Miracle-dz/UniFAR-FTUs huggingface dataset:
LRb signals act within a distributed network of leptin‐responsive neurones to mediate leptin action

The adipose tissue‐derived hormone, leptin, acts via its receptor (LRb) in the brain to regulate energy balance and neuroendocrine function. In order to understand leptin action we have explored the physiological function of LRb signalling pathways, defining important roles for signal transducer and activator of transcription‐3 (STAT3) in positive signalling and for LRbTyr985‐mediated feedback inhibition in leptin signal attenuation. As the cells on which leptin acts are not homogeneous, but rather represent a broadly distributed network of neurones with divergent projections and functions, it is also crucial to consider how each of these populations responds to LRb signals to contribute to leptin action. While well‐known LRb‐expressing neurones within the arcuate nucleus of the hypothalamus mediate crucial effects on satiety and energy expenditure, other populations of LRb‐expressing neurones in the ventral tegmental area and elsewhere likely control the mesolimbic dopamine system. Additional populations of LRb‐expressing neurones likely contribute to other aspects of neuroendocrine regulation. It will be important to define the molecular mechanisms by which leptin acts to regulate neurophysiology in each of these LRb‐expressing neural populations in order to understand the totality of leptin action.
[Dynamic anatomy].

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Family history and the risk of cancer: genetic factors influencing multiple cancer sites

A number of co-aggregations of cancers at different sites has been reported, including recognized syndromes (e.g., Li-Fraumeni), and aggregations between cancers at breast, stomach and ovary, between cancers at prostate, urinary tract and other sites, as well as between several tobacco-related neoplasms. In a network of case–control studies from Italy and Switzerland, including more than 12,000 cases of 13 different cancers, after controlling for multiple testing, significant associations emerged between oral and pharyngeal cancer and family history of laryngeal cancer (relative risk (RR): 3.3); esophageal cancer and family history of oral and pharyngeal cancer RR: 4.1; breast cancer and family history of colorectal cancer (RR: 1.5) and of hemolymphopoietic cancers (RR: 1.7); ovarian cancer and family history of breast cancer (RR: 2.3); and prostate cancer and family history of bladder cancer (RR: 3.4). Shared exposures to environmental factors within families account for some of the observed aggregations, together with heritable, and hence, genetic factors.
Synthesis and Experimental Validation of the Novel LQ-NEMCSI Adaptive Strategy on an Electronic Throttle Valve

This paper is concerned with the design of a novel adaptive controller, namely the linear quadratic new extended minimal control synthesis with integral action (LQ-NEMCSI). We present for the first time the analytical proof of asymptotic stability of the controller and experimental evidence of the algorithm effectiveness for controlling an electronic throttle body: an element of any drive-by-wire system in automotive engineering, affected by many nonlinear perturbations.
Microwave exposure induces Hsp70 and confers protection against hypoxia in chick embryos

To determine if microwave exposure could elicit a biological effect in the absence of thermal stress, studies were designed in which chick embryos were exposed to athermal microwave radiation (915 MHz) to look for induction of Hsp70, a protein produced during times of cellular stress that aids in the protection of cellular components. Levels of Hsp70 were found to increase within 2 h, with maximum expression (∼30% higher than controls) typically occurring by 3 h from the start of exposure. Other embryos were exposed to microwave radiation prior to being subjected to hypoxic stress, and were found to have significantly higher survival (P < 0.05) following re‐oxygenation than non‐exposed controls. The results of these studies indicate that not only can athermal microwave exposures activate the stress protein response pathway; they can also enhance survivability following exposure to a subsequent, potentially lethal stress. From a public health standpoint, it is important that more studies be performed to determine if repeated exposures, a condition likely to be found in cell phone use, are still beneficial. J. Cell. Biochem. 86: 490–496, 2002. © 2002 Wiley‐Liss, Inc.
Determinants of Myelosuppression in the Treatment of Non‐small Cell Lung Cancer with Cisplatin‐containing Chemotherapy

Data on 16 potential risk factors for myelosuppression were assessed in 134 patients who received either vindesine and cisplatin (VP) or mitomycin C, vindesine and cisplatin (MVP) for inoperable stage III or IV non‐small cell lung cancer in a randomized trial. Determinant factors for myelosuppression were evaluated by using univariate analysis and the logistic regression model. Recursive partitioning and amalgamation (RPA) was also used to define patient subgroups frequently suffering from severe bone marrow toxicity. Overall, 33 (25%) of 134 patients experienced at least one episode of grade 4 leukopenia. In univariate analysis, age, body surface area, serum creatinine, and pretreatment hemoglobin concentration were associated with severe leukopenia. A multivariate analysis using the logistic regression method showed that only raised creatinine level was an independent predictor for grade 4 leukopenia (P=0.049). The RPA model generated three distinct subgroups based on age, body surface area and regimen. The three subgroups were distinguished by the frequency of severe (grade 4) leukopenia (50%, 25%, and 2.4%, respectively) (P<0.001). Grade 4 leukopenia occurred more frequently in patients in class 3 (age ≥65 years and treatment with MVP). The RPA model was useful in identifying the risk factors for myelosuppression induced by cisplatin‐based chemotherapy, and in defining patient subgroups with elevated risk of toxicity.
Diagnostic accuracies for celiac disease of four tissue transglutaminase autoantibody tests using human antigen.

Celiac disease (CD), a genetic, immunologically mediated small bowel enteropathy that causes malabsorption, is one of the more common disorders in Western countries and is frequently underdiagnosed because of its protean presentations (1). Early diagnosis and treatment with a gluten-free diet may reduce the risk for nutritional (2), bone (3), and obstetric complications (4), as well as malignancies (5)(6) and increased mortality rates (7)(8). Histologic demonstration of a flat small intestinal mucosa, together with clinical improvement when patients are on a gluten-free diet, continues to be the gold standard for its diagnosis. The serologic detection of anti-endomysium antibodies (EmAs) is used to support the diagnosis and to screen populations at risk; the sensitivity and specificity of these tests are 70–95% and 100%, respectively (9). The identification of tissue transglutaminase (tTG) as the main antigen of EmAs (10) allows a new diagnostic approach to CD. A large number of ELISA methods, mainly based on commercially available guinea pig tTG, have been produced; however, these methods have a lower diagnostic accuracy than EmAs (11)(12)(13). Assuming that possible interspecies differences could be responsible for such discrepancies, the use of human tTG antigen was recently suggested (14). The first aim of this study was to clarify the diagnostic accuracy of four commercially available anti-human tTG-IgA ELISA methods in both controls and EmA-positive CD patients. The second aim was to compare anti-tTG results obtained by these different methods and their feasibility in practice. The study population consisted of 34 untreated, newly diagnosed, and ambulatory EmA-positive CD patients (26 women and 8 men; median age, 36 years; range 23–65 years) seen consecutively at the University Department of Internal Medicine between May and September 2000. The diagnosis was made in all cases by the typical histologic appearance …
Sources of resistance and susceptibility to Septoria tritici blotch of wheat

Summary An association genetics analysis was conducted to investigate the genetics of resistance to Septoria tritici blotch, caused by the fungus Zymoseptoria tritici (alternatively Mycosphaerella graminicola), in cultivars and breeding lines of wheat (Triticum aestivum) used in the UK between 1860 and 2000. The population was tested with Diversity Array Technology (DArT) and simple‐sequence repeat (SSR or microsatellite) markers. The lines formed a single population with no evidence for subdivision, because there were several common ancestors of large parts of the pedigree. Quantitative trait loci (QTLs) controlling Septoria resistance were postulated on 11 chromosomes, but 38% of variation was not explained by the identified QTLs. Calculation of best linear unbiased predictions (BLUPs) identified lineages of spring and winter wheat carrying different alleles for resistance and susceptibility. Abundant variation in Septoria resistance may be exploited by crossing well‐adapted cultivars in different lineages to achieve transgressive segregation and thus breed for potentially durable quantitative resistance, whereas phenotypic selection for polygenic quantitative resistance should be effective in breeding cultivars with increased resistance. The most potent allele reducing susceptibility to Septoria, on chromosome arm 6AL, was associated with reduced leaf size. Genes which increase susceptibility to Septoria may have been introduced inadvertently into UK wheat breeding programmes from cultivars used to increase yield, rust resistance and eyespot resistance between the 1950s and 1980s. This indicates the need to consider trade‐offs in plant breeding when numerous traits are important and to be cautious about the use of non‐adapted germplasm.
Prospective analysis of cerebral infarction after carotid endarterectomy and carotid artery stent placement by using diffusion-weighted imaging.

BACKGROUND AND PURPOSE Small emboli arising from a friable plaque during carotid endarterectomy (CEA) and carotid artery stent placement (CAS) constitute a potentially important cause of periprocedural ischemic complications. To evaluate the frequency and significance of cerebral ischemic lesions of embolic origin after CEA and CAS, we examined patients with moderate to severe carotid stenosis by using diffusion-weighted (DW) imaging. METHODS Twenty-four patients undergoing 26 CEAs and 20 patients undergoing 22 CAS were prospectively studied with pre- and post-treatment DW imaging of the brain within 7 days (mean, 2.3 days) before and within 7 days (mean, 3.2 days) after treatment. DW images were analyzed by two neuroradiologists blinded to the clinical results after CEA and CAS. Any new hyperintense lesion on DW image was interpreted as a post-treatment ischemic lesion. We compared post-treatment ischemic lesions with change in neurologic status, presence of plaque ulcerations, and severity of stenosis and compared the frequency of overall post-treatment complications between the two procedures. RESULTS In 25 (96%) of 26 CEAs, post-operative brain DW images were unchanged. In one patient (4%), a new single asymptomatic hyperintensity was observed in the striatocapsule on the surgical side. In 14 (64%) of 22 CAS procedures, post-operative brain DW images were unchanged. In eight CAS cases (36%), new hyperintensities were seen on DW images. Among them, two were symptomatic with a major neurologic deficit lasting more than 7 days. Post-treatment brain or retinal major stroke rates were 4% (n = 1) for CEA and 14% (n = 3) for CAS. Overall symptomatic complication rates were 19.2% and 13.6%, respectively. CONCLUSION Rate of ischemic brain lesions was significantly lower after CEA than after CAS, although most of these brain lesions were silent. Also, CEA is a safer procedure carrying a lower risk of post-operative cerebral ischemia. CAS, however, may be a comparable procedure considering the total complication rate and can be a more reliable procedure with advances in neuroprotective means.
The interpretation of Spatial 'At': An Experimental Study

This paper presents an experimental study on the interpretation of the spatialpreposition at in adult speakers, based on a variant of the Truth ValueJudgment Task. It is shown that speakers can interpret at as denoting a spatialrelation that stands in the “lexical entailment” relation with other spatial prepositions(e.g. inside, in front of, on top of, behind). For instance, if multiplelocated entities are involved in this relation, then they may occupy locationsthat can be “internal”, “external”, or placed on different verses of the samedirection, e.g. in front or behind a certain landmark object. It is discussed whichsemantic hypothesis correctly predicts these findings, and what the implicationscould be, for a theory of spatial prepositions and their Semantics.
Physiology and treatment of pain.

http://ccn.aacnjournals. org understand the principles of pain management. The pain experience can be functionally divided into acute and chronic types. Acute and chronic pain are due to different physiological mechanisms and thus require different treatments. In addition, children, adults, and elderly persons have both subtle and sharp differences in the perception of pain. Much of the nursing literature on pain is focused on common interventions but does not explain the physiological mechanisms of pain and the vastly different types of pain that patients may have. Thus, in this article, we review theories of pain and examine the physiology of pain, with emphasis on the types of pain and their manifestations. To provide the best possible care for patients experiencing pain, nurses must understand the physiology of pain, the different types of pain and their varied manifestations, the diversity of patients’ responses, and the rationale for choices of pain control methods.
Histological chorioamnionitis in relation to clinical presentation at 14-40 weeks of gestation.

This study examines the prevalence of histological inflammation of the fetal membranes according to gestational age and mode of clinical presentation in a series of 179 consecutive placentas evaluated in a single centre. The frequency of histological inflammation between clinical groups was compared and relation between the prevalence of inflammation and gestational age examined using regression analysis. One hundred and seventy-nine placentas were examined. Histological inflammation was present in 65 (38%) cases including 37/52 (71%) pregnancies presenting with spontaneous preterm labour and delivery (PTL), 23/36 (64%) with preterm prelabour rupture of membranes (PPROM), 1/20 (5%) with vaginal bleeding but no contractions (PVB), 1/13 (8%) with intrauterine death but no labour (IUD), 1/28 (4%) with iatrogenic delivery, 0/4 with termination of pregnancy and 2/20 (10%) delivering spontaneously at term. The prevalence of histological inflammation was significantly higher in those with PTL or PPROM compared to the other groups (P<0.0001). The frequency of histological inflammation was associated with gestational age (F=57.2, P<0.0001, R=0.91), with a peak prevalence (>90%) at 20-24 weeks' gestation.
HIV-1 protease and reverse transcriptase mutations for drug resistance surveillance

Objectives:Monitoring regional levels of transmitted HIV-1 resistance informs treatment guidelines and provides feedback on the success of HIV-1 prevention efforts. Surveillance programs for estimating the frequency of transmitted resistance are being developed in both industrialized and resource-poor countries. However, such programs will not produce comparable estimates unless a standardized list of drug-resistance mutations is used to define transmitted resistance. Methods:In this paper, we outline considerations for developing a list of drug-resistance mutations for epidemiologic estimates of transmitted resistance. First, the mutations should cause or contribute to drug resistance and should develop in persons receiving antiretroviral therapy. Second, the mutations should not occur as polymorphisms in the absence of therapy. Third, the mutation list should be applicable to all group M subtypes. Fourth, the mutation list should be simple, unambiguous, and parsimonious. Results:Applying these considerations, we developed a list of 31 protease inhibitor-resistance mutations at 14 protease positions, 31 nucleoside reverse transcriptase inhibitor-resistance mutations at 15 reverse transcriptase positions, and 18 non-nucleoside reverse transcriptase inhibitor-resistance mutations at 10 reverse transcriptase positions. Conclusions:This list, which should be updated regularly using the same or similar criteria, can be used for genotypic surveillance of transmitted HIV-1 drug resistance.
Lung Function and Cardiovascular Risk: Relationship With Inflammation-Sensitive Plasma Proteins

Background—The inverse relationship between pulmonary function and incidence of cardiovascular disease remains largely unexplained. This prospective study explored the hypothesis of a relationship with inflammation-sensitive plasma proteins. Methods and Results—Forced vital capacity (FVC) and plasma levels of fibrinogen, &agr; 1-antitrypsin, haptoglobin, ceruloplasmin, and orosomucoid were determined in 5064 healthy men aged 28 to 61 years. All-cause mortality, cardiovascular mortality, and incidence of myocardial infarction were monitored over a mean follow-up period of 18.4 years. Low FVC (fourth quartile) was associated with higher protein levels and with increased incidences of myocardial infarction and cardiovascular death. Adjustments for protein levels reduced the age-adjusted relative risks (RRs) for myocardial infarction (from 1.99, 95% CI 1.5 to 2.6, to 1.70, 95% CI 1.3 to 2.2) and cardiovascular death (from 2.71, 95% CI 1.9 to 3.9, to 2.28, 95% CI 1.6 to 3.3) among men with low FVC, corresponding to ≈25% of the excess risk. The risk factor–adjusted RRs were reduced from 1.45 (95% CI 1.1 to 1.9) to 1.38 (95% CI 1.1 to 1.8) and from 1.96 (95% CI 1.4 to 2.8) to 1.85 (95% CI 1.3 to 2.7) for myocardial infarction and cardiovascular death, respectively, corresponding to ≈10% to 15% of the excess risk. Among men with low FVC, the risk factor–adjusted RR for myocardial infarction was 2.5 (95% CI 1.7 to 3.6) for those with high protein levels (≥2 proteins in top quartile) and 1.7 (95% CI 1.1 to 2.4) for those with low protein levels (≤1 protein in top quartile; reference, top quartile of FVC and low protein levels). Conclusions—FVC is significantly and inversely associated with plasma levels of inflammation-sensitive plasma proteins. This relationship contributes to but cannot fully explain the increased cardiovascular risk among men with low FVC.
Failure matters: unsuccessful cytogenetics and unperformed cytogenetics are associated with a poor prognosis in a population‐based series of acute myeloid leukaemia

Unsuccessful cytogenetics (UC) in patients with acute myeloid leukaemia (AML) treated on different SWOG trials was recently reported to be associated with increased age and dismal outcome. To ascertain whether this holds true also in unselected patients with AML, we retrieved all cytogenetic reports in cases from the population‐based Swedish AML Registry. Between 1997 and 2006, 1737 patients below 80 yr of age without myelosarcoma or acute promyelocytic leukaemia received intensive treatment. The frequencies of UC and unperformed cytogenetics (UPC) were 2.1% and 20%, respectively. The early death rates differed between the cytogenetic subgroups (P = 0.006) with the highest rates in patients with UC (14%) and UPC (12%) followed by high‐risk (HR) AML, intermediate risk (IR) and standard risk (SR) cases successfully karyotyped (8.6%, 5.9%, and 5.8%, respectively). The complete remission rate was lower in UC and UPC and HR compared with the other risk groups (P < 0.001). The overall five‐year survival rates were 25% for UC and 22% for UPC, whereas the corresponding frequencies for SR, IR and HR AML patients without UC and UPC were 64%, 31% and 15%, respectively. In conclusion, lack of cytogenetic data translates into a poor prognosis.
Skeletal Muscle Content of Membrane Glycoprotein PC-1 in Obesity: Relationship to Muscle Glucose Transport

Membrane glycoprotein PC-1, an inhibitor of insulin signaling, produces insulin resistance when overexpressed in cells transfected with PC-1 cDNA. In the present study, we determined whether PC-1 plays a role in the insulin resistance of skeletal muscle in obesity. Rectus abdominus muscle biopsies were taken from patients undergoing elective surgery. Subjects included both NIDDM patients (n = 14) and nondiabetic patients (n = 34) across a wide range of BMI values (19.5–90.1). Insulin-stimulated glucose transport was measured in incubated muscle strips, and PC-1 content, enzymatic activity, and insulin receptor content were measured in solubilized muscle extracts. Increasing BMI correlated with both an increase in the content of PC-1 in muscle (r = 0.55, P < 0.001) and a decrease in insulin stimulation of muscle glucose transport (r = −0.58, P = 0.008). NIDDM had no effect on either PC-1 content or glucose transport for any given level of obesity. Insulin stimulation of muscle glucose transport was negatively related to muscle PC-1 content (r = −0.68, P = 0.001) and positively related to insulin receptor content (r = 0.60, P = 0.005). Multivariate analysis indicated that both skeletal muscle PC-1 content and insulin receptor content, but not BMI, were independent predictors of insulin-stimulated glucose transport. Muscle PC-1 content accounted for 42% and insulin receptor content for 17% of the variance in glucose transport values. These studies raise the possibility that increased expression of PC-1 and a decreased insulin receptor content in skeletal muscle may be involved in the insulin resistance of obesity.
Cut-and-paste for impulsive gravitational waves with 
Λ
: The geometric picture

Impulsive gravitational waves in Minkowski space were introduced by Roger Penrose at the end of the 1960s, and have been widely studied over the decades. Here we focus on non-expanding waves which later have been generalised to impulses travelling in all constant-curvature backgrounds, that is also the (anti-)de Sitter universe. While Penrose's original construction was based on his vivid geometric `scissors-and-paste' approach in a flat background, until now a comparably powerful visualisation and understanding have been missing in the ${\Lambda\not=0}$ case. In this work we provide such a picture: The (anti-)de Sitter hyperboloid is cut along the null wave surface, and the `halves' are then re-attached with a suitable shift of their null generators across the wave surface. This special family of global null geodesics defines an appropriate comoving coordinate system, leading to the continuous form of the metric. Moreover, it provides a complete understanding of the nature of the Penrose junction conditions and their specific form. These findings shed light on recent discussions of the memory effect in impulsive waves.