A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

death - Top 30 Publications

LncRNA HANR Promotes Tumorigenesis and Increase of Chemoresistance in Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world and the third leading cause of cancer-related death. Critical roles for long non-coding RNAs (lncRNAs) have recently been demonstrated for a variety of cancers, including hepatocellular carcinoma. However, the effect and mechanism of lncRNAs in HCC tumorigenesis and chemoresistance have not been extensively characterized.

Membranous and Cytoplasmic Expression of PD-L1 in Ovarian Cancer Cells.

Expression of programmed death-ligand 1 (PD-L1) on tumor cells represents a powerful immune evasion pathway, but the role of intracellular or cytoplasmic PD-L1 has not been investigated in ovarian cancer cells.

Socioeconomic Inequalities in Frailty among Older Adults: Results from a 10-Year Longitudinal Study in the Netherlands.

Frailty is an important risk factor for adverse outcomes in older people. Substantial variation in frailty prevalence between socioeconomic groups exists, but longitudinal evidence for the association between socioeconomic position (SEP) and frailty is scarce.

Bladder Metastases from Breast Cancer: Managing the Unexpected. A Systematic Review.

Breast cancer (BrC) has the highest incidence among females world over and it is one of the most common causes of death from cancer overall. Its high mortality is mostly due to its propensity to rapidly spread to other organs through lymphatic and blood vessels in spite of proper treatment. Bladder metastases from BrC are rare, with 50 cases having been reported in the last 60 years. This review aims to discuss some critical points regarding this uncommon condition. First, we performed a systematic review of the literature in order to draw a clinical and pathological profile of this entity. On this basis, its features in terms of diagnostic issues, imaging techniques, and survival are critically examined. Most bladder metastases from BrC are secondary lobular carcinoma, which mimic very closely the rare variant of urothelial cancer with lobular carcinoma-like features (uniform cells with an uncohesive single-cell, diffusely invasive growth pattern); thus, immunohistochemistry is mandatory to arrive at a correct diagnosis. This article summarizes the current knowledge regarding the incidence, clinical presentation, diagnosis, prognosis, and treatment of bladder metastases in patients with BrC.

Hepatitis C and Its Metabolic Complications in Kidney Disease.

Evidence has been accumulated during the last decade showing that HCV infection plays an important activity at hepatic and extra-hepatic level. Chronic HCV is associated with a large spectrum of extra-hepatic manifestations including lympho-proliferative diseases and metabolic abnormalities (such as insulin resistance and fatty liver disease).

High risk of hepatocellular carcinoma and death in patients with immune-tolerant-phase chronic hepatitis B.

High serum HBV DNA levels are associated with high risks of hepatocellular carcinoma (HCC) and cirrhosis in patients with chronic hepatitis B (CHB). Although the immune-tolerant (IT) phase is characterised by high circulating HBV DNA levels, it remains unknown whether antiviral treatment reduces risks of HCC and mortality.

SIFD as a novel cause of severe fetal hydrops and neonatal anaemia with iron loading and marked extramedullary haemopoiesis.

SIFD describes a heritable, syndromic condition characterised principally by sideroblastic anaemia (SA) with immunodeficiency, fevers and developmental delay, arising in mutations within the TRNT1 gene. Other clinical manifestations of SIFD include cardiomyopathy, seizures, sensorineural hearing loss, renal dysfunction, metabolic abnormalities, hepatosplenomegaly and retinitis pigmentosa.Presentation of SIFD is variable but typically in early childhood with SA or with fever. In this report, we extend the described SIFD phenotype. We describe a kindred in which the index case presented with fetal hydrops, and early neonatal death, and the second child had severe anaemia at delivery. Both cases had prominent extramedullary erythropoiesis and numerous circulating nucleated red blood cells.

Evidence for brain glucose dysregulation in Alzheimer's disease.

It is unclear whether abnormalities in brain glucose homeostasis are associated with Alzheimer's disease (AD) pathogenesis.

Amyloid beta synaptotoxicity is Wnt-planar cell polarity dependent and blocked by fasudil.

Synapse loss is the basis of the cognitive decline indicative of dementia. In the brains of Alzheimer's disease (AD) sufferer's amyloid beta (Aβ) peptides aggregate to form senile plaques but as soluble peptides that are toxic to synapses. We previously demonstrated that Aβ induces Dickkopf-1 (Dkk1), which in turn activates the Wnt-planar cell polarity (Wnt-PCP) pathway to drive tau pathology and neuronal death.

Live or let die: Neuroprotective and anti-cancer effects of nutraceutical antioxidants.

Diet sources are closely involved in the pathogenesis of diverse neuropsychiatric disorders and cancers, in addition to inherited factors. Currently, natural products or nutraceuticals (commonly called medical foods) are increasingly employed for adjunctive therapy of these patients. However, the potential molecular mechanisms of the nutrient efficacy remain elusive. In this review, we summarized the neuroprotective and anti-cancer mechanisms of nutraceuticals. It was concluded that the nutraceuticals exerted neuroprotection and suppressed tumor growth possibly through the differential modulations of redox homeostasis. In addition, the balance between reactive oxygen species (ROS) production and ROS elimination was manipulated by multiple molecular mechanisms, including cell signaling pathways, inflammation, transcriptional regulation and epigenetic modulation, which were involved in the therapeutic potential of nutraceutical antioxidants against neurological diseases and cancers. We specifically proposed that ROS scavenging was integral in the neuroprotective potential of nutraceuticals, while alternation of ROS level (either increase or decrease) or disruption of redox homeostasis (ROS addiction) constituted the anti-cancer property of these compounds. We also hypothesized that ROS-associated ferroptosis, a novel type of lipid ROS-dependent regulatory cell death, was likely to be a critical mechanism for the nutraceutical antioxidants. Targeting ferroptosis is advantageous to develop new nutraceuticals with more effective and lower adverse reactions for curing patients with neuropsychiatric diseases or carcinomas.

New methods to optimally detect episodes of non-metabolic heart rate variability reduction as an indicator of psychological stress in everyday life.

Cardiovascular disease is the leading cause of death in the western world. Frequent or chronic reductions in heart rate variability (HRV) are a powerful predictor of cardiovascular disease. Psychological stress has been suggested to be an important factor in the development of reduced HRV. Recently, Verkuil et al. (2016) introduced a laboratory-based method to measure additional HRV reduction in everyday life, and reductions in HRV related to psychological stress. In the current paper, we discuss alternative methods to detect additional HRV reductions, in real life data sets without the necessity of laboratory-based calibration, and even in existing data sets. All of these methods use a subset of 24h' worth of HRV and movement data to do so: either the first 10min of every hour, the full 24h, a combination of 10min from three consecutive hours, or a classification of level of movement. We also present a method to visualize HRV and movement data to be able to detect episodes of reduced additional HRV optically. The method that used the full 24h' worth of data detected the largest percentage of episodes of reduced additional HRV that actually match with self-reported stress levels, making this method the most promising.

Sphingosine kinase 1 in breast cancer.

Breast cancer affects 1 out of 8 women in the US and is the second highest cause of death from cancer for women, leading to considerable research examining the causes, progression, and treatment of breast cancer. Over the last two decades, sphingosine-1-phosphate (S1P), a potent sphingolipid metabolite, has been implicated in many processes important for breast cancer including growth, progression, transformation and metastasis, and is the focus of this review. In particular, one of the kinases that produces S1P, sphingosine kinase 1 (SphK1), has come under increasing scrutiny as it is commonly upregulated in breast cancer cells and has been linked with poorer prognosis and progression, possibly leading to resistance to certain anti-cancer therapies. In this review, we will also discuss preclinical studies of both estrogen receptor (ER) positive as well as triple-negative breast cancer mouse models with inhibitors of SphK1 and other compounds that target the S1P axis and have shown good promise in reducing tumor growth and metastasis. It is hoped that in the future this will lead to development of novel combination approaches for effective treatment of both conventional hormonal therapy-resistant breast cancer and triple-negative breast cancer.

CCN1 sensitizes esophageal cancer cells to TRAIL-mediated apoptosis.

TRAIL is one of the best anti-cancer molecules in our body. It kills a variety of cancer cells that are resistant to conventional chemotherapy, without causing much negative impact on normal cells, because its death receptors are almost exclusively found on cancer cells. However, some cancer cells are not sensitive to TRAIL treatment, even though they express its death receptors. A second molecule is needed to help TRAIL to complete its mission. Finding such molecules now becomes a top priority in cancer research. Our study shows that CCN1 is such a molecule. CCN1 was highly expressed in the esophageal epithelium of the patients suffering from gastroesophageal reflux disease, but faded away as the situation worsened towards adenocarcinoma. Treating the tumor cells with CCN1 resulted in apoptosis, while the same treatment to the normal cells only nourished cell growth. It was TRAIL that mediated this process. Apparently, CCN1 altered the expression profile of TRAIL and its receptors in tumor cells, namely, activating TRAIL and its death receptors and shutting down its decoy receptors. CCN1 and TRAIL worked as a team to put the cancer cells to death, as elimination of either one failed apoptosis.

Long Noncoding RNAs: New Players in Ischaemia-reperfusion Injury.

Long noncoding RNAs (lncRNAs) constitute a new class of noncoding RNAs that interfere with gene expression. It has been shown that lncRNAs exert comprehensive effects on biological processes and are associated with numerous diseases such as cancer. However, the possible role of lncRNAs in ischaemia/reperfusion (I/R) injury have received relatively little attention. Accumulating evidence indicates that lncRNAs are also involved in the progression of I/R injury such as myocardial, cerebral, hepatic, renal and mesenteric I/R injury. In this review, we summarise the current knowledge of lncRNAs in I/R injury, attempting to better explain the molecular mechanism of I/R injury and provide new directions for its therapy.

Impact of Pre-Diabetes on Coronary Plaque Composition and Clinical Outcome in Patients With Acute Coronary Syndromes: An Analysis From the PROSPECT Study.

The aim of this study was to investigate the impact of pre-diabetes (pre-DM) on coronary plaque characteristics and ischemic outcomes in patients with acute coronary syndromes (ACS).

The relationship between fibrinogen and in-hospital mortality in patients with type A acute aortic dissection.

Fibrinogen plays an important role in hemostasis and thrombosis and is proven to have prognostic significance in patients with cardiovascular disease. We examined the utility of fibrinogen as a prognostic indicator for patients with type A acute aortic dissection (AAD).

End-stage renal disease after pediatric heart transplantation: A 25-year national cohort study.

End-stage renal disease (ESRD), defined as the need for chronic dialysis and/or kidney transplantation (KTx), is a known complication after heart transplant (HTx). However, factors associated with ESRD are not well elucidated. The objectives of this study were to determine the prevalence, risk factors, and outcomes associated with ESRD after pediatric HTx.

2017 ACC Expert Consensus Decision Pathway on the Management of Mitral Regurgitation: A Report of the American College of Cardiology Task Force on Expert Consensus Decision Pathways.

Mitral regurgitation (MR) is a complex valve lesion that can pose significant management challenges for the cardiovascular clinician. This Expert Consensus Document emphasizes that recognition of MR should prompt an assessment of its etiology, mechanism, and severity, as well as indications for treatment. A structured approach to evaluation based on clinical findings, precise echocardiographic imaging, and when necessary, adjunctive testing, can help clarify decision making. Treatment goals include timely intervention by an experienced heart team to prevent left ventricular dysfunction, heart failure, reduced quality of life, and premature death.

New digital adherence devices could prevent millions of strokes from atrial fibrillation by the end of the next century.

The effectiveness and safety of a pharmacologic intervention is highly dependent on patient's capability to follow the recommended treatment regimen. Non-adherence to pharmacologic treatments is associated with worsening conditions including hospitalization and death. This is a significant burden to healthcare systems on a global scale with non-adherence rates being as high (or higher) as 50% in the first treatment year. The most common causes for non-adherence are forgetfulness, busy lifestyle or complexity and changes in therapeutic schedules. In conditions like atrial fibrillation (AFib) this leads to a drastic increase in event rates, e.g. strokes. Patients diagnosed with AFib are strongly recommended to receive anticoagulant treatments for stroke prevention. Treatments with Vitamin K antagonists or novel oral anticoagulants (NOACs) can dramatically lower the risk of ischemic strokes in the presence of AFib. Non-adherence can expose the patients to an increased stroke risk. This is especially true for NOACs, due to their short half-life. Patients have to take these medications once or twice daily for adequate stroke prevention, i.e., single non-use of the medication can already diminish or reset the anticoagulative effect. Adherence devices could help improve patient's compliance by reminder or feedback function. They have shown to be successful in a number of clinical trails. Especially, newer devices that make use of digital technologies show promising results but are not used broadly in clinical practice. Here we provide evidence for our hypothesis that newly available adherence devices might increase adherence rates and thereby reduce the number of strokes in patients with AFib.

Could lung cancer exosomes induce apoptosis of natural killer cells through the p75NTR-proNGF-sortilin axis?

Lung cancer is the leading cause of cancer-related death worldwide. Tumor exosomes play an important role in the development of lung cancer. Previous studies indicated that tumor exosomes derived from lung cancer cells contained abundant sortilin. Sortilin is a member of the vacuolar protein sorting 10 protein (VPS10P) family of receptors that act as co-receptors for p75NTR and play an independent role in cell death induced by proNGF. Recently, a study showed that proNGF could mediate the death of natural killer (NK) cells through binding to the p75NTR-sortilin complex. However, it has not been reported, to our knowledge, that lung cancer cells induce NK cell apoptosis through a p75NTR-proNGF-sortilin mechanism. As a secreted protein, lung cancer cells may release some proNGF into the tumor microenvironment. We therefore hypothesized that lung cancer cells may promote the apoptosis of NK cells through releasing exosomal sortilin and proNGF. To test this hypothesis, experiments involving the production of exosomal sortilin and proNGF in lung cancer cells and the expression of p75NTR in NK cells are required based upon previously established experiments using fluorescent components. Such experiments may provide insight into the potential mechanism by which lung cancer cells promote apoptosis of NK cells through a p75NTR-proNGF-sortilin pathway.

The colon revisited or the key to wellness, health and disease.

The hypothesis being advanced in this paper is that there is a new medical paradigm emerging from the biomedical research carried out in this century, mainly due to the explosion of the so called "omics" and associated techniques. The main idea is that there is a common pathway from wellbeing and health to chronic disease ("chronopathy") and even to death, which comprises following steps: 1) unhealthy diet, sedentary life style and permanent exposition to xenobiotics and all kinds of noxious stimuli;→2) intestinal dysbiosis;→3) alteration of the intestinal mucus layer (especially that of the colon);→4) disruption of the endothelial tight junctions;→5) metabolic endotoxemia+bacterial translocation;→6) inflammation;→7) exacerbation of the enteric nervous system (ENS) and consequent maladaptation and malfunctioning of the colon;→8) epigenetic manifestations;→9) "chronopathy" and premature death. Therefore, in order to maintain a good health or to improve or even reverse chronic diseases in a person, the main outcome to look for is a homeostatic balance of the intestinal microbiota (eubiosis), most of which is located in the colon. Lynn Margulis was one of the main scientists to highlight the importance of the role played by bacteria not only in the origin of all biological species now present on earth, but also on their role in global homeostasis. Bacteria do not rely on other living beings for their existence, while the latter depend completely on the former. Humans are no exemption, and new evidence emerges each day about the pivotal role of intestinal microbiota in human health, disease and, in general, in its wellbeing. The following facts about intestinal microbiota are nowadays generally accepted: there are about 10 times more bacteria in the gut than human cells in every human being; the microbioma is about 100-150 times bigger that the human genome, and there is a clear link between intestinal microbiota and many of the most common chronic diseases, from obesity and diabetes to depression and Parkinson disease and different kinds of cancer. The main implication of this theory is that we should become a sort of microbiota farmers, that is, we ought to be more conscious of our intestinal microbiota, take care of it and monitor it permanently. Thus, as part of our good life habits (healthy eating, physical exercise), we should probably undergo periodic seasons of fasting and colon cleansing, as it was common in older times.

The Pathophysiology of Dry Eye Disease: What We Know and Future Directions for Research.

Clinical and laboratory studies performed over the past few decades have discovered that dry eye is a chronic inflammatory disease that can be initiated by numerous extrinsic or intrinsic factors that promote an unstable and hyperosmolar tear film. These changes in tear composition, in some cases combined with systemic factors, lead to an inflammatory cycle that causes ocular surface epithelial disease and neural stimulation. Acute desiccation activates stress signaling pathways in the ocular surface epithelium and resident immune cells. This triggers production of innate inflammatory mediators that stimulate the production of matrix metalloprotease, inflammatory cell recruitment, and dendritic cell maturation. These mediators, combined with exposure of autoantigens, can lead to an adaptive T cell-mediated response. Cornea barrier disruption develops by protease-mediated lysis of epithelial tight junctions, leading to accelerated cell death; desquamation; an irregular, poorly lubricated cornea surface; and exposure and sensitization of epithelial nociceptors. Conjunctival goblet cell dysfunction and death are promoted by the T helper 1 cytokine interferon gamma. These epithelial changes further destabilize the tear film, amplify inflammation, and create a vicious cycle. Cyclosporine and lifitegrast, the 2 US Food and Drug Administration-approved therapies, inhibit T-cell activation and cytokine production. Although these therapies represent a major advance in dry eye therapy, they are not effective in improving discomfort and corneal epithelial disease in all patients. Preclinical studies have identified other potential therapeutic targets, biomarkers, and strategies to bolster endogenous immunoregulatory pathways. These discoveries will, it is hoped, lead to further advances in diagnostic classification and treatment.

A traditional American Indian death ritual: Developing nursing knowledge through aesthetic exposure.

The theoretical and practical application of Boykin and Schoenhofer's Nursing as Caring: A Model for Transforming Practice (2001) provided a framework for the exploration of an aesthetic project of quilting, which was undertaken in order to explain the death journey for a cherished mentor of American Indian nursing students. In particular, the nursing situation was used to guide the making of the quilt sampler. Aesthetics nested into the teaching-learning process became another way to help students solidify their professional self-identity as caring persons. This research has implications for the intentional development of studying quilting as an aesthetic way to express valuable lessons learned while caring for patients and telling stories. This idea of quilting opens up a line of enquiry into caring that can be expressed through a new and creative medium.

Safety and efficacy of the cervical pessary combined with vaginal progesterone for the prevention of spontaneous preterm birth.

The aim of this study was to evaluate the safety and efficacy of the combined treatment of cervical pessary and endovaginal progesterone for the prevention of spontaneous preterm birth (SPB) in women with a short cervical length (CL) between 20 and 24 weeks of gestation.

Clinical relevance of peroxisome proliferator-activated receptor-γ gene polymorphisms with sepsis.

Peroxisome proliferator-activated receptor-γ (PPARγ) is a regulator of inflammation. This study aimed to explore associations between PPARγ gene single-nucleotide polymorphisms (SNPs) and susceptibility to and clinical outcome of sepsis in the North China Han population.

A multicenter prospective evaluation study of endoscopic ultrasound-guided hepaticogastrostomy combined with antegrade stenting (with video).

EUS-guided hepaticogastrostomy (EUS-HGS) is often indicated for advanced stage patients because it prevents the adverse events associated with EUS-HGS procedures, and provides long stent patency. EUS-guided antegrade stenting (AS) has been developed as an advanced technique. Thus, to prevent adverse events and achieve, long stent patency, EUS-AS combined with EUS-HGS (EUS-HGAS) has been reported. The aim of this study was to evaluate the technical feasibility and efficacy of EUS-HGAS in a multicenter, prospective study.

Pregnancy prior to recurrent pregnancy loss more often complicated by post-term birth and perinatal death.

The cause of recurrent pregnancy loss remains often unknown. Possibly, pathophysiological pathways are shared with other pregnancy complications.

Type I interferon enhances necroptosis of Salmonella Typhimurium-infected macrophages by impairing antioxidative stress responses.

Salmonella enterica serovar Typhimurium exploits the host's type I interferon (IFN-I) response to induce receptor-interacting protein (RIP) kinase-mediated necroptosis in macrophages. However, the events that drive necroptosis execution downstream of IFN-I and RIP signaling remain elusive. In this study, we demonstrate that S Typhimurium infection causes IFN-I-mediated up-regulation of the mitochondrial phosphatase Pgam5 through RIP3. Pgam5 subsequently interacts with Nrf2, which sequesters Nrf2 in the cytosol, thereby repressing the transcription of Nrf2-dependent antioxidative genes. The impaired ability to respond to S Typhimurium-induced oxidative stress results in reactive oxygen species-mediated mitochondrial damage, energy depletion, transient induction of autophagy, and autophagic degradation of p62. Reduced p62 levels impair interaction of p62 with Keap1, which further decreases Nrf2 function and antioxidative responses to S Typhimurium infection, eventually leading to cell death. Collectively, we identify impaired Nrf2-dependent redox homeostasis as an important mechanism that promotes cell death downstream of IFN-I and RIP3 signaling in S Typhimurium-infected macrophages.

Natural killer T-cell immunotherapy in combination with chemotherapy-induced immunogenic cell death targets metastatic breast cancer.

Natural killer T (NKT) cells are glycolipid-reactive lymphocytes that promote cancer control. In previous studies, NKT-cell activation improved survival and antitumor immunity in a post-surgical mouse model of metastatic breast cancer. Herein, we investigated whether NKT-cell activation could be combined with chemotherapeutic agents to augment therapeutic outcomes. Gemcitabine and cyclophosphamide analogs enhanced the potential immunogenicity of 4T1 mammary carcinoma cells by increasing the expression of antigen-presenting molecules (MHC-I, MHC-II, and CD1d) and promoting exposure or release of immunogenic cell death markers (calreticulin, HMGB1 and ATP). In 4T1 primary tumor and post-surgical metastasis models, BALB/c mice were treated with cyclophosphamide or gemcitabine. NKT cells were then activated by transfer of dendritic cells loaded with the glycolipid antigen α-galactosylceramide (α-GalCer). Chemotherapeutic treatments did not impact NKT-cell activation but enhanced recruitment into primary tumors. Cyclophosphamide, gemcitabine, or α-GalCer-loaded dendritic cell monotherapies decreased tumor growth in the primary tumor model, and reduced metastatic burden and prolonged survival in the metastasis model. Combining chemotherapeutics with NKT cell activation therapy significantly enhanced survival, with surviving mice exhibiting attenuated tumor growth following a second tumor challenge. The frequency of myeloid derived suppressor cells was reduced by gemcitabine, cyclophosphamide, or α-GalCer-loaded dendritic cell treatments; cyclophosphamide also reduced the frequency of regulatory T cells. Individual treatments increased immune cell activation, cytokine polarization, and cytotoxic responses, although these readouts were not enhanced further by combining therapies. These findings demonstrate that NKT-cell activation therapy can be combined with gemcitabine or cyclophosphamide to target tumor burden and enhance protection against tumor recurrence.

Lung cancer, genetic predisposition and smoking: the Nordic Twin Study of Cancer.

We aimed to disentangle genetic and environmental causes in lung cancer while considering smoking status.