Miracle-dz/UniFAR-FTUs huggingface dataset:
δ-Generalized Labeled Multi-Bernoulli Simultaneous Localization and Mapping with an Optimal Kernel-Based Particle Filtering Approach

Under realistic environmental conditions, heuristic-based data association and map management routines often result in divergent map and trajectory estimates in robotic Simultaneous Localization And Mapping (SLAM). To address these issues, SLAM solutions have been proposed based on the Random Finite Set (RFS) framework, which models the map and measurements such that the usual requirements of external data association routines and map management heuristics can be circumvented and realistic sensor detection uncertainty can be taken into account. Rao–Blackwellized particle filter (RBPF)-based RFS SLAM solutions have been demonstrated using the Probability Hypothesis Density (PHD) filter and subsequently the Labeled Multi-Bernoulli (LMB) filter. In multi-target tracking, the LMB filter, which was introduced as an efficient approximation to the computationally expensive δ-Generalized LMB (δ-GLMB) filter, converts its representation of an LMB distribution to δ-GLMB form during the measurement update step. This not only results in a loss of information yielding inferior results (compared to the δ-GLMB filter) but also fails to take computational advantages in parallelized implementations possible with RBPF-based SLAM algorithms. Similar to state-of-the-art random vector-valued RBPF solutions such as FastSLAM and MH-FastSLAM, the performances of all RBPF-based SLAM algorithms based on the RFS framework also diverge from ground truth over time due to random sampling approaches, which only rely on control noise variance. Further, the methods lose particle diversity and diverge over time as a result of particle degeneracy. To alleviate this problem and further improve the quality of map estimates, a SLAM solution using an optimal kernel-based particle filter combined with an efficient variant of the δ-GLMB filter (δ-GLMB-SLAM) is presented. The performance of the proposed δ-GLMB-SLAM algorithm, referred to as δ-GLMB-SLAM2.0, was demonstrated using simulated datasets and a section of the publicly available KITTI dataset. The results suggest that even with a limited number of particles, δ-GLMB-SLAM2.0 outperforms state-of-the-art RBPF-based RFS SLAM algorithms.
Characterisation of endogenous players in fibroblast growth factor‐regulated functions of hypothalamic tanycytes and energy‐balance nuclei

The mammalian hypothalamus regulates key homeostatic and neuroendocrine functions ranging from circadian rhythm and energy balance to growth and reproductive cycles via the hypothalamic‐pituitary and hypothalamic‐thyroid axes. In addition to its neurones, tanycytes are taking centre stage in the short‐ and long‐term augmentation and integration of diverse hypothalamic functions, although the genetic regulators and mediators of their involvement are poorly understood. Exogenous interventions have implicated fibroblast growth factor (FGF) signalling, although the focal point of the action of FGF and any role for putative endogenous players also remains elusive. We carried out a comprehensive high‐resolution screen of FGF signalling pathway mediators and modifiers using a combination of in situ hybridisation, immunolabelling and transgenic reporter mice, aiming to map their spatial distribution in the adult hypothalamus. Our findings suggest that β‐tanycytes are the likely focal point of exogenous and endogenous action of FGF in the third ventricular wall, utilising FGF receptor (FGFR)1 and FGFR2 IIIc isoforms, but not FGFR3. Key IIIc‐activating endogenous ligands include FGF1, 2, 9 and 18, which are expressed by a subset of ependymal and parenchymal cells. In the parenchymal compartment, FGFR1‐3 show divergent patterns, with FGFR1 being predominant in neuronal nuclei and expression of FGFR3 being associated with glial cell function. Intracrine FGFs are also present, suggestive of multiple modes of FGF function. Our findings provide a testable framework for understanding the complex role of FGFs with respect to regulating the metabolic endocrine and neurogenic functions of hypothalamus in vivo.
MHC-mismatched Allotransplantation of Induced Pluripotent Stem Cell-Derived Cardiomyocyte Sheets to Improve Cardiac Function in A Primate Ischemic Cardiomyopathy Model.

BACKGROUND Although allogeneic induced pluripotent stem cell (iPSC)-derived cardiomyocytes (CMs) exhibit potential in cardiomyogenesis for heart failure, whether major histocompatibility complex (MHC) -matched allogenic iPSC implantation (MMAI) minimizes immune rejection for cell survival or functional recovery remains unknown. We herein explored whether MMAI with an iPSC-CM sheet is stable for a longer period and therapeutically more effective than MHC-mismatched AI in a primate ischemic cardiomyopathy model. METHODS Green fluorescent protein (GFP)-transfected iPSC-CM sheets, derived from cynomolgus macaques with homozygous MHC haplotypes ''HT1'', were transplanted on the left ventricle (LV), generated by ligating the left anterior descending (LAD) artery for 2 weeks in an ischemic model with or without heterozygous HT1 as MMAI and MHC-mismatched AI. Sham models were made by opening chest at 14 days after LAD ligation without any treatment. RESULTS Stereomicroscopy revealed that at 4 months post transplantation, GFP intensity was higher in the MMAI group than in the MHC-mismatched AI group and the sham group. Immunohistochemistry staining revealed that host immune reaction with CD3-positive cells was stronger in MHC-mismatched AI than in MMAI at 3 months. Cardiac function improved both in MMAI and MHC-mismatched AI at 1 month after transplantation and was preserved until 6 months, whereas in the sham group, functional deterioration progressed over time. CONCLUSION Although MHC-homo-iPSCs are preferred to avoid immune rejection, MHC-mismatched iPSC-CMs can also induce comparable cardiac functional recovery at late follow-up, suggesting that MHC-mismatched iPSC-based cardiac regenerative therapy with immunosuppressants is a feasible option for treating heart failure in clinical settings.
A Meta-Analysis of Odor Thresholds and Odor Identification in Autism Spectrum Disorders

Autism Spectrum Disorders (ASD) are often accompanied by atypical visual, auditory, and tactile sensory behavior. Evidence also suggests alterations of the olfactory system, but the pattern of findings appears mixed. To quantify this pattern systematically, we conducted a meta-analysis. Studies were included if they examined olfactory function (i.e., odor threshold, or odor identification) in ASD compared with healthy age-matched control groups. We also coded for the potential moderators gender, age, and IQ. Articles were identified through computerized literature search using Web of Science, PubMed, and Scopus databases. A total of 11 articles compared odor threshold and/or odor identification between cases and controls (for threshold, n = 143 ASD and 148 controls; and for identification, n = 132 ASD and 139 controls). Effects sizes showed a substantial heterogeneity. As a result, the 95% prediction intervals were wide and ranged between a large negative and a large positive effect size for odor threshold, [-1.86, 2.05], and for odor identification, [-1.51, 2.52]. Exploratory analyses suggested that age and IQ may be potential moderators. To conclude, the large heterogeneity is consistent with the notion of both hyposensitivity and hypersensitivity in individuals with ASD. However, future research needs to predict and test the specific direction of the effect to provide convincing evidence for atypical olfactory functions in ASD.
Motivated Reflection on Attitude-Inconsistent Information

The mere thought effect is defined in part by the tendency of self-reflective thought to heighten the generation of and reflection on attitude-consistent thoughts. By focusing on individuals’ fears of invalidity, we explored the possibility that the mere opportunity for thought sometimes motivates reflection on attitude-inconsistent thoughts. Across three experiments, dispositional and situational fear of invalidity was shown to heighten reflection on attitude-inconsistent thoughts. This heightened reflection, in turn, interacted with individuals’ thought confidence to determine whether attitude-inconsistent thoughts were assimilated or refuted and consequently whether individuals’ attitudes and behavioral intentions depolarized or polarized following a sufficient opportunity for thought, respectively. These findings emphasize the impact of motivational influences on thought reflection and generation, the importance of thought confidence in the assimilation and refutation of self-generated thought, and the dynamic means by which the mere thought bias can impact self-persuasion.
Functional Characterization of the Gene Cluster from Pseudomonas syringae pv. phaseolicola NPS3121 Involved in Synthesis of Phaseolotoxin

ABSTRACT Pseudomonas syringae pv. phaseolicola is the causal agent of halo blight disease of beans (Phaseolus vulgaris L.), which is characterized by water-soaked lesions surrounded by a chlorotic halo resulting from the action of a non-host-specific toxin known as phaseolotoxin. This phytotoxin inhibits the enzyme ornithine carbamoyltransferase involved in arginine biosynthesis. Different evidence suggested that genes involved in phaseolotoxin production were clustered. Two genes had been previously identified in our laboratory within this cluster: argK, which is involved in the immunity of the bacterium to its own toxin, and amtA, which is involved in the synthesis of homoarginine. We sequenced the region around argK and amtA in P. syringae pv. phaseolicola NPS3121 to determine the limits of the putative phaseolotoxin gene cluster and to determine the transcriptional pattern of the genes comprising it. We report that the phaseolotoxin cluster (Pht cluster) is composed of 23 genes and is flanked by insertion sequences and transposases. The mutation of 14 of the genes within the cluster lead to a Tox− phenotype for 11 of them, while three mutants exhibited low levels of toxin production. The analysis of fusions of selected DNA fragments to uidA, Northern probing, and reverse transcription-PCR indicate the presence of five transcriptional units, two monocistronic and three polycistronic; one is internal to a larger operon. The site for transcription initiation has been determined for each promoter, and the putative promoter regions were identified. Preliminary results also indicate that the gene product of phtL is involved in the regulation of the synthesis of phaseolotoxin.
Place of preimplantation diagnosis in genetic practice

Preimplantation genetic diagnosis (PGD) is currently one of the practical options available for couples at‐risk to avoid the birth of children with genetic and chromosomal disorders. Despite its novelty, PGD has already become an alternative to traditional prenatal diagnosis, allowing establishing only unaffected pregnancies avoiding the risk for pregnancy termination. Indications for PGD have currently expanded beyond those practices in prenatal diagnosis, such as late‐onset diseases with genetic predisposition, and preimplantation HLA typing with the purpose of establishing potential donor progeny for stem cell treatment of siblings, which makes PGD also an important compliment to prenatal diagnosis. The fact that more than 1,000 apparently healthy unaffected children have been born after PGD suggests its accuracy, reliability, and safety. PGD is presently an excellent option for carriers of balanced translocations, and appears to be of special value for avoiding age‐related aneuploidies in patients of advanced reproductive age. The accumulated experience of thousands of PGD cycles for poor prognosis in vitro fertilization (IVF) patients provides strong evidence of the improvement of clinical outcome, particularly obvious from the reproductive history of patients. This makes of practical relevance to inform couples at‐risk about availability of PGD option, so they make their own choice in avoiding the birth of affected offspring and having healthy children of their own. © 2005 Wiley‐Liss, Inc.
Not-so-working Memory: Drift in Functional Magnetic Resonance Imaging Pattern Representations during Maintenance Predicts Errors in a Visual Working Memory Task

Working memory (WM) is critical to many aspects of cognition, but it frequently fails. Much WM research has focused on capacity limits, but even for single, simple features, the fidelity of individual representations is limited. Why is this? One possibility is that, because of neural noise and interference, neural representations do not remain stable across a WM delay, nor do they simply decay, but instead, they may “drift” over time to a new, less accurate state. We tested this hypothesis in a functional magnetic resonance imaging study of a match/nonmatch WM recognition task for a single item with a single critical feature: orientation. We developed a novel pattern-based index of “representational drift” to characterize ongoing changes in brain activity patterns throughout the WM maintenance period, and we were successfully able to predict performance on the match/nonmatch recognition task using this representational drift index. Specifically, in trials where the target and probe stimuli matched, participants incorrectly reported more nonmatches when their activity patterns drifted away from the target. In trials where the target and probe did not match, participants incorrectly reported more matches when their activity patterns drifted toward the probe. On the basis of these results, we contend that neural noise does not cause WM errors merely by degrading representations and increasing random guessing; instead, one means by which noise introduces errors is by pushing WM representations away from the target and toward other meaningful (yet incorrect) configurations. Thus, we demonstrate that behaviorally meaningful drift within representation space can be indexed by neuroimaging.
TIP30 inhibits oligodendrocyte precursor cell differentiation via cytoplasmic sequestration of Olig1

Differentiation of oligodendrocyte precursor cells (OPCs) is a prerequisite for both developmental myelination and adult remyelination in the central nervous system. The molecular mechanisms underlying OPC differentiation remain largely unknown. Here, we show that the thirty‐kDa HIV‐1 Tat interacting protein (TIP30) is a negative regulator in oligodendrocyte development. The TIP30−/− mice displayed an increased myelin protein level at postnatal day 14 and 21. By using a primary OPC culture system, we demonstrated that overexpression of TIP30 dramatically inhibited the stage progression of differentiating OPCs, while knockdown of TIP30 enhanced the differentiation of oligodendroglial cells remarkably. Moreover, overexpression of TIP30 was found to sequester the transcription factor Olig1 in the cytoplasm and weaken its nuclear translocation due to the interaction between TIP30 and Olig1, whereas knockdown of TIP30 led to more Olig1 localized in the nucleus in the initiation stage during OPC differentiation. In the cuprizone‐induced demyelination model, there was a dramatic increase in NG2‐expressing cells with nuclear location of Olig1 in the corpus callosum during remyelination. In contrast, within chronic demyelinated lesions in multiple sclerosis, TIP30 was abnormally expressed in NG2‐expressing cells, and few nuclear Olig1 was observed in these cells. Taken together, our findings suggest that TIP30 plays a negative regulatory role in oligodendroglial differentiation. GLIA 2015;63:684–698
Hemodynamic Effects of a New Inotropic Compound, PST-2744, in Dogs With Chronic Ischemic Heart Failure

Inotropic agents for acute decompensated heart failure are associated with a lack of efficacy or increased mortality. New compounds are needed to support patients with acute exacerbations of heart failure. This study examined the hemodynamic effects of a new inotropic agent (PST-2744) in dogs with chronic ischemic heart failure. Eight mongrel dogs at low risk for postmyocardial infarction (MI) sudden death entered the protocol. Dogs were studied after ischemic left ventricular dysfunction was induced by repeated injections of latex microspheres into the circumflex artery until the ejection fraction reached 35%. Hemodynamic parameters were measured at baseline and peak drug effect (PST-2744 5 &mgr;g·kg−1·min−1). In 5 animals, PST-2744 effects were compared with dobutamine. Heart rates, PR intervals and QT intervals were unchanged following PST-2744 administration. PST-2744 increased contractility (+dP/dt) by 56% from 1881 ± 282 mm Hg/s to 2939 ± 734 mm Hg/s (P < 0.01). The inotropic effect of PST-2744 was equal to that produced by 5-&mgr;g·kg−1·min−1 dobutamine (56% increase in +dP/dt), but peak heart rates were significantly higher with dobutamine (129 ± 24 bpm PST-2744 versus 160 ± 6 bpm 5-&mgr;g·kg−1·min−1 dobutamine, P < 0.002). No arrhythmias or conduction delays were seen with either compound. PST-2744 is an effective inotropic agent without positive chronotropic effect in subjects with stable moderate left ventricular dysfunction.
Prevalence of gca, a gene involved in synthesis of A-band common antigen polysaccharide in Pseudomonas aeruginosa

Two distinct forms of lipopolysaccharide are expressed by Pseudomonas aeruginosa. These forms are known as the A band and the B band. In an attempt to obtain a better understanding of A-band lipopolysaccharide synthesis, a previously isolated A-band gene known as the gca gene (GDP-D-mannose conversion protein for A-band common antigen polysaccharide) was sequenced and analyzed. Previous protein expression data from our laboratory, along with nucleotide sequence analysis from the present study, suggest that the Gca protein is encoded by the open reading frame ORF36.5. Amino acid homology reveals that this protein may be functioning as a dehydratase or as a bifunctional enzyme, facilitating the conversion of GDP-D-mannose to GDP-D-rhamnose. The distribution of this gca gene among the 20 P. aeruginosa O serotypes, clinical isolates, and other Pseudomonas species was also examined. Southern hybridization results revealed that the gca gene is present and conserved on a 1.6-kb KpnI fragment among all 20 O serotypes with the exception of serotype O12. In addition, the gca gene is not universally found among all pseudomonads; however, probe-reactive profiles are similar to that of P. aeruginosa when the gca gene is present. Primers were designed from the gca nucleotide sequence, and PCR amplification of a 700-bp product was found with each of the 20 O serotypes. Because of the conservation of this gene, gca may be useful as a diagnostic tool for detecting the presence of P. aeruginosa as well as other Pseudomonas species.
Utility of the Canadian Occupational Performance Measure in community-based brain injury rehabilitation

Primary objective: To investigate the clinical utility of the Canadian Occupational Performance Measure (COPM) for community-based individuals with acquired brain injury (ABI). Methods and procedures: Thirty-four individuals with ABI (M = 5.32 years post-injury, SD = 3.92) were administered the COPM with self- and relative ratings of performance and satisfaction obtained. Relatives completed the Brain Injury Community Rehabilitation Outcome 39 (BICRO-39) scales. Measures of awareness of deficits, emotional status and cognitive function were obtained. A sub-group of participants was randomly allocated into a no-intervention group (n = 15) or an 8-week treatment group (n = 10). Initial assessments and 8-week follow-up assessments were conducted. Main outcomes and results: A pre- and post-assessment comparison for the treatment group identified a significant improvement on most COPM ratings (p < 0.05), but not the BICRO-39 (p > 0.05). However, self-ratings of satisfaction improved for the no-intervention group (p < 0.05). Self-ratings of satisfaction were significantly correlated with anxiety (r = −0.42, p < 0.05), although there were no other significant associations between COPM ratings and awareness, mood state and cognitive function. Conclusions: The findings generally support the utility of the COPM in community-based rehabilitation; however, the need for self-ratings to be interpreted in the context of other outcome indicators is recommended.
Salmonella enterica Serovar Typhimurium Pathogenicity Island 2 Is Necessary for Complete Virulence in a Mouse Model of Infectious Enterocolitis

ABSTRACT Salmonella species cause a wide range of disease in multiple hosts. Salmonella enterica serovar Typhimurium causes self-limited intestinal disease in humans and systemic typhoid-like illness in susceptible mice. The prevailing dogma in murine S. enterica serovar Typhimurium pathogenesis is that distinct virulence mechanisms—Salmonella pathogenicity islands 1 and 2 (SPI1 and SPI2)—perform distinct roles in pathogenesis, the former being important for invasion and intestinal disease and the latter important for intracellular survival and systemic persistence and disease. Although evidence from bovine infections has suggested that SPI2 has a role in ileal disease, there is no evidence that SPI2 is important for inflammation in a disease that more closely recapitulates human colitis. Using S. enterica serovar Typhimurium strains that lack functional type III secretion systems, we demonstrate that SPI2 is essential for complete virulence in murine infectious enterocolitis. Using a recently characterized murine model (M. Barthel,S. Hapfelmeier, L. Quintanilla-Martinez, M. Kremer, M. Rohde, M. Hogardt, K. Pfeffer, H. Russmann, and W. D. Hardt, Infect. Immun. 71:2839-2858, 2003), we demonstrate that SPI1 mutants are unable to cause intestinal disease 48 h after infection and that SPI2-deficient bacteria also cause significantly attenuated typhlitis. We show that at the peak of inflammation in the cecum, SPI2 mutants induce diminished intercellular adhesion molecule 1 expression and neutrophil recruitment but that wild-type and mutant Salmonella are similarly distributed in the lumen of the infected organ. Finally, we demonstrate that attenuation of intestinal inflammation is accompanied by resolution of typhlitis in the mutant, but not wild-type, infections. Collectively, these results indicate that SPI2 is needed for enterocolitis, as well as for systemic disease.
Intracellular Neutrophil Oxidants: From Laboratory Curiosity to Clinical Reality

The phagocyte NADPH oxidase is responsible for the neutrophil’s great capacity to produce reactive oxygen species (ROS). The NADPH oxidase can be assembled in the plasma membrane, as well as in membranes of intracellular vesicles, giving neutrophils the ability to direct ROS production to distinct subcellular sites. Neutrophil ROS contribute to microbial killing, trigger formation of neutrophil extracellular traps and appear to partake in inflammation control. Consequently, function-disrupting mutations in the NADPH oxidase lead to chronic granulomatous disease, characterized by severe infections and inflammatory disorders. Recent experimental data and description of a novel chronic granulomatous disease subtype (p40phox-deficiency) imply that ROS generated in intracellular compartments are key for NETosis and for controlling inflammatory signaling. We foresee boosted interest in intracellular ROS production. To fully understand where and how such ROS function, however, limitations of assay systems to measure ROS need to be appreciated, and the development of novel techniques/reagents would be highly useful.