Crowd Counting with Decomposed Uncertainty

Research in neural networks in the field of computer vision has achieved remarkable accuracy for point estimation. However, the uncertainty in the estimation is rarely addressed. Uncertainty quantification accompanied by point estimation can lead to a more informed decision, and even improve the prediction quality. In this work, we focus on uncertainty estimation in the domain of crowd counting. With increasing occurrences of heavily crowded events such as political rallies, protests, concerts, etc., automated crowd analysis is becoming an increasingly crucial task. The stakes can be very high in many of these real-world applications. We propose a scalable neural network framework with quantification of decomposed uncertainty using a bootstrap ensemble. We demonstrate that the proposed uncertainty quantification method provides additional insight to the crowd counting problem and is simple to implement. We also show that our proposed method exhibits the state of the art performances in many benchmark crowd counting datasets.Comment: Accepted in AAAI 2020 (Main Technical Track

siRNA knockdown of SPHK1 in vivo protects mice from systemic, type-I Allergy.

Systemic anaphylaxis is considered to be a typical immediate hypersensitivity response, determined by the activation of immune cells,
via antigen-induced aggregation of IgE-sensitized FcεRI cells. Perhaps most the important cells, in the immediate hypersensitivity responses, are mast cells. We have previously shown that SPHK1 plays a key role in the intracellular signaling pathways triggered by FceRI aggregation on human
mast cells. More recently, we performed a genome-wide gene expression profiling of human mast cells, sensitized with IgE alone, or stimulated by FcεRI aggregation. We found that sphingosine kinase 1 (SPHK1) was one
of genes activated at the earlier stages of mast cell activation, including during sensitization. Moreover, SPHK1 has been shown, by us and others, to be a key player in the intracellular signaling pathways triggered by
several immune-receptors, including fMLP, C5a, and Fcg- and Fcereceptors. Here we have investigated the in vivo role of SPHK1 in allergy, using a specific siRNA to knockdown SPHK1 in vivo. Our results support a role for
SPHK1 in the inflammatory responses that share clinical, immunological, and histological features of type I hypersensitivity. Thus, mice pretreated with the siRNA for SPHK1 were protected from the IgE mediated allergic
reactions including: temperature changes, histamine release, cytokine production, cell-adhesion molecule expression, and immune cell infiltration into the lungs

Synthetic Routes to Pyrroloiminoquinone Alkaloids. A Direct Synthesis of Makaluvamine C

Makaluvamine C is a pyrroloiminoquinone which has been isolated from marine sponges. This molecule has been synthesized in 13 steps from p-anisidine. The key steps in this synthesis include an intramolecular nucleophilic aromatic substitution mediated by potassiumtert-butoxide, the selective reduction of a dinitro ester using catalytic hydrogenation, and the novel use of Fremy\u27s salt to synthesize an iminoquinone from an amino phenol. The synthesis of makaluvamine C has been achieved from p-anisidine in 13.1% overall yield

The trypanosome transcriptome is remodelled during differentiation but displays limited responsiveness within life stages.

BACKGROUND: Trypanosomatids utilise polycistronic transcription for production of the vast majority of protein-coding mRNAs, which operates in the absence of gene-specific promoters. Resolution of nascent transcripts by polyadenylation and trans-splicing, together with specific rates of mRNA turnover, serve to generate steady state transcript levels that can differ in abundance across several orders of magnitude and can be developmentally regulated. We used a targeted oligonucleotide microarray, representing the strongly developmentally-regulated T. brucei membrane trafficking system and approximately 10% of the Trypanosoma brucei genome, to investigate both between-stage, or differentiation-dependent, transcriptome changes and within-stage flexibility in response to various challenges. RESULTS: 6% of the gene cohort are developmentally regulated, including several small GTPases, SNAREs, vesicle coat factors and protein kinases both consistent with and extending previous data. Therefore substantial differentiation-dependent remodeling of the trypanosome transcriptome is associated with membrane transport. Both the microarray and qRT-PCR were then used to analyse transcriptome changes resulting from specific gene over-expression, knockdown, altered culture conditions and chemical stress. Firstly, manipulation of Rab5 expression results in co-ordinate changes to clathrin protein expression levels and endocytotic activity, but no detectable changes to steady-state mRNA levels, which indicates that the effect is mediated post-transcriptionally. Secondly, knockdown of clathrin or the variant surface glycoprotein failed to perturb transcription. Thirdly, exposure to dithiothreitol or tunicamycin revealed no evidence for a classical unfolded protein response, mediated in higher eukaryotes by transcriptional changes. Finally, altered serum levels invoked little transcriptome alteration beyond changes to expression of ESAG6/7, the transferrin receptor. CONCLUSION: While trypanosomes regulate mRNA abundance to effect the major changes accompanying differentiation, a given differentiated state appears transcriptionally inflexible. The implications of the absence of a transcriptome response in trypanosomes for both virulence and models of life cycle progression are discussed.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Testing the Drosophila maternal haploid gene for functional divergence and a role in hybrid incompatibility

Crosses between Drosophila simulans females and Drosophila melanogaster males produce viable F1 sons and poorly viable F1 daughters. Unlike most hybrid incompatibilities, this hybrid incompatibility violates Haldane’s rule, the observation that incompatibilities preferentially affect the heterogametic sex. Furthermore, it has a different genetic basis than hybrid lethality in the reciprocal cross, with the causal allele in Drosophila melanogaster being a large species-specific block of complex satellite DNA on its X chromosome known as the 359-bp satellite, rather than a protein-coding locus. The causal allele(s) in Drosophila simulans are unknown but likely involve maternally expressed genes or factors since the F1 females die during early embryogenesis. The maternal haploid (mh) gene is an intriguing candidate because it is expressed maternally and its protein product localizes to the 359-bp repeat. We found that this gene has diverged extensively between Drosophila melanogaster and Drosophila simulans. This observation led to the hypothesis that Drosophila melanogaster mh may have coevolved with the 359-bp repeat and that hybrid incompatibility thus results from the absence of a coevolved mh allele in Drosophila simulans. We tested for the functional divergence of mh by creating matched transformants of Drosophila melanogaster and Drosophila simulans orthologs in both Drosophila melanogaster and Drosophila simulans strains. Surprisingly, we find that Drosophila simulans mh fully complements the female sterile phenotype of Drosophila melanogaster mh mutations. Contrary to our hypothesis, we find no evidence that adding a Drosophila melanogaster mh gene to Drosophila simulans increases hybrid viability

Association between primary hypothyroidism and metabolic syndrome and the role of C reactive protein: a cross–sectional study from South India

<p>Abstract</p> <p>Background</p> <p>Hypothyroidism (sub-clinical and overt) and metabolic syndrome are recognized risk factors for atherosclerotic cardiovascular disease. This study is an effort to identify the proposed association between these two disease entities and the risk factors involved in this association.</p> <p>Methods</p> <p>A cross – sectional study from a tertiary care teaching hospital in Chennai city, South India. 420 patients with metabolic syndrome (NCEP – ATP III criteria) were included in the study group. 406 appropriately age and sex matched controls having no features of metabolic syndrome (0 out of the 5 criteria) were compared with the study group. The study extended over a 5 year period. TSH, FT4 were measured for both the groups using electrochemiluminescence immuno assay. HsCRP was measured for all the patients in the study group. The baseline characteristics between the groups were compared with Student's't' test. Chi-square test was used to analyze the association between metabolic syndrome and hypothyroidism (overt and sub-clinical). Logistic regression analysis was applied to identify the association between hypothyroidism and the patient characteristics in the study group.</p> <p>Results</p> <p>Of the 420 patients in the study group, 240 were females (57.1%), 180 were males (42.9%) with mean age 51 ± 9.4 years. Of the 406 patients in the control group, 216 were females (53.2%), 190 males (46.8%) with mean age 49 ± 11.2 years. In the study group, 92 had sub-clinical hypothyroidism (SCH) (21.9%), 31 were overtly hypothyroid (7.4%) and 297 were euthyroid (70.7%). In the control group 27 patients had sub-clinical hypothyroidism (6.6%), 9 patients had overt hypothyroidism (2.2%) and 370 patients were euthyroid (91.2%). On comparison SCH (P < 0.001) and overt hypothyroidism (P < 0.001) were significantly associated with the study group as compared to the control group. Logistic regression analysis recognized the association between female gender (P = 0.021) and HsCRP (P = 0.014) with sub-clinical hypothyroidism and female gender (P = 0.01) with overt hypothyroidism in the study group.</p> <p>Conclusion</p> <p>Hypothyroidism is associated with metabolic syndrome and females are more at risk. Metabolic syndrome patients with a raised HsCRP are at significant risk of having sub-clinical hypothyroidism.</p