The fly pharyngeal sense organs lie at the transition between external and internal nutrient sensing mechanisms. Here, we investigate the function of pharyngeal sweet gustatory receptor neurons (GRNs), demonstrating that they express a subset of the nine previously identified sweet receptors and respond to stimulation with a panel of sweet compounds. We show that pox-neuro (poxn) mutants lacking taste function in the legs and labial palps have intact pharyngeal sweet taste, which is both necessary and sufficient to drive preferred consumption of sweet compounds by prolonging ingestion. Moreover, flies putatively lacking all sweet taste show little preference for nutritive or non-nutritive sugars in a short-term feeding assay. Together, our data demonstrate that pharyngeal sense organs play an important role in directing sustained consumption of sweet compounds, and suggest that post-ingestive sugar sensing does not effectively drive food choice in a simple short-term feeding paradigm.

Biomedical signal monitoring systems have been rapidly advanced with electronic and information technologies in recent years. However, most of the existing physiological signal monitoring systems can only record the signals without the capability of automatic analysis. In this paper, we proposed a novel brain-computer interface (BCI) system that can acquire and analyze electroencephalogram (EEG) signals in real-time to monitor human physiological as well as cognitive states, and, in turn, provide warning signals to the users when needed. The BCI system consists of a four-channel biosignal acquisition/amplification module, a wireless transmission module, a dual-core signal processing unit, and a host system for display and storage. The embedded dual-core processing system with multitask scheduling capability was proposed to acquire and process the input EEG signals in real time. In addition, the wireless transmission module, which eliminates the inconvenience of wiring, can be switched between radio frequency (RF) and Bluetooth according to the transmission distance. Finally, the real-time EEG-based drowsiness monitoring and warning algorithms were implemented and integrated into the system to close the loop of the BCI system. The practical online testing demonstrates the feasibility of using the proposed system with the ability of real-time processing, automatic analysis, and online warning feedback in real-world operation and living environments.

SUMMARY The Drosophila pharyngeal taste organs are poorly characterized despite their location at important sites for monitoring food quality. Functional analysis of pharyngeal neurons has been hindered by the paucity of molecular tools to manipulate them, as well as their relative inaccessibility for neurophysiological investigations. Here, we generate receptor-to-neuron maps of all three pharyngeal taste organs by performing a comprehensive chemoreceptor-GAL4/LexA expression analysis. The organization of pharyngeal neurons reveals similarities and distinctions in receptor repertoires and neuronal groupings compared to external taste neurons. We validate the mapping results by pinpointing a single pharyngeal neuron required for feeding avoidance of L-canavanine. Inducible activation of pharyngeal taste neurons reveals functional differences between external and internal taste neurons and functional subdivision within pharyngeal sweet neurons. Our results provide road maps of pharyngeal taste organs in an insect model system for probing the role of these understudied neurons in controlling feeding behaviors.

miRNAs have emerged as master regulators of cancer-related events. miRNA dysregulation also occurs in Kaposi sarcoma (KS). Exploring the roles of KS-associated miRNAs should help to identify novel angiogenesis and lymphangiogenesis pathways. In the present study, we show that Kaposi sarcoma-associated herpesvirus (KSHV), the etiological agent of KS, induces global miRNA changes in lymphatic endothelial cells (LECs). Specifically, the miR-221/miR-222 cluster is down-regulated, whereas miR-31 is upregulated. Both latent nuclear antigen (LANA) and Kaposin B repress the expression of the miR-221/miR-222 cluster, which results in an increase of endothelial cell (EC) migration. In contrast, miR-31 stimulates EC migration, so depletion of miR-31 in KSHV-transformed ECs reduces cell motility. Analysis of the putative miRNA targets among KSHV-affected genes showed that ETS2 and ETS1 are the downstream targets of miR-221 and miR-222, respectively. FAT4 is one of the direct targets of miR-31. Overexpression of ETS1 or ETS2 alone is sufficient to induce EC migration, whereas a reduction in FAT4 enhances EC motility. Our results show that KSHV regulates multiple miRNAmRNA networks to enhance EC motility, which eventually contributes to KS progression by promoting the spread of malignant KS progenitor cells. Targeting IntroductionKaposi sarcoma-associated herpesvirus (KSHV) was identified in 1994. 1 KSHV is also associated with 2 other human B-cell leukemias, primary effusion lymphoma (PEL) and multicentric Castleman disease. 2 Kaposi sarcoma (KS) is one of the few human cancers derived from a lymphatic endothelial cell (LEC) lineage, 3,4 and typically appears as colored lesions or patches on the skin, although it can spread to internal organs. 2 This disease has been recognized as a highly disseminated and angiogenic tumor. 4 Analyzing KSHV clonality at different stages of KS has shown that KS begins as a polyclonal disease and then evolves into a mono/oligoclonal disease involving infected spindle cells. 5 This model therefore implies that the spreading of a few malignant spindle cells in patients' bodies occurs during tumor progression. Moreover, distal metastasis, such as pulmonary KS, can be observed in AIDS-KS patients and causes diffused lung disease. Tumor cells of KSHV-associated B-cell neoplasias (PEL and multicentric Castleman disease) are also able to migrate into body cavities. 6 The ability of KSHV to induce cell migration and invasion is therefore important to disease progression.In vitro, KSHV infects both micro-and macrovascular endothelial cells (ECs), and these cells are useful when studying the role of KSHV in the pathogenesis of KS. 7,8 KSHV has also become a powerful tool that aids in the study of EC biology. 9 KSHV infects both LECs and blood vessel ECs (BECs) of microvascular origin in vitro. 3,4 After infection, KSHV stimulates EC invasiveness by inducing extracellular matrix metalloproteinases (MMPs) such as MMP-1, MMP-2, and MMP-9. 10 Because the majority of cells in KS lesions and in KSHV-infected...

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