Desfechos obstétricos adversos durante a COVID-19: uma série de casos retrospectiva / Adverse obstetric outcomes during COVID-19: a retrospective case series / Resultados obstétricos adversos durante el COVID-19: serie de casos retrospectiva

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.

Strong activation of p53 by actinomycin D and nutlin-3a overcomes the resistance of cancer cells to the pro-apoptotic activity of the FAS ligand.

The FAS ligand (FASLG) is expressed on lymphocytes, which employ it to activate death receptors on target cells. Cancer cells are generally resistant to apoptosis triggered by FASLG. In this work, we found a way to circumvent this resistance by treatment with actinomycin D (ActD) and nutlin-3a (Nut3a). We selected this drug combination based on our transcriptomic data showing strong activation of proapoptotic genes, including those for receptor-mediated apoptosis, in cells exposed to actinomycin D and nutlin-3a. To test our hypothesis, we pre-exposed cancer cell lines to this drug combination for 45 h and then treated them with recombinant FASLG. This almost instantaneously killed most cells. Actinomycin D and nutlin-3a strongly cooperated in the sensitization because the effect of the drugs acting solo was not as spectacular as the drug combination, which together with FASLG killed more than 99% of cells. Based on the caspase activation pattern (caspase-8, caspase-9, caspase-10), we conclude that both extrinsic and intrinsic pro-apoptotic pathways were engaged. In engineered p53-deficient cells, this pro-apoptotic effect was completely abrogated. Therefore, the combination of ActD + Nut3a activates p53 in an extraordinary way, which overcomes the resistance of cancer cells to apoptosis triggered by FASLG. Interestingly, other combinations of drugs, e.g., etoposide + nutlin-3a, actinomycin D + RG7112, and actinomycin D + idasanutlin had a similar effect. Moreover, normal human fibroblasts are less sensitive to death induced by ActD + Nut3a + FASLG. Our findings create the opportunity to revive the abandoned attempts of cancer immunotherapy employing the recombinant FAS ligand.

Sphingolipid metabolism and regulated cell death in malignant melanoma.

Malignant melanoma (MM) is a highly invasive and therapeutically resistant skin malignancy, posing a significant clinical challenge in its treatment. Programmed cell death plays a crucial role in the occurrence and progression of MM. Sphingolipids (SP), as a class of bioactive lipids, may be associated with many kinds of diseases. SPs regulate various forms of programmed cell death in tumors, including apoptosis, necroptosis, ferroptosis, and more. This review will delve into the mechanisms by which different types of SPs modulate various forms of programmed cell death in MM, such as their regulation of cell membrane permeability and signaling pathways, and how they influence the survival and death fate of MM cells. An in-depth exploration of the role of SPs in programmed cell death in MM aids in unraveling the molecular mechanisms of melanoma development and holds significant importance in developing novel therapeutic strategies.

New substituted benzoxazine derivatives as potent inducers of membrane permeability and cell death.

The search for new agents targeting different forms of cell death is an important research focus for developing new and potent antitumor therapies. As a contribution to this endeavor, we have designed and synthesized a series of new substituted 3,4-dihydro-2H-1,4-benzoxazine derivatives. These compounds have been evaluated for their efficacy against MCF-7 breast cancer and HCT-116 colon cancer cell lines. Overall, substituting this heterocycle led to improved antiproliferative activity compared to the unsubstituted derivative 1. The most active compounds, 2b and 4b, showed IC50 values of 2.27 and 3.26 µM against MCF-7 cells and 4.44 and 7.63 µM against HCT-116 cells, respectively. To investigate the mechanism of action of the target compounds, the inhibition profile of 8 kinases involved in cell signaling was studied highlighting residual activity on HER2 and JNK1 kinases. 2b and 4b showed a consistent binding mode to both receptor kinases, establishing significant interactions with known and catalytically important domains and residues. Compounds 2b and 4b exhibit potent cytotoxic activity by disrupting cell membrane permeability, likely triggering both inflammatory and non-inflammatory cell death mechanisms. This dual capability increases their versatility in the treatment of different stages or types of tumors, providing greater flexibility in clinical applications.

Lipidomic analyses reveal potential biomarkers for predicting death and heart failure after acute myocardial infarction.

Background Acute myocardial infarction (AMI) and postmyocardial infarction heart failure (pMIHF) have high mortality rates worldwide. This study aimed to explore lipidomic profiles and identify potential biomarkers for the prediction of death and heart failure (HF) after AMI. Methods All serum samples were collected at Xuanwu Hospital, Capital Medical University, and their clinical characteristics and lipidomic profiles were analyzed in different groups. LC-MS/MS was used for lipidomic analyses, and underlying biomarkers were screened by receiver operating characteristic (ROC) curve analysis. Results Lipidomic analyses of the survival and nonsurvival groups revealed that the decrease of the content of SM (d18:1/22:0), PE (P-20:1/18:0), PC (18:2), LPE (18:2), PE (P-20:0/18:0), LPC (18:0) and PC (20:0/20:3) while increase of the content of PG (18:1/18:1) could increase the risk of death after AMI. In parallel, the lipidomic analysis of the HF and non-HF groups revealed that the decrease of the content of PC (20:3/20:4), LPC (20:3), LPC (18:0), LPC (18:2), LPC (20:0), LPC (18:3), LPE (16:1) and PC (18:2/20:3) could increase the risk of HF after AMI. Conclusion Several lipids could be potential biomarkers for the prediction of death and HF after AMI.

Life expectancy in relation to societal development level: significant discordant factors.

OBJECTIVES: The aim of this study is to determine the interdependence between life expectancy and numerous social indicators, i.e., to determine the factors that encourage an increase or decrease in life expectancy. METHODS: Pearson coefficients as well as linear and logarithmic trends and correlations between the dependent variable of life expectancy and numerous independent variables were calculated and analysed. The calculations were carried out for all countries in the world for which data is available. Based on the strength of the correlations between life expectancy and numerous indicators, we have tried to determine the reasons for the different values of life expectancy in the various countries. RESULTS: Important factors for achieving high life expectancy values are economic development and healthcare spending but the spread of "diseases of the modern era", such as obesity or diabetes, have a significant negative impact on life expectancy. Other important limiting factors for life expectancy are large income inequalities, a higher share of private healthcare expenditure in total healthcare expenditure and lower total healthcare expenditure. Less developed societies can significantly increase their life expectancy by providing clean water and safe sanitation and by combating various infectious diseases (especially HIV). CONCLUSIONS: Life expectancy is a meaningful indicator of the state of social development and accurately reflects the general state of a particular society. It has been shown that GDP per capita (PPP) is a key determinant of life expectancy, while other important factors play the role of a further modifier.

End of Life Care Practices at a Tertiary Cancer Centre in India: An Observational Study.

PURPOSE: To assess the End of life care (EOLC ) practices and the magnitude of futile care in a tertiary cancer center. To find out the barriers in provision of good EOLC in cancer patients. METHODS: An observational study was done on 129 patients. Patients were enrolled using the palliative prognostic index (PPI) in the end of life stages. Socio-demographic and clinical details were recorded. Detailed counselling done by the palliative physician or the oncologist was recorded. The barriers in provision of care were recorded. RESULTS: In this study initial experience of 129 patients were analyzed. PPI score was >6 (survival shorter than 3 weeks) in 85 (65.89%) ; 34 (26.36%) had PPI score between >4 to 6 (survival between 3 to 6 weeks); and 10 (7.75%) patients had PPI score less than equal to 4( survival more than 6 weeks).77 (59.69%) patients preferred home as their place for EOLC while 41(31.78%) preferred hospital, 7 (5.43%) preferred hospice while 4 (3.10%) opted ICU for their EOLC . The most common barrier associated was caregiver related in 34 case, followed by physician related in 14 cases and patients related in 3 cases, because of hope of being cured in hospital, social stigma, fear of worsening of symptoms at home, denial. CONCLUSION: EOLC is the least studied part of patient care with various barriers. With proper communication and a good palliative care support, futile treatment can be avoided. With healthy communication we can empower family members and patients for a good EOLC.

Death from Failed Protection? An Evolutionary-Developmental Theory of Sudden Infant Death Syndrome.

Sudden infant death syndrome (SIDS) has been mainly described from a risk perspective, with a focus on endogenous, exogenous, and temporal risk factors that can interact to facilitate lethal outcomes. Here we discuss the limitations that this risk-based paradigm may have, using two of the major risk factors for SIDS, prone sleep position and bed-sharing, as examples. Based on a multipronged theoretical model encompassing evolutionary theory, developmental biology, and cultural mismatch theory, we conceptualize the vulnerability to SIDS as an imbalance between current physiologic-regulatory demands and current protective abilities on the part of the infant. From this understanding, SIDS appears as a developmental condition in which competencies relevant to self-protection fail to develop appropriately in the future victims. Since all of the protective resources in question are bound to emerge during normal infant development, we contend that SIDS may reflect an evolutionary mismatch situation-a constellation in which certain modern developmental influences may overextend the child's adaptive (evolutionary) repertoire. We thus argue that SIDS may be better understood if the focus on risk factors is complemented by a deeper appreciation of the protective resources that human infants acquire during their normal development. We extensively analyze this evolutionary-developmental theory against the body of epidemiological and experimental evidence in SIDS research and thereby also address the as-of-yet unresolved question of why breastfeeding may be protective against SIDS.

Silibinin Induces Both Apoptosis and Necroptosis with Potential Anti-tumor Efficacy in Lung Cancer.

BACKGROUND: Lung cancer incidence is steadily on the rise, posing a growing threat to human health. The search for therapeutic drugs from natural active substance and elucidating their mechanism have been the focus of anti-tumor research. OBJECTIVE: In our work, Silibinin (SiL) was chosen as a possible substance that could inhibit lung cancer. and its effects on inducing tumor cell death have been studied. METHODS: CCK-8 analysis and morphological observation were used to assess the cytotoxic impacts of SiL on lung cancer cells in vitro. The alterations in mitochondrial membrane potential (MMP) and apoptosis rate of cells were detected by flow cytometry. The level of lactate dehydrogenase (LDH) release out of cells was measured. The expression changes of apoptosis or necroptosis-related proteins were detected using western blotting. Protein interactions among RIPK1, RIPK3 and MLKL were analyzed using the co-immunoprecipitation technique. In vivo, SiL was evaluated for its antitumor effects using LLC tumor-bearing mice with mouse lung cancer. RESULTS: With an increased dose of SiL, the proliferation ability of A549 cells was considerably inhibited, and the accompanying cell morphology changed. The results of flow cytometry showed that after SiL treatment, MMP levels decreased, and the proportion of cells undergoing apoptosis increased. The proteins associated with apoptosis were upregulated and activated. The amount of LDH released from the cells increased following SiL treatment, accompanied by augmented expression and phosphorylation levels of necroptosis-related proteins. The co-IP assay further confirmed necrosome formation induced by SiL. Furthermore, Necrosulfonamide (an MLKL inhibitor) increased the apoptotic rate of SiL-treated cells and aggravated the cytotoxic effect of SiL, indicating that necroptosis blockade could switch cell death to apoptosis and increase the inhibitory effect of SiL on A549 cells. In LLC-bearing mice, gastric administration of SiL significantly inhibited tumor growth. CONCLUSIONS: This study helped clarify the anti-tumor mechanism of SiL against lung cancer, elucidating its role in dual induction of apoptosis and necroptosis. In particular, necroptosis blockade could switch cell death to apoptosis and increase the inhibitory effect of SiL. Our work provided an experimental basis for the research on cell death induced by SiL and revealed its possible applications for improving the management of lung cancer.

Effectiveness of Rational Emotive Behavior Therapy on Death Anxiety and Depression During the COVID-19 Disease: A Historical Approach.

This research study investigated the effectiveness of Rational Emotive Behavior Therapy (REBT) on depression and anxiety during the coronavirus disease 2019 (COVID-19) pandemic in Nigeria. REBT is used in correcting irrational beliefs and behaviors. This study adopted a randomized pretest, post-test, control group design. Two trial-tested instruments covering; depression, anxiety, and irrational beliefs were for data collection. Data obtained with the instruments were analyzed using mean, standard deviation, and analysis of variance. The study revealed that REBT was effective in reducing depression and death anxiety in COVID-19 patients. The result of this study also showed that the introduction of REBT helped to curb the spread of COVID-19 disease by letting Nigerians to know that the existence, mode of spread, and consequences of the disease is real and not a myth.

Co-Twin Prognosis After Single Intrauterine Fetal Death at a Tertiary Care Hospital in India: A Retrospective Observational Study.

INTRODUCTION: Twin pregnancy is associated with an increased risk of perinatal morbidity. Besides, if intrauterine death of a single twin occurs, it increases the morbidity of the surviving co-twin perinatally and postnatally. AIM:  The objective of this study was to determine the incidence of single intrauterine fetal death (SIUFD) in a twin pregnancy and fetal outcome defined in dimensions according to the complications in the surviving co-twin. MATERIAL AND METHODS: Data on twin pregnancies were collected retrospectively for a period of five years (from 2015 to 2019) from the labour room records of the Central Records Department (CRD) at the Postgraduate Institute of Medical Education and Research, Chandigarh, India. Cases with SIUFD were studied individually and neonatal follow-up was taken post delivery for up to three to eight years. Inclusion criteria were SIUFD in twin pregnancies after 14 weeks gestation, chorionicity pre-defined by early trimester ultrasonography. Exclusion criteria were higher-order pregnancy and monoamniotic twins. RESULTS: A total of 1246 (4.273%) twin deliveries were conducted in the study period. Of these, 107 (8.587%) pregnancies had SIUFD with co-twin surviving in utero. Among these, 77 (72%) were dichorionic diamniotic (DCDA) twin pregnancies and 30 (28%) were monochorionic diamniotic (MCDA) twin pregnancies. The incidence of SIUFD was 8.5%. Preterm birth was the most common complication observed in our study and was found in 53.5% and 58.3% of participants in DCDA and MCDA twins, respectively. Early neonatal death (within 24 hours of life) of the surviving twin was found in 29.2% monochorionic twins with SIUFD. SIUFD at < 28 weeks gestation led to a greater number of early neonatal deaths of surviving twins. The incidence of neurodevelopmental disorders (cerebral palsy, developmental delay, epilepsy) in our population after birth was 7.5% (n=93). CONCLUSION: Twin pregnancies with SIUFD have an increased incidence of preterm labour, increased neonatal death of the surviving twin, and neurodevelopmental disorders (cerebral palsy, developmental delay, epilepsy). Monochorionicity and SIUFD at <28 weeks gestation are associated with increased neonatal deaths in co-twin. The Incidence of neurodevelopmental disorders is not directly associated with chorionicity, but developmental delay is more profoundly seen in the monochorionic group.

Cardiac Tamponade and Myocardial Infarction: A Case Report.

In recent times, there has been a concerning rise in the incidence of sudden death among individuals in middle age. Predominantly, cardiovascular diseases emerge as the leading cause behind such untimely fatalities. Myocardial infarction and its subsequent complications stand out as the most frequently encountered scenarios in these tragic events. Despite being a relatively uncommon occurrence, cardiac tamponade represents one of the rare yet fatal complications that can ensue following a myocardial infarction. This condition manifests when the pericardial cavity becomes filled with either blood or blood clots, impeding the heart's normal functioning. Typically, patients experiencing cardiac tamponade are often reported to have succumbed to sudden death, with a preceding history of chest pain being a common indicator. The definitive diagnosis of cardiac tamponade usually occurs during post-mortem examinations. We consider the case of a 38-year-old man who was discovered unconscious at his residence and was pronounced dead upon arrival at the hospital. Subsequent autopsy findings unveiled the presence of both blood and blood clots within the pericardial cavity, in conjunction with a rupture in the right ventricle and occlusion of the left coronary artery. Histopathological analysis further confirmed the root cause of this tragic event as an acute myocardial infarction.

Research landscape of genetics in dilated cardiomyopathy: insight from a bibliometric analysis.

Background: Dilated cardiomyopathy (DCM) is a heterogeneous myocardial disorder with diverse genetic or acquired origins. Notable advances have been achieved in discovering and understanding the genetics of DCM. This study aimed to depict the distribution of the main research forces, hotspots, and frontiers in the genetics of DCM, thus shaping future research directions. Methods: Based on the documents published in the Web of Science Core Collection database from 2013 to 2022, co-authorship of authors, institutions, and countries/regions, co-citation of references, and co-occurrence of keywords were conducted respectively to present the distribution of the leading research forces, research hotspots, and emerging trends in the genetics of DCM. Results: 4,141 documents were included, and the annual publications have steadily increased. Seidman, Christine E, Meder, Benjamin, Sinagra, Gianfranco were the most productive authors, German Centre for Cardiovascular Research was the most productive institution, and the USA, China, and Germany were the most prolific countries. The co-occurrence of keywords has generated 8 clusters, including DCM, lamin a/c, heart failure, sudden cardiac death, hypertrophic cardiomyopathy, cardiac hypertrophy, arrhythmogenic cardiomyopathy, and next-generation sequencing. Frequent keywords with average publication time after 2019 mainly included arrhythmogenic cardiomyopathy, whole-exome sequencing, RBM 20, phenotype, risk stratification, precision medicine, genotype, and machine learning. Conclusion: The research landscape of genetics in DCM is continuously evolving. Deciphering the genetic profiles by next-generation sequencing and illustrating pathogenic mechanisms of gene variants, establishing innovative treatments for heart failure and improved risk stratification for SCD, uncovering the genetic overlaps between DCM and other inherited cardiomyopathies, as well as identifying genotype-phenotype correlations are the main research hotspots and frontiers in this field.

Programmed cell death 1 inhibitor sintilimab plus concurrent chemoradiotherapy for locally advanced pancreatic adenocarcinoma.

BACKGROUND: Pancreatic adenocarcinoma, a malignancy that arises in the cells of the pancreas, is a devastating disease with unclear etiology and often poor prognosis. Locally advanced pancreatic cancer, a stage where the tumor has grown significantly but has not yet spread to distant organs, presents unique challenges in treatment. This article aims to discuss the current strategies, challenges, and future directions in the management of locally advanced pancreatic adenocarcinoma (LAPC). AIM: To investigate the feasibility and efficacy of programmed cell death 1 (PD-1) inhibitor sintilimab plus concurrent chemoradiotherapy for LAPC. METHODS: Eligible patients had LAPC, an Eastern cooperative oncology group performance status of 0 or 1, adequate organ and marrow functions, and no prior anticancer therapy. In the observation group, participants received intravenous sintilimab 200 mg once every 3 wk, and received concurrent chemoradiotherapy (concurrent conventional fractionated radiotherapy with doses planning target volume 50.4 Gy and gross tumor volume 60 Gy in 28 fractions and oral S-1 40 mg/m2 twice daily on days 1-14 of a 21-d cycle and intravenous gemcitabine 1000 mg/m2 on days 1 and 8 of a 21-d cycle for eight cycles until disease progression, death, or unacceptable toxicity). In the control group, participants only received concurrent chemoradiotherapy. From April 2020 to November 2021, 64 participants were finally enrolled with 34 in the observation group and 30 in the control group. RESULTS: Thirty-four patients completed the scheduled course of chemoradiotherapy, while 32 (94.1%) received sintilimab plus concurrent chemoradiotherapy with 2 patients discontinuing sintilimab in the observation group. Thirty patients completed the scheduled course of chemoradiotherapy in the control group. Based on the Response Evaluation Criteria in Solid Tumors guidelines, the analysis of the observation group revealed that a partial response was observed in 11 patients (32.4%), stable disease was evident in 19 patients (55.9%), and 4 patients (11.8%) experienced progressive disease; a partial response was observed in 6 (20.0%) patients, stable disease in 18 (60%), and progressive disease in 6 (20%) in the control group. The major toxic effects were leukopenia and nausea. The incidence of severe adverse events (AEs) (grade 3 or 4) was 26.5% (9/34) in the observation group and 23.3% (7/30) in the control group. There were no treatment-related deaths. The observation group demonstrated a significantly longer median overall survival (22.1 mo compared to 15.8 mo) (P < 0.05) and progression-free survival (12.2 mo vs 10.1 mo) (P < 0.05) in comparison to the control group. The occurrence of severe AEs did not exhibit a statistically significant difference between the observation group and the control group (P > 0.05). CONCLUSION: Sintilimab plus concurrent chemoradiotherapy was effective and safe for LAPC patients, and warrants further investigation.

Diagnosis and management of arrhythmogenic cardiomyopathy: a case report.

Background: Arrhythmogenic cardiomyopathy (ACM) is a genetically determined myocardial atrophy which progressively extends from the epicardium towards the endocardium, resulting in wall thinning. It is one of the leading causes of sudden death in young people. Postmortem studies demonstrate that up to 70-80% of the cases have biventricular involvement. Variable penetrance and expressivity results in a wide phenotypic spectrum, challenging diagnostic accuracy of advanced multimodality imaging tools. Prompt recognition, non-invasive imaging, risk stratification for sudden cardiac death (SCD), and preventive measures are paramount to improve prognosis. Case summary: Here, we present a 22-year-old Black male who was referred to our electrophysiology clinic with palpitations, remote syncope, and a family history of SCD. Over 3 years, he developed gradually worsening symptomatic palpitations. While physical exam and transthoracic echocardiography were unremarkable, his cardiac magnetic resonance imaging was consistent with biventricular ACM. Genetic testing confirmed ACM, revealing double heterozygosity in DSG2 and PKP2. Given the elevated estimated risk of life-threatening dysrhythmias, a subcutaneous cardiac defibrillator was successfully implanted. Discussion: Frequently, patients with ACM have more than one mutation in the same gene (compound heterozygosity) or in a second gene (double heterozygosity). Genetic counselling is strongly recommended for family members of the proband. The diagnosis of ACM may be mimicked by other diseases (cardiac sarcoidosis, dilated cardiomyopathy, amyloidosis), thus genetic testing can be useful to determine the presence of the disease. The present report provides an overview of the clinical course, diagnostic criteria, risk stratification, and prognostication for patients with ACM.

Cardiac arrest and cardiogenic shock complicating ST-segment elevation myocardial infarction in China: A retrospective multicenter study.

Background: Data on the effect of cardiac arrest (CA), cardiogenic shock (CS), and their combination on the prognosis of Chinese patients with ST-segment elevation myocardial infarction (STEMI) are limited. The present study sought to evaluate the clinical outcomes of STEMI complicated by CA and CS, and to identify the risk factors for CA or CS. Methods: This study included 7468 consecutive patients with STEMI in China. The patients were divided into 4 groups (CA + CS, CA only, CS only, and No CA or CS). The endpoints were 30-day all-cause death and major adverse cardiovascular events. A Cox proportional hazards regression analysis was performed. Results: CA, CS, and their combination were noted in 332 (4.4 %), 377 (5.0 %), and 117 (1.6 %) among all patients. During the 30-day follow-up, 817 (10.9 %) all-cause deaths and 964 (12.9 %) major adverse cardiovascular events occurred, and the incidence of all-cause mortality (3.6 %, 62.3 %, 74.1 %, 83.3 %) and major adverse cardiovascular events (5.4 %, 67.1 %, 75.0 %, and 87.2 %) significantly increased in the No CA or CS, CS only, CA only, and CA + CS groups, respectively. In the multivariate Cox regression models, compared with the No CA or CS group, the CA + CS, CA, and CS-only groups were associated with an increased risk of all-cause death and major adverse cardiovascular events. Patients with CA + CS had the highest risk of all-cause death (hazard ratio [HR], 25.259 [95 % confidence interval (CI) 19.221-33.195]) and major adverse cardiovascular events (HR 19.098, 95%CI 14.797-24.648). Conclusions: CA, CS, and their combination were observed in approximately 11 % of Chinese patients with STEMI, and were associated with increased risk for 30-day mortality and major adverse cardiovascular events in Chinese patients with STEMI.

Hepatocyte programmed cell death: the trigger for inflammation and fibrosis in metabolic dysfunction-associated steatohepatitis.

By replacing and removing defective or infected cells, programmed cell death (PCD) contributes to homeostasis maintenance and body development, which is ubiquitously present in mammals and can occur at any time. Besides apoptosis, more novel modalities of PCD have been described recently, such as necroptosis, pyroptosis, ferroptosis, and autophagy-dependent cell death. PCD not only regulates multiple physiological processes, but also participates in the pathogenesis of diverse disorders, including metabolic dysfunction-associated steatotic liver disease (MASLD). MASLD is mainly classified into metabolic dysfunction-associated steatotic liver (MASL) and metabolic dysfunction-associated steatohepatitis (MASH), and the latter putatively progresses to cirrhosis and hepatocellular carcinoma. Owing to increased incidence and obscure etiology of MASH, its management still remains a tremendous challenge. Recently, hepatocyte PCD has been attracted much attention as a potent driver of the pathological progression from MASL to MASH, and some pharmacological agents have been proved to exert their salutary effects on MASH partly via the regulation of the activity of hepatocyte PCD. The current review recapitulates the pathogenesis of different modalities of PCD, clarifies the mechanisms underlying how metabolic disorders in MASLD induce hepatocyte PCD and how hepatocyte PCD contributes to inflammatory and fibrotic progression of MASH, discusses several signaling pathways in hepatocytes governing the execution of PCD, and summarizes some potential pharmacological agents for MASH treatment which exert their therapeutic effects partly via the regulation of hepatocyte PCD. These findings indicate that hepatocyte PCD putatively represents a new therapeutic point of intervention for MASH.

IoT-based emergency cardiac death risk rescue alert system.

The use of technology in healthcare is one of the most critical application areas today. With the development of medical applications, people's quality of life has improved. However, it is impractical and unnecessary for medium-risk people to receive specialized daily hospital monitoring. Due to their health status, they will be exposed to a high risk of severe health damage or even life-threatening conditions without monitoring. Therefore, remote, real-time, low-cost, wearable, and effective monitoring is ideal for this problem. Many researchers mentioned that their studies could use electrocardiogram (ECG) detection to discover emergencies. However, how to respond to discovered emergencies in household life is still a research gap in this field.•This paper proposes a real-time monitoring of ECG signals and sending them to the cloud for Sudden Cardiac Death (SCD) prediction.•Unlike previous studies, the proposed system has an additional emergency response mechanism to alert nearby community healthcare workers when SCD is predicted to occur.

Effectiveness of transarterial chemoembolization in combination with lenvatinib and programmed cell death protein-1 inhibition for unresectable hepatocellular carcinoma.

This editorial comments on the study by Ma et al, which delves into the efficacy and predictive factors associated with the combination of transarterial chemoembolization, lenvatinib, and programmed cell death protein-1 inhibition for the management of unresectable hepatocellular carcinoma. Analysing data from a retrospective study involving 102 patients, the treatment showcased a median overall survival (OS) of 26.43 months and a median progression-free survival (PFS) of 10.07 months. Notably, the objective response rate and disease control rate reached 61.76% and 81.37%, respectively. Specific factors such as Barcelona Clinic Liver Cancer (BCLC) Classification B-stage, early neutrophil-to-lymphocyte ratio response, and early alpha-fetoprotein response (> 20% decrease) correlated with superior OS and PFS. The triple therapy exhibited promising efficacy, particularly in BCLC B-stage disease, with prognostic markers aiding in patient stratification. Acknowledging the retrospective nature of the study design, future research should address this limitation and incorporate longer follow-up periods for a comprehensive evaluation of long-term outcomes.