Miracle-dz/UniFAR-FTUs huggingface dataset:
Spectrum of heart failure in older patients: results from the National Heart Failure project.

BACKGROUND The elderly make up the majority of patients with heart failure (HF), but information on this segment of the HF population is lacking because clinical trials typically enroll younger patients and population-based studies lack clinical detail. We sought to describe a contemporary national sample of elderly patients with HF and to examine the sample for age-related trends in clinical characteristics. METHODS We studied the charts of 800 Medicare patients per state who were hospitalized with a principal diagnosis of HF between April 1998 and March 1999. There were 34,587 patients in the sample after exclusion of patients who were <65 years old, repeat discharges, discharges to another acute care facility or against medical advice, or receiving long-term hemodialysis. RESULTS Comorbidity was common. About one third of patients had chronic obstructive pulmonary disease, about 40% had diabetes, more than half had coronary heart disease, and more than half had a history of hypertension, but comorbidity rates declined with age. Left ventricular ejection fraction was <40% in only 50.4% of patients in whom it was assessed. Associated laboratory abnormalities were relatively constant across the age spectrum, but renal insufficiency was more common with advancing age. The likelihood that patients were in long-term care facilities before admission rose quite steeply with age. CONCLUSIONS Elderly patients with HF are a heterogeneous group and appear to differ substantially from patients enrolled in clinical trials. Evidence-based guidance for treatment in the context of multiple comorbid conditions, poor renal function, HF with preserved left ventricular systolic function, and residence in long-term care facilities is urgently needed.
Renin-angiotensin system, hypertrophy and gene expression in cardiac myocytes.

In response to humoral and mechanical stimuli, the myocardium adapts to increased work load through hypertrophy of individual muscle cells. Myocardial hypertrophy is characterized by an increase in cell size in the absence of cell division and is accompanied by changes in gene expression. Angiotensin II (ANG II), the effector peptide of the renin-angiotensin system (RAS), regulates volume and electrolyte homeostasis and is involved in cardiac and vascular growth in rats. In this review, the role of RAS on the myocyte protein synthesis (myocyte hypertrophy) and on the induction of gene expression will be discussed in rat cardiomyocytes in culture. The traditional RAS can be considered as a system in which circulating ANG II is delivered to target tissues or cells. However, a local RAS has also been described in cardiac cells and evidence has been accumulated for autocrine and/or paracrine pathways by which biological actions of ANG II can be mediated. These actions of ANG II are primarily mediated through ANG II receptors of the subtype I (AT1-R). When evaluating the effects of ANG II in situ, both changes in circulating levels and local production have to be taken into account. Discrepant findings on the in vitro effect of ANG II on the protein synthesis in cardiac myocytes are described and can be at least partly be attributed to methodological problems such as assay of the de novo protein synthesis, isolation and the separation procedure of cardiac myocytes. The ANG II-induced hypertrophic effect also depends on the existence of non-myocytes in a cardiocyte culture. In rat cardiocytes ANG II also causes induction of many immediately-early genes (c-fos, c-jun, jun-B, Egr-1 and c-myc) and induces also late markers of cardiac hypertrophy (skeletal alpha-actin and atrial natriuretic peptide expression) and growth factors (TGF-beta1 gene expression). In vivo ANG II via AT1-R, causes not only ventricular hypertrophy, independently of blood pressure, but also a shift to the fetal phenotype of the myocardium. Angiotensin-converting enzyme inhibitors and ANG II receptor antagonists of the subtype I not only induce the regression, but also prevent the development of cardiac hypertrophy in experimental rat models.
Effect of parity in age adjustment factors in the Italian Holstein Friesian cattle breed.

Inclusion of parity in multiplicative adjustment factors for age at calving was investigated for the Italian Holstein Friesian cattle breed. Separated age adjustment factors for first, second, third and later parities are necessary because cows of the same age but different parity have different production. Differences in production were particularly evident for first and second parity cows of same age. If parity is not accounted for, first lactation mature equivalent production can be underestimated. Because progeny testing is based on first lactation production, underestimation of a fraction of mature equivalent records may be reflected in genetic indexes.
Dark Chocolate Effect on Platelet Activity, C-Reactive Protein and Lipid Profile: A Pilot Study

Background: Dark chocolate (DC) is one of the richest sources of flavonoids. Since DC has been demonstrated to have beneficial effects on the cardiovascular system, our study examined its effect on platelet reactivity, inflammation, and lipid levels in healthy subjects. Methods: In 28 healthy volunteers, we analyzed the effect of one week of DC (providing 700 mg of flavonoids/day). The primary outcome was to determine the effects of DC consumption on platelet activity measured by flow cytometry (adenosine diphosphate [ADP]- and arachidonic acid [AA]-induced total and activated glycoprotein (GP) IIb/IIIa as well as P-selectin expression). In addition to this, we measured the effect of DC on high-sensitivity C-reactive protein (hsCRP), high-density lipid cholesterol (HDL) and low-density lipid cholesterol (LDL) levels. Results: Following seven days of regular DC ingestion, LDL fell by 6% (120 ± 38 vs 112 ± 37 mg/dL, P < 0.018) and HDL rose by 9% (66 ± 23 vs 72 ± 26 mg/dL, P < 0.0019). ADP- and AA-induced activated GPIIb/IIIa expression was reduced by DC [27.3 ± 27.8 vs 17.4 ± 20.5 mean fluorescence intensity (MFI), P < 0.006; and 9.2 ± 6.5 vs. 6.1 ± 2.2 MFI, P < 0.005, respectively]. DC reduced hsCRP levels in women (1.8 ± 2.1 vs. 1.4 ± 1.7 mg/dL, P < 0.04). Conclusions: One week of DC ingestion improved lipid profiles and decreased platelet reactivity within the total group while reducing inflammation only in women. Regular dark chocolate ingestion may have cardioprotective properties. Further long-term research is warranted to evaluate the effect of flavonoids on cardiovascular health and to determine whether DC's beneficial effects are related to flavonoids or some yet unknown component. This research is based on a larger study which was presented at the American Heart Association Scientific Sessions 2007.
Physical work and strain involved in manual sorting of postal parcels.

A field study was conducted to assess cardiorespiratory and musculoskeletal stress and strain and work output during manual sorting of postal parcels, and to detect the effects of parcel sorting on the maximal muscle strength and endurance. The volunteer subjects comprised 32 healthy male sorters with mean (+/- s.d.) age of 34 +/- 7 years at five different sorting sites. Each subject was studied during one evening work shift. During the shift of 391 +/- 46 min the subjects manually sorted 1173 +/- 630 parcels and walked 4.7 +/- 2.3 km with and without the load. While sorting, heart rate was 101 +/- 18 beats min-1. In the heaviest tasks the oxygen consumption was 1.2 +/- 0.41 min-1, and no elevated blood lactate concentrations were found. Work postures in which the back was bent forward averaged 24% of the time for sorting. The overall cardiorespiratory rating and local ratings of perceived exertion for arms, back, and legs did not exceed the 'somewhat strong' level during the work shift. The maximal static strength both for the right and left hand-grip muscles was, on average, 3% lower (p less than 0.05) after the work shift than before the shift. No significant differences were found in the static or dynamic endurance times for the hand-grip muscles when the results obtained after the work shift were compared to the baseline values. At sorting centres the stress and strain on the cardiorespiratory and musculoskeletal system was evaluated to remain within acceptable limits for healthy male sorters.
On the predictive power of meta-features in OpenML

Abstract The demand for performing data analysis is steadily rising. As a consequence, people of different profiles (i.e., nonexperienced users) have started to analyze their data. However, this is challenging for them. A key step that poses difficulties and determines the success of the analysis is data mining (model/algorithm selection problem). Meta-learning is a technique used for assisting non-expert users in this step. The effectiveness of meta-learning is, however, largely dependent on the description/characterization of datasets (i.e., meta-features used for meta-learning). There is a need for improving the effectiveness of meta-learning by identifying and designing more predictive meta-features. In this work, we use a method from exploratory factor analysis to study the predictive power of different meta-features collected in OpenML, which is a collaborative machine learning platform that is designed to store and organize meta-data about datasets, data mining algorithms, models and their evaluations. We first use the method to extract latent features, which are abstract concepts that group together meta-features with common characteristics. Then, we study and visualize the relationship of the latent features with three different performance measures of four classification algorithms on hundreds of datasets available in OpenML, and we select the latent features with the highest predictive power. Finally, we use the selected latent features to perform meta-learning and we show that our method improves the meta-learning process. Furthermore, we design an easy to use application for retrieving different meta-data from OpenML as the biggest source of data in this domain.
Nitric oxide contributes to the development of a post‐injury Th2 T‐cell phenotype and immune dysfunction

Severe injury induces immune dysfunction resulting in increased susceptibility to opportunistic infections. Previous studies from our laboratory have demonstrated that post‐burn immunosuppression is mediated by nitric oxide (NO) due to the increased expression of macrophage inducible nitric oxide synthase (iNOS). In contrast, others suggest that injury causes a phenotypic imbalance in the regulation of Th1‐ and Th2 immune responses. It is unclear whether or not these apparently divergent mediators of immunosuppression are interrelated. To study this, C57BL/6 mice were subjected to major burn injury and splenocytes were isolated 7 days later and stimulated with antiCD3. Burn injury induced NO‐mediated suppression of proliferative responses that was reversed in the presence of the NOS inhibitor L‐monomethyl‐L‐arginine and subsequently mimicked by the addition of the NO donor, S‐nitroso‐N‐acetyl‐penicillamine (SNAP). SNAP also dose‐dependently suppressed IFN‐γ and IL‐2 (Th1), but not IL‐4 and IL‐10 (Th2) production. Delaying the addition of SNAP to the cultures by 24 h prevented the suppression of IFN‐γ production. The Th2 shift in immune phenotype was independent of cGMP and apoptosis. The addition of SNAP to cell cultures also induced apoptosis, attenuated mitochondrial oxidative metabolism and induced mitochondrial membrane depolarization. However, these detrimental cellular effects of NO were observed only at supra‐physiologic concentrations (>250 µM). In conclusion, these findings support the concept that NO induces suppression of cell‐mediated immune responses by selective action on Th1 T cells, thereby promoting a Th2 response. J. Cell. Physiol. 208: 418–427, 2006. © 2006 Wiley‐Liss, Inc.
Five Configurations of Opportunism in International Market Entry

We investigate the conditions under which opportunism occurs in international market entry. Examining 133 entries into new markets by 38 Chinese exporters, we uncover instances of opportunistic behaviour on the part of importers. We study five variables affecting such behaviour: managerial experience, market entry share; market distance, young age, and network size. While we find no single variable on its own associated with opportunism, we do find that in concert they form five configurations of opportunism. In one configuration, even older firms with experienced managers and a large network are subject to partners behaving opportunistically when they are entering a distant market. We conclude that simplistic predictions based on the presence of a single antecedent should make way for a configurational approach whereby a set of conditions must be in place for opportunism to materialize.
Apoptosis induced by hyperthermia in Dunn osteosarcoma cell line in vitro

The effect of hyperthermia at 43.5oC for 1h on Dunn osteosarcoma cells was studied. With sham-heated cells (37oC, 1h) as the control, the hyperthermia treated cells were divided into five groups. Time 0 group was the cells that were harvested immediately after heated at 43.5oC for 1h. Whereas time 3, 6, 12, and 24h groups were the cells that were collected respectively after reincubation at 37oC for the above different time periods. The appearance of hyperthermiainduced apoptosis of Dunn osteosarcoma cells was demonstrated to be time dependent. With the confocal microscopic study and TUNEL staining, the morphological characteristics of apoptosis, condensed nuclei and fragmented nuclei were obvious when reincubated at 37oC for 6h after hyperthermic treatment. This hyperthermia-induced apoptosis was further confirmed by flow cytometric analysis on DNA contents. The sub-G1 region that was proposed as a marker of apoptotic cells was most significantly elevated at 6h after hyperthermic treatment and, thereafter, decreased to the levels of control values by 24h, as the apoptotic cells underwent secondary necrosis and degraded to debris. The DNA strand breaks, considered as the key biochemical event of apoptosis, were detected by the TUNEL assay. This study indicated that hyperthermia (43.5oC for 1h) can induce apoptotic changes on osteosarcoma cells in vitro very rapidly (within 6h after treatment), and its occurrence might not be detected if the samples are not taken at several early time points after hyperthermia.
Pulmonary arterial hypertension

Key points PAH is defined by RHC showing a pre-capillary PH. Clinical suspicion of PH should arise in the case of symptoms such as dyspnoea without overt signs of specific heart or lung disease. RHC is required to confirm the diagnosis of PAH, to assess the severity of the haemodynamic impairment and to test the vasoreactivity of the pulmonary circulation. Variables that have been shown to predict prognosis in IPAH include baseline NYHA functional classification, history of right heart failure, baseline 6-minute walk distance, and baseline haemodynamics. FPAH segregates as an autosomal dominant trait, but with markedly reduced penetrance. Germline BMPR2 mutations have been detected in at least 60% of the families studied to date, as well as in cases of so-called IPAH. Basic PAH therapy includes oxygen, diuretics and warfarin. Chronic treatment with oral CCBs should be considered for PAH patients who respond to acute vasodilator challenge. Cohort analysis of IPAH patients receiving continuous intravenous epoprostenol, as compared to historical control groups, clearly demonstrated clinical benefits in NYHA functional class III and IV patients. Two double-blind, randomised, placebocontrolled trials have supported the efficacy of oral bosentan in patients with PAH class III. One double-blind, randomised placebocontrolled trial has supported the efficacy of oral sildenafil in patients with symptomatic PAH. Lung transplantation is the ultimate alternative for severe PAH cases who cannot be managed medically. Educational aims To improve awareness of PAH. To describe the novel classification of PH. To provide information regarding the therapeutic approach of PAH. Summary Pulmonary arterial hypertension (PAH) is a rare condition characterised by elevated pulmonary arterial resistance, leading to right heart failure. PAH can be sporadic (idiopathic PAH), familial or related to other conditions. Echocardiography is the investigation of choice for non-invasive screening. Measurement of haemodynamic parameters during right heart catheterisation (RHC) is mandatory to establish the diagnosis. Recent advances in the management of PAH include prostaglandins, endothelin receptor antagonists and PDE5 inhibitors. Lung transplantation is the last option for patients who deteriorate despite medical treatment. This review aims to update the reader on all these aspects of PAH.
Activation of the muscarinic K+ channel by P2‐purinoceptors via pertussis toxin‐sensitive G proteins in guinea‐pig atrial cells.

1. Whole‐cell voltage clamp and cell‐attached patch‐clamp techniques were applied to single atrial myocytes enzymatically dissociated from adult guinea‐pig hearts. 2. In whole‐cell clamp conditions, external applications, of ATP activated the muscarinic K+ (KACh) current, identified by its inward rectification, its reversal potential near the calculated K+ equilibrium potential (EK) and its relaxation properties during step changes of whole‐cell membrane potential. Theophylline, an antagonist for Pi‐purinoceptors, did not affect the action of ATP on the KACh current, indicating that the response was evoked through P2‐purinoceptors. 3. The concentration‐response relationship for ATP was well described by a Hill equation with a half‐maximal concentration of 1.84 microM and a Hill coefficient of 0.94. ATP (100 microM) produced a maximal increase of the KACh current to 10.92 microA microF‐1, which corresponds to 44.9 and 80.9% of the maximal increases evoked by ACh (10 microM) and adenosine (100 microM), respectively. 4. The activation of KACh current gradually declined to a steady level despite the continuous presence of ATP (desensitization). Recovery from the desensitization was relatively rapid with a half‐time of approximately 1.5 min. 5. The activation of KACh current by ATP was completely abolished by pre‐incubating myocytes with pertussis toxin (PTX, 5 micrograms ml‐1), indicating that P2‐purinoceptors are coupled to PTX‐sensitive G proteins to activate the KACh channel. 6. In the cell‐attached patch recording, ATP (5 microM) applied to the pipette solution enhanced the activity of a channel with single‐channel conductance of 52.7 +/‐ 0.9 pS (mean +/‐ S.E.M., n = 10), reversal potential near EK and mean open time of 1.1 +/‐ 0.1 ms. These conductance and kinetic properties are identical to those of the KACh channel in the heart. In contrast, ATP applied to the bath solution did not significantly affect the basal activity of KACh channel openings. These observations suggest that the mechanism coupling the P2‐purinoceptor to the activation of the KACh channel involves membrane‐delimited component(s) rather than soluble second messenger(s). 7. These results strongly suggest a direct coupling of the P2‐purinoceptor to the KACh channel through PTX‐sensitive G proteins, analogous to the coupling mechanism of the muscarinic ACh receptor and Pi‐purinoceptor to this channel.
[The effects of polygoni multiflori total glycosides on the experimentally atherosclerotic formation in apoE-deficient mice].

OBJECTIVE To study the effect of polygoni multiflori total glycosides (PMTG) on the expressions of ICAM-1 and VCAM-1 in the apoE-deficienct (ApoE-/-)mice with experimental atherosclerosis (AS) and underlying mechanism. METHOD Thirty-two female apoE-deficienct mice were randomized into four groups: high dose PMTG group (150 mg x kg(-1) x d(-1)), low dose PMTG group (25 mg x kg(-1) x d(-1)), atorvastatin positive control group (5 mg x kg(-1) x d(-1)) and model group. At the end of the tenth week of treatment, all mice were killed. The serum levels of total cholesterol (TC), triglyceride(TG), high-density lipoprotein-cholesterol (HDL-C) were measured by enzyme dynamics method. Light microscopy were adopted to assess the degree of atherosclerotic plaque of aortic wall and image analysis was performed with computer. The expressions of ICAM-1 and VCAM-1 were studied by SABC imunohistochemistry. RESULT In comparison with the model group, (1) PMTG reduced the levels of serum TC and TG significantly (P < 0.01), but elevated HDL level obviously (P < 0.01) . (2) PMTG increased the levels of serum NO and the anti-oxidation capacities significantly (P < 0.05 and P < 0.01), but reduced the levels of serum MDA markedly (P < 0.01). (3) PMTG reduced also the extent of atherosclerotic plaque of aorta areas were (P < 0.05). (4) PMTG deregulated the expressions of ICAM-1 and VCAM-1 in aortic wall. CONCLUSION PMTG could inhibit the occurrence and development of atherosclerotic lesions by the regulating lipid metabolism and anti-oxidation and deregulating the of expressiona of ICAM-1 and VCAM-1 in AopE-/- mice in aortic wall.
Collaborative Regulation of Escherichia coli Glutamate-Dependent Acid Resistance by Two AraC-Like Regulators, GadX and GadW (YhiW)

ABSTRACT An important feature of Escherichia coli pathogenesis is an ability to withstand extremely acidic environments of pH 2 or lower. This acid resistance property contributes to the low infectious dose of pathogenic E. coli species. One very efficient E. coli acid resistance system encompasses two isoforms of glutamate decarboxylase (gadA and gadB) and a putative glutamate:γ-amino butyric acid (GABA) antiporter (gadC). The system is subject to complex controls that vary with growth media, growth phase, and growth pH. Previous work has revealed that the system is controlled by two sigma factors, two negative regulators (cyclic AMP receptor protein [CRP] and H-NS), and an AraC-like regulator called GadX. Earlier evidence suggested that the GadX protein acts both as a positive and negative regulator of the gadA and gadBC genes depending on environmental conditions. New data clarify this finding, revealing a collaborative regulation between GadX and another AraC-like regulator called GadW (previously YhiW). GadX and GadW are DNA binding proteins that form homodimers in vivo and are 42% homologous to each other. GadX activates expression of gadA and gadBC at any pH, while GadW inhibits GadX-dependent activation. Regulation of gadA and gadBC by either regulator requires an upstream, 20-bp GAD box sequence. Northern blot analysis further indicates that GadW represses expression of gadX. The results suggest a control circuit whereby GadW interacts with both the gadA and gadX promoters. GadW clearly represses gadX and, in situations where GadX is missing, activates gadA and gadBC. GadX, however, activates only gadA and gadBC expression. CRP also represses gadX expression. It does this primarily by repressing production of sigma S, the sigma factor responsible for gadX expression. In fact, the acid induction of gadA and gadBC observed when rich-medium cultures enter stationary phase corresponds to the acid induction of sigma S production. These complex control circuits impose tight rein over expression of the gadA and gadBC system yet provide flexibility for inducing acid resistance under many conditions that presage acid stress.