Miracle-dz/UniFAR-FTUs huggingface dataset:
Microbes and mass extinctions: paleoenvironmental distribution of microbialites during times of biotic crisis

Widespread development of microbialites characterizes the substrate and ecological response during the aftermath of two of the ‘big five’ mass extinctions of the Phanerozoic. This study reviews the microbial response recorded by macroscopic microbial structures to these events to examine how extinction mechanism may be linked to the style of microbialite development. Two main styles of response are recognized: (i) the expansion of microbialites into environments not previously occupied during the pre‐extinction interval and (ii) increases in microbialite abundance and attainment of ecological dominance within environments occupied prior to the extinction. The Late Devonian biotic crisis contributed toward the decimation of platform margin reef taxa and was followed by increases in microbialite abundance in Famennian and earliest Carboniferous platform interior, margin, and slope settings. The end‐Permian event records the suppression of infaunal activity and an elimination of metazoan‐dominated reefs. The aftermath of this mass extinction is characterized by the expansion of microbialites into new environments including offshore and nearshore ramp, platform interior, and slope settings. The mass extinctions at the end of the Triassic and Cretaceous have not yet been associated with a macroscopic microbial response, although one has been suggested for the end‐Ordovician event. The case for microbialites behaving as ‘disaster forms’ in the aftermath of mass extinctions accurately describes the response following the Late Devonian and end‐Permian events, and this may be because each is marked by the reduction of reef communities in addition to a suppression of bioturbation related to the development of shallow‐water anoxia.
Effects of papillary muscles and trabeculae on left ventricular quantification: increased impact of methodological variability in patients with left ventricular hypertrophy

Background Accurate quantification of left ventricular mass and ejection fraction is important for patients with left ventricular hypertrophy. Although cardiac magnetic resonance imaging has been proposed as a standard for these indices, prior studies have variably included papillary muscles and trabeculae in myocardial volume. This study investigated the contribution of papillary muscles and trabeculae to left ventricular quantification in relation to the presence and pattern of hypertrophy. Methods Cardiac magnetic resonance quantification was performed on patients with concentric or eccentric hypertrophy and normal controls (20 per group) using two established methods that included papillary muscles and trabeculae in myocardium (method 1) or intracavitary (method 2) volumes. Results Among all patients, papillary muscles and trabeculae accounted for 10.5% of ventricular mass, with greater contribution with left ventricular hypertrophy than normals (12.6 vs. 6.2%, P < 0.001). Papillary muscles and trabeculae mass correlated with ventricular wall mass (r = 0.53) and end-diastolic volume (r = 0.52; P < 0.001). Papillary muscles and trabeculae inclusion in myocardium (method 1) yielded smaller differences with a standard of mass quantification from linear ventricular measurements than did method 2 (P < 0.001). Method 1 in comparison with method 2 yielded differences in left ventricular mass, ejection fraction and volume in all groups, especially in patients with hypertrophy: the difference in ventricular mass index was three-fold to six-fold greater in hypertrophy than normal groups (P < 0.001). Difference in ejection fraction, greatest in concentric hypertrophy (P < 0.001), was independently related to papillary muscles and trabeculae mass, ventricular wall mass, and smaller ventricular volume (R2 = 0.56, P < 0.001). Conclusion Established cardiac magnetic resonance methods yield differences in left ventricular quantification due to variable exclusion of papillary muscles and trabeculae from myocardium. The relative impact of papillary muscles and trabeculae exclusion on calculated mass and ejection fraction is increased among patients with hypertrophy-associated left ventricular remodeling.
Isolation of alkali‐tolerant benzene‐degrading bacteria from a contaminated aquifer

Aims: To isolate benzene‐degrading strains from neutral and alkaline groundwaters contaminated by benzene, toluene, ethylbenzene, xylenes (BTEX) from the SIReN aquifer, UK, and to test their effective pH range and ability to degrade TEX.
Knowledge and attitude on HIV/AIDS among married women of reproductive age attending a teaching hospital

Acquired immunodeficiency disease syndrome (AIDS) though a disease only about 20 years old now has evolved into a pandemic affecting millions of people worldwide. By the end of 2001 25 million people had already died of AIDS. In India the cumulative number of AIDS cases reported as on June 2002 was 36160 which is supposed to be only the tip of the iceberg. The important characteristic of HIV scenario in India is its heterogenicity the prevalence varying in different states. Pondicherry is among the hardest hit regions. Based on the seroprevalence among antenatal clinic attendees Pondicherry comes under the high prevalence category (=> 1%) indicative of a generalized epidemic. Heterosexual transmission being the commonest route of spread the only way to check its transmission is by increasing awareness regarding the modes of spread and methods of prevention of this disease among people particularly those belonging to the sexually active age groups. In this context this study was conducted to examine the extent of awareness of its determinants as well as the attitude of married women in reproductive age group towards HIV/AIDS in Pondicherry. (excerpt)
Diagnostic performance of clinical tests for sacroiliac joint pain

Abstract Background: An updated review of the diagnostic clinical tests available for sacroiliac joint (SIJ) pain has yet to be undertaken. Objective: To evaluate the diagnostic performance of clinical tests for SIJ pain based on a systematic review. Methods: Five electronic databases were searched. Studies that examined the SIJ pain provocation tests with sensitivity and specificity data in patients (age ⩾18 years) with non-specific, non-pregnancy related low back pain and/or buttock pain, with or without lower extremity symptoms, were selected. Studies related to SIJ dysfunction were excluded. The Quality Assessment of Diagnostic Accuracy Studies (QUADAS) tool has been used to evaluate the quality of all included studies. Results: Six studies were included in this systematic review and the QUADAS scores are similar for all selected studies. The diagnostic performance of most clinical tests was poor with low specificity (0·03–0·95), sensitivity (0·08–0·90), and positive likelihood ratio (0·3–1·4), when used in isolation. The thigh thrust is the most sensitive test (0·88), the distraction test is most specific (0·81), and the compression test has the strongest positive likelihood ratio (2·20). Three or more positive pain provocation tests showed optimal sensitivity (0·85–0·94) and specificity (0·78–0·79) values with high positive likelihood ratios (4·02–4·29). Conclusion: Pain location below the lumbosacral junction overlying the SIJ with at least three or more positive SIJ pain provocation tests (thigh thrust, distraction, and compression) should be considered for the clinical diagnosis of SIJ pain.
Human-centred integration of a stand-alone manufacturing facility in a networked product development environment

Recent advances in Internet technology have led to the concept of networked product development. This includes geographically separated teams, co-located over wide area networks for the design, manufacture and marketing of products. Such a distributed environment consists of humans, software and manufacturing machines. Previous research in networked product development assumed that all manufacturing facilities were already networked and remotely accessible, and excluded the non-networked machines. This paper presents a human-centred methodology for virtual integration of stand-alone facilities into a networked environment. The methodology is based on a modified Open Systems Interconnection (OSI) model and has been realised through a hybrid architecture which includes stand-alone machines, humans and software agents. A laboratory-based experiment was carried out to validate the integration methodology for a stand-alone injection moulding machine. The role of humans in the integration process at different s.
Left ventricular geometry and endogenous ouabain in a Flemish population

Background Endogenous ouabain, an endogenous digitalis-like steroid, is synthesized in the adrenal glands and possibly in the hypothalamus. In vitro and in vivo, endogenous ouabain triggers growth and proliferation of cardiomyocytes. Objective We therefore investigated the association between left ventricular structure and function and plasma endogenous ouabain in a general population. Methods We randomly recruited 536 individuals from a general population (50.7% women, mean age 53.1 years). Measurements included echocardiographic left ventricular structure and function, blood pressure, plasma endogenous ouabain, and the 24-h urinary excretion of sodium. Results The geometric mean plasma endogenous ouabain was 95.5 pmol/l (interquartile range 79.4–120.2 pmol/l). We expressed effect sizes for a 1-SD increase in plasma endogenous ouabain (0.21 on the logarithmic scale), while accounting for important covariables. For a 1-SD increment in plasma endogenous ouabain, SBP, left ventricular posterior wall, the interventricular septum, and relative wall thickness increased by 1.59 mmHg (P = 0.009), 0.138 mm (P = 0.003), 0.152 mm (P = 0.013), and 0.71 × 10−2 (P = 0.008), respectively. In a sensitivity analysis, involving 431 individuals aged 29–71 years (10–90th percentile interval), a 1-SD increase in plasma endogenous ouabain was associated with opposite trends in ejection fraction (+0.90%, P = 0.005) and left ventricular systolic longitudinal strain (−0.48%, P = 0.011). Moreover, in individuals whose sodium excretion was above median (160 mmol/24 h), the aforementioned associations reached a higher level of statistical significance. Conclusion Our population-based study suggested that endogenous ouabain might have a trophic effect on the myocardium, independent of blood pressure and other covariables. The clinical implication of these findings remains to be elucidated.
Left ventricular hypertrophy increases cardiovascular risk independently of in-office and out-of-office blood pressure values

Objectives Previous studies have shown that left ventricular hypertrophy (LVH) represents a cardiovascular risk factor independently of clinic blood pressure (BP). The present study was aimed at determining the impact of LVH on the incidence of cardiovascular morbid and fatal events taking into account not only classical risk factors but also home and ambulatory BP values, which have been shown to have an important independent prognostic impact. Methods In 1716 patients belonging to the ‘Pressioni Arteriose Monitorate E Loro Associazioni’ population of Monza, we quantified left ventricular mass index and identified LVH by standard cutoff values. We also measured clinic, home and 24-h ambulatory BPs together with serum glucose and lipids. Results During a follow-up of 148 months, the rate of fatal and nonfatal (hospitalizations) cardiovascular events as well as of all-cause death was markedly greater (four-fold to five-fold) in patients as compared with those without LVH. In LVH individuals, the increased risk remained significant even when data were adjusted for a large number of other confounding factors including home BP, 24-h mean BP and ambulatory BP. Results were similar when left ventricular mass was indexed by height and body surface area. A 10% increase in left ventricular mass index was associated with a significant increase in cardiovascular risk or all-cause deaths. In multivariate analysis, left ventricular mass index was always an independent predictor of cardiovascular events and death for any cause. Conclusion Our data provide evidence that LVH is an important risk factor even when the contribution of different BPs to risk is fully taken into account.
The Effects of Plastazote® and Aliplast®/Plastazote® Orthoses on Plantar Pressures in Elderly Persons With Diabetic Neuropathy

High plantar pressures often lead to ulcers and amputation in persons with diabetic neuropathy. Orthoses, worn with diabetic shoes, are prescribed to decrease plantar pressures. The purpose of this study was to determine the effect of Plastazote® and Aliplast®/Plastazote® orthoses in decreasing plantar pressures. Eight men and eight women (mean age, 68 ± 6 years), with diabetic neuropathy were separated into two groups of eight, matched by body mass index and history of or current foot ulceration. One group wore custom Plastazote orthoses, the other, custom Aliplast/Plastazote orthoses, for 3 months. Plantar pressures were measured during walking with and without orthoses at predetermined velocity immediately after orthosis fabrication, at 1 month, after orthosis adjustment deemed necessary by the orthotist, and after 3 months of wear. Plantar pressure variables were recorded for six plantar regions of the foot: heel, medial midfoot, lateral midfoot, metatarsal one and big toe, metatarsals two and three and corresponding toes, and metatarsals four and five and corresponding toes. Repeated measures ANOVAs identified significant differences in peak pressure, maximum mean pressure, pressure time integral, mean force, and contact area between groups and orthosis condition (with vs. without) immediately after fabrication. Separate repeated measures ANOVAs identified significant differences in the same variables for group, orthosis condition, and time between 1 and 3 months. Walking with shoes and either orthosis significantly decreased all plantar pressure variables and increased contact areas compared with walking with shoes without orthoses under the big toe and metatarsals two and three immediately after fabrication. Peak pressure under the big toe decreased 27% and that under metatarsals two and three decreased 41% when wearing orthoses. Peak pressure also significantly decreased under the heel and metatarsals four and five (25% and 35%, respectively). No variables differed between orthosis groups or with time wearing orthoses. Wearing custom-made orthoses reduced plantar pressures by increasing contact area. Plastazote alone and Aliplast/Plastazote are equally effective in decreasing pressures at time of fabrication, at 1 month after 9 of 16 pairs of orthoses were adjusted for wear, and after orthoses wear for an additional 2 months.
Molecular mechanisms of experimental glomerulonephritis: an overview

Summary: Most glomerular diseases are autoimmune in nature with injury occurring as a consequence of antibody reacting with antigens on glomerular cell membranes or in glomerular matrix, or immune complex formation occurring on or near glomerular cell membrnes. Many of the structural and functional consequences of these events result from the response of resident glomerular cells to the injury, or may be induced by inflammatory effector cells derived from the circulation. In terms of glomerular cells, injury to the glomerular epithelial cell (GEC) may be induced by: (i) non‐complement fixing antibodies which mimic the glomerular lesions of minimal change nephrotic syndrome/focal glomerular sclerosis; or (ii) by antibodies which fix complement leading to GEC attack by C5b‐9 resulting in a lesion analogous to membranous nephropathy. C5b‐9 also mediates antibody induced injury to the mesangial cell resulting in a mesangioproliferative glomerulonephritis (IgA nephropathy, systemic lupus erythematosus; SLE) as well as to the glomerular endothelial cell (thrombotic microangiopathy, haemolytic uraemic syndrome). the effects of C5b‐9 may be lytic (mesangial cell, glomerular endothelial cell; GEN) or sublytic (GEC) resulting in stimulation of local oxident and protease production. Both lytic and sublytic effects are substantially modulated by cell‐bound complement regulatory proteins such as CD59 and Crry. When fixed or planted antigens are present in larger quantities and accessible to the circulation, complement activation generates chemotactic factors leading to neutrophil infiltration and producing injury through the myeloperoxidase (MPO)‐H2‐O2‐halide system, a mechanism substantially augmented by platelet‐neutrophil interaction (post‐infectious glomerulonephritis [GN], SLE). Macrophages may also be localized in glomeruli by either immune adherence mechanisms or as a consequence of cell mediated immune reactions in the glomerulus. Macrophages differ from neutrophils in producing large amounts of transforming growth factor‐β (TGF‐β) and procoagulants which contribute to crescent formation rapidly progressive glomerulonephritis (RPGN).
Perindopril and indapamide reverse coronary microvascular remodelling and improve flow in arterial hypertension

Objectives Patients and animal models of arterial hypertension are characterized by structural and functional abnormalities of the coronary microcirculation. Using a translational approach, we ascertained whether antihypertensive treatment can reverse microvascular remodelling and improve myocardial perfusion. Methods In 20 hypertensive patients with left ventricular hypertrophy, blood pressure, left ventricular mass index and myocardial blood flow were measured at baseline and after 6 months of treatment with perindopril + indapamide. In spontaneously hypertensive rats, blood pressure, coronary flow and histomorphometry of intramural coronary arterioles were measured after 8 weeks of treatment with placebo or perindopril + indapamide. Results In patients, treatment decreased blood pressure (161 ± 10/96 ± 5 to 136 ± 12/81 ± 6 mmHg; P < 0.0001) and left ventricular mass index (93 ± 16 to 85 ± 17 g/m2; P < 0.01) while increasing baseline (0.69 ± 0.13 to 0.88 ± 0.36 ml/min per g; P < 0.05) and hyperaemic myocardial blood flow (1.42 ± 0.32 to 1.94 ± 0.99 ml/min per g; P < 0.05). In rats treated with perindopril + indapamide (n = 11), blood pressure was 93 ± 18/55 ± 18 mmHg compared to 215 ± 18/161 ± 17 mmHg in placebo (n = 6; P < 0.001), baseline flow was unchanged whilst hyperaemic coronary flow was 19.89 ± 3.50 vs. 12.15 ± 0.99 ml/min per g, respectively (P < 0.01). The medial area of intramural arterioles was 1613 ± 409 with perindopril + indapamide and 8118 ± 901 μm2 with placebo (P < 0.001). Conclusion In patients with arterial hypertension and left ventricular hypertrophy, perindopril + indapamide reduced blood pressure and left ventricular mass index and improved resting and hyperaemic myocardial blood flow. Data in rats provide evidence that the improvement in coronary flow observed after treatment is due to reverse remodelling of intramural coronary arterioles and improved microvascular function.
Transgenic expression of human matrix metalloproteinase-9 augments monocrotaline-induced pulmonary arterial hypertension in mice

Objectives Pulmonary arterial hypertension (PAH) is characterized by intimal lesions, right ventricular hypertrophy, and adventitial thickening of pulmonary arteries with progressive pulmonary hypertension. This investigation was aimed to examine the effects of transgenic expression of human matrix metalloproteinase-9 (MMP-9) in the pathogenesis of PAH. Methods PAH was induced using serial subcutaneous administration of monocrotaline (MCT). Right ventricular pressure was measured through the right jugular vein using a 1.4F Millar Mikro-tip catheter-transducer. Zymography, western blotting, and quantitative reverse transcription PCR (qRT-PCR) were carried out for MMP-9. Immunohistochemistry was performed for α-smooth muscle actin (α-SMA) and Mac-3 antigen. Results Measurement of right ventricular pressure demonstrated 2.5-fold and 3.7-fold elevation after the administration of MCT in wild-type and MMP-9 transgenic mice, respectively. Zymography, western blotting, and qRT-PCR depicted increased activity and expression of MMP-9 after treatment with MCT, which were augmented in transgenic mice. There was marked pulmonary inflammation with extensive infiltration of mononuclear cells, which was more intense in MMP-9 transgenic mice. SMA and Mac-3 staining demonstrated hypertrophy of pulmonary arteries with occlusion of precapillary vessels and extensive infiltration of macrophages, respectively. All these changes were aggravated in MCT-treated MMP-9 transgenic mice when compared to normal littermates. Conclusion Our study demonstrated that the MCT-induced PAH in mouse is a reproducible and potentially valuable animal model for the human disease. Our results further demonstrated that MMP-9 plays a significant role in the pathogenesis of PAH and effective blocking of MMP-9 could provide an option in the therapeutic intervention of human PAH.
Mononuclear Alkali Metal Organoperoxides Stabilized by an NNNN-Macrocycle and Short Hydrogen Bonds from ROOH Molecules.

A series of light alkali metal organoperoxides [MOOR] (M=Li, Na, K; R=tBu, CMe2 Ph) were isolated in mononuclear form, aided by the tetradentate and neutral NNNN-type macrocycle Me4 TACD (L; Me4 [12]aneN4 =1,4,7,10-tetramethyl-1,4,7,10-tetraazacyclododecane) and strong hydrogen bonds from additional ROOH molecules. The Na and K compounds are characterized by short O-H⋅⋅⋅O contacts, in the case of the Na derivative as short as 2.41 Å.
Combined effects of office and 24-h blood pressure on aortic stiffness in human hypertension

Objective Aortic stiffness, a prognostically adverse marker of arteriosclerosis, is critically dependent on blood pressure (BP). Office BP may not always reflect BP behaviour away from the medical environment, and it is uncertain whether office or out-of-office BP values are stronger determinants of arterial stiffness. Methods Twenty-four-hour BP and carotid-to-femoral pulse wave velocity (PWV) – a direct measure of aortic stiffness – were measured in 539 never-treated hypertensive patients and in 71 normotensive individuals. Results Sustained hypertensive patients had a higher age and heart-rate-adjusted aortic PWV than normotensive individuals (9.7 ± 2 vs. 8.5 ± 2 m/s, P < 0.001), even after further adjustment for office mean pressure as a measure of distending pressure (P = 0.018). The higher aortic PWV in white-coat hypertensive patients as compared with normotensive individuals (9.3 ± 2 vs. 8.5 ± 2 m/s, P = 0.026) did not hold after adjustment for office mean pressure (P = 0.16). To examine the independent effect of office BP on aortic PWV beyond the influence of 24-h BP, patients were classified according to the difference between observed and predicted office systolic BP (the latter determined by regressing 24-h BP on office BP). Despite having comparable 24-h BP values (131/82 vs. 131/84 mmHg), the patients with higher-than-predicted office BP had higher aortic PWV than those with lower-than-predicted office BP (10.1 ± 2 vs. 9.2 ± 2 m/s, P < 0.001). Similarly, after regressing office BP on 24-h BP, the group with higher-than-predicted 24-h BP also had higher aortic PWV (9.9 ± 2 vs. 9.5 ± 2 m/s, P < 0.05) despite having identical office BP (152/95 vs. 152/96 mmHg). In a multivariate regression model, both 24-h and office mean BP independently predicted aortic PWV. Conclusions Both office and out-of-office BP are independent predictors of aortic PWV in hypertension. Elevated BP values over the 24 h are associated with increased isobaric aortic stiffness.