Learning Using Privileged Information for Food Recognition

10.1145/3343031.3350870ACM MM 2019557-56

Heterogeneous Fusion of Semantic and Collaborative Information for Visually-Aware Food Recommendation

10.1145/3394171.3413598ACM Multimedia 202

Longitudinal analyses of CLL in mice identify leukemia-related clonal changes including a Myc gain predicting poor outcome in patients

Chronic lymphocytic leukemia (CLL) is a B-cell malignancy mainly occurring at an advanced age with no single major genetic driver. Transgenic expression of TCL1 in B cells leads after a long latency to a CLL-like disease in aged Eµ-TCL1 mice suggesting that TCL1 overexpression is not sufficient for full leukemic transformation. In search for secondary genetic events and to elucidate the clonal evolution of CLL, we performed whole exome and B-cell receptor sequencing of longitudinal leukemia samples of Eµ-TCL1 mice. We observed a B-cell receptor stereotypy, as described in patients, confirming that CLL is an antigen-driven disease. Deep sequencing showed that leukemia in Eµ-TCL1 mice is mostly monoclonal. Rare oligoclonality was associated with inability of tumors to develop disease upon adoptive transfer in mice. In addition, we identified clonal changes and a sequential acquisition of mutations with known relevance in CLL, which highlights the genetic similarities and therefore, suitability of the Eµ-TCL1 mouse model for progressive CLL. Among them, a recurrent gain of chromosome 15, where Myc is located, was identified in almost all tumors in Eµ-TCL1 mice. Interestingly, amplification of 8q24, the chromosomal region containing MYC in humans, was associated with worse outcome of patients with CLL

Chd7 is indispensable for mammalian brain development through activation of a neuronal differentiation programme.

Mutations in chromatin modifier genes are frequently associated with neurodevelopmental diseases. We herein demonstrate that the chromodomain helicase DNA-binding protein 7 (Chd7), frequently associated with CHARGE syndrome, is indispensable for normal cerebellar development. Genetic inactivation of Chd7 in cerebellar granule neuron progenitors leads to cerebellar hypoplasia in mice, due to the impairment of granule neuron differentiation, induction of apoptosis and abnormal localization of Purkinje cells, which closely recapitulates known clinical features in the cerebella of CHARGE patients. Combinatory molecular analyses reveal that Chd7 is required for the maintenance of open chromatin and thus activation of genes essential for granule neuron differentiation. We further demonstrate that both Chd7 and Top2b are necessary for the transcription of a set of long neuronal genes in cerebellar granule neurons. Altogether, our comprehensive analyses reveal a mechanism with chromatin remodellers governing brain development via controlling a core transcriptional programme for cell-specific differentiation

Devastating Decline of Forest Elephants in Central Africa.

African forest elephants– taxonomically and functionally unique–are being poached at accelerating rates, but we lack range-wide information on the repercussions. Analysis of the largest survey dataset ever assembled for forest elephants (80 foot-surveys; covering 13,000 km; 91,600 person-days of fieldwork) revealed that population size declined by ca. 62% between 2002–2011, and the taxon lost 30% of its geographical range. The population is now less than 10% of its potential size, occupying less than 25% of its potential range. High human population density, hunting intensity, absence of law enforcement, poor governance, and proximity to expanding infrastructure are the strongest predictors of decline. To save the remaining African forest elephants, illegal poaching for ivory and encroachment into core elephant habitat must be stopped. In addition, the international demand for ivory, which fuels illegal trade, must be dramatically reduced

Estimated change in elephant dung density (/km²) distribution during 2002–2011 across the Central African forests.

<p>Results are shown as a percentage of the total area of potential elephant habitat overall (A & B) and by country (C & D) for the predictive model with variables: (A & C) survey year, Human Influence Index, corruption and the presence/absence of guards, and (B & D) survey year, proximity to road, human population density, corruption and the presence/absence of guards. The dung density (per km²) intervals are unequal and correspond to the following elephant population categories: extremely low density (0–100), very low (100–250), low (250–500), medium (500–1,000), high (1,000–3,000) and very high (3,000–7,500). With the loss of very high elephant populations in 2011, there is a significant shift into the lower density intervals over the nine years.</p

Elephant dung density and range reduction across the Central African forests.

<p>Predictions are shown for (A) 2002 and (B) 2011 for the model with variables: survey year∧, Human Influence Index***, corruption*** and the presence/absence of guards***, and (C) 2002 and (D) 2011 for the model with variables: survey year∧, proximity to road∧, human population density***, corruption*** and the presence/absence of guards*** (P-values are: ‘***’ <0.001 and ‘∧’ <0.1). Increasingly darker shades of green correspond to higher densities, grey represents extremely low elephant density range (the first interval: 0–100 elephant dung piles/km²) and white is non-habitat (80 survey sites outlined in red). Cutpoints are: 0; 100; 250; 500; 1,000; 1,500; 3,000; 5,000; and 7,500 dung piles/km². Countries 1–5 are: Cameroon; Central African Republic; Republic of Congo; DRC; Gabon.</p