asymptomatic. Neurological event, myocardial infarction and death during early follow-up were monitored. Major adverse cardiovascular events (MACE), major limb events (MALE), and all-cause mortality were compared for patients with a CEA for an asymptomatic carotid stenosis versus those with a symptomatic stenosis. RESULTS: Among the 190 patients included, 86 (51%) had a CEA for an asymptomatic stenosis and 84 (49%) for a symptomatic stenosis. During the first 30 days, the rate of all-cause death or ischemic stroke was similar in both groups (1%, p=0.986). After 30 days, there were a total of 35 MACE (21.3%) and 15 MALE (9.1%) during mean follow-up of 53 (22.6) months. Overall cardiovascular morbidity and mortality was 30.4%, and did not differ between groups (p=0.565). New ischemic stroke occurred in 11 patients (9.1%) and was significantly more frequent in the asymptomatic group (9 (14.8%) vs 2 (3.6%) in the symptomatic group, (OR: 4.96; CI 95% [1.04-23.77]; p = 0.013)). Overall all-cause mortality was 24% in both groups (p=0.93) CONCLUSION: The occurrence of ischemic stroke of carotid origin prior to revascularization does not appear to be associated with an excess risk of cardiovascular morbidity or mortality or all-cause mortality after surgery.
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OBJECTIVE: To develop and validate a score to predict the 90-day risk of hospitalization/death in patients with low respiratory tract infections (LRTIs) with the aim to support clinical decision making on vaccine (co)-administration. METHODS: We formed a cohort of patients aged 18 years or older being diagnosed with LRTIs in the period between January 1, 2012 and December 31, 2022. Each patient was followed until occurrence of respiratory-related hospitalization/death up to the end of the study period (December 31, 2022). Along with age and sex, forty determinants were adopted to assemble the respiratory tract infection(RTI)-Health Search(HS)core using the development sub-cohort. The prediction accuracy of the score was therefore assessed in the validation sub-cohort. RESULTS: We identified 252,319 patients being diagnosed with LRTIs (females: 54.7%; mean age: 60 (SD:18.1)). When the risk of LRTIs-related hospitalizations/deaths was estimated via RTI-HScore, its predicted value was equal to 1.4% over a 90-day event horizon. The score showed explained variation and discrimination accuracy were equal to 45% (95% CI: 44-47%) and 81% (95% CI: 79-84%), respectively. The calibration slope did not significantly differ from the unit (p=0.8314). CONCLUSIONS: The RTI-HScore was featured by good accuracy for prediction of LRTIs-related complications over a 90-day follow-up. Such a tool might therefore support general practitioners to enhance patients' care by facilitating approaches for (co)-administration of vaccines for respiratory infections through a score-based decision support system.
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BACKGROUND: This study aimed to analyze the current status of brain death/death by neurologic criteria (BD/DNC) determination in Korea over a decade, identifying key areas for improvement in the process. METHODS: We conducted a retrospective analysis of data from the Korea Organ Donation Agency spanning 2011 to 2021, focusing on donors whose donations were not completed. The study reviewed demographics, medical settings, diagnoses, and outcomes, with particular emphasis on cases classified as nonbrain death and those resulting in death by cardiac arrest during the BD/DNC assessment. RESULTS: Of the 5047 patients evaluated for potential brain death from 2011 to 2021, 361 were identified as noncompleted donors. The primary reasons for noncompletion included nonbrain death (n = 68, 18.8%), cardiac arrests during the BD/DNC assessment process (n = 80, 22.2%), organ ineligibility (n = 151, 41.8%), and logistical and legal challenges (n = 62, 17.2%). Notably, 25 (36.8%) of them failed to meet the minimum clinical criteria, and 7 of them were potential cases of disagreement between the two clinical examinations. Additionally, most cardiac arrests (n = 44, 55.0%) occurred between the first and second examinations, indicating management challenges in critically ill patients during the assessment period. CONCLUSIONS: Our study highlights significant challenges in the BD/DNC determination process, including the need for improved consistency in neurologic examinations and the management of critically ill patients. The study underscores the importance of refining protocols and training to enhance the accuracy and reliability of brain death assessments, while also ensuring streamlined and effective organ donation practices.
RÉSUMÉ
AIMS: Limited literature shows the existence of sex differences in the long-term prognosis of heart failure (HF) patients with frailty. In this study, whether sex differences exist in the impact of frailty on death from cardiovascular causes in patients with HF was investigated by conducting a retrospective cohort study. METHODS AND RESULTS: Data from the National Health and Nutrition Examination Survey (NHANES) study (2009-2018) were used to conduct a retrospective cohort study of 958 participants with HF. Patients were grouped based on sex and frailty index (FI). The relationship between death from cardiovascular causes and baseline frailty was assessed by Cox proportional hazard analysis and the Kaplan-Meier (K-M) plot. The study population had an age of 67.3 ± 12.3. Among them, around 54.5% were male. A median follow-up of 3.6 years was performed. After that, females who died from cardiovascular causes exhibited higher baseline FI values, while males did not show this trend (P < 0.05; P = 0.1253). Cox regression analysis demonstrated a significant association between FI and cardiovascular mortality in females (most frail: hazard ratio (HR) = 3.65, 95% confidence interval (CI): 1.07 ~ 12.39, P < 0.05; per 1-unit increase in FI: HR = 1.78, 95% CI: 1.33 ~ 2.39, P < 0.001). A dose-response association between FI and cardiovascular mortality was presented by restricted cubic splines. CONCLUSIONS: Frailty is related to an increased risk of cardiovascular mortality in HF patients, particularly female patients.