Miracle-dz/UniFAR-FTUs huggingface dataset:
Triiodothyronine: a link between the insulin resistance syndrome and blood pressure?

OBJECTIVE Overall obesity is associated with elevated serum triiodothyronine concentrations and insulin resistance. Oral triiodothyronine is known to induce hypertension in laboratory rats, while triiodothyronine also increases the expression of genes encoding for enzymes involved in the synthesis and secretion of insulin by pancreatic beta cells. We investigated the hypothesis that central obesity and insulin resistance are linked with an increased blood pressure and insulin production through elevated free serum triiodothyronine concentrations. DESIGN A cross-sectional study of 47 healthy euthyroid subjects (17 men, 30 women; 34 +/- 15 years, mean +/- SD). METHODS The waist:hip ratio was used as measure of central obesity, and insulin-stimulated glucose disposal during a hyperinsulinaemic euglycaemic clamp was used as measure of insulin sensitivity. Insulin production was calculated from the insulin clearance during the clamp and fasting insulin concentrations. RESULTS Free serum triiodothyronine concentrations correlated, independent of age and gender, positively with systolic and diastolic blood pressure, insulin production and fasting insulin. There was only a borderline significant correlation of free serum triiodothyronine with the waist-to-hip ratio, and no correlation with insulin sensitivity as assessed during the clamp. The correlations of free serum triiodothyronine with blood pressure, insulin production and fasting insulin were independent of the waist:hip ratio and insulin sensitivity. CONCLUSION Our hypothesis of free serum triiodothyronine as an intermediate factor in the insulin resistance syndrome is refuted by these data, but we identified free serum triiodothyronine concentrations as a new determinant of blood pressure, insulin production, and fasting insulin in healthy euthyroid subjects.
Parental Characteristics in Relation to Depressive Disorders

Summary Using a reliable and valid measure of reported parental care and overprotection (the Parental Bonding Instrument) patients with two types of depressive disorder were compared with a control group, and the relationships to depressive experience examined in a non-clinical group as well. Bipolar manic-depressive patients scored like controls whereas neurotic depressives reported less parental care and greater maternal overprotection. Depressive experience in the non-clinical group was negatively associated with low parental care and weakly associated with parental overprotection.
Fall detection via human posture representation and support vector machine

Accidental falls of elderly people are a major cause of fatal injuries, especially for those living alone. We present a novel vision–based fall detection approach that analyzes an extracted human body using described human postures. First, a human body extracted by a background subtraction technique is located by a minimum area-enclosing ellipse. Then, a normalized directional histogram is developed around the center of the ellipse to represent a human posture by multi-directional statistical analysis. After that, 12 static and 8 dynamic features are derived from the normalized directional histogram. These features are fed into a directed acyclic graph support vector machine to distinguish four closely related human postures (standing, crouching, lying, and sitting). A fall-like accident is detected by counting the occurrences of lying postures in a short temporal window. After conducting majority voting, a fall event is determined by immobility verification. From the experimental results, an overall accuracy of 97.1% is obtained for recognition of the four postures, and only 1.0% of postures are misclassified as lying postures. Our fall detection system achieves up to 95.2% fall detection accuracy on a public fall dataset.
The Unfolded Protein Response and the Phosphorylations of Activating Transcription Factor 2 in the trans-Activation of il23a Promoter Produced by β-Glucans*

Background: Phagocytosis and Th17 immune response control fungal invasion. Results: β-Glucans mobilize nuclear C/EBP homologous protein (CHOP) and increase activating transcription factor 2 (ATF2) binding to the il23a promoter. Conclusion: β-Glucans direct proapoptotic CHOP to phagosomal vesicles and induce ATF2-dependent il23a transcription. Significance: The mechanisms underlying the unfolded protein response and the trans-activation of il23a elicited by β-glucans are ascertained. Current views on the control of IL-23 production focus on the regulation of il23a, the gene encoding IL-23 p19, by NF-κB in combination with other transcription factors. C/EBP homologous protein (CHOP), X2-Box-binding protein 1 (XBP1), activator protein 1 (AP1), SMAD, CCAAT/enhancer-binding protein (C/EBPβ), and cAMP-response element-binding protein (CREB) have been involved in response to LPS, but no data are available regarding the mechanism triggered by the fungal mimic and β-glucan-containing stimulus zymosan, which produces IL-23 and to a low extent the related cytokine IL-12 p70. Zymosan induced the mobilization of CHOP from the nuclear fractions to phagocytic vesicles. Hypha-forming Candida also induced the nuclear disappearance of CHOP. Assay of transcription factor binding to the il23a promoter showed an increase of Thr(P)-71–Thr(P)-69-activating transcription factor 2 (ATF2) binding in response to zymosan. PKC and PKA/mitogen- and stress-activated kinase inhibitors down-regulated Thr(P)-71–ATF2 binding to the il23a promoter and il23a mRNA expression. Consistent with the current concept of complementary phosphorylations on N-terminal Thr-71 and Thr-69 of ATF2 by ERK and p38 MAPK, MEK, and p38 MAPK inhibitors blunted Thr(P)-69–ATF2 binding. Knockdown of atf2 mRNA with siRNA correlated with inhibition of il23a mRNA, but it did not affect the expression of il12/23b and il10 mRNA. These data indicate the following: (i) zymosan decreases nuclear proapoptotic CHOP, most likely by promoting its accumulation in phagocytic vesicles; (ii) zymosan-induced il23a mRNA expression is best explained through coordinated κB- and ATF2-dependent transcription; and (iii) il23a expression relies on complementary phosphorylation of ATF2 on Thr-69 and Thr-71 dependent on PKC and MAPK activities.
Have family income mobility patterns changed?

We examine the mobility of individuals in the United States based on equivalent family income-that is, total income of all family members adjusted for family size according to the equivalence scale implicit in the U.S. poverty line. Our analysis, which tracks movements across quintiles, centers on four questions: How much movement is there across the family income distribution? How has this mobility changed over time? To what extent are the movements attributable to factors related to changes in family composition versus events in the labor markets? In light of major socioeconomic changes occurring in the quarter-century under study, have the determinants of mobility changed over time? Our findings indicate that mobility rates in the 1980s differed little from those in the 1970s. However, individuals in families headed by a young person or a person without a college education were less likely to experience upward mobility in the 1980s than in the 1970s.
X-Ray Studies of Phonon Softening in TiSe 2

M. Holt,1,2 P. Zschack,2 Hawoong Hong,2 M. Y. Chou,3 and T. -C. Chiang1,2,* 1Department of Physics, University of Illinois at Urbana-Champaign, 1110 West Green Street, Urbana, Illinois 61801-3080 2Frederick Seitz Materials Research Laboratory, University of Illinois at Urbana-Champaign, 104 South Goodwin Avenue, Urbana, Illinois 61801-2902 3School of Physics, Georgia Institute of Technology, Atlanta, Georgia 30332-0430 (Received 13 November 2000)
Measurement of S‐phase duration of adult stem cells in the flatworm Macrostomum lignano by double replication labelling and quantitative colocalization analysis

Platyhelminthes are highly attractive models for addressing fundamental aspects of stem cell biology in vivo. These organisms possess a unique stem cell system comprised of neoblasts that are the only proliferating cells during adulthood. We have investigated Ts (S‐phase duration) of neoblasts during homoeostasis and regeneration in the flatworm, Macrostomum lignano. A double immunohistochemical technique was used, performing sequential pulses with the thymidine analogues CldU (chlorodeoxyuridine) and IdU (iododeoxyuridine), separated by variable chase times in the presence of colchicine. Owing to the localized nature of the fluorescent signals (cell nuclei) and variable levels of autofluorescence, standard intensity‐based colocalization analyses could not be applied to accurately determine the colocalization. Therefore, an object‐based colocalization approach was devised to score the relative number of double‐positive cells. Using this approach, Ts (S‐phase duration) in the main population of neoblasts was ∼13 h. During early regeneration, no significant change in Ts was observed.
Methylation status of the CpG islands in vitamin D and calcium-sensing receptor gene promoters does not explain the reduced gene expressions in parathyroid adenomas.

AIM The exact mechanism causing decreased expression of the vitamin D receptor (VDR) and calcium-sensing receptor (CASR) genes in parathyroid adenoma is not known, but methylation of promoter regions is often detected during epigenetic downregulation of gene expression. We investigated whether epigenetic silencing is involved in the decreased expression of VDR and CASR. EXPERIMENTAL DESIGN Real-time PCR and immunohistochemistry confirmed the downregulation of the VDR and CASR genes at transcriptional and translational levels. Bisulfite-converted DNA samples from parathyroid adenomas with control samples were analyzed for methylation in the promoter region of VDR and CASR genes. RESULTS There was no significant methylation in the promoter regions of VDR and CASR genes in parathyroid adenomatous tissues. CONCLUSIONS Methylation-mediated silencing of VDR and CASR promoter does not appear to be associated with reduced expression, indicating the involvement of other factors in specific suppression of VDR and CASR in parathyroid adenomas.
Sonic hedgehog signalling in neurons of adult ventrolateral nucleus tractus solitarius

The transmembrane receptor Patched (Ptc) mediates the action of the diffusing factor Sonic hedgehog (Shh), which is implicated in establishing morphogenetic gradients during embryonic development. Whereas alteration of Ptc function is associated with developmental abnormalities and brain tumors, its functional activity and roles in the adult brain have yet to be elucidated. Here we describe the complementary pattern of Shh and Ptc expression in the rat dorsal vagal motor nucleus and the ventrolateral nucleus tractus solitarius (vNTS), respectively. Those two interconnected structures regulate the cardiorespiratory function during hypoxia. Bath application of a subnanomolar concentration of aminoterminal Shh protein (ShhN) to a slice preparation of the vNTS induces a rapid decrease in neuronal firing followed by a bursting activity that propagates in the neuronal network. Intracellular current injections show that bursts result from an action on the neuronal membrane electro‐responsiveness. Both inhibiting and bursting effects are blocked by the monoclonal Shh antibody 5E1 and may require the Ptc binding site of ShhN. Thus, ShhN acting on specific neuronal sites controls electrophysiological properties of differentiated neurons of the vNTS. We speculate on a retrocontrol of cardiorespiratory signals in the vNTS, by Shh generated in dorsal vagal motoneurons.
Hallmarks of opium poisoning in infants and toddlers

Accidental opium intoxication in children is an extremely dangerous poisoning if it remains undiagnosed and untreated. The classic triad of miosis, decreased level of consciousness and bradypnea, which are the hallmarks of opiate intoxication, are used for the diagnosis of opium poisoning in adults and children. Little attention has been paid to the signs of opium intoxication in children and no published study has explored the frequency of hallmarks of this type of poisoning in the paediatric population. We conducted a study in order to evaluate the prevalence of major signs of opium poisoning in infants and toddlers. In this study, a total of 228 infants and 82 toddlers who had been admitted to Loghman Hakim Hospital as a result of opium poisoning between 2001 and 2009 were evaluated, retrospectively. The most usual sign of opium poisoning was miosis (90%) followed by a decreased level of consciousness (88.4%), bradypnea (28.4%) and seizure (10.3%). The prevalence of the triad of miosis, bradypnea and a decreased level of consciousness was 25.2%. Miosis in association with decreased level of consciousness was detected in 82.6% of our patients. Bradypnea was present in 74 infants and 14 toddlers, which shows a statistically significant difference (P = 0.01). The mean age and weight of the patients with bradypnea were significantly less than those without bradypnea (P = 0.008 and P = 0.0001, respectively). Bradypnea and seizure were significantly more common in females (36.7% versus 26%; P = 0.05 and 15.2% versus 6.5%; P = 0.01, respectively). Miosis in association with a decreased level of consciousness is the most useful indicator of opium poisoning in infants and toddlers. Furthermore, seizure is a more common feature of this type of poisoning in infants, especially in those who are less than 1 month old.
Regional myocyte hypertrophy parallels regional myocardial dysfunction during post-infarct remodeling.

After large myocardial infarction (MI), left-ventricular (LV) remodeling is characterized by cavity dilatation, eccentric hypertrophy, and regional mechanical dysfunction. We wished to correlate cellular hypertrophy chronically after MI with in vivo function on a regional basis within non-infarcted myocardium. Twelve sheep were studied. Seven underwent coronary ligation to create an anteroapical MI. Magnetic resonance imaging (MRI) was performed once in controls, and prior to and 8 weeks after infarction, for measurement of LV mass, volumes, ejection fraction, and regional intramyocardial circumferential shortening (%S). Myocyte morphometric indices (cell volume, length, cross-sectional area, width, and length/width ratios) were measured from myocytes isolated from regions adjacent to (within 2 cm of the infarct border) and remote from the infarct and at corresponding loci in the control animals. From baseline to 8 weeks after infarction in the infarcted animals, end-diastolic volume increased from (mean+/-s.d.) 1.9+/-0.4 ml/kg to 2.6+/-0.4 ml/kg (P<0.02) and EF fell from 49+/-6 to 35+/-6% (P<0.02). LV mass trended upwards from 2.2+/-0.4 to 2.6+/-0.4 g/kg (P=n.s.). Regionally, %S in the region adjacent to the infarct fell (from 19+/-3 to 13+/-3%, P<0.003) while remote %S did not change. Cell volume in adjacent non-infarcted regions was greater than that in remote non-infarcted regions (3.8+/-0.9x10(4) micrometer3 v 2.6+/-0. 8x10(4) micrometer3, P<0.006) and this difference (+1.2+/-0.7x10(4) micrometer3) was greater than the corresponding regional difference in controls (+0.4+/-0.2x10(4) micrometer3, P<0.05). Similarly, myocytes in adjacent non-infarcted regions were longer (138.0+/-10.1 micrometer) than in remote regions (123.7+/-10.1 micrometer, P<0.002), and this difference (+14.3+/-7.2 micrometer) was greater than that in controls (-1.4+/-5.6 micrometer, P<0.003). Adjacent %S correlated inversely with adjacent myocyte cell volume (r=-0.72, P<0.009) and cell length (r=-0.70, P<0.02). In mechanically dysfunctional non-infarcted regions adjacent to chronic transmural myocardial infarction in the remodeled LV, disproportionate cellular hypertrophy occurs, predominantly due to an increase in cell length. Mechanical dysfunction in these regions correlates with cell lengthening and hypertrophy.
Asymmetrical extra-hippocampal grey matter loss related to hippocampal atrophy in patients with medial temporal lobe epilepsy

Background: Structural neuroimaging studies have consistently shown a pattern of extra-hippocampal atrophy in patients with left and right drug-refractory medial temporal lobe epilepsy (MTLE). However, it is not yet completely understood how extra-hippocampal atrophy is related to hippocampal atrophy. Moreover, patients with left MTLE often exhibit more intense cognitive impairment, and subtle brain asymmetries have been reported in patients with left MTLE versus right MTLE but have not been explored in a controlled study. Objectives: To investigate the association between extra-hippocampal and hippocampal atrophy in patients with MTLE, and the effect of side of hippocampal atrophy on extra-hippocampal atrophy. Methods: Voxel-based morphometry analyses of magnetic resonance images of the brain were performed to determine the correlation between regional extra-hippocampal grey matter volume and hippocampal grey matter volume. The results from 36 patients with right and left MTLE were compared, and results from the two groups were compared with those from 49 healthy controls. Results: Compared with controls, patients with MTLE showed a more intense correlation between hippocampal grey matter volume and regional grey matter volume in locations such as the contralateral hippocampus, bilateral parahippocampal gyri and frontal and parietal areas. Compared with right MTLE, patients with left MTLE exhibited a wider area of atrophy related to hippocampal grey matter loss, encompassing both the contralateral and ipsilateral hemispheres, particularly affecting the contralateral hippocampus. Conclusions: Our results suggest that left hippocampal atrophy is associated with a larger degree of extra-hippocampal atrophy. This may help to explain the more intense cognitive impairment usually observed in these patients.
Opposite Roles of Human Pancreatitis-Associated Protein and REG1A Expression in Hepatocellular Carcinoma: Association of Pancreatitis-Associated Protein Expression with Low-Stage Hepatocellular Carcinoma, β-Catenin Mutation, and Favorable Prognosis

Purpose: Pancreatitis-associated protein (PAP) and regenerating protein 1 α (Reg1A) are up-regulated during the pancreas regeneration. This study is to investigate the clinicopathologic denotation of their expression in hepatocellular carcinoma (HCC). Experimental Design: PAP and REG1A mRNA levels were measured in 265 surgically removed unifocal primary HCCs using reverse transcription-PCR. Results: PAP and REG1A mRNAs were detected in 97 (36.6%) and 55 (20.8%) HCCs, respectively, including 46 with coexpression but in none of the 219 nontumorous livers. HCCs with PAP expression correlated with low-stage tumors without evidence of vascular invasion (P = 0.013) but the REG1A expression did not. By a combination analysis, HCCs with PAP expression alone showed the lowest frequency of p53 mutation (P < 0.036), the highest rates of grade 1 and low-stage tumors (P < 0.007 and P < 0.001, respectively), less frequent early tumor recurrence (P = 0.051), and hence a better 5-year survival (P = 0.044) than groups expressing PAP and REG1A, REG1A alone, and neither PAP or REG1A. Besides, PAP expressing HCCs had significantly frequent β-catenin mutation, regardless of REG1A expression, P < 0.00001. In the subset of HCCs that has no mutations of p53 and β-catenin but showed PAP expression, coexpression of REG1A and PAP was associated with more frequent vascular invasion than PAP expression alone (P < 0.005). Conclusions: These data suggest that PAP expression designate a subset of low-grade, low-stage HCC with frequent β-catenin mutation and hence more favorable prognosis, whereas further genetic or epigenetic alterations, such as p53 mutation and REG1A expression, lead to more advanced HCCs.
Marginal Analyses of Clustered Data When Cluster Size Is Informative

Summary. We propose a new approach to fitting marginal models to clustered data when cluster size is in‐ formative. This approach uses a generalized estimating equation (GEE) that is weighted inversely with the cluster size. We show that our approach is asymptotically equivalent to within‐cluster resampling ( Hoffman, Sen, and Weinberg, 2001 , Biometrika73, 13–22), a computationally intensive approach in which replicate data sets containing a randomly selected observation from each cluster are analyzed, and the resulting estima‐ tes averaged. Using simulated data and an example involving dental health, we show the superior performa‐ nce of our approach compared to unweighted GEE, the equivalence of our approach with WCR for large sam‐ ple sizes, and the superior performance of our approach compared with WCR when sample sizes are small.
Influence of Land-Surface Evapotranspiration on the Earth's Climate

Calculations with a numerical model of the atmosphere show that the global fields of rainfall, temperature, and motion strongly depend on the land- surface evapotranspiration. This confirms the long-held idea that the surface vegetation, which produces the evapotransporation, is an important factor in the earth's climate.
Restoration of Rostral Ventrolateral Medulla Cystathionine-γ Lyase Activity Underlies Moxonidine-Evoked Neuroprotection and Sympathoinhibition in Diabetic Rats

We recently demonstrated a fundamental role for cystathionine-γ lyase (CSE)–derived hydrogen sulfide (H2S) in the cardioprotective effect of the centrally acting drug moxonidine in diabetic rats. Whether a downregulated CSE/H2S system in the rostral ventrolateral medulla (RVLM) underlies neuronal oxidative stress and sympathoexcitation in diabetes has not been investigated. Along with addressing this question, we tested the hypothesis that moxonidine prevents the diabetes-evoked neurochemical effects by restoring CSE/H2S function within its major site of action, the RVLM. Ex vivo studies were performed on RVLM tissues of streptozotocin (55 mg/kg, i.p.) diabetic rats treated daily for 3 weeks with moxonidine (2 or 6 mg/kg; gavage), H2S donor sodium hydrosulfide (NaHS) (3.4 mg/kg, i.p.), CSE inhibitor DL-propargylglycine (DLP) (37.5 mg/kg, i.p.), a combination of DLP with moxonidine, or their vehicle. Moxonidine alleviated RVLM oxidative stress, neuronal injury, and increased tyrosine hydroxylase immunoreactivity (sympathoexcitation) by restoring CSE expression/activity as well as heme oxygenase-1 (HO-1) expression. A pivotal role for H2S in moxonidine-evoked neuroprotection is supported by the following: 1) NaHS replicated the moxonidine-evoked neuroprotection, and the restoration of RVLM HO-1 expression in diabetic rats; and 2) DLP abolished moxonidine-evoked neuroprotection in diabetic rats, and caused RVLM neurotoxicity, reminiscent of a diabetes-evoked neuronal phenotype, in healthy rats. These findings suggest a novel role for RVLM CSE/H2S/HO-1 in moxonidine-evoked neuroprotection and sympathoinhibition, and as a therapeutic target for developing new drugs for alleviating diabetes-evoked RVLM neurotoxicity and cardiovascular anomalies.