Miracle-dz/UniFAR-FTUs huggingface dataset:
The ever increasing role of percutaneous interventions in coronary revascularisation.

Balloon angioplasty was developed as the first non-surgical method to treat coronary artery stenosis, thanks to the pioneering work by Andreas Gruentzig from 1977 to 1986. The method is based on mechanical stenosis relief by balloon dilatation. Vessel wall stretch, as well as plaque compaction and redistribution, are the main mechanisms of angioplasty lumen gain. The technique had a relatively high acute vessel closure rate that dictated its performance with standby emergency coronary artery bypass grafting (CABG). Stenosis recurrence four to five months after a successful procedure was relatively frequent, and was common to balloon angioplasty as well as other means of percutaneous revascularisation that developed in parallel. Restenosis after balloon angioplasty was mainly attributed to passive recoil of the initially stretched vessel wall, although plaque increase, later defined as intimal hyperplasia, also played a role. Despite all its shortcomings, percutaneous interventions in the 80s made modification of coronary stenosis with diseased vessel reformation possible for the first time in history. Thanks to this development, patients were offered the option of open arteries, at least in cases without restenosis.
Plaque burden in HIV-infected patients is associated with serum intestinal microbiota-generated trimethylamine

Objective:Some intestinal microbiota-generated metabolites of phosphatidylcholine are recognized to be proatherogenic. As the HIV population is vulnerable to cardiovascular disease and can develop intestinal dysbiosis associated with systemic inflammation, we investigated the novel relationship between microbiota-derived metabolites of phosphatidylcholine and coronary atherosclerosis in HIV. Design/Methods:One hundred and fifty-five HIV-infected and 67 non-HIV-infected individuals without known history of cardiovascular disease were previously recruited to assess coronary plaque by computed tomography angiography. In the current study, we evaluate whether serum choline, trimethylamine (TMA), or trimethylamine-N-oxide (TMAO) levels are associated with plaque features. Results:Young, asymptomatic HIV-infected patients (age 47 ± 7 years) demonstrated significantly higher prevalence of plaque (53 vs. 35%, P = 0.01) and number of total plaque segments (1.8 ± 2.5 vs. 1.2 ± 2.2, P = 0.03) when compared with well matched noninfected individuals with similar comorbidities. TMA was significantly associated with calcium score (r = 0.22, P = 0.006), number of total (r = 0.20, P = 0.02) and calcified (r = 0.18, P = 0.03) plaque segments, and calcium plaque volume (r = 0.19, P = 0.02) and mass (r = 0.22, P = 0.009) in the HIV cohort only. In multivariate modeling among HIV-infected patients, TMA remained significantly associated with calcium score (P = 0.008), number of total (P = 0.005) and calcified (P = 0.02) plaque segments, and calcium plaque volume (P = 0.01) and mass (P = 0.007), independent of Framingham risk score. In contrast, there was no association of TMAO to coronary plaque features in either cohort. Conclusion:A link between TMA and atherosclerosis has not previously been established. The current study suggests that TMA may be a nontraditional risk factor related to the number of plaque segments and severity of calcified plaque burden in HIV.
Surface antigenic determinants of mammalian "hepadnaviruses" defined by group- and class-specific monoclonal antibodies

The hepatitis B-like viruses (human hepatitis B virus, woodchuck hepatitis virus, ground squirrel hepatitis virus, and duck hepatitis B virus) are hepatotropic DNA viruses which have been referred to collectively as "hepadnaviruses. " Using a murine monoclonal antibody (101-2) to the surface antigen of woodchuck hepatitis virus, we have shown that the surface antigens of mammalian hepadnaviruses (HBsAg, WHsAg, and GSHsAg) are antigenically related via a common determinant (HV/101). Furthermore, analysis with other monoclonal antibodies to WHsAg revealed that WHsAg and GHsAg are antigenically distinct, although the antigens had more determinants in common with each other than with HBsAg. The hepadnavirus group-specific antibody (101-2) reacted with HBsAg subtypic variants in a group-specific rather than subtype-specific manner. In conjunction with observations with an HBsAg-specific, group-reactive monoclonal antibody (BX259), the present data suggest that there are at least two group-reactive epitopes of HBsAg: one which is virus specific (HBV/259) and one which is common to two other mammalian hepadnaviruses (HV/101).
SPIKE1 Activates ROP GTPase to Modulate Petal Growth and Shape1

SPIKE1 activates ROP GTPase proteins to regulate anisotropic cell expansion and petal anisotropic growth by affecting the organization of cortical microtubule arrays in Arabidopsis. Plant organ growth and final shape rely on cell proliferation and, particularly, on cell expansion that largely determines the visible growth of plant organs. Arabidopsis (Arabidopsis thaliana) petals serve as an excellent model for dissecting the coordinated regulation of patterns of cell expansion and organ growth, but the molecular signaling mechanisms underlying this regulation remain largely unknown. Here, we demonstrate that during the late petal development stages, SPIKE1 (SPK1), encoding a guanine nucleotide exchange factor, activates Rho of Plants (ROP) GTPase proteins (ROP2, ROP4, and ROP6) to affect anisotropic expansion of epidermal cells in both petal blades and claws, thereby affecting anisotropic growth of the petal and the final characteristic organ shape. The petals of SPK1 knockdown mutants were significantly longer but narrower than those of the wild type, associated with increased anisotropic expansion of epidermal cells at late development stages. In addition, ROP2, ROP4, and ROP6 are activated by SPK1 to promote the isotropic organization of cortical microtubule arrays and thus inhibit anisotropic growth in the petal. Both knockdown of SPK1 and multiple rop mutants caused highly ordered cortical microtubule arrays that were transversely oriented relative to the axis of cell elongation after development stage 11. Taken together, our results suggest a SPK1-ROP-dependent signaling module that influences anisotropic growth in the petal and defines the final organ shape.
Genetic relationships among populations of Aedes aegypti from Uruguay and northeastern Argentina inferred from ISSR‐PCR data

Aedes aegypti (L.) (Diptera: Culicidae), the main vector of yellow fever and dengue viruses, was eradicated from Argentina between 1955 and 1963, but reinvaded the country in 1986. In Uruguay, the species was reintroduced in 1997. In this study we used highly polymorphic inter‐simple sequence repeats (ISSR) markers to analyse the genetic structure of Ae. aegypti populations from Uruguay and northeastern Argentina to identify possible colonization patterns of the vector. Overall genetic differentiation among populations was high (FST = 0.106) and showed no correlation with geographic distance, which is consistent with the short time since the reintroduction of the species in the area. Differentiation between pairs of Argentine populations (FST 0.072 to 0.221) was on average higher than between Uruguayan populations (FST−0.044 to 0.116). Bayesian estimation of population structure defined four genetic clusters and most populations were admixtures of two of them: Mercedes and Treinta y Tres (Uruguay) were mixtures of clusters 1 and 3; Salto (Uruguay) and Paraná (Argentina) of clusters 1 and 4; Fray Bentos (Uruguay) of clusters 2 and 3, and Gualeguaychú (Argentina) of clusters 2 and 3. Posadas and Buenos Aires in Argentina were fairly genetically homogeneous. Our results suggest that Ae. aegypti recolonized Uruguay from bordering cities in Argentina via bridges over the Uruguay River and also from Brazil.
It Takes a Confounded Face to Pop Out of a Crowd

It is widely reported that a picture of an angry face seems to figuratively pop out of an array of happy faces, although all of these reports are based on a single experiment by Hansen and Hansen. Pop out, when it occurs, indicates that an observer has located the target by means of a preattentive, parallel search. Hansen and Hansen concluded that it was the affect displayed by the face which caused it to pop out from its surrounding distracters. However, Hansen and Hansen's angry faces contained extraneous dark areas which were introduced when they transformed Ekman and Friesen's photographs of angry and happy faces into black-on-white sketches. When the original artifact-free gray-scaled versions of angry and happy faces were used no evidence for pop out was found. All target faces were found during a serial, self-terminating search regardless of their expression. The angry face in Hansen and Hansen's experiments may have popped out from a crowd of happy faces because of a contrast artifact inadvertently introduced when they created their stimuli.
High-Resolution Versus Standard-Resolution Cardiovascular MR Myocardial Perfusion Imaging for the Detection of Coronary Artery Disease

Background— Although accelerated high-spatial-resolution cardiovascular MR (CMR) myocardial perfusion imaging has been shown to be clinically feasible, there has not yet been a direct comparison with standard-resolution methods. We hypothesized that higher spatial resolution detects more subendocardial ischemia and leads to greater diagnostic accuracy for the detection coronary artery disease. This study compared the diagnostic accuracy of high-resolution and standard-resolution CMR myocardial perfusion imaging in patients with suspected coronary artery disease. Methods and Results— A total of 111 patients were recruited to undergo 2 separate perfusion-CMR studies at 1.5 T, 1 with standard-resolution (2.5×2.5 mm in-plane) and 1 with high-resolution (1.6×1.6 mm in-plane) acquisition. High-resolution acquisition was facilitated by 8-fold k-t broad linear speed-up technique acceleration. Two observers visually graded perfusion in each myocardial segment on a 4-point scale. Segmental scores were summed to produce a perfusion score for each patient. All patients underwent invasive coronary angiography and coronary artery disease was defined as stenosis ≥50% luminal diameter (quantitative coronary angiography). CMR data were successfully obtained in 100 patients. In patients with coronary artery disease (n=70), more segments were determined to have subendocardial ischemia with high-resolution than with standard-resolution acquisition (279 versus 108; P<0.001). High-resolution acquisition had a greater diagnostic accuracy than standard resolution for identifying single-vessel disease (area under the curve, 0.88 versus 0.73; P<0.001) or multivessel disease (area under the curve, 0.98 versus 0.91; P=0.002) and overall (area under the curve, 0.93 versus 0.83; P<0.001). Conclusions— High-resolution perfusion-CMR has greater overall diagnostic accuracy than standard-resolution acquisition for the detection of coronary artery disease in both single- and multivessel disease and detects more subendocardial ischemia.
Productivity Losses Among Treated Depressed Patients Relative to Healthy Controls

Objectives: Estimate the productivity-related cost of depression in an employed population. Methods: By using administrative data, annual short-term disability (STD) and absenteeism costs ($2005) were compared for patients with depression and treated with antidepressants and for a matched control group without depression. Results: Mean annual STD costs were $1038 among treated depressed patients versus $325 among controls and $1685 among a subgroup of severely depressed treated patients versus $340 among their controls. After controlling for demographic and employment characteristics, treated patients with depression had STD costs that were $356 higher per patient and those with severe depression had costs that were $861 higher. The marginal impact of treated depression on absenteeism was $377. Conclusions: Even when depressed patients are treated with antidepressants, there are substantial productivity losses. Therapies that can better manage depression may provide opportunities for savings to employers.
Cell cycle‐dependent abundance, stability and localization of FtsA and FtsQ in Caulobacter crescentus

Coordination between cell division and DNA replication is ensured by checkpoints that act through proteins required for cell division. Following a block in DNA replication, transcription of the cell division progression genes ftsA and ftsQ is prevented in Caulobacter crescentus. One requirement for this checkpoint is that FtsA and/or FtsQ should be limiting for division in the next cell cycle. We show that the number of FtsA and FtsQ molecules fluctuates such that their concentration is low in swarmer and stalked cells, peaks in pre‐divisional cells, and then dramatically decreases after cell division. Despite constitutive expression from an inducible promoter, FtsA and FtsQ levels still vary during the cell cycle, and the half‐life of FtsA increases from 13 min in swarmer cells to 55 min in stalked cell types, confirming cell type‐specific degradation. The post‐division degradation of FtsA and FtsQ in swarmer cells reduces their concentration to 7% and 10% of their maximal level, respectively, strongly suggesting that de novo synthesis of both proteins is required for each division cycle. The localization of FtsA and FtsQ is also cell type‐specific. FtsA and FtsQ are recruited to the midcell during a short period in late pre‐divisional cells, consistent with the demonstrated requirement of FtsA for late stages of cell division. As previously reported for FtsZ, constitutive expression of FtsA causes cell division defects. These results indicate that the tight control of FtsA, and probably FtsQ, by cell cycle transcription, proteolysis, and localization are critical for optimal cell division and the coordination of cell division with the DNA replication cycle.
Hydrocortisone effects on cardiovascular variability in septic shock: A spectral analysis approach*

Rational:Septic shock may be associated with a loss in cardiovascular variability and adrenal dysfunction. Objectives:To investigate the relationship between cardiovascular autonomic modulation and adrenal function during sepsis. Measurement and Main Results:Seventy-five volunteers with septic shock and six healthy volunteers were prospectively included in the study. Cardiovascular variability was assessed by spectral analysis of heart rate and diastolic blood pressure signals, which included computation of normalized low (LFnu) and high frequency (HFnu) components. Cardiovascular variability was investigated in patients and healthy volunteers immediately before and 1 hr after a single bolus of 50 mg of hydrocortisone (study phase I); in patients according to adrenal function (study phase II); and in patients with septic shock and adrenal insufficiency, before and 72 hrs after a treatment with 50 mg every 6 hrs of hydrocortisone and 50 &mgr;g daily of fludrocortisone or their placebos (study phase III). As compared to healthy volunteers, patients had decreased LFnu-HR (.16 ± .05 vs. .23 ± .07 p = .01) and LFnu-DBP (.18 ± .11 vs. .28 ± .02 p = .01) and, after hydrocortisone, they had a greater increase in LFnu-DBP (p = .01). As compared to patients with normal adrenal function, those with adrenal failure had decreased LFnu-HR (.1 ± .01 vs. .2 ± .15 p = .01) and LFnu-DBP (.008 ± .01 vs. .14 ± .22 p = .0003). In patients with adrenal failure, as compared to placebos, hydrocortisone plus fludrocortisone increased significantly LFnu-DBP (p = .02) and low frequency/high volume ratio (p = .009). Conclusion:In septic shock, the loss in cardiovascular variability is more marked in patients with adrenal insufficiency and is partly restored by exogenous administration of corticosteroids.
ANMCO Position Paper: long-term follow-up of patients with pulmonary thromboembolism

Abstract Venous thromboembolism (VTE), including pulmonary embolism and deep venous thrombosis, is the third most common cause of cardiovascular death. The management of the acute phase of VTE has already been described in several guidelines. However, the management of the follow-up (FU) of these patients has been poorly defined. This consensus document, created by the Italian cardiologists, wants to clarify this issue using the currently available evidence in VTE. Clinical and instrumental data acquired during the acute phase of the disease are the cornerstone for planning the FU. Acquired or congenital thrombophilic disorders could be identified in apparently unprovoked VTE during the FU. In other cases, an occult cancer could be discovered after a VTE. The main targets of the post-acute management are to prevent recurrence of VTE and to identify the patients who can develop a chronic thromboembolic pulmonary hypertension. Knowledge of pathophysiology and therapeutic approaches is fundamental to decide the most appropriate long-term treatment. Moreover, prognostic stratification during the FU should be constantly updated on the basis of the new evidence acquired. Currently, the cornerstone of VTE treatment is represented by both the oral and the parenteral anticoagulation. Novel oral anticoagulants should be an interesting alternative in the long-term treatment.
Dendritic cells with TGF-β1 differentiate naïve CD4+CD25− T cells into islet-protective Foxp3+ regulatory T cells

CD4+CD25+Foxp3+ regulatory T cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natural) or differentiated in the periphery outside the thymus (induced). Here we show that β-cell peptide-pulsed dendritic cells (DCs) from nonobese diabetic (NOD) mice can effectively induce CD4+CD25+Foxp3+ T cells from naïve islet-specific CD4+CD25− T cells in the presence of TGF-β1. These induced, antigen-specific T regs maintain high levels of clonotype-specific T cell receptor expression and exert islet-specific suppression in vitro. When cotransferred with diabetogenic cells into NOD scid recipients, T regs induced with DCs and TGF-β1 prevent the development of diabetes. Furthermore, in overtly NOD mice, these cells are able to significantly protect syngeneic islet grafts from established destructive autoimmunity. These results indicate a role for DCs in the induction of antigen-specific CD4+CD25+Foxp3+ T cells that can inhibit fully developed autoimmunity in a nonlymphopoenic host, providing an important potential strategy for immunotherapy in patients with autoimmune diabetes.
Epizootiologic patterns of diabetes mellitus in cats: 333 cases (1980-1986).

Medical records from 333 cats with diabetes mellitus were studied retrospectively, using epidemiologic methods to determine the incidence of and risk factors for diabetes mellitus in this species. Abstracts were derived, using the Veterinary Medical Data Program with its 17 participating academic institutions in the United States and Canada. A reference population of 135,651 cats was derived from the same hospital population and time span (July 1980 to June 1986). The incidence of diabetes mellitus in cats was determined to be 2.45 cases/1,000 cat-years-of-risk during the 6-year study period. Breed had no detectable effect on risk for diabetes mellitus. In contrast, body weight, age, gender, and neutering had a significant (P less than or equal to 0.01) effect. Body weight of cats was categorized as being less than or greater than or equal to 6.8 kg. The higher body weight, probably indicating obesity, contributed a 2.2-fold increase in risk, even after adjustment for age and gender (adjusted odds ratio). The etiologic fraction for high body weight was 3.8%, suggesting that an estimated 3.8% of cases of diabetes mellitus was attributable to this factor alone. Over 50% of diabetic cats were greater than 10 years old, and the etiologic fraction for age greater than 7 years alone was 73.5%. Age was a significant (P less than 0.001) and the most important single risk factor for development of the disease in cats, with adjusted odds ratios of 8.3 and 14.4 for age 7 to 10 years and greater than 10 years, respectively. (ABSTRACT TRUNCATED AT 250 WORDS)
An Overview of an Emergency Department Short Stay Ward in Hong Kong

Objectives To describe the structure and service pattern of a short stay ward (SSW) named as Emergency Observation and Pre-admission Ward (EOPW) in Hong Kong. The effectiveness of the EOPW was to be examined. Methods This was a retrospective observational cohort study. The facilities, staffing and operation of the EOPW were described. Consecutive patients admitted to the EOPW in the year 2006 were retrieved from the hospital computer database. Admission diagnoses, length of stay (LOS) and destination of disposal were the main outcome variables measured. The ICD coded admission diagnoses were categorised into 24 diagnosis-related groups. Different diagnosis-related groups were compared with respect to the selected efficacy cutoff points of LOS less than 24 hours and hospital admission rate less than 30% respectively. Results The service of the 30-bed short stay ward as started in year 2003 was a pilot project in Hong Kong. In year 2006, 10,111 patients were admitted and the mean age was 54.2 years. The five commonest diagnosis-related groups were psychiatric disease, chest pain, dizziness, musculoskeletal pain and poisoning. The overall hospital admission rate and the mean LOS were 26.8% and 23.4 hours respectively and were below the efficacy cutoff points. Musculoskeletal pain, chronic obstructive pulmonary disease and acute urinary retention were the three diagnostic groups with both LOS and hospital admission rate above the efficacy cutoff points. Conclusion This first SSW in Hong Kong was demonstrated to be effective according to the analysis result of the 2006 data. SSW has become an integral part of emergency medicine and provided an alternative way of effective management in contrast to traditional inpatient management for various selected disease conditions.
Is There a Chastity Belt on Perception?

Can one’s ability to perform an action, such as hitting a softball, influence one’s perception? According to the action-specific account, perception of spatial layout is influenced by the perceiver’s abilities to perform an intended action. Alternative accounts posit that purported effects are instead due to nonperceptual processes, such as response bias. Despite much confirmatory research on both sides of the debate, researchers who promote a response-bias account have never used the Pong task, which has yielded one of the most robust action-specific effects. Conversely, researchers who promote a perceptual account have rarely used the opposition’s preferred test for response bias, namely, the postexperiment survey. The current experiments rectified this. We found that even for people naive to the experiment’s hypothesis, the ability to block a moving ball affected the ball’s perceived speed. Moreover, when participants were explicitly told the hypothesis and instructed to resist the influence of their ability to block the ball, their ability still affected their perception of the ball’s speed.