Miracle-dz/UniFAR-FTUs huggingface dataset:
Influence of antimicrobial chemotherapy and smoking status on the plasma concentrations of vitamin C, vitamin E, beta-carotene, acute phase reactants, iron and lipid peroxides in patients with pulmonary tuberculosis.

SETTING Inflammation-related oxidative stress has been implicated in the pathogenesis of lung fibrosis and dysfunction in patients with pulmonary tuberculosis. OBJECTIVE To investigate the effects of antimicrobial chemotherapy and smoking status on the plasma concentrations of the anti-oxidative nutrients vitamin C, vitamin E and beta-carotene, as well as those of iron, lipid peroxides and the acute phase reactants C-reactive protein (CRP) and ferritin. DESIGN A total of 41 patients with active pulmonary tuberculosis were studied at the outset and after 6 months of antimicrobial chemotherapy. RESULTS Initial plasma concentrations of vitamin C and beta-carotene were low, returning to normal values after chemotherapy in the non-smokers, but not in the smokers, while those of vitamin E remained low throughout in both groups. Ferritin and CRP concentrations decreased significantly following chemotherapy, with the former higher in smokers than in non-smokers. Serum lipid peroxides were elevated in patients with pulmonary tuberculosis and were unaffected by chemotherapy or smoking habits, while iron levels were not significantly affected by chemotherapy. Although residual dysfunction and infiltration were evident, pulmonary function (FEV1) and radiographic score improved equally in both smokers and non-smokers following antimicrobial chemotherapy. CONCLUSIONS Even after 6 months of apparently successful antimicrobial chemotherapy, pulmonary tuberculosis is associated with increased oxidative stress, which is unrelated to cigarette smoking and characterized by increased levels of circulating lipid peroxides and low concentrations of plasma vitamin E.
Identification and Characterization of a Common Set of Complex I Assembly Intermediates in Mitochondria from Patients with Complex I Deficiency*

Deficiencies in the activity of complex I (NADH: ubiquinone oxidoreductase) are an important cause of human mitochondrial disease. Complex I is composed of at least 46 structural subunits that are encoded in both nuclear and mitochondrial DNA. Enzyme deficiency can result from either impaired catalytic efficiency or an inability to assemble the holoenzyme complex; however, the assembly process remains poorly understood. We have used two-dimensional Blue-Native/SDS gel electrophoresis and a panel of 11 antibodies directed against structural subunits of the enzyme to investigate complex I assembly in the muscle mitochondria from four patients with complex I deficiency caused by either mitochondrial or nuclear gene defects. Immunoblot analyses of second dimension denaturing gels identified seven distinct complex I subcomplexes in the patients studied, five of which could also be detected in nondenaturing gels in the first dimension. Although the abundance of these intermediates varied among the different patients, a common constellation of subcomplexes was observed in all cases. A similar profile of subcomplexes was present in a human/mouse hybrid fibroblast cell line with a severe complex I deficiency due to an almost complete lack of assembly of the holoenzyme complex. The finding that diverse causes of complex I deficiency produce a similar pattern of complex I subcomplexes suggests that these are intermediates in the assembly of the holoenzyme complex. We propose a possible assembly pathway for the complex, which differs significantly from that proposed for Neurospora, the current model for complex I assembly.
Treatment of Resistant Port‐Wine Stains with a Variable‐Pulse Pulsed Dye Laser

BACKGROUND The conventional pulsed dye laser (PDL), operating at a wavelength of 585 nm and a pulse duration of 0.45 ms, usually does not achieve complete clearance in the majority of port-wine stains (PWSs). OBJECTIVE In this study, we demonstrate the efficacy of a variable-pulse pulsed dye laser (VPPDL) equipped with cryogen spray cooling (CSC) in the treatment of PWS that have become resistant to PDL treatment. METHODS Forty Asian patients with Fitzpatrick skin types III to IV were enrolled in this study. All patients had previously been treated by the PDL at least eight times (mean, 12.8±5.9) and had reached a treatment plateau. A VPPDL with a wavelength of 595 nm and a spot size of 7 mm was used. The patients were treated with fluences between 9 and 15 J/cm2 and pulse durations of 1.5 to 10 ms. Four treatments were administered at 8-week intervals for each lesion. Three months after the last treatment, all patients were evaluated for the degree of improvement by two independent clinicians. RESULTS Eight patients had excellent improvement, 9 had good improvement, 11 had fair improvement, and 12 had poor improvement. No complications were observed during the course of laser treatment. Vessels larger than 30 μm were not seen in the biopsy specimens obtained after the final treatment. CONCLUSION The VPPDL is more effective than the PDL and the VPPDL should be used for treating PDL-resistant PWSs. Nonetheless, vessels less than 30 μm in diameter are resistant to both PDL and VPPDL treatment.
The Guanine Nucleotide-Binding Switch in Three Dimensions

Guanine nucleotide–binding proteins regulate a variety of processes, including sensual perception, protein synthesis, various transport processes, and cell growth and differentiation. They act as molecular switches and timers that cycle between inactive guanosine diphosphate (GDP)–bound and active guanosine triphosphate (GTP)–bound states. Recent structural studies show that the switch apparatus itself is a conserved fundamental module but that its regulators and effectors are quite diverse in their structures and modes of interaction. Here we will try to define some underlying principles.
Polyoma virus middle‐T‐transformed PECAM‐1 deficient mouse brain endothelial cells proliferate rapidly in culture and form hemangiomas in mice

Wild‐type mouse brain endothelial (bEND) cells transformed with the polyoma virus middle‐T proliferate rapidly in culture and form hemangiomas in mice. These cells express high levels of platelet/endothelial cell adhesion molecule‐1 (PECAM‐1), a molecule shown to be important during hemangioma formation. In this study, we have examined the ability of polyoma virus middle‐T‐transformed mouse bEND cells prepared from PECAM‐1−/− mice to proliferate in culture and form hemangiomas in mice. We show that these cells express a number of endothelial cell markers and share a similar morphology with PECAM‐1+/+ bEND cells. PECAM‐1−/− bEND cells exhibit a limited ability to form tubes in Matrigel and rapidly form hemangioma when injected into nude mice, very similar to PECAM‐1+/+ bEND cells. These cells, however, have increased proliferation, slower migration, altered endothelial cell adhesion molecule expression, and are less adherent when compared to PECAM‐1+/+ bEND cells. Therefore, lack of PECAM‐1 expression impacts polyoma middle‐T‐transformed endothelial cell proliferative, adhesive, and migratory properties without impacting their ability to rapidly form hemangiomas in mice or poorly organize to capillary‐like structures in Matrigel. © 2005 Wiley‐Liss, Inc.
Inducible nitric oxide synthase (iNOS) in endotoxemia: chimeric mice reveal different cellular sources in various tissues

The aim of these experiments was to determine the contribution of leukocyte‐derived iNOS to total iNOS expression induced by lipopolysaccharide (LPS). By transferring bone marrow between iNOS+/+ and iNOS–/– mice, we created chimeric mice in which iNOS expression was limited to either circulating leukocytes (leukocyte‐iNOS mice) or parenchymal cells (parenchyma‐iNOS mice). Analysis of congenic markers demonstrated that >95% of thymocytes in chimeric mice were of donor origin. Also, following LPS treatment, iNOS mRNA was detectable in blood from leukocyte‐iNOS mice but not parenchyma‐iNOS mice. Together these findings indicated that the host marrow had been replaced entirely by donor cells. In the lung, at least 50% of the LPS‐induced iNOS mRNA was derived from leukocytes, and immunohistochemical analysis indicated that leukocytes were the main source of iNOS protein. In contrast in the liver, colon, and muscle, iNOS expression was derived predominantly from parenchymal cells. This divergence is potentially explained by the high level of leukocyte recruitment to the lung, relative to the other tissues. Plasma levels of NOS byproducts indicated that parenchymal iNOS was the dominant source of systemic iNOS activity. These findings indicate that in tissues other than the lung, parenchymal cells are the principal source of iNOS during endotoxemia.
Update article Sentence processing is uniquely human

In this article, we will focus on three fundamental issues concerning language processing in the human brain, and update recent advances made by functional neuroimaging and magnetic stimulation studies of language. First, we will provide the first experimental evidence that the neural basis of sentence comprehension is indeed specialized. Specifically, our recent functional magnetic resonance imaging (fMRI) study has clarified that the human left prefrontal cortex (PFC) is more specialized in the syntactic processes of sentence comprehension than other domain-general processes such as short-term memory. Second, the distinction between explicit and implicit syntactic processes will be clarified, based on our fMRI studies that elucidate syntactic specialization in the left PFC. Third, we will advance a hypothesis stating that distinct subregions of the left PFC are recruited for the syntactic integration of lexico-semantic information. The current direction of research in the neuroscience of language is beginning to reveal the uniqueness of the human mind. # 2003 Elsevier Science Ireland Ltd and Japan Neuroscience Society. All rights reserved.
Bile duct obstruction due to portal biliopathy in extrahepatic portal hypertension: surgical management

Varices can develop in and around the bile duct in the presence of portal hypertension, especially when it is caused by extrahepatic portal vein thrombosis. The term ‘portal biliopathy’ is used to describe changes in the bile duct due to these varices, which may cause bile duct obstruction. This paper reviews experience of the surgical management of patients with symptomatic portal biliopathy.
Modulation du système de récompense par le risque et le type de récompenses chez l’homme sain et chez des joueurs pathologiques : une approche intégrative combinant enregistrements intracrâniens, mesures hormonales et IRMf

Comment notre cerveau traite l’information de la recompense, et comment un tel traitement est influence par des parametres tels que la probabilite et le risque sont devenues des questions cruciales des neurosciences cognitives. De plus, des recherches recentes suggerent un effet modulateur d’un certain nombre d’hormones sur le cerveau et sur le comportement, et egalement qu’un dysfonctionnement du systeme de recompense pourrait expliquer des comportements addictifs tels que le jeu pathologique. Durant cette these, nous avons eu recours a de l’EEG stereotaxique (SEEG) et a une combinaison d’Imagerie a Resonnance Magnetique fonctionnelle (IRMf) et d’endocrinologie pour realiser trois etudes s’interessant au traitement de la recompense chez des sujets sains, chez des patients souffrant d’epilepsie chez qui des macroelectrodes ont ete implantees, et chez des joueurs pathologiques. Ensemble, nos etudes ameliorent la comprehension de nouveaux aspects du traitement de la recompense chez les sujets sains, chez les patients epileptiques, et chez les joueurs pathologiques
Venous Identity Is Lost but Arterial Identity Is Not Gained During Vein Graft Adaptation

Objectives—Ephrin ligands and Eph receptors are signaling molecules that are differentially expressed on arteries and veins during development. We examined whether Eph-B4, a venous marker, and Ephrin-B2, an arterial marker, are regulated during vein graft adaptation in humans and aged rats. Methods and Results—Eph-B4 transcripts and immunodetectable protein are downregulated in endothelial and smooth muscle cells of patent vein grafts in both humans and in aged rats, whereas Ephrin-B2 transcripts and protein are not strongly induced. Other markers of arterial identity, including dll4 and notch-4, are also not induced during vein graft adaptation in aged rats. Because VEGF-A is upstream of the Ephrin–Eph pathway, and expression of VEGF-A is induced only at early time points after exposure of the vein to the arterial environment, we inhibited VEGF-A in vein grafts using an siRNA-based approach. Vein grafts treated with siRNA directed against VEGF-A demonstrated a thicker intima-media containing α-actin, consistent with arterialization, but did not contain Eph-B4 or Ephrin-B2. Conclusions—Venous identity is preserved in the veins of aged animals, but is lost during adaptation to the arterial circulation; arterial markers are not induced. Markers of vessel identity are plastic in adults and their selective regulation may mediate vein graft adaptation to the arterial environment in aged animals and humans.
Maternal undernutrition upregulates apoptosis in offspring nephrogenesis

Maternal undernutrition (MUN) results in growth-restricted newborns with reduced nephron numbers that is associated with increased risk of hypertension and renal disease. The total adult complement of nephrons is set during nephrogenesis suggesting that MUN affects the staged development of nephrons in as yet unknown manner. A possible cause may be the increased renal apoptosis; therefore, we investigated whether apoptotic signaling and cell death were increased in MUN rat kidneys. Pregnant rat dams were fed an ad libitum diet [control] or were 50% food restricted (MUN) starting at embryonic day (E) 10. Male offspring kidneys (n = 5 each, MUN and control) were analyzed for mRNA using quantitative PCR (E20) and for protein expression using Western blotting and immunohistochemistry (E20 and postnatal day 1, P1). Apoptosis was measured by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Upregulation of pro-apoptotic protein expression was detected at E20 (Fas receptor, caspase 9) and at P1 (caspase 3, Bax). The anti-apoptotic factor Bcl2 was significantly decreased in P1 kidneys. Kidney TUNEL showed apoptotic nuclei significantly increased in the P1 nephrogenic zone (MUN 3.3 + 0.3 v. C 1.6 + 0.5, P = 0.002). The majority of apoptotic nuclei co-localized to mesenchyme and pretubular aggregates in the nephrogenic zone. Differential regulation of apoptosis in mesenchyme and pretubular aggregates following parturition suggests a mechanism for nephropenia in gestational programming of the kidney.
Human papillomavirus update with a particular focus on cervical disease

Summary Human papillomavirus (HPV) is a common viral infection of squamous epithelial tissues, but its importance has only recently been recognised by the medical community. HPVs are now realised to consist of many genotypes and are associated with a diverse spectrum of clinical manifestations. Within the genital tract, some diseases have been recognised since antiquity; for example, genital warts which are caused by HPV types distinct from those causing genital cancer. However, others (such as cervical cancer), although recognised centuries ago as linked to sexual activity, have only been associated with oncogenic HPVs relatively recently, with the tools of molecular biology. We now understand that genital HPV infections are the most common sexually transmitted viral infections, are largely transient, asymptomatic and of no consequence. This virus manifests as more than just benign warts. Chronic carriage of with oncogenic genotypes (over years and in a minority of patients), together with other cofactors (host and/or exogenous) in complex pathways not totally understood, result in severe dysplasia or, ultimately, carcinogenesis. As it takes time for precursor lesions to develop and there are effective screening programmes for their detection and treatment, HPV‐related neoplastic disease of the cervix is largely a preventable reproductive health issue of women. Yet, on a global scale, cervical cancer is the second most common cancer of women, with the majority of cases occurring in developing countries. Although HPV is noncultivatable by traditional diagnostic virological methods, successfully applied molecular biology techniques have underpinned development of vaccines which are now in phase II/III clinical trials. Successful vaccination ultimately has the greatest potential to impact upon the global burden of disease from genital HPV infection. However, the outcome from reduction in incidence of dysplasia and neoplasia will take years to eventuate; consequently, various cervical cancer prevention strategies still need to be endorsed and maintained in the meantime.
Living an uncertain future: An ethnography of displacement, health, psychosocial well-being and the search for durable solutions among Iraqi refugees in Egypt

by NADIA ROSE EL-SHAARAWI This dissertation examines the effects of prolonged urban displacement on the self-identified health and psycho-social well-being of Iraqi refugees in Egypt. In addition, this study considers the ways in which refugees seek to mitigate the effects of displacement through interactions with institutions and policies. Within this, I focus on the process of seeking third-country resettlement and the implications and effects of this process for psycho-social well-being. Using a mixed-methods approach, this dissertation draws on field research with Iraqi refugees that includes participant observation, personcentered interviews with refugees (n=110), interviews with service providers and archival research. This study has three main aims: (1) to take a person-centered view of the refugee resettlement process and foreground health and psycho-social well-being in that inquiry; (2) to look at ways in which people attempt to manage states of insecurity; uncertainty and liminality and implications for their health; and (3) to document the situation of Iraqi refugees in Egypt – who have been almost ignored in the discussion of Iraqi forced migration in the region. A key finding of this dissertation is the
Expression of monocyte subsets and angiogenic markers in relation to carotid plaque neovascularization in patients with pre-existing coronary artery disease and carotid stenosis

Abstract Aim. To characterize blood monocyte subsets in patients with different degrees of carotid atherosclerosis and pathological carotid plaque neovascularization. Methods. Assessment of carotid plaque neovascularization using contrast ultrasonography and flow cytometric quantification of monocyte subsets and their receptors involved in inflammation, angiogenesis, and tissue repair was done in 40 patients with carotid stenosis ≥ 50% and CAD (CS > 50), 40 patients with carotid stenosis < 50% and documented CAD (CS < 50), 40 hypercholesterolaemic controls (HC group), and 40 normocholesterolaemic controls (NC). Results. CS > 50 and CS < 50 groups had increased counts of Mon1 (‘classical’ CD14++ CD16-CCR2 + cells) compared to HCs (P = 0.03, and P = 0.009). Mon3 (‘non-classical’ CD14 + CD16++ CCR2- cells) were only increased in CS < 50 compared with HCs (P < 0.01). Both CS>50 and CS < 50 groups showed increased expression of proinflammatory interleukin-6 receptor on Mon1 and Mon2 (‘intermediate’ CD14++ CD16 + CCR2+ cells); TLR4, proangiogenic Tie2 on all subsets (P < 0.01 for all). In multivariate regression analysis only high Mon1 count was a significant predictor of carotid stenosis (P = 0.04) and intima-media thickness (P = 0.02). In multivariate regression analysis only the Mon1 subset was significantly associated with severe, grade 2 neovascularization (P = 0.034). Conclusion. In this pilot study classical monocytes (Mon1) represent the only monocyte subset predictive of the severity of carotid and systemic atherosclerosis, such as carotid intima-media thickness, degree of carotid stenosis, and presence of carotid intraplaque neovascularization.
Neurogenetics of Slow Axonal Transport: From Cells to Animals

Slow axonal transport is a multivariate phenomenon implicated in several neurodegenerative disorders. Recent reports have unraveled the molecular basis of the transport of certain slow component proteins, such as the neurofilament subunits, tubulin, and certain soluble enzymes such as Ca2+/calmodulin-dependent protein kinase IIa (CaM kinase IIa), etc., in tissue cultured neurons. In addition, genetic analyses also implicate microtubule-dependent motors and other housekeeping proteins in this process. However, the biological relevance of this phenomenon is not so well understood. Here, the authors have discussed the possibility of adopting neurogenetic analyses in multiple model organisms to correlate molecular level measurements of the slow transport phenomenon to animal behavior, thus facilitating the investigation of its biological efficacy.
Simulating Ordinal Data

The increasing use of ordinal variables in different fields has led to the introduction of new statistical methods for their analysis. The performance of these methods needs to be investigated under a number of experimental conditions. Procedures to simulate from ordinal variables are then required. In this article, we deal with simulation from multivariate ordinal random variables. We propose a new procedure for generating samples from ordinal random variables with a prespecified correlation matrix and marginal distributions. Its features are examined and compared with those of its main competitors. A software implementation in R is also provided along with examples of its application.