A privacy-preserving method using secret key for convolutional neural network-based speech classification

In this paper, we propose a privacy-preserving method with a secret key for convolutional neural network (CNN)-based speech classification tasks. Recently, many methods related to privacy preservation have been developed in image classification research fields. In contrast, in speech classification research fields, little research has considered these risks. To promote research on privacy preservation for speech classification, we provide an encryption method with a secret key in CNN-based speech classification systems. The encryption method is based on a random matrix with an invertible inverse. The encrypted speech data with a correct key can be accepted by a model with an encrypted kernel generated using an inverse matrix of a random matrix. Whereas the encrypted speech data is strongly distorted, the classification tasks can be correctly performed when a correct key is provided. Additionally, in this paper, we evaluate the difficulty of reconstructing the original information from the encrypted spectrograms and waveforms. In our experiments, the proposed encryption methods are performed in automatic speech recognition~(ASR) and automatic speaker verification~(ASV) tasks. The results show that the encrypted data can be used completely the same as the original data when a correct secret key is provided in the transformer-based ASR and x-vector-based ASV with self-supervised front-end systems. The robustness of the encrypted data against reconstruction attacks is also illustrated.Comment: To appear in the 31st European Signal Processing Conference (EUSIPCO 2023

Extra-embryonic endoderm cells derived from ES cells induced by GATA Factors acquire the character of XEN cells

<p>Abstract</p> <p>Background</p> <p>Three types of cell lines have been established from mouse blastocysts: embryonic stem (ES) cells, trophoblast stem (TS) cells, and extra-embryonic endoderm (XEN) cells, which have the potential to differentiate into their respective cognate lineages. ES cells can differentiate <it>in vitro </it>not only into somatic cell lineages but into extra-embryonic lineages, including trophectoderm and extra-embryonic endoderm (ExEn) as well. TS cells can be established from ES cells by the artificial repression of <it>Oct3/4 </it>or the upregulation of <it>Cdx2 </it>in the presence of FGF4 on feeder cells. The relationship between these embryo-derived XEN cells and ES cell-derived ExEn cell lines remains unclear, although we have previously reported that overexpression of <it>Gata4 </it>or <it>Gata6 </it>induces differentiation of mouse ES cells into extra-embryonic endoderm in vitro.</p> <p>Results</p> <p>A system in which GATA factors were conditionally activated revealed that the cells continue to proliferate while expressing a set of extra-embryonic endoderm markers, and, following injection into blastocysts, contribute only to the extra-embryonic endoderm lineage <it>in vivo</it>. Although the <it>in vivo </it>contribution is limited to cells of parietal endoderm lineage, Gata-induced extra-embryonic endoderm cells (gExEn) can be induced to differentiate into visceral endoderm-like cells <it>in vitro </it>by repression of <it>Gata6</it>. During early passage, the propagation of gExEn cells is dependent on the expression of the <it>Gata6 </it>transgene. These cells, however, lose this dependency following establishment of endogenous <it>Gata6 </it>expression.</p> <p>Conclusion</p> <p>We show here that Gata-induced extra-embryonic endoderm cells derived from ES cells mimic the character of XEN cells. These findings indicate that Gata transcription factors are sufficient for the derivation and propagation of XEN-like extra-embryonic endoderm cells from ES cells.</p

Sox7 is dispensable for primitive endoderm differentiation from mouse ES cells

Abstract Background Primitive endoderm is a cell lineage segregated from the epiblast in the blastocyst and gives rise to parietal and visceral endoderm. Sox7 is a member of the SoxF gene family that is specifically expressed in primitive endoderm in the late blastocyst, although its function in this cell lineage remains unclear. Results Here we characterize the function of Sox7 in primitive endoderm differentiation using mouse embryonic stem (ES) cells as a model system. We show that ectopic expression of Sox7 in ES cells has a marginal effect on triggering differentiation into primitive endoderm-like cells. We also show that targeted disruption of Sox7 in ES cells does not affect differentiation into primitive endoderm cells in embryoid body formation as well as by forced expression of Gata6. Conclusions These data indicate that Sox7 function is supplementary and not essential for this differentiation from ES cells

Sox7 is dispensable for primitive endoderm differentiation from mouse ES cells.

BACKGROUND: Primitive endoderm is a cell lineage segregated from the epiblast in the blastocyst and gives rise to parietal and visceral endoderm. Sox7 is a member of the SoxF gene family that is specifically expressed in primitive endoderm in the late blastocyst, although its function in this cell lineage remains unclear. RESULTS: Here we characterize the function of Sox7 in primitive endoderm differentiation using mouse embryonic stem (ES) cells as a model system. We show that ectopic expression of Sox7 in ES cells has a marginal effect on triggering differentiation into primitive endoderm-like cells. We also show that targeted disruption of Sox7 in ES cells does not affect differentiation into primitive endoderm cells in embryoid body formation as well as by forced expression of Gata6. CONCLUSIONS: These data indicate that Sox7 function is supplementary and not essential for this differentiation from ES cells

Hemodynamic and autonomic response to acute hemorrhage in streptozotocin-induced diabetic rats

<p>Abstract</p> <p>Background</p> <p>The various autonomic control systems lead to characteristic changes in heart rate (HR) and blood pressure (BP) during acute hemorrhage. However, cardiovascular autonomic neuropathy due to diabetes mellitus may interfere with the normal compensation for hemorrhage.</p> <p>Materials and methods</p> <p>A controlled graded bleeding (6 - 36% loss of estimated total blood volume: ETBV) was performed in streptozotocin-induced diabetic rats (STZ rats) under a conscious state. Hemodynamic and autonomic responses to acute hemorrhage were examined using analysis of BP-HR variability. The effects of dextran treatment after hemorrhage were also examined.</p> <p>Results</p> <p>A significant reduction in mean arterial pressure began at 12% ETBV loss in STZ rats and 18% in the control rats, respectively. When blood loss reached 18% of TEBV, the decrease in HR was prominent in STD rats due to the activation of a parasympathetic drive, as indicated by the increase in high frequency (HF; 0.75~3.0 Hz) power in HR variability, while in the control rats this response was not observed. The administration of dextran prevented the activation of the parasympathetic drive in STZ rats during hemorrhaging. In the control rats, the dextran treatment sustained the initial increase in HR with reduced HF power in HR variability.</p> <p>Conclusion</p> <p>STZ rats showed different hemodynamic and autonomic responses to acute hemorrhage from the control rats. STZ rats were prone to develop bradycardiac hypotension characterized by marked parasympathetic activation during hemorrhaging. This finding suggests enhancement of the Bezold-Jarisch reflex in STZ rats. Dextran treatment to maintain a normovolemic hemorrhage state inhibits this reflex.</p

Premedication with midazolam in intellectually disabled dental patients: intramuscular or oral administration? A retrospective study

Background: The use of midazolam for dental care in patients with intellectual disability is poorly documented. The purpose of this study was to determine which method of premedication is more effective for these patients, 0.15 mg/kg of intramuscular midazolam or 0.3 mg/kg of oral midazolam. Material and Methods: This study was designed and implemented as a non-randomized retrospective study. The study population was composed of patients with intellectual disability who required dental treatment under ambulatory general anesthesia from August 2009 through April 2013. Patients were administered 0.15 mg/kg of midazolam intramuscularly (Group IM) or 0.3 mg/kg orally (Group PO). The predictor variable was the method of midazolam administration. The outcome variables measured were Observer’s Assessment of Alertness/ Sedation (OAA/S) Scale scores, the level of cooperation when entering the operation room and for venous cannulation, post-anesthetic agitation and recovery time. Results: Midazolam was administered intramuscularly in 23 patients and orally in 21 patients. More patients were successfully sedated with no resistance behavior during venous cannulation in Group PO than in Group IM ( p =0.034). There were no differences in demographic data and other variables between the groups. Conclusions: The results of this study suggest that oral premedication with 0.3 mg/kg of midazolam is more effective than 0.15 mg/kg of midazolam administered intramuscularly, in terms of patient resistance to venous cannulation. If both oral and intramuscular routes of midazolam are acceptable in intellectually disabled patients, the oral route is recommended

Rex1/Zfp42 is dispensable for pluripotency in mouse ES cells

Research articl

The evolutionally-conserved function of group B1 Sox family members confers the unique role of Sox2 in mouse ES cells.

BACKGROUND: In mouse ES cells, the function of Sox2 is essential for the maintenance of pluripotency. Since the Sox-family of transcription factors are well conserved in the animal kingdom, addressing the evolutionary origin of Sox2 function in pluripotent stem cells is intriguing from the perspective of understanding the origin of pluripotency. RESULTS: Here we approach this question using a functional complementation assay in inducible Sox2-null ES cells. Assaying mouse Sox proteins from different Groups, we found that only Group B1 and Group G proteins were able to support pluripotency. Interestingly, invertebrate homologs of mammalian Group B1 Sox proteins were able to replace the pluripotency-associated function of mouse Sox2. Moreover, the mouse ES cells rescued by the Drosophila SoxNeuro protein are able to contribute to chimeric embryos. CONCLUSIONS: These data indicate that the function of mouse Sox2 supporting pluripotency is based on an evolutionally conserved activity of the Group B1 Sox family. Since pluripotent stem cell population in developmental process could be regarded as the evolutional novelty in vertebrates, it could be regarded as a co-optional use of their evolutionally conserved function

Pancreatic β Cell–specific Expression of Thioredoxin, an Antioxidative and Antiapoptotic Protein, Prevents Autoimmune and Streptozotocin-induced Diabetes

The cytotoxicity of reactive oxygen intermediates (ROIs) has been implicated in the destruction of pancreatic β cells in insulin-dependent diabetes mellitus (IDDM). Thioredoxin (TRX), a redox (reduction/oxidation)-active protein, has recently been shown to protect cells from oxidative stress and apoptosis. To elucidate the roles of oxidative stress in the development of autoimmune diabetes in vivo, we produced nonobese diabetic transgenic mice that overexpress TRX in their pancreatic β cells. In these transgenic mice, the incidence of diabetes was markedly reduced, whereas the development of insulitis was not prevented. Moreover, induction of diabetes by streptozotocin, an ROI-generating agent, was also attenuated by TRX overexpression in β cells. This is the first direct demonstration that an antioxidative and antiapoptotic protein protects β cells in vivo against both autoimmune and drug-induced diabetes. Our results strongly suggest that oxidative stress plays an essential role in the destruction of β cells by infiltrating inflammatory cells in IDDM