Off-site primary percutaneous coronary intervention in a new centre is safe: comparing clinical outcomes with a hospital with surgical backup

Objectives

To evaluate the procedural and clinical outcomes of a new primary percutaneous coronary intervention (PPCI) centre without surgical back-up (off-site PCI) and to investigate whether these results are comparable with a high volume on-site PCI centre in the Netherlands.

Background

Controversy remains about the safety and efficacy of PPCI in off-site PCI centres.

Methods

We retrospectively analysed clinical and procedural data as well as 6?month follow-up of 226 patients diagnosed with ST-elevated myocardial infarction (STEMI) who underwent PPCI at VieCuri Medical Centre Venlo and 115 STEMI patients who underwent PPCI at Catharina Hospital Eindhoven.

Results

PPCI patients in VieCuri Medical Centre had similar procedural and clinical outcomes to those in Catharina Hospital. Overall there were no significant differences. The occurrence of procedural complications was low in both groups (8.4?% VieCuri vs. 12.3?% Catharina Hospital). In the VieCuri group there was one procedural-related death. No patients in either group needed emergency surgery. At 30 days, 17 (7.9?%) patients in the VieCuri group and 9 (8.1?%) in the Catharina Hospital group had a major adverse cardiac event.

Conclusion

Performing PPCI in an off-site PCI centre is safe and effective. The study results show that the procedural and clinical outcomes of an off-site PPCI centre are comparable with an on-site high-volume PPCI centre.

     

Thyrotropin-releasing hormone receptor expression in thyroid follicular cells: a new paracrine role of C-cells?

Thyrotropin-releasing hormone (TRH) synthesized in the hypothalamus has the capability of inducing the release of thyroid-stimulating hormone (TSH) from the anterior pituitary, which in turn stimulates the production of thyroid hormones in the thyroid gland. Immunoreactivity for TRH and TRH-like peptides has been found in some tissues outside the nervous system, including thyroid. It has been demonstrated that thyroid C-cells express authentic TRH, affecting thyroid hormone secretion by follicular cells. Therefore, C-cells could have a paracrine role in thyroid homeostasis. If this hypothesis is true, follicular cells should express TRH receptors (TRH-Rs) for the paracrine modulation carried out by C-cells. In order to elucidate whether or not C-cell TRH production could act over follicular cells modulating thyroid function, we studied TRH-Rs expression in PC C13 follicular cells from rat thyroid, by means of immunofluorescence technique and RT-PCR analysis. We also investigated the possibility that C-cells present TRH-Rs for the autocrine control of its own TRH production. Our results showed consistent expression for both receptors, TRH-R1 and TRH-R2, in 6-23 C-cells, and only for TRH-R2 in PC C13 follicular cells. Our data provide new evidence for a novel intrathyroidal regulatory pathway of thyroid hormone secretion via paracrine/autocrine TRH signaling.     

A new subclade of mtDNA haplogroup C1 found in icelanders: Evidence of pre‐columbian contact?

Although most mtDNA lineages observed in contemporary Icelanders can be traced to neighboring populations in the British Isles and Scandinavia, one may have a more distant origin. This lineage belongs to haplogroup C1, one of a handful that was involved in the settlement of the Americas around 14,000 years ago. Contrary to an initial assumption that this lineage was a recent arrival, preliminary genealogical analyses revealed that the C1 lineage was present in the Icelandic mtDNA pool at least 300 years ago. This raised the intriguing possibility that the Icelandic C1 lineage could be traced to Viking voyages to the Americas that commenced in the 10th century. In an attempt to shed further light on the entry date of the C1 lineage into the Icelandic mtDNA pool and its geographical origin, we used the deCODE Genetics genealogical database to identify additional matrilineal ancestors that carry the C1 lineage and then sequenced the complete mtDNA genome of 11 contemporary C1 carriers from four different matrilines. Our results indicate a latest possible arrival date in Iceland of just prior to 1700 and a likely arrival date centuries earlier. Most surprisingly, we demonstrate that the Icelandic C1 lineage does not belong to any of the four known Native American (C1b, C1c, and C1d) or Asian (C1a) subclades of haplogroup C1. Rather, it is presently the only known member of a new subclade, C1e. While a Native American origin seems most likely for C1e, an Asian or European origin cannot be ruled out.     

Is there a primary role of the mitochondrial genome in Alzheimer’s disease?

The “mitochondrial cascade hypothesis” could explain many of the biochemical, genetic and pathological features of sporadic Alzheimer’s disease (AD). Somatic mutations in mitochondrial DNA (mtDNA) could cause energy failure, increased oxidative stress and accumulation of amyloid β, which in a vicious cycle reinforces mtDNA damage and oxidative stress. Despite the evidence of mitochondrial dysfunction in AD, and despite the cognitive impairment frequently reported in patients with mtDNA mutation, no causative mutation in the mtDNA have been linked to AD. Indeed, results of studies on the role of mtDNA polymorphisms or haplogroups in AD are controversial. In this minireview, we summarize the actual knowledge about the involvement of mtDNA in AD pathology.     

Presenilin-1 regulates induction of hypoxia inducible factor-1α: altered activation by a mutation associated with familial Alzheimer's disease

Background

The pathogenesis of HIV-associated dementia (HAD) is poorly understood. To date, detailed proteomic fingerprinting directly from autopsied brain tissues of HAD and HIV non-dementia patients has not been performed.

Result

Here, we have analyzed total proteins from the frontal cortex of 9 HAD and 5 HIV non-dementia patients. Using 2-Dimensional differential in-gel electrophoresis (2-DIGE) to analyze the brain tissue proteome, 76 differentially expressed proteins (p < 0.05; fold change>1.25) were identified between HAD and HIV non-dementia patients, of which 36 protein spots (based on 3D appearance of spots on the images) were chosen for the mass spectrometry analysis. The large majority of identified proteins were represented in the energy metabolic (mitochondria) and signal transduction pathways. Furthermore, over 90% of the protein candidates are common to both HAD and other non-viral neurodegenerative disease, such as Alzheimer's disease. The data was further validated using specific antibodies to 4 proteins (CA2, GS, CKMT and CRMP2) by western blot (WB) in the same samples used for 2D-DIGE, with additional confirmation by immunohistochemitsry (IHC) using frontal lobe tissue from different HAD and HIV+ non-dementia patients. The validation for all 4 antibodies by WB and IHC was in concordance with the DIGE results, lending further credence to the current findings.

Conclusion

These results suggest not only convergent pathogenetic pathways for the two diseases but also the possibility of increased Alzheimer's disease (AD) susceptibility in HAD patients whose life expectancy has been significantly increased by highly active antiretroviral therapy.     

The scaling of colony size with nest volume in termites: a role in population dynamics?

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The role of noise in a predator–prey model with Allee effect

The existence and implications of alternative stable states in ecological systems have been investigated extensively within deterministic models. However, it is known that natural systems are undeniably subject to random fluctuations, arising from either environmental variability or internal effects. Thus, in this paper, we study the role of noise on the pattern formation of a spatial predator–prey model with Allee effect. The obtained results show that the spatially extended system exhibits rich dynamic behavior. More specifically, the stationary pattern can be induced to be a stable target wave when the noise intensity is small. As the noise intensity is increased, patchy invasion emerges. These results indicate that the dynamic behavior of predator–prey models may be partly due to stochastic factors instead of deterministic factors, which may also help us to understand the effects arising from the undeniable susceptibility to random fluctuations of real ecosystems.     

The role of major virulence factors of AIEC involved in inflammatory bowl disease—a mini-review

Applied Microbiology and Biotechnology - Adherent-invasive Escherichia coli (AIEC) has recently attracted more attention because it is closely related to the pathogenicity of human inflammatory...     

Hearing impairment in patients with 3243A→G mtDNA mutation: phenotype and rate of progression

The relationship between the phenotype and the genotype is complex in diseases caused by mutations in mitochondrial DNA (mtDNA). The 3243A-->G mutation in mtDNA frequently leads to sensorineural hearing impairment (HI), a phenotype that can be assessed in severity by audiometry; hence, consecutive audiograms can give an estimate of the rate of HI progression.We examined the audiological phenotype of 38 patients (14 men, 24 women; mean age: 45+/-14 years) who possessed the 3243A-->G mutation and who belonged to a population-based cohort ascertained in the province of Northern Ostrobothnia, Finland. The subjects took part in an otorhinolaryngologic examination, including audiometry. Factors modulating the severity of HI were analyzed, and the rate of HI progression was calculated. The better ear hearing level (BEHL) at frequencies 0.5, 1, 2, and 4 kHz (BEHL0.5-4kHz) was greater than 20 dB suggesting HI in 28 patients (74%). A good correlation (r=0.428, P=0.009) was found between BEHL0.5-4kHz and the degree of the mutant heteroplasmy. BEHL0.5-4kHz was worse in men than in women, and women outnumbered men among patients with normal hearing or mild HI. In addition, 181 consecutive audiograms were reviewed from 24 patients with HI. The rate of HI progression was calculated to be 2.9 dB/year in men and 1.5 dB/year in women, being clearly faster than the rates that have been observed in the corresponding age group in the general population. A high degree of mutant heteroplasmy, male gender, and age were found to increase the severity of HI. Phenotypic difference by gender may thus be a more universal phenomenon in mitochondrial diseases, not only being associated with Leber's hereditary optic neuropathy. This study provides the first estimate of the rate of disease progression among patients with the 3243A-->G mutation.     

A novel I247T missense mutation in the haptoglobin 2 β-chain decreases the expression of the protein and is associated with ahaptoglobinemia

We have identified a novel base substitution at codon 247 in the -chain of the haptoglobin 2 (Hp²) allele in a Ghanaian with the Hp0 (ahaptoglobinemic) phenotype. The heterozygous TC substitution caused reduced expression of the protein when the mutant was transfected into COS7 cells. The base substitution resulted in a missense change of the non-polar amino acid isoleucine to the polar amino acid threonine at a position in the -chain that is highly conserved among several species. We had previously identified a mutation in the Hp gene promoter region for the same individual, which gives her genotype as –61CHp²/–61CHp²(I247T). Since the –61C mutation also leads to low Hp expression, the genotype represents the first and most definitive ahaptoglobinemic case reported in Africa.     

Evaluation of the role of cytokines in autoimmune disease: The importance of TNFα in rheumatoid arthritis

Cytokines and growth factors are involved in all important biological processes. Hence it is anticipated that they will be of importance in autoimmune disease. The pathogenesis of autoimmune diseases involves a number of stages, initiation, perpetuation and tissue damage, each of which involves different cell and molecular interactions. In this review, we will discuss an outline of the cytokine involvement in the various stages of autoimmune development, prior to focusing on the analysis of cytokines in rheumatoid arthritis. Cytokines exert their effect via high affinity cell surface receptors. Thus an understanding of cytokines involves the analysis of receptor expression, and also of cytokine inhibitors. Currently there is only adequate knowledge of these aspects in rheumatoid arthritis (RA), and as such the emphasis of this review is on RA. One of the major reasons for being interested in the role of cytokines in autoimmunity is to define possible therapeutic targets. There is now considerable evidence that TNFα is such a target in RA, and the effect of anti TNFα monoclonal antibody therapy in RA is discussed.     

Identification of a new point mutation in the human xanthine dehydrogenase gene responsible for a case of classical type I xanthinuria

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Revealing the role of predator interference in a predator–prey system with disease in prey population

Predation on a species subjected to an infectious disease can affect both the infection level and the population dynamics. There is an ongoing debate about the act of managing disease in natural populations through predation. Recent theoretical and empirical evidence shows that predation on infected populations can have both positive and negative influences on disease in prey populations. Here, we present a predator–prey system where the prey population is subjected to an infectious disease to explore the impact of predator on disease dynamics. Specifically, we investigate how the interference among predators affects the dynamics and structure of the predator–prey community. We perform a detailed numerical bifurcation analysis and find an unusually large variety of complex dynamics, such as, bistability, torus and chaos, in the presence of predators. We show that, depending on the strength of interference among predators, predators enhance or control disease outbreaks and population persistence. Moreover, the presence of multistable regimes makes the system very sensitive to perturbations and facilitates a number of regime shifts. Since, the habitat structure and the choice of predators deeply influence the interference among predators, thus before applying predators to control disease in prey populations or applying predator control strategy for wildlife management, it is essential to carefully investigate how these predators interact with each other in that specific habitat; otherwise it may lead to ecological disaster.     

The role of in vitro cultivation on asymbiotic trait variation in a single species of arbuscular mycorrhizal fungus

Cultivating arbuscular mycorrhizal (AM) fungi in vitro is an efficient way to produce material for industry and research. However, such artificial growing conditions may impose selective pressure on fungi grown in vitro over many generations. We hypothesized that isolates subjected to long term propagation in vitro may develop increasingly ruderal traits. We proposed a predictive framework for the effect of in vitro cultivation on asymbiotic AM fungal traits. Using photomicrography and image processing, we analyzed morphology and growth traits for 14 isolates representing an in vitro cultivation gradient from 0 to >80 generations in vitro. We investigated the range of trait variation among asymbiotic growth of arbuscular mycorrhizal (AM) fungus isolates (Rhizoglomus irregulare). Spore dormancy was strongly associated with in vitro cultivation. We observed extremely high levels of inter-isolate variation for most fungal traits, but this was not related to time in vitro. Our results indicate that intra-specific diversity may have a strong ecological role in AM fungal communities.     

Coralligenous “atolls”: Discovery of a new morphotype in the Western Mediterranean Sea

Coralligenous habitat and rhodoliths beds are very important in terms of biodiversity in the Mediterranean Sea. During an oceanographic campaign, carried out in northern Cap Corse, new coralligenous structures have been discovered. These structures, never previously identified in the Mediterranean Sea, are named “coralligenous atolls” because of their circular shape. The origin and growth dynamics of these atolls are still unknown but their form does not appear to result from hydrodynamic action and an anthropogenic origin also seems unlikely. However, this kind of shape seems rather closer to that of other circular structures (e.g. pockmarks) the origin of which is related to gaseous emissions. Further studies are needed to confirm this hypothesis through chemical analysis.     

The incidence of ΔF508 CF mutation,and associated haplotypes,in a sample of English CF families

Summary Data are presented for ΔF508 screening and KM19/XV2c haplotype analysis of 195 cystic fibrosis (CF) chromosomes from the British Caucasian population. We report the frequency of ΔF508 in this group to be 80% and find pronounced disequilibrium between the deletion and the KM 2, XV 1 haplotype. Haplotype analysis of 71 normal chromosomes is also presented. We report one individual who had meconium ileus and who does not have the ΔF508 mutation on either chromosome.     

The potential role of variations in juvenile hip geometry on the development of Legg-Calvé-Perthes disease: a biomechanical investigation

Legg-Calvé-Perthes disease (LCP) is one of the most poorly understood diseases in paediatric orthopaedics. One common trait of LCP is the marked morphological difference between healthy and pathological hips, early deviations of which (i.e. prior to disease onset) have been suggested to lead to the overload and collapse of the epiphysis. Here, the impact of common variations in geometry is investigated with a finite element model of a juvenile femur under single leg standing and landing. Here, the impact of typical variations in geometry is investigated with a finite element model of a juvenile femur under single leg standing and landing. The variations appear to have only a limited effect on the stress distribution in the femoral epiphysis even during high impact activities. This suggests that, for this individual at least, they would be unlikely to cause epiphyseal overload and collapse, even in the presence of a skeletally immature epiphysis.