Miracle-dz/UniFAR-FTUs huggingface dataset:
Cerebral Microbleeds: Do They Really Predict Macrobleeding?

There is growing evidence linking microbleeds to macrobleeding in selected patient populations. Yet, prospective data in unselected populations are scarce. The high prevalence of microbleeds and relatively low incidence of symptomatic intracerebral haemorrhage suggest that it may be a specific sub-group of persons with microbleeds developing macrobleeding. This may be related to the severity and nature of the underling vascular pathology. Future studies should therefore use a longitudinal design and not only focus on microbleed presence, but also on location and number of microbleeds.
Determinants of Adiposity during Preweaning Postnatal Growth in Appropriately Grown and Growth-Restricted Term Infants

The distribution and quantity of adipose tissue are markers of morbidity risk in children and adults. Poor intrauterine growth and accelerated postnatal growth are believed to add to these risks. The aim of this study was to assess adipose tissue content and distribution at birth and 6 wk in relation to intrauterine growth restriction, postnatal growth, and infant diet. We measured weight, length, and head circumference and adipose content and distribution using magnetic resonance imaging at 6 wk of age in appropriately grown for gestational age (AGA) and growth-restricted (GR) infants and compared this with birth data. By 6 wk, GR infants showed complete catch-up in comparison to AGA infants in relation to head growth and adiposity. Catch-up in length and weight was not complete. Accelerated linear growth, but not accelerated weight gain, was associated with a highly significant increase in adiposity (r = 0.57, p = 0.001) regardless of AGA/GR status. The highest adiposity at 6 wk, allowing for baseline variables and linear growth, was seen in exclusively breast-fed GR infants (mean, 95% confidence interval: 33.5%, 29.51–37.5). Adipose tissue distribution remained constant and was unrelated to growth and diet. Reduced birth adiposity (B = –0.185, p = 0.003), but not low birth head size (B = 0.32, p = 0.093), was a significant predictor of accelerated postnatal head growth (R2 = 0.29, adjusted R2 = 0.23, p = 0.012). Increasing adiposity appears to be an inevitable accompaniment of accelerated linear growth. Low total adipose tissue quantity at birth appears to direct nutrition toward head growth. Adipose tissue may be involved in the signaling of catch-up growth.
Recovery Algorithms for Vector-Valued Data with Joint Sparsity Constraints

Vector-valued data appearing in concrete applications often possess sparse expansions with respect to a preassigned frame for each vector component individually. Additionally, different components may also exhibit common sparsity patterns. Recently, there were introduced sparsity measures that take into account such joint sparsity patterns, promoting coupling of nonvanishing components. These measures are typically constructed as weighted $\ell_1$ norms of componentwise $\ell_q$ norms of frame coefficients. We show how to compute solutions of linear inverse problems with such joint sparsity regularization constraints by fast thresholded Landweber algorithms. Next we discuss the adaptive choice of suitable weights appearing in the definition of sparsity measures. The weights are interpreted as indicators of the sparsity pattern and are iteratively updated after each new application of the thresholded Landweber algorithm. The resulting two-step algorithm is interpreted as a double-minimization scheme for a suitable target functional. We show its $\ell_2$-norm convergence. An implementable version of the algorithm is also formulated, and its norm convergence is proven. Numerical experiments in color image restoration are presented.
Evidence for a Role of Mast Cells in the Evolution to Congestive Heart Failure

Mast cells are believed to be involved in the pathophysiology of heart failure, but their precise role in the process is unknown. This study examined the role of mast cells in the progression of heart failure, using mast cell-deficient (WBB6F1-W/Wv) mice and their congenic controls (wild-type [WT] mice). Systolic pressure overload was produced by banding of the abdominal aorta, and cardiac function was monitored over 15 wk. At 4 wk after aortic constriction, cardiac hypertrophy with preserved left ventricular performance (compensated hypertrophy) was observed in both W/Wv and WT mice. Thereafter, left ventricular performance gradually decreased in WT mice, and pulmonary congestion became apparent at 15 wk (decompensated hypertrophy). In contrast, decompensation of cardiac function did not occur in W/Wv mice; left ventricular performance was preserved throughout, and pulmonary congestion was not observed. Perivascular fibrosis and upregulation of mast cell chymase were all less apparent in W/Wv mice. Treatment with tranilast, a mast cell–stabilizing agent, also prevented the evolution from compensated hypertrophy to heart failure. These observations suggest that mast cells play a critical role in the progression of heart failure. Stabilization of mast cells may represent a new approach in the management of heart failure.
moz regulates Hox expression and pharyngeal segmental identity in zebrafish

In vertebrate embryos, streams of cranial neural crest (CNC) cells migrate to form segmental pharyngeal arches and differentiate into segment-specific parts of the facial skeleton. To identify genes involved in specifying segmental identity in the vertebrate head, we screened for mutations affecting cartilage patterning in the zebrafish larval pharynx. We present the positional cloning and initial phenotypic characterization of a homeotic locus discovered in this screen. We show that a zebrafish ortholog of the human oncogenic histone acetyltransferase MOZ (monocytic leukemia zinc finger) is required for specifying segmental identity in the second through fourth pharyngeal arches. In moz mutant zebrafish, the second pharyngeal arch is dramatically transformed into a mirror-image duplicated jaw. This phenotype resembles a similar but stronger transformation than that seen in hox2 morpholino oligo (hox2-MO) injected animals. In addition, mild anterior homeotic transformations are seen in the third and fourth pharyngeal arches of moz mutants. moz is required for maintenance of most hox1-4 expression domains and this requirement probably at least partially accounts for the moz mutant homeotic phenotypes. Homeosis and defective Hox gene expression in moz mutants is rescued by inhibiting histone deacetylase activity with Trichostatin A. Although we find early patterning of the moz mutant hindbrain to be normal, we find a late defect in facial motoneuron migration in moz mutants. Pharyngeal musculature is transformed late, but not early, in moz mutants. We detect relatively minor defects in arch epithelia of moz mutants. Vital labeling of arch development reveals no detectable changes in CNC generation in moz mutants, but later prechondrogenic condensations are mispositioned and misshapen. Mirror-image hox2-dependent gene expression changes in postmigratory CNC prefigure the homeotic phenotype in moz mutants. Early second arch ventral expression of goosecoid (gsc) in moz mutants and in animals injected with hox2-MOs shifts from lateral to medial, mirroring the first arch pattern. bapx1, which is normally expressed in first arch postmigratory CNC prefiguring the jaw joint, is ectopically expressed in second arch CNC of moz mutants and hox2-MO injected animals. Reduction of bapx1 function in wild types causes loss of the jaw joint. Reduction of bapx1 function in moz mutants causes loss of both first and second arch joints, providing functional genetic evidence that bapx1 contributes to the moz-deficient homeotic pattern. Together, our results reveal an essential embryonic role and a crucial histone acetyltransferase activity for Moz in regulating Hox expression and segmental identity, and provide two early targets, bapx1 and gsc, of moz and hox2 signaling in the second pharyngeal arch.
Novel Competitive Inhibitor of NAD(P)H Oxidase Assembly Attenuates Vascular O2− and Systolic Blood Pressure in Mice

We previously reported enhanced expression of the p67phox and gp91phox components of NAD(P)H oxidase in angiotensin (Ang) II–induced hypertension, suggesting de novo assembly in response to Ang II. To examine the direct involvement of NAD(P)H oxidases in Ang II–induced O2− production, we designed a chimeric peptide that inhibits p47phox association with gp91phox in NAD(P)H oxidase (gp91ds-tat). This was achieved by linking a 9-amino acid peptide (aa) derived from HIV-coat protein (tat) to a 9-aa sequence of gp91phox (known to interact with p47phox). As a control, we constructed a chimera containing tat and a scrambled gp91 sequence (scramb-tat). We found that gp91ds-tat decreased O2− levels in aortic rings treated with Ang II (10 pmol/L) but had no effect on either the O2−-generating enzyme xanthine oxidase or potassium superoxide–generated O2−. We infused vehicle, Ang II (0.75 mg · kg−1 · d−1), Ang II+gp91ds-tat (10 mg · kg−1 · d−1), or Ang II+scramb-tat intraperitoneally in C57Bl/6 mice and measured systolic blood pressure (SBP) on days 0, 3, 5, and 7 of infusion. SBP increased by day 3 in mice given Ang II and Ang II+scramb-tat but was significantly lower with Ang II+gp91-tat. On day 7, SBP was still significantly inhibited in mice given Ang II+gp91ds-tat, whereas Ang II–induced O2− production was inhibited throughout the aorta as detected by dihydroethidium staining, consistent with the ability of this inhibitor to block the various vascular NAD(P)H oxidase isoforms. These data support the hypothesis that inhibition of the interaction of p47phox and gp91phox (or its homologues) can block O2− production and attenuate blood pressure elevation in mice.
Secrecy Capacity of a Class of Broadcast Channels with an Eavesdropper

We study the security of communication between a single transmitter and many receivers in the presence of an eavesdropper for several special classes of broadcast channels. As the first model, we consider the degraded multireceiver wiretap channel where the legitimate receivers exhibit a degradedness order while the eavesdropper is more noisy with respect to all legitimate receivers. We establish the secrecy capacity region of this channel model. Secondly, we consider the parallel multireceiver wiretap channel with a less noisiness order in each subchannel, where this order is not necessarily the same for all subchannels, and hence the overall channel does not exhibit a less noisiness order. We establish the common message secrecy capacity and sum secrecy capacity of this channel. Thirdly, we study a class of parallel multireceiver wiretap channels with two subchannels, two users and an eavesdropper. For channels in this class, in the first (resp., second) subchannel, the second (resp., first) receiver is degraded with respect to the first (resp., second) receiver, while the eavesdropper is degraded with respect to both legitimate receivers in both subchannels. We determine the secrecy capacity region of this channel, and discuss its extensions to arbitrary numbers of users and subchannels. Finally, we focus on a variant of this previous channel model where the transmitter can use only one of the subchannels at any time. We characterize the secrecy capacity region of this channel as well.
American Journal of Epidemiology Original Contribution Prisoner Survival inside and outside of the Institution: Implications for Health- Care Planning

which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The life expectancy of persons cycling through the prison system is unknown. The authors sought to determine the 15.5-year survival of 23,510 persons imprisoned in the state of Georgia on June 30, 1991. After linking prison and mortality records, they calculated standardized mortality ratios (SMRs). The cohort experienced 2,650 deaths during follow-up, which were 799 more than expected SMRs varied by race, with black men exhibiting lower relative mortality than white men. Black men were the only demographic subgroup to experience significantly lower mortality while incarcerated (SMR ¼ 0.66, 95% CI: 0.58, 0.76), while white men experienced elevated mortality while incarcerated (SMR ¼ 1.28, 95% CI: 1.10, 1.48). Four causes of death (homicide, transportation, accidental poisoning, and suicide) accounted for 74% of the decreased mortality during incarceration, while 6 causes (human immunodefi-ciency virus infection, cancer, cirrhosis, homicide, transportation, and accidental poisoning) accounted for 62% of the excess mortality following release. Adjustment for compassionate releases eliminated the protective effect of incarceration on mortality. These results suggest that the low mortality inside prisons can be explained by the rarity of deaths unlikely to occur in the context of incarceration and compassionate releases of moribund patients. As a consequence of political pressure to increase punishment for crime, the United States leads the world in rates of incarceration (1). The length of time that a particular prisoner serves behind bars may depend on both structural factors (the laws of the state, the conduct of the jury and judge, underlying racism, etc.) and individual factors (the particular crime committed; educational level, which in turn affects the ability to afford skilled legal counsel) (2). A multitude of causes, including high rates of substance abuse, engagement in risky sexual behaviors, intermittent home-lessness, and poor access to mental health care, can explain why the 10.7 million persons who spent at least a portion of the year 2006 in a US prison or jail (3) are believed to have poorer health on average than the general population (4, 5). For example, the prevalence of human immunodeficiency virus (HIV) infection among US prisoners is 3.8 times that for US adults as a whole (6, 7). Many predictors of criminal activity are also predictors of poor health outcomes. Numerous studies have demonstrated that the period immediately following release, especially the first month, is …
EVALUATION OF THE CHELATING EFFECT OF METHANOLIC EXTRACT OF CORIANDRUM SATIVUM AND ITS FRACTIONS ON WISTAR RATS POISONED WITH LEAD ACETATE

Background: The rate of lead poisoning has decreased in recent years due to increased health control in industries that use this metal. However, it is still a public health problem worldwide. The use of various plants with chelating properties has been a topic of research today. In traditional medicine, it is said that Coriandrum sativum has chelating properties, but there is no scientific evidence to support this fact. The purpose of this research is to evaluate the chelating effect of methanol extract of coriander and its fractions on Wistar rats intoxicated with lead. Materials and Methods: In this research, male Wistar rats were poisoned with 50 mg/kg of lead acetate and treated with 50 mg/kg of methanol extract and its fractions. The extract and its fractions were administered to four treatment groups. Positive and negative controls were established. Hemoglobin, hematocrit and lead concentrations were analyzed; liver was evaluated histologically in control and treatment groups. Results: The methanol extract of coriander presented a LD50 >1000 mg/dL. The group administered with the methanol extract showed significant difference in the levels of hemoglobin and hematocrit compared to the negative control group. Lead concentration in treatment groups showed a decrease compared to the positive control. Histological evaluation of tissue showed less damage in groups administered with methanolic extract and its fractions compared to the positive control which presented structural alterations. Conclusion: Coriander extracts protect liver and lower lead concentration in rats intoxicated with lead in contrast to the positive control group.
PD-L1 on Tumor Cells Is Induced in Ascites and Promotes Peritoneal Dissemination of Ovarian Cancer through CTL Dysfunction

Purpose: Ovarian cancer often progresses by disseminating to the peritoneal cavity, but how the tumor cells evade host immunity during this process is poorly understood. Programmed cell death 1 ligand 1 (PD-L1) is known to suppress immune system and to be expressed in cancer cells. The purpose of this study is to elucidate the function of PD-L1 in peritoneal dissemination. Experimental Design: Ovarian cancer cases were studied by microarray and immunohistochemistry. PD-L1 expression in mouse ovarian cancer cell line in various conditions was assessed by flow cytometry. PD-L1–overexpression cell line and PD-L1–depleted cell line were generated, and cytolysis by CTLs was analyzed, and alterations in CTLs were studied by means of timelapse and microarray. These cell lines were injected intraperitoneally to syngeneic immunocompetent mice. Results: Microarray and immunohistochemistry in human ovarian cancer revealed significant correlation between PD-L1 expression and peritoneal positive cytology. PD-L1 expression in mouse ovarian cancer cells was induced upon encountering lymphocytes in the course of peritoneal spread in vivo and coculture with lymphocytes in vitro. Tumor cell lysis by CTLs was attenuated when PD-L1 was overexpressed and promoted when it was silenced. PD-L1 overexpression inhibited gathering and degranulation of CTLs. Gene expression profile of CTLs caused by PD-L1–overexpressing ovarian cancer was associated with CTLs exhaustion. In mouse models, PD-L1 depletion resulted in inhibited tumor growth in the peritoneal cavity and prolonged survival. Conclusion: PD-L1 expression in tumor cell promotes peritoneal dissemination by repressing CTL function. PD-L1–targeted therapy is a promising strategy for preventing and treating peritoneal dissemination. Clin Cancer Res; 19(6); 1363–74. ©2012 AACR.
Post-event Processing Predicts Impaired Cortisol Recovery Following Social Stressor: The Moderating Role of Social Anxiety

There is growing evidence that individuals with social anxiety show impaired cortisol recovery after experiencing social evaluative stressors. Yet, little is known regarding the cognitive processes underlying such impaired cortisol recovery. The present study examined the effect of post-event processing (PEP), referred to as repetitive thinking about social situations, on cortisol recovery following a social stressor. Forty-two non-clinical university students (23 women, 19 men, mean age = 22.0 ± 2.0 years) completed the Trier Social Stress Test (TSST), followed by a thought sampling procedure which assessed the frequency of PEP reflecting the TSST. A growth curve model showed PEP and social anxiety interactively predicted cortisol recovery. In particular, PEP predicted impaired cortisol recovery in those with low levels of social anxiety but not in those with high levels of social anxiety, which contradicted the initial hypothesis. These findings suggest that PEP is differentially associated with cortisol recovery depending on levels of social anxiety. The possible mechanisms underlying these findings were discussed in terms of protective inhibition framework.
The effects of stimulus competition and voluntary attention on colour-graphemic synaesthesia

Colour-graphemic synaesthetes experience vivid colours when reading letters, digits and words. We examined the effect of stimulus competition and attention on these unusual colour experiences in 14 synaesthetes and 14 non-synaesthetic controls. Participants named the colour of hierarchical local–global stimuli in which letters at each level elicited synaesthetic colours that were congruent or incongruent with the display colour. Synaesthetes were significantly slower to name display colours when either level was incongruent than when both levels were congruent. This effect was significantly reduced when synaesthetes focused attention on one level while the congruency of letters at the ignored level was varied. These findings suggest that competition between multiple inducers and mechanisms of voluntary attention influence colour-graphemic synaesthesia.
A Transcriptome—Targeting EcoChip for Assessing Functional Mycodiversity

A functional biodiversity microarray (EcoChip) prototype has been developed to facilitate the analysis of fungal communities in environmental samples with broad functional and phylogenetic coverage and to enable the incorporation of nucleic acid sequence data as they become available from large-scale (next generation) sequencing projects. A dual probe set (DPS) was designed to detect a) functional enzyme transcripts at conserved protein sites and b) phylogenetic barcoding transcripts at ITS regions present in precursor rRNA. Deviating from the concept of GeoChip-type microarrays, the presented EcoChip microarray phylogenetic information was obtained using a dedicated set of barcoding microarray probes, whereas functional gene expression was analyzed by conserved domain-specific probes. By unlinking these two target groups, the shortage of broad sequence information of functional enzyme-coding genes in environmental communities became less important. The novel EcoChip microarray could be successfully applied to identify specific degradation activities in environmental samples at considerably high phylogenetic resolution. Reproducible and unbiased microarray signals could be obtained with chemically labeled total RNA preparations, thus avoiding the use of enzymatic labeling steps. ITS precursor rRNA was detected for the first time in a microarray experiment, which confirms the applicability of the EcoChip concept to selectively quantify the transcriptionally active part of fungal communities at high phylogenetic resolution. In addition, the chosen microarray platform facilitates the conducting of experiments with high sample throughput in almost any molecular biology laboratory.