Miracle-dz/UniFAR-FTUs huggingface dataset:
Animal Models of Inhibin Action

The physiology of inhibin has been investigated using rodent and ruminant animal models in both in vitro and in vivo studies. Inhibin was originally deﬁned as a substance that causes selective suppression of follicle-stimulating hormone (FSH) secretion by pituitary gonadotropes. Although this deﬁnition is still valid, it fails to encompass the breadth of inhibin’s actions. In addition to its endocrine action on pituitary FSH secretion, inhibin has a local paracrine action in its target tissues. The inhibin a subunit appears to play an important role in determining whether inhibin or activin is produced in cells. More recently, transgenic and knockout mouse models have highlighted the importance of inhibin for fertility and the inhibin a subunit for tumor suppression. Whether inhibin exerts its effects by a direct action on the gonad or by regulating FSH secretion, it is clear that inhibin is essential for normal reproductive function. In this article, we review the rodent and ruminant models employed to investigate inhibin physiology and examine the potential of inhibin-based vaccines to enhance gonadal function.
Testosterone, Hemostasis, and Cardiovascular Diseases in Men

Men have a higher incidence of cardiovascular disease (CVD) than women, and adverse thrombotic events increase with age. Recent experimental cross-sectional, and case-control studies have shown that testosterone may affect the hemostatic/ﬁbrinolytic system in men in several ways. It has been hypothesized that physiological doses of testosterone would have a beneﬁcial effect on tissue factor-induced thrombin generation and the development of CVD. The search for eternal youth has created a market for testosterone treatment in aging men during the last few years. However, whether testosterone supplementation could be useful in the treatment of testosterone-deﬁcient elderly men is still controversial. The present review focuses on the coagulation system and CVD from the perspective of testosterone.
Tissue Factor in Infection and Severe Inflammation

In the pathogenesis of vascular disease, inﬂammation and coagulation play a pivotal role. Increasing evidence points to an extensive cross-talk between these two systems, whereby inﬂammation not only leads to activation of coagulation, but coagulation also considerably affects inﬂammatory activity. Tissue factor (TF) plays an important role at the crossroad of coagulation and inﬂammation, as the principal initiator of coagulation and an important modulator of inﬂammation. Proinﬂammatory cytokines can induce TF expression on mononuclear cells and endothelial cells and thereby commence pathways that lead to thrombin generation. Simultaneously, TF may bind to cellular receptors, which may affect the production and release of inﬂammatory mediators. There is increasing experimental evidence that TF inhibition may have beneﬁcial effects in disease states in which the combination of coagulation and inﬂammation plays a prominent role.
Physiology of Breathing and Respiratory Control during Sleep

Studies of respiratory control during sleep have revealed that multiple sites of central CO 2 chemosensitivity exist within the brainstem, and different chemosensory sites may function only during certain sleep states. In general, chemical control of respiratory function, related to both hypercapnia and hypoxia, appears to be blunted during sleep. The decline in respiratory activity during sleep is particularly marked in the muscles of the upper airway. A variety of neuromechanical factors originating in the lungs, chest wall, and upper airway also modify respiratory function during sleep. Cardiorespiratory function seems to be less stable during sleep, and arousal responses represent a ﬁnal element in the control system that preserves cardiorespiratory function by terminating the sleep state and restoring more effective control mechanisms.
Extracellular Matrix of the Cumulus-Oocyte Complex

The mammalian oocyte is surrounded by several layers of cumulus granulosa cells that nurture the oocyte during its development and actively participate in the process of ovulation. After the ovulatory luteinizing hormone surge, a distinctive program of extracellular matrix production is initiated in the cumulus–oocyte complex. This process known as cumulus expansion or muciﬁcation involves synthesis of a backbone of long hyaluronan oligosaccharide chains that are cross-linked by a complex of hyaluronan binding cell surface and extracellular matrix proteins and proteoglycans. Active components of the cumulus matrix are synthesized directly by cumulus cells under the control of endocrine-and oocyte-derived factors, secreted by mural granulosa cells, or enter the follicle in blood plasma. Appropriate composition and assembly of the cumulus matrix is essential for ovulation, efﬁcient passage of the oocyte through the oviduct, and for fertilization. This review describes the critical components and their functional roles in the cumulus matrix, as well as the molecular regulation of cumulus matrix gene expression.
Evidence supporting New Geophysics

In the last decade a New Geophysics has been proposed, whereby the crust and uppermost ~400 km of the mantle of the Earth are so pervaded by closely‐spaced stress‐aligned microcracks (intergranular films of hydrated melt in the mantle) that in situ rocks verge on failure by fracturing, and hence are critical‐systems that impose a range of fundamentally‐new properties on conventional sub‐critical geophysics. Enough of these new properties have been observed to confirm that New Geophysics is a new understanding of fluid/rock deformation with important implications and applications. Evidence supporting New Geophysics has been published in a wide variety of publications. Here, for clarification, we summarise in one document the evidence supporting New Geophysics.
Nonspecific Interstitial Pneumonia

Nonspeciﬁc interstitial pneumonia (NSIP) describes a histopathologic pattern that can be seen in patients with immunodeﬁciency, drug or environmental exposures, and connective tissue diseases. The clinical diagnosis of NSIP, however, should be reserved for idiopathic cases in which no causative factor is identiﬁed. Patients typically present with cough, dyspnea, restrictive pulmonary physiology with decreased gas transfer, and ground-glass inﬁltrates on high-resolution computed tomography (HRCT). Response to immunosuppressive therapy is often successful; however, patients with progressive disease are at increased risk of subsequent mortality and should be considered for alternative treatment strategies such as lung transplantation.
Percutaneous Techniques for Cervical Pain of Discal Origin

Cervical discogenic pain is an important cause of suffering and disability in the adult population. Pain management in cervical disc herniation relies initially on conservative care (rest, physiotherapy, and oral medications). Once conservative treatment has failed, different percutaneous minimally invasive radiological procedures can be applied to relief pain. This article offers a systematic review on the percutaneous minimally invasive techniques that can be advocated for the treatment of cervical pain of discal origin. Periradicular steroid injection under image guidance (computed tomography or magnetic resonance imaging) is the ﬁrst technique to be considered. The steroid injection aims at reducing the periradicular inﬂammation and thus relieves the radicular pain. The steroid injections present satisfying short-term results, but pain can recur in the long term. Whenever the steroid injections fail to relieve pain from a contained cervical disc herniation, the more invasive percutaneous disc decompression techniques should be proposed. Percutaneous radiofrequency nucleoplasty is the most often applied technique on the cervical level with a low risk of thermal damage. When the indications and instructions are respected, radiofrequency nucleoplasty presents accepted safety and efﬁcacy levels.
Oculomotor Disorders

Ocular misalignment and nystagmus result in the visual symptoms of binocular diplopia and oscillopsia, and are frequently encountered in neurological practice. Correct localization of the underlying problem is the ﬁrst step to accurate diagnosis, and requires a systematic approach and knowledge of the ocular motor pathways and actions of the extraocular muscles. This article contains three segments: The ﬁrst outlines the diagnostic approach with attention to ﬁne historical and examination details helpful in localization; the second describes common localizations of diplopia including extraocular muscle, neuromuscular junction, cranial nerve and nuclei, and supranuclear structures with attention to examination features characteristic for each location; and the third describes the types of acquired nystagmus and their treatments.
Current Insights on the Pathogenesis of Pulmonary Arterial Hypertension

Regardless of the initial trigger, the elevated pulmonary arterial pressure and vascular resistance in patients with pulmonary arterial hypertension are primarily caused by remodeling and thrombosis of small-and medium-sized pulmonary arteries and arterioles, as well as sustained vasoconstriction. The process of pulmonary vascular remodeling involves all layers of the vessel wall and is complicated by cellular heterogeneity within each compartment. Indeed, each cell type (endothelial cells, smooth muscle cells, and ﬁbroblasts), as well as inﬂammatory cells and platelets, may play signiﬁcant roles in this condition. Recent studies have emphasized the relevance of several mediators in this condition, including prostaglandin-I 2 (prostacyclin), nitric oxide, endothelin-1, angiopoietin-1, 5-hydroxytryptamine (serotonin), cytokines, chemokines, and members of the transforming growth factor beta (TGF-b ) superfamily. Targeting some of these dysfunctional pathways (prostacyclin, nitric oxide, and endothelin-1) has been beneﬁcial in subjects displaying pulmonary arterial hypertension.
Standardization and Clinical Utility of Thrombin-Generation Assays

Thrombin generation is a key process that determines the extent of a hemostatic plug or a thrombotic process. The ensuing thrombin burst is crucial for the formation of a stable ﬁbrin clot. During its active life, thrombin exerts a multitude of highly regulated actions on the blood and the vessel wall, including the clotting of ﬁbrinogen. The inappropriate generation of thrombin may lead to pathologic processes, foremost of which are hemorrhagic or thrombotic diseases. The coagulation system is usually investigated by means of two in vitro classic clotting tests, the activated partial thromboplastin time (APTT) and prothrombin time (PT), which assess only time to initiation of clot formation and do not entirely reﬂect global hemostatic balance. The APTT and PT permit identiﬁcation of connectivity between the component activities identiﬁed as required for plasma coagulation and deﬁne the concept of intrinsic and extrinsic coagulation pathways, which converge at the point of formation of the prothrombinase complex. However, the mechanisms established by in vitro tests are not always mirrored in the human pathologies associated with bleeding or thrombosis. The recent development of newer tests based on the continuous registration of thrombin generation under in vitro conditions that mimic more closely what occurs in vivo prompt a reinvestigation of the balance between procoagulants and anticoagulants in patients with various hemostatic disorders. Throm-bin-generation assays not only provide an overall assessment of hemostasis but also target potential extrahemostatic effects of the generated thrombin, a potent agonist of a multitude of cellular activation pathways. Moreover, estimation of an individual’s thrombin-generation potential may correlate more closely with a hypercoagulable or hypocoagulable phenotype when compared with traditional coagulation tests. In this review, we discuss to what extent thrombin generation can be expected to reﬂect the clotting function of blood, the development and use of different thrombin-generation assay systems suitable for detecting changes in the kinetics of thrombin generation, and the clinical utility of thrombin generation.
Platelets and Endothelial Cells

The pathogenesis of atherosclerosis, the leading cause of morbidity and mortality in industrial countries, is multifactorial. Atherogenesis, the development of atherosclerotic lesions, is initiated by a mechanical or functional injury of the endothelium. The function of the endothelium is inﬂuenced by multiple factors as a consequence of cell–cell interactions. Cell–cell communication between endothelial cells with platelets has only recently begun to receive systematic study. In recent years it has been established that platelet–endothelial interactions are involved at all stages of atherosclerotic disease. This article reviews the interactions between endothelial cells and platelets in the context of their role to initiate and accelerate atherothrombosis, as well as in acute thrombotic occlusion (e.g., at the site of atherosclerotic plaque rupture or subsequent to coronary angioplasty). From a mechanistic standpoint, platelets and endothelial cells communicate on multiple levels. Cross-talk may occur over a distance (paracrine signaling), via transient interactions (so-called give-and-go mechanism), or through receptor-mediated cell–cell adhesion. Platelets may release or transfer substances that inﬂuence endothelial cell function, and vice versa. Among many others, adhesion molecules, such as P-selectin (CD62P), are of special interest because of their role in modulating interactions between blood cells and the endothelium, and also because of the possible use of the soluble form as a plasma predictor of adverse cardiovascular events. In addition to dietary, cholesterol and lipid lowering, and other pharmaceutical approaches, antiplatelet therapy plays an important part in the treatment of atherosclerosis and its multifactorial clinical manifestations. Understanding the speciﬁc interactions between platelets and the endothelium may lead to the development of novel therapeutic strategies.
Treatment Failure in Patients with Ventilator-Associated Pneumonia

Ventilator-associated pneumonia (VAP) is one of the most important infectious diseases in the intensive care unit (ICU). In some series the attributable mortality of VAP may reach 30%, and the adequacy of the initial empirical treatment greatly inﬂuences the prognosis. Treatment failure can be anticipated in (cid:1) 30 to 40% of patients developing pneumonia during mechanical ventilation and this situation is associated with an adverse outcome in terms of morbidity. For these reasons, the lack of response to empirical antibiotic treatment should be recognized early in the course of VAP, and a clear strategy for clarifying the causes of failure should be implemented. Resolution of VAP depends not only on the accuracy of microbial diagnosis but also on comorbidities, the response of the host to the infection, concomitant infections, and the correct clinical diagnosis. Treatment failure can be deﬁned by the pattern of resolution of VAP, which is clearly established in the literature.
Pragmatics and Adult Language Disorders: Past Achievements and Future Directions

In this article, the current state of our knowledge of pragmatic disorders in adults with language impairment is assessed. A brief historical background of clinical pragmatics is presented, and the place of adult language pathology within the development of this ﬁeld is discussed. A comprehensive review is undertaken of pragmatic deﬁcits in adults with language impairments of diverse etiologies. Speciﬁcally, pragmatic deﬁcits are examined in adults with left-hemisphere damage, often resulting in aphasia, and in adults with right-hemisphere damage, traumatic brain injury, schizophrenia, and neurodegenerative disorders (principally, Alzheimer’s disease). Although many pragmatic phenomena have been examined in these clinical populations, studies have also tended to neglect important areas of pragmatic functioning in adults with these disorders. Several such areas are identiﬁed within a wider discussion of how researchers and clinicians can best pursue future investigations of pragmatics in adults with language impairment.
Influenza and Cardiovascular Disease: Does Swine-Origin, 2009 H1N1 Flu Virus Represent a Risk Factor, an Acute Trigger, or Both?

Inﬂuenza infection has become an important focus of both public and medical attention because of high-level perceived clinical and public health effects, enormously ampliﬁed by the current and ongoing 2009 H1N1 ﬂu pandemic, sustained by the swine-origin inﬂuenza A (H1N1) virus (S-OIV). The current transmission of this virus among humans appears much higher than that traditionally observed with seasonal inﬂuenza, raising several outbreaks of febrile respiratory infection ranging in severity from self-limited to severe, even life-threatening disease. Reliable biological and clinical evidence support a signiﬁcant association between inﬂuenza infection and cardiovascular disorders, so that S-IOV might also be regarded as a potential multifaceted bioweapon able to affect the function of the cardiovascular system through a kaleidoscope of humoral, biological, and biochemical mechanisms. In acute coronary ischemic episodes, on one hand, it seems reasonable to consider any acute inﬂuenza virus infection as a precipitating factor that is the ﬁnal event propelling predisposed individuals (e.g., those with preexisting coronary artery disease) over a threshold that precipitates the development of infarction in synergy with other well-known triggers. On the other hand, inﬂuenza virus-induced endothelial dysfunction, modiﬁcation of lipoprotein metabolism, atherosclerotic plaque outgrowth, and inﬂammation additionally support the role of inﬂuenza infection as a strong cardiovascular risk factor. Comprehensive information regarding the 2009 H1N1 infection remains limited, so that it seems unreasonable to draw deﬁnitive conclusions. Nevertheless, current recorded mortality data would lead us to conclude that this new virus might represent a sinister threat to humankind, with cardiovascular mortality risk highlighting an additional crucial role for
On the convergence of general projection methods for solving convex feasibility problems with applications to the inverse problem of image recovery

Abstract For an arbitrary family of closed convex sets with nonempty intersection in a Hilbert space, we consider the classical convex feasibility problem. We study the convergence property of the recently introduced unified projection algorithm B-EMOPP for solving this problem. For this, a new general control strategy is proposed, which we call the ‘quasi-coercive control’. Under mild assumptions, we prove the convergence of B-EMOPP using these new control strategies as well as various other strategies. Several known results are extended and improved. The proposed algorithm is then applied to the inverse problem of image recovery.
On the nonlinear analysis of optical flow

We utilize the methods of computational topology to the database of optical flow created by Roth and Black from range images, and demonstrate a qualitative topological analysis of spaces of $3 \times 3, 5 \times 5$ and $7 \times 7$ optical flow patches. We experimentally prove that there exist subspaces of the spaces of the three sizes high-contrast patches that are topologically equivalent to a circle and a three circles model, respectively. The Klein bottle is the quotient space described as the square $[0,1] \times [0,1]$ with sides identified by the relations $(0, y)\sim (1, y)$ for $y\in [0, 1]$ and $(x, 0) \sim (1-x, 1)$ for $ x\in [0, 1]$. For the space of $3 \times 3$ optical flow patches we found a subspace having the same homology as that of the Klein bottle. As the size of patches increases, the Klein bottle feature of the spaces of $5 \times 5$ and $7 \times 7$ optical flow patches gradually disappears.
Fetal Programming of Adipose Tissue: Effects of Intrauterine Growth Restriction and Maternal Obesity/High-Fat Diet

A newly recognized primary cause of obesity epidemic is the developmental programming effects of (1) intrauterine growth-restricted (IUGR) newborns exposed in utero to undernutrition, and (2) normal or excessive weight newborns exposed to maternal obesity and high-fat (HF) diets. The mechanisms contributing to offspring obesity have been extensively studied in animal models with adipose tissue identiﬁed as one of the principal targets of programming. IUGR and HF offspring exhibit programmed adipocytes, such that an intrinsic enhanced lipogenesis and adipocyte proliferation contribute to the development of obesity. This is attributed to early induction of adipogenic transcription factor peroxisome proliferator-activated receptor (PPAR) g , whose activity is enhanced under limited or excess nutrient availability. Nonetheless, this occurs via different mechanisms involving PPAR g coregulators: In IUGR, it is upregulation of coactivators, whereas in HF newborns, it is downregulation of corepressors. Thus preventive therapeutic interventions will require target-speciﬁc modalities that depend on the primary etiology.
Cartilage MRI T2 Relaxation Time Mapping: Overview and Applications

The sensitivity of magnetic resonance imaging to biochemical and biophysical changes in the extracellular matrix of articular cartilage give it the potential to noninvasively detect the earliest changes of cartilage damage. The transverse relaxation time (T2) of cartilage has been shown to be a sensitive parameter for evaluation of early degeneration in articular cartilage, particularly changes in water and collagen content and tissue anisotropy. Although initial application has been in microimaging of small cartilage explants, in vivo techniques have been developed for cartilage T2 mapping of human joints. In addition to potential application in development of new pharmaceuticals and surgical techniques for preserving cartilage, in vivo cartilage T2 mapping can improve understanding of arthritis, cartilage aging, and response of cartilage to exercise.
Visual Orbit and Individual Masses of the Single-lined Spectroscopic Binary 94 AQR A (HD 219834A; MCA 74)

By combining our improved visual orbit with the last spectroscopic solution of the single-lined spectroscopic binary, MCA 74 (ADS 16672Aa, Ab; HD 219834A), we derived its orbital solution to have a period of 6.321 years. Using the Gaia parallax, a systemic mass of 1.87 ± 0.09 and a mass ratio of q = 0.725 were obtained, which yielded individual masses of 1.07 ± 0.06 and 0.80 ± 0.04 for the main and the secondary components, respectively. The mass and the absolute magnitude of +3.52 confirm that the primary is a late G5–G8 subgiant, while the same parameters of the secondary (Mv = +6.52) suggest that it is an early K2–K3 dwarf.