The Impact of Counter-Rumor Strategy and Source on Non-Professional Investors' Judgments over Social Media

Non-professional investors often rely on information obtained from social media to make investment decisions. Extant literature has not examined the most effective strategy for the target company to counter the rumors so that investors will be more willing to continue investing in the target firm. Drawing on source credibility theory and the moral intensity model, I propose that the most effective strategy would vary given different agents who are selected to counter the rumor. After conducting a 2 x 3 (counter-rumor source x counter-rumor strategy) experiment with 272 non-professional investors recruited from Amazon Mechanical Turk, my study shows that when an internal agent (e.g., the CEO) acts as a counter-rumor source, shareholders are more willing to invest in the company when the internal agent utilizes a denial strategy rather than a reassociation or a questioning strategy. In contrast, when an external agent (e.g., a famous food blogger) serves as the counter-rumor source, the external agent can also use a questioning strategy in addition to a denial strategy to motivate shareholders to be more willing to invest in the company; however, the external agent still needs to avoid from engaging a reassociation strategy. Moderated serial-mediation analysis shows that the persuasiveness of the counter-rumor information and investors' perceived rumor intensity serially mediate the effect of counter-rumor source on investors' willingness to invest, and this effect is conditioned on the different strategy used to counter the rumor. Overall, the main effect of counter-rumor source suggests that external agents are perceived as more persuasive, which leads investors to perceive less rumor intensity, making them more willing to invest in the target company. The results of my paper can thus inform companies' social media policy

Law of Balance and Stationary Distribution of Stochastic Gradient Descent

The stochastic gradient descent (SGD) algorithm is the algorithm we use to train neural networks. However, it remains poorly understood how the SGD navigates the highly nonlinear and degenerate loss landscape of a neural network. In this work, we prove that the minibatch noise of SGD regularizes the solution towards a balanced solution whenever the loss function contains a rescaling symmetry. Because the difference between a simple diffusion process and SGD dynamics is the most significant when symmetries are present, our theory implies that the loss function symmetries constitute an essential probe of how SGD works. We then apply this result to derive the stationary distribution of stochastic gradient flow for a diagonal linear network with arbitrary depth and width. The stationary distribution exhibits complicated nonlinear phenomena such as phase transitions, broken ergodicity, and fluctuation inversion. These phenomena are shown to exist uniquely in deep networks, implying a fundamental difference between deep and shallow models.Comment: Preprin

A Kinesin-13 Family Kinesin in Trypanosoma Brucei Regulates Cytokinesis and Cytoskeleton Morphogenesis by Promoting Microtubule Bundling

The early branching eukaryote Trypanosoma brucei divides uni-directionally along the longitudinal cell axis from the cell anterior toward the cell posterior, and the cleavage furrow ingresses along the cell division plane between the new and the old flagella of a dividing bi-flagellated cell. Regulation of cytokinesis in T. brucei involves actomyosin-independent machineries and trypanosome-specific signaling pathways, but the molecular mechanisms underlying cell division plane positioning remain poorly understood. Here we report a kinesin-13 family protein, KIN13-5, that functions downstream of FPRC in the cytokinesis regulatory pathway and determines cell division plane placement. KIN13-5 localizes to multiple cytoskeletal structures, interacts with FPRC, and depends on FPRC for localization to the site of cytokinesis initiation. Knockdown of KIN13-5 causes loss of microtubule bundling at both ends of the cell division plane, leading to mis-placement of the cleavage furrow and unequal cytokinesis, and at the posterior cell tip, causing the formation of a blunt posterior. In vitro biochemical assays demonstrate that KIN13-5 bundles microtubules, providing mechanistic insights into the role of KIN13-5 in cytokinesis and posterior morphogenesis. Altogether, KIN13-5 promotes microtubule bundle formation to ensure cleavage furrow placement and to maintain posterior cytoskeleton morphology in T. brucei

SGD with a Constant Large Learning Rate Can Converge to Local Maxima

Previous works on stochastic gradient descent (SGD) often focus on its success. In this work, we construct worst-case optimization problems illustrating that, when not in the regimes that the previous works often assume, SGD can exhibit many strange and potentially undesirable behaviors. Specifically, we construct landscapes and data distributions such that (1) SGD converges to local maxima, (2) SGD escapes saddle points arbitrarily slowly, (3) SGD prefers sharp minima over flat ones, and (4) AMSGrad converges to local maxima. We also realize results in a minimal neural network-like example. Our results highlight the importance of simultaneously analyzing the minibatch sampling, discrete-time updates rules, and realistic landscapes to understand the role of SGD in deep learning.Comment: ICLR 2022 Spotligh

The Microtubule Quartet Protein SNAP1 in Trypanosoma Brucei Facilitates Flagellum and Cell Division Plane Positioning by Promoting Basal Body Segregation

The unicellular protozoan Trypanosoma brucei has a single flagellum that is involved in cell motility, cell morphogenesis, and cell division. Inheritance of the newly assembled flagellum during the cell cycle requires its correct positioning, which depends on the faithful duplication or segregation of multiple flagellum-associated cytoskeletal structures, including the basal body, the flagellum attachment zone, and the hook complex. Along the flagellum attachment zone sites a set of four microtubules termed the microtubule quartet (MtQ), whose molecular function remains enigmatic. We recently reported that the MtQ-localized protein NHL1 interacts with the microtubule-binding protein TbSpef1 and regulates flagellum inheritance by promoting basal body rotation and segregation. Here, we identified a TbSpef1- and NHL1-associated protein named SNAP1, which co-localizes with NHL1 and TbSpef1 at the proximal portion of the MtQ, depends on TbSpef1 for localization and is required for NHL1 localization to the MtQ. Knockdown of SNAP1 impairs the rotation and segregation of the basal body, the elongation of the flagellum attachment zone filament, and the positioning of the newly assembled flagellum, thereby causing mis-placement of the cell division plane, a halt in cleavage furrow ingression, and an inhibition of cytokinesis completion. Together, these findings uncover a coordinating role of SNAP1 with TbSpef1 and NHL1 in facilitating flagellum positioning and cell division plane placement for the completion of cytokinesis

Primary spleen extranodal NK/T cell lymphoma, nasal type, with bone marrow involvement and CD30 positive expression: a case report and literature review

AIMS: Primay spleen NK/T cell lymphoma is very rare. We report a case of 39-years-old male of primary splenic NK/T cell lymphoma with bone marrow involvement and CD30 positive expression. CASE DESCRIPTION: The patient had high fever for 2 months, and CT scan revealed a diffuse splenomegaly without hepatomegaly. The diagnosis was established by splenectomy specimen and bone marrow biopsy. Normal spleen structure was destroyed by the diffusely infiltrated neoplastic cells, and one of the splenic hilar lymph nodes was involved. The lymphomatous cells were mainly medium-sized, mixed with small and large cells with pleomorphic nuclei and conspicuous nucleoli. Angiocentric growth pattern was present, with mitotic figures and apoptotic bodies easily being found. These neoplastic cells demonstrated a typical immunophenotype of CD2, CD3ε, CD7, CD4, CD56, TIA-1, Granzyme B, CD30 positive, and CD5, CD8, CD20, CD79a negative. The Epstein-Barr virus encoded RNAs (EBERs) genomes were also found in tumor cells by in situ hybridization, while no clonal rearrangement of the T cell receptor-γ genes (TCRG) was found. Biopsy of bone marrow revealed scattered atypical cells presented with a predominantly intrasinusoidal distribution. A diagnosis as primary spleen NK/T cell lymphoma, nasal type (ENKTL) with CD30 expression and bone marrow involvement was finally made. The patient received chemotherapy and was still alive 6 months after splenectomy. CLINICAL SIGNIFICANCE: Primary spleen ENKTL is very rare, it should be made with the combination of clinical feature, PET-CT image, and pathological characteristics, and should be distinguished from other lymphomas or leukemia involved in spleen. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/13000_2014_16

Editorial: Celebrating Microbial Diversity: The Many Cell Cycles of Eukaryotic Microbes.

Editorial on the Research Topic Celebrating Microbial Diversity: The Many Cell Cycles of Eukaryotic MicrobesCM: ERC research grant ‘Plasmocycle’. ZL: NIH R01 grant AI101437. MB: Swiss National Science Foundation 31003A_179321

An Essential Farnesylated Kinesin in Trypanosoma brucei

Kinesins are a family of motor proteins conserved throughout eukaryotes. In our present study we characterize a novel kinesin, KinesinCaaX, orthologs of which are only found in the kinetoplastids and not other eukaryotes. KinesinCaaX has the CVIM amino acids at the C-terminus, and CVIM was previously shown to be an ideal signal for protein farnesylation in T. brucei. In this study we show KinesinCaaX is farnesylated using radiolabeling studies and that farnesylation is dependent on the CVIM motif. Using RNA interference, we show KinesinCaaX is essential for T. brucei proliferation. Additionally RNAi KinesinCaaX depleted T. brucei are 4 fold more sensitive to the protein farneysltransferase (PFT) inhibitor LN-59, suggesting that KinesinCaaX is a target of PFT inhibitors' action to block proliferation of T. brucei. Using tetracycline-induced exogenous tagged KinesinCaaX and KinesinCVIMdeletion (non-farnesylated Kinesin) expression lines in T. brucei, we demonstrate KinesinCaaX is farnesylated in T. brucei cells and this farnesylation has functional effects. In cells expressing a CaaX-deleted version of Kinesin, the localization is more diffuse which suggests correct localization depends on farnesylation. Through our investigation of cell cycle, nucleus and kinetoplast quantitation and immunofluorescence assays an important role is suggested for KinesinCaaX in the separation of nuclei and kinetoplasts during and after they have been replicated. Taken together, our work suggests KinesinCaaX is a target of PFT inhibition of T. brucei cell proliferation and KinesinCaaX functions through both the motor and farnesyl groups