Miracle-dz/UniFAR-FTUs huggingface dataset:
Local narrowband UVB phototherapy vs. local PUVA in the treatment of chronic hand eczema

Background: Hand eczema is a chronic skin disorder characterized by a poor response to conventional therapies. Although local PUVA has been proven to be effective in the treatment of chronic hand eczema, little is known about the efficacy and safety of local narrowband UVB (TL‐01) for this condition. The aim of our study was to compare the efficacy and safety of local narrowband UVB phototherapy with paint‐PUVA in patients with chronic hand eczema of dry and dyshidrotic types unresponsive to conventional therapies.
Sinus Microbiome Diversity Depletion and Corynebacterium tuberculostearicum Enrichment Mediates Rhinosinusitis

Enrichment of Corynebacterium tuberculostearicum caused by depletion of the sinus microbiome contributes to chronic rhinosinusitis. Nosing in on Chronic Sinusitis If the frequency of ads for sinus-clearing drugs tells us anything, sinusitis is a widespread problem that directly affects an individual’s quality of life. Indeed, chronic rhinosinusitis (CRS), which is defined as sinusitis lasting longer than 12 weeks, affects more than 30 million Americans. CRS is characterized by persistent mucosal inflammation and microbial infection, which can be expected to perturb the mucosal microbiota; however, the contribution of sinus microbiota to CRS remains unclear. Now, Abreu et al. identify both a potential pathogenic species that is more prevalent in CRS patients than in healthy controls as well as a bacterial candidate that may protect against this pathogenic species. The authors performed comparative microbiome profiling of patients with CRS and healthy controls. They found reduced bacterial diversity in the CRS patients, with specific depletion of lactic acid bacteria and a relative increase in Corynebacterium tuberculostearicum. In a murine model, C. tuberculostearicum contributed to the development of sinusitis in the absence of a normal microbiota. Moreover, Lactobacillus sakei was sufficient to protect against C. tuberculostearicum–induced sinusitis, even when the microbiome was depleted. If these effects are consistent in humans, L. sakei may serve as a new therapeutic for CRS. Persistent mucosal inflammation and microbial infection are characteristics of chronic rhinosinusitis (CRS). Mucosal microbiota dysbiosis is found in other chronic inflammatory diseases; however, the relationship between sinus microbiota composition and CRS is unknown. Using comparative microbiome profiling of a cohort of CRS patients and healthy subjects, we demonstrate that the sinus microbiota of CRS patients exhibits significantly reduced bacterial diversity compared with that of healthy controls. In our cohort of CRS patients, multiple, phylogenetically distinct lactic acid bacteria were depleted concomitant with an increase in the relative abundance of a single species, Corynebacterium tuberculostearicum. We recapitulated the conditions observed in our human cohort in a murine model and confirmed the pathogenic potential of C. tuberculostearicum and the critical necessity for a replete mucosal microbiota to protect against this species. Moreover, Lactobacillus sakei, which was identified from our comparative microbiome analyses as a potentially protective species, defended against C. tuberculostearicum sinus infection, even in the context of a depleted sinus bacterial community. These studies demonstrate that sinus mucosal health is highly dependent on the composition of the resident microbiota as well as identify both a new sino-pathogen and a strong bacterial candidate for therapeutic intervention.
Short-term effects of air pollution on hospital admissions of respiratory diseases in Europe: a quantitative summary of APHEA study results. Air Pollution and Health: a European Approach.

The Air Pollution and Health: a European Approach (APHEA) project is a coordinated study of the short-term effects of air pollution on mortality and hospital admissions. Five West European cities (i.e., London, Amsterdam, Rotterdam, Paris, Milano) contributed several years of hospital admissions data for all respiratory causes. In the current study, the authors describe the results obtained from the quantitative pooling (meta-analysis) of local analyses. The diagnostic group was defined by ICD 460-519. The age groups studied were 15-64 y (i.e., adults) and 65+ y (elderly). The air pollutants studied were sulfur dioxide; particles (i.e., Black Smoke or total suspended particles); ozone; and nitrogen dioxide. The pollutants were obtained from existing fixed-site monitors in a standardized manner. We used Poisson models and standardized confounder models to examine the associations between daily hospital admissions and air pollution. We conducted quantitative pooling by calculating the weighted means of local regression coefficients. We used a fixed-effects model when no heterogeneity could be detected; otherwise, we used a random-effects model. When possible, the authors investigated the factors correlated with heterogeneity. The most consistent and strong finding was a significant increase of daily admissions for respiratory diseases (adults and elderly) with elevated levels of ozone. This finding was stronger in the elderly, had a rather immediate effect (same or next day), and was homogeneous over cities. The elderly were affected more during the warm season. The Sulfur dioxide daily mean was available in all cities, and it was not associated consistently with an adverse effect. Effects were present in areas in which more than one station was used in the assessment of daily exposure. Some significant associations were observed, although no conclusion that related to an overall particle effect could be drawn. The effect of Black Smoke was significantly stronger with high nitrogen dioxide levels on the same day, but nitrogen dioxide itself was not associated with admissions. The ozone results were in good agreement with the results of similar U.S. studies. The coherence of the results of this study and other results gained under different conditions strengthens the argument for causality.
Eighteen Month Follow-up of Patients Diverted to Mental Health Facilities from the Magistrates Court

Abstract In 1991 we carried out a 6-week pilot study providing an on-site psychiatry service to a large inner city magistrates' court. This is an 18-month follow-up of the 22 patients for whom psychiatric or social care was arranged. The majority of these patients were still being seen by district psychiatric services or other agencies to whom referrals were made.
Food-Grade Bacteria Expressing Elafin Protect Against Inflammation and Restore Colon Homeostasis

Lactic acid–producing bacteria engineered to produce the antiprotease Elafin restore colon homeostasis in mice with colitis and protect human tissue from inflammation. Bugs Deliver Drug and Keep the Gut Happy Elafin is a natural protease inhibitor that is normally expressed by the human intestine and protects the gut from insults. Elafin expression is lost in patients suffering from inflammatory bowel diseases such as Crohn’s disease and ulcerative colitis. In a new study, Motta et al. tested whether delivery of human Elafin directly into the gut would protect from inflammatory insults and restore gut homeostasis. They commandeered helpful, safe bacteria that are commonly present in the gut and in food products and genetically modified the bacteria so that they would produce Elafin. They introduced the human Elafin gene into Lactococcus lactis and Lactobacillus casei, two bacteria present in dairy food. When given orally to mice, the two strains of genetically modified bacteria were detected a few hours later at the surface of the intestine, where they produced human Elafin. In different mouse models of acute or chronic intestinal inflammation, oral treatment with Elafin-expressing food-grade bacteria protected the gut from inflammatory damage. Elafin-expressing bacteria were also able to protect cultured human intestinal cells from inflammatory insults and to restore homeostasis and physiological functions. This approach may offer a safe, cost-effective long-term treatment for inflammatory bowel diseases. Elafin, a natural protease inhibitor expressed in healthy intestinal mucosa, has pleiotropic anti-inflammatory properties in vitro and in animal models. We found that mucosal expression of Elafin is diminished in patients with inflammatory bowel disease (IBD). This defect is associated with increased elastolytic activity (elastase-like proteolysis) in colon tissue. We engineered two food-grade strains of lactic acid bacteria (LAB) to express and deliver Elafin to the site of inflammation in the colon to assess the potential therapeutic benefits of the Elafin-expressing LAB. In mouse models of acute and chronic colitis, oral administration of Elafin-expressing LAB decreased elastolytic activity and inflammation and restored intestinal homeostasis. Furthermore, when cultures of human intestinal epithelial cells were treated with LAB secreting Elafin, the inflamed epithelium was protected from increased intestinal permeability and from the release of cytokines and chemokines, both of which are characteristic of intestinal dysfunction associated with IBD. Together, these results suggest that oral delivery of LAB secreting Elafin may be useful for treating IBD in humans.
Asymptotic spectral efficiency of LMMSE multi-user multi-signature MC-CDMA in frequency-selective Rayleigh fading

We present an asymptotic analysis of a multi-signature multi-carrier CDMA communications system. Such a system is suited to scalable data rate services with decentralized control. Specifically, we derive the asymptotic SINR at the output of a multi-user linear minimum mean squared error (LMMSE) receiver and the asymptotic sum spectral efficiency of both the LMMSE and optimal receivers. Simulation studies demonstrate that the asymptotic results closely predict the performance of practical finite systems.
A New Approach to Drug Discovery

Natural products are an inexhaustible source for drug discovery. However, the validation and selection of primary screening assays are vital to guarantee a selection of extracts or molecules with relevant pharmacological action and worthy of following up. The assay must be rapid, simple, easy to implement, and produce quick results and preferably at a low cost. In this work, we developed and validated a colorimetric microtiter assay using the resazurin viability dye. The parameters of the resazurin method for high-throughput screening (HTS) using natural extracts against Aspergillus fumigatus were optimized and set up. The extracts plus RPMI-1640 modified medium containing the spores and 0.002% resazurin were added per well. The fluorescence was read after 24 to 30 h of incubation. The resazurin proved to be as suitable as Alamar Blue for determining the minimal inhibitory concentration of different antifungals against A. fumigatus and effective to analyze fungicidal and fungistatic compounds. An HTS of 12 000 microbial extracts was carried out against two A. fumigatus strains, and 2.7% of the extracts displayed antifungal activity. Our group has been the first to use this methodology for screening a collection of natural extracts to identify compounds with antifungal activity against the medically important human pathogen A. fumigatus.
Clonal Evolution of Preleukemic Hematopoietic Stem Cells Precedes Human Acute Myeloid Leukemia

Exome sequencing and single-cell analysis reveals that a clonal progression of mutations in hematopoietic stem cells precedes human acute myeloid leukemia. Getting to the Root of Acute Myeloid Leukemia Acute myeloid leukemia (AML) is an aggressive clonal malignancy of bone marrow progenitor cells caused by the accumulation of multiple mutations in a single lineage of cells. In the bone marrow, most cells are short-lived and the frequency of mutations is low, making it tough to explain how such a lineage of cells with multiple mutations could arise. In a new study, Jan et al. now propose a model in which AML develops by serial acquisition of mutations in long-lived self-renewing hematopoietic stem cells (HSCs). The authors directly tested their clonal evolution model by sequencing the exomes (the protein-coding regions of the genome) of AML cells and residual HSCs taken from patients with AML. First, they identified the coding mutations present in six AML patient samples by exome sequencing. Then, using cell surface markers to isolate rare residual HSCs by flow cytometry, the researchers discovered leukemia-associated mutations in the HSCs. Finally, the authors performed single-cell assays targeted to the identified mutations to determine the genotype of individual HSCs. They detected multiple cell clones in the HSC pool that contained some, but not all, of the mutations seen in the AML cells. Furthermore, the authors were able to determine the order of acquisition of the mutations that preceded development of AML. These results offer fresh insights into the early stages of AML and pinpoint preleukemic HSCs as an important therapeutic target to prevent relapse and to ensure durable clinical remission after chemotherapy. Given that most bone marrow cells are short-lived, the accumulation of multiple leukemogenic mutations in a single clonal lineage has been difficult to explain. We propose that serial acquisition of mutations occurs in self-renewing hematopoietic stem cells (HSCs). We investigated this model through genomic analysis of HSCs from six patients with de novo acute myeloid leukemia (AML). Using exome sequencing, we identified mutations present in individual AML patients harboring the FLT3-ITD (internal tandem duplication) mutation. We then screened the residual HSCs and detected some of these mutations including mutations in the NPM1, TET2, and SMC1A genes. Finally, through single-cell analysis, we determined that a clonal progression of multiple mutations occurred in the HSCs of some AML patients. These preleukemic HSCs suggest the clonal evolution of AML genomes from founder mutations, revealing a potential mechanism contributing to relapse. Such preleukemic HSCs may constitute a cellular reservoir that should be targeted therapeutically for more durable remissions.
Effects of Aluminium Chloride Exposure on the Histology of the Cerebral Cortex of Adult Wistar Rats

Aluminium (Al) is presents in many manufactured foods, medicines and is also added to drinking water for purification purposes. Human exposure to Al has been increasing over the last decades. Al exposure and neurological impairments demonstrate mixed findings. The cerebral cortex is a sheet of neural tissue that is outer-most to the cerebrum of the mammalian brain and it plays a key role in memory, attention, perceptual awareness, thought, language, and consciousness.The objectives of this study was to investigate the possible effects that aluminium Chloride could have on the histology of cerebral cortex. Total of twenty adult wistar rats were used for this experiment. The wistar rats were divided into five groups; group I was the control, group II received 475mg/Kg, group III received 950mg/kg, group IV received 1,425mg/kg and group V received 1,900mg/kg via oral intubation for a duration of Eight weeks. The wistar rats were humanly sacrificed and the brain was removed and immediately fixed in bouin fluid. The histological observations of the aluminium treated groups revealed extensive neuronal vacuolation and necrosis (neuro-degeneration) of the cerebral cortex of wistar rats.Based on our observations, we therefore conclude that Aluminium chloride exposure has neurodegenerative effects on the histology of cerebral cortex of adult wistar rats especially at higher dose. Therefore, caution should be taken in its usage.
Flow Cytometry Enables a High-Throughput Homogeneous Fluorescent Antibody-Binding Assay for Cytotoxic T Cell Lytic Granule Exocytosis

We developed a homogeneous phenotypic fluorescence end-point assay for cytotoxic T lymphocyte lytic granule exocytosis. This flow cytometric assay measures binding of an antibody to a luminal epitope of a lysosomal membrane protein (LAMP-1) that is exposed by exocytosis to the extracellular solution. Washing to remove unbound antibody is not required. Confirming the assay’s ability to detect novel active compounds, we screened at a concentration of 50 µM a synthetic diversity library of 91 compounds in a 96-well plate format, identifying 17 compounds that blocked by 90% or more. The actions of six structurally related tetracyano-hexahydroisoindole compounds that inhibited by ~90% at a concentration of 10 µM were investigated further. Four reduced elevations in intracellular Ca2+; it is likely that depolarization of the cells’ membrane potential underlies the effect for at least two of the compounds. Another compound was found to be a potent inhibitor of the activation of the mitogen-activated protein (MAP) kinase ERK. Finally, we transferred the assay to a 384-well format and screened the Prestwick Compound Library using high-throughput flow cytometry. Our results indicate that our assay will likely be a useful means of screening libraries for novel compounds with important biological activities.
Rett Syndrome Clinical And Biological Aspects Studies On 130 Swedish Females

Find loads of the rett syndrome clinical and biological aspects studies on 130 swedish females book catalogues in this site as the choice of you visiting this page. You can also join to the website book library that will show you numerous books from any types. Literature, science, politics, and many more catalogues are presented to offer you the best book to find. The book that really makes you feels satisfied. Or that's the book that will save you from your job deadline.
Lipoxin A4 Regulates Natural Killer Cell and Type 2 Innate Lymphoid Cell Activation in Asthma

The pro-resolving mediator lipoxin A4 regulates natural killer cells and type 2 innate lymphoid cells in severe asthma. ILCs Catch Their Breath Focusing on your breath is one of the most basic meditation techniques. But for people with asthma, breathing can be anything but relaxing. Asthma is a chronic inflammatory disease, but attacks can be triggered by everything from allergens to cold to exercise. However, much still remains to be learned about the dysregulation that allows this inflammation to continue. Now, Barnig et al. suggest that differences in innate lymphoid cells (ILCs) may contribute to asthma pathogenesis. The authors look at two types of ILCs—natural killer (NK) cells and type 2 ILCs (ILC2s)—in the context of severe asthma. They find that NK cells may down-modulate the airway inflammatory response by inducing eosinophil apoptosis, whereas ILC2s promote airway inflammation through the secretion of interleukin-13 (IL-13). Intriguingly, despite their disparate function, both NK cells and ILC2s express the receptor for lipoxin A4, which functions in resolving inflammation. Indeed, lipoxin A4 increased the ability of NK cells to induce eosinophil apoptosis and decreased IL-13 production from the ILC2 population. Furthermore, lipoxin A4 production was decreased in severe asthmatics, suggesting this as a new line of potential therapies. Increasing lipoxin A4 may help severe asthmatics breathe easy. Asthma is a prevalent disease of chronic inflammation in which endogenous counterregulatory signaling pathways are dysregulated. Recent evidence suggests that innate lymphoid cells (ILCs), including natural killer (NK) cells and type 2 ILCs (ILC2s), can participate in the regulation of allergic airway responses, in particular airway mucosal inflammation. We have identified both NK cells and ILC2s in human lung and peripheral blood in healthy and asthmatic subjects. NK cells were highly activated in severe asthma, were linked to eosinophilia, and interacted with autologous eosinophils to promote their apoptosis. ILC2s generated antigen-independent interleukin-13 (IL-13) in response to the mast cell product prostaglandin D2 alone and in a synergistic manner with the airway epithelial cytokines IL-25 and IL-33. Both NK cells and ILC2s expressed the pro-resolving ALX/FPR2 receptors. Lipoxin A4, a natural pro-resolving ligand for ALX/FPR2 receptors, significantly increased NK cell–mediated eosinophil apoptosis and decreased IL-13 release by ILC2s. Together, these findings indicate that ILCs are targets for lipoxin A4 to decrease airway inflammation and mediate the catabasis of eosinophilic inflammation. Because lipoxin A4 generation is decreased in severe asthma, these findings also implicate unrestrained ILC activation in asthma pathobiology.
From the Southern Association for Vascular Surgery Prospective randomized trial of ACUSEAL ( Gore-Tex ) vs Finesse ( Hemashield ) patching during carotid endarterectomy : Long-term outcome

Background: Several studies have reported that carotid endarterectomy with patch angioplasty is superior to primary closure. Conventional polytetrafluoroethylene (Gore-Tex, W. L. Gore & Associates, Flagstaff, Ariz) patching has been shown to have results similar to autogenous saphenous vein patching; however, it requires a longer hemostasis time. This study examined the long-term clinical outcome and incidence of restenosis after carotid endarterectomy using the new ACUSEAL (Gore-Tex) patching vs Hemashield Finesse (Boston Scientific Corp, Natick, Mass) patching. Methods: The study randomized 200 patients (1:1) undergoing carotid endarterectomy to 100 with ACUSEAL patching and 100 with Hemashield-Finesse patching. All patients underwent immediate and 1-month postoperative duplex ultrasound studies, which were repeated at 6-month intervals. Kaplan-Meier analysis was used to estimate the freedom from stroke, stroke-free survival, and the risk of restenosis for both groups. Results: The demographic and clinical characteristics, the mean operative diameter of the internal carotid artery, and the length of the arteriotomy were similar in both groups. The mean hemostasis time was 5.1 for the ACUSEAL patching vs 3.7 minutes for Finesse patching (P .01); however, the mean operative times were similar for both groups (P .61). The incidence of ipsilateral stroke was 2% for ACUSEAL patching (both early perioperative strokes) vs 3% for Finesse patching (2 early and 1 late stroke) at a mean follow-up of 21 months. The respective cumulative stroke-free rates at 1, 2, and 3 years were 98%, 98%, and 98% for ACUSEAL patching vs 97%, 97%, and 97% for Finesse patching (P .7). The respective cumulative stroke-free survival rates at 1, 2, and 3 years were 97%, 92%, and 88% for ACUSEAL patching vs 96%, 96%, and 91% for Finesse patching (P .6). The respective freedom from >70% carotid restenosis at 1, 2, and 3 years was 98%, 96%, and 89% for ACUSEAL patching vs 92%, 85%, and 79% for Finesse patching (P .04). Conclusions: Carotid endarterectomy with ACUSEAL patching and Finesse patching had similar stroke-free rates and stroke-free survival rates. The mean hemostasis time for the ACUSEAL patch was 1.4 minutes longer than that for the Finesse patch; however, the Finesse patch had higher restenosis rates than the ACUSEAL patch. (J Vasc Surg 2008;48: 99-103.)