Demonstration of a Bosonic Quantum Classifier with Data Reuploading.

In a single qubit system, a universal quantum classifier can be realized using the data reuploading technique. In this study, we propose a new quantum classifier applying this technique to bosonic systems and successfully demonstrate it using a silicon-based photonic integrated circuit. We established a theory of quantum machine learning algorithm applicable to bosonic systems and implemented a programmable optical circuit combined with an interferometer. Learning and classification using part of the implemented optical quantum circuit with uncorrelated two photons resulted in a classification with a success probability of 94±0.8% in the proof of principle experiment. As this method can be applied to an arbitrary two-mode N-photon system, further development of optical quantum classifiers, such as extensions to quantum entangled and multiphoton states, is expected in the future.

Apparent diffusion coefficient (ADC) values of serous, endometrioid, and clear cell carcinoma of the ovary: pathological correlation.

BACKGROUND: Primary epithelial ovarian cancer is divided into several subtypes. The relationships between apparent diffusion coefficient (ADC) values and their subtypes have not yet been established. PURPOSE: To investigate whether ADC values of epithelial ovarian cancer vary according to histologic tumor cellularity and evaluate the difference of clear cell carcinoma (CCC), high-grade serous carcinoma (HGSC), and endometrioid carcinoma (EC). MATERIAL AND METHODS: This retrospective study included 51 cases of epithelial ovarian cancer (17 CCC, 20 HGSC, and 14 EC) identified by magnetic resonance imaging with pathological confirmation. All patients underwent diffusion-weighted imaging and the ADC values of lesions were measured. We counted the tumor cells in three high-power fields and calculated the average for each case. The Spearman's correlation coefficient test was used to analyze correlation between ADC values and tumor cellularity. The ADC values of HGSC, EC, and CCC were compared using the Steel-Dwass test. RESULTS: The ADC values of all cases were significantly inversely correlated with tumor cellularity (rs = -0.761; P < 0.001). The mean ± SD ADC values (×10-3 mm2/s) of CCC, HGSC, and EC were 1.24 ± 0.17 (range 0.98--1.65), 0.84 ± 0.10 (range 0.67--1.06), and 0.84 ± 0.10 (range 0.67--1.07). The mean ± SD tumor cellularity of CCC, HGSC, and EC was 162.88 ± 63.28 (range 90.33--305.67), 440.60 ± 119.86 (range 204.67--655.67), and 461.02 ± 81.86 (range 333.33--602.33). CONCLUSION: There is a significant inverse correlation between ADC values and tumor cellularity in epithelial ovarian cancer. The mean ADC value of CCC was higher than those of HGSC and EC, seemingly due to the low cellularity of CCC.

Observation of nonlinear interference on a silicon photonic chip.

Photonic integrated circuits represent a promising platform for applying quantum information science to areas such as quantum computation, quantum communication, and quantum metrology. While the linear optical approach has greatly contributed to this field, it is often possible to improve the functionality and scalability by making use of nonlinear processes. One interesting phenomenon is the interference between two nonlinear optical processes, where the interference occurs by removing the information as to which of two processes have occurred. In this Letter, we demonstrate a nonlinear interferometer in the pair-photon generation regime by using spontaneous four-wave mixing in an integrated silicon photonic chip. We observe a nonlinear interference in the production rate of photon pairs generated from two different four-wave mixing waveguides. We obtain an interference visibility of 96.8%. This work shows the possibility of integrating and controlling nonlinear-optical-interference components for silicon quantum photonics.

Nuclear inverse polarity papillary lesions lacking myoepithelial cells: A report of two cases.

Here, cases of a 68- (Case 1) and a 44-year-old (Case 2) female are presented. They had an abnormality in the breast, and came to our hospital for further examination and treatment. Radiologically, malignancy could not completely excluded so breast excision was performed. Histologically, both cases revealed papillary neoplastic lesions lined by fibrovascular core and nuclear inverse polarity without atypia. Loss of myoepithelial cells was observed by HE, p63, and calponin. Previous report indicate CK5/6, ER, p63 and MUC3 are important for distinguishing between papillary lesions according to the differential index (based on Allred score) of ([ER total score] + [MUC3 total score])/([CK5/6 total score] + [p63 total score] + 1). Based on this analysis, our two cases had benign lesions. However, based on immunopositivity for cell-cycle marker Cyclin-D1, Case 1 was negative, and Case 2 was about 70% positive. Additionally, the Ki-67 index was <1% in both cases, and no evidence of disease was observed after a maximum 62 months of follow-up in both cases, despite lack of additional treatment. Thus, we propose that lack of myoepithelial cells in papillary lesions do not necessarily indicate malignancy and are thought to be, at the most, uncertain malignant potential.

Quantum interference of pulsed time-bin entanglement generated from silicon ring resonator.

We demonstrate a pulsed operation of an entangled photon pair source that is based on a silicon ring resonator. Time-bin entangled photon pairs at telecommunication wavelengths are generated via spontaneous four-wave mixing, which is excited by a pulsed pump laser. The entanglement between the generated photon pair is analyzed by using asymmetric Mach-Zehnder interferometers followed by single-photon detectors, resulting in non-classical interference with a visibility exceeding a classical limit. The reason for the degradation of the interference visibility is discussed using the theoretical model with experimental parameters. Our experimental results show successful pulsed generation of entanglement, which represents an important step towards a synchronized quantum network based on silicon photonics.

Inferior Epigastric Artery Injury due to Femoral Venipuncture for Neuroendovascular Intervention: Two Cases Requiring Transcatheter Arterial Embolization.

Objective: Injury to the inferior epigastric artery (IEA) caused by femoral puncture may lead to retroperitoneal hematoma. We report on two cases of IEA injury due to femoral venipuncture for neuroendovascular intervention that resulted in hemorrhagic shock and required transcatheter arterial embolization. Case Presentations: A 67-year-old woman and a 71-year-old man receiving dual antiplatelet therapy sustained injury to a branch of the IEA in the process of right femoral venipuncture for neuroendovascular intervention. In both cases, stent placement in the intracranial artery was accomplished as intended with systemic heparinization throughout the procedure; however, the patients became hypotensive during the procedure, and contrast-enhanced CT scans taken after the stenting revealed extravasation of contrast from the IEA and retroperitoneal hematoma. Transcatheter arterial embolization of the bleeding branch of the IEA was performed with the left femoral approach, and subsequent angiography confirmed the disappearance of the extravasation of contrast. Conclusion: Femoral venipuncture for neuroendovascular intervention in patients receiving antithrombotic agents may cause IEA injury requiring transcatheter arterial embolization. The risk of IEA injury may be reduced by using the femoral head as a reference, performing ultrasound-guided puncture, and confirming the course of the IEA by femoral angiography before venipuncture.

The common aspects of pathophysiolgy of alcoholism and depression.

Recent biological studies suggest the existence of the common pathophysiological aspects in alcoholism and depression. Postmortem studies have revealed the impairment of cAMP signaling in the patients with alcoholism. The similar alteration of cAMP signaling was also reported in postmortem brains of depressed patients. In this study, we supported the notion that neurogenesis would be essential in pathophysiology of both alcoholism and depression. Alcohol affected the function of neural stem cells (NSCs) and decreased neurogenesis at doses which did not affects cell survival, and treatment of antidepressant or moodstabilizer rescued the alcohol-induced suppression of neurogenesis. As the key mechanism of NSC differentiation change by ethanol and psychotropics, we focused on the transcriptional repressor, NRSF/REST activity change. Our in vitro studies demonstrated the NRSF/REST activation by ethanol and suppressive effect of antidepressants and lithium against its activation by ethanol. We further described the ERK reduction and ER stress in the cellular mechanism of NRSF/REST activation. All these findings suggested that cAMP-CREB cascade reduction and NRSF/REST activation may be common underlying mechanisms in the pathophysiology of alcoholism and depression.

Ni(0)-Catalyzed Three-Component Coupling Reaction of Tetrafluoroethylene and N-Sulfonyl-Substituted Imines with Silanes via Aza-Nickelacycles.

A nickel-catalyzed three-component coupling reaction of tetrafluoroethylene (TFE) and N-sulfonyl-substituted imines with silanes that furnishes a variety of fluorine-containing amines is disclosed. Stoichiometric experiments revealed that the aza-nickelacycles generated upon oxidative cyclization of TFE and N-sulfonyl-substituted imines on Ni(0) were identified as the key intermediates in this catalytic reaction. A single-crystal X-ray diffraction analysis of such an aza-nickelacycle revealed that the O atom of the N-sulfonyl group stabilizes the key intermediate via coordination to the nickel center.

Neuroprotective effects of Yi-Gan San against beta amyloid-induced cytotoxicity on rat cortical neurons.

INTRODUCTION: Recent clinical studies have demonstrated that Yi-Gan San (YGS, Yokukan-San in Japanese), a Chinese herbal medicine, alleviates various dementia-related symptoms. However, Chinese herbal medicines have rarely been investigated scientifically and the underlying mechanism of YGS remains uncertain. In this study, we investigated the effect of YGS on beta amyloid protein (Abeta)-induced cytotoxicity in a primary culture of rat cortical neurons. METHODS: Cortical neurons prepared from rat embryos were exposed to Abeta in the presence or absence of YGS. The protective effect of YGS was measured as the % of control (unexposed neurons) by using MTT assay and LDH assay. RESULTS: Abeta significantly decreased the number of surviving cortical neurons at a dose of 20 microM and higher. In the presence of 20 microM Abeta, YGS concentrations of 10(-5) g/L (W/V) and higher significantly increased the number of viable neurons. CONCLUSION: Our study demonstrated a neuroprotective effect of Yi-Gan San against Abeta-induced cytotoxicity. Since according to traditional herbal medicine beliefs, YGS most likely exerts its clinical effects not through a single constituent but as a mixture of several herbal ingredients, the true mechanism of this neuroprotective action remains unclear. However, our results suggest that this Chinese herbal medicine might be a valuable treatment for clinical symptoms associated with dementia having fewer side effects and possible additional neuroprotective effects in the elderly.

[The analysis of impairment and repair of neural network by ethanol: in vitro and in vivo studies using neurons and neural stem cells].

Recent clinical neuroimaging studies have suggested the morphological brain changes occur and progress in the course of alcoholism and depression. The abnormality of neurogenesis has emerged as a potential epidemiological mechanism of these diseases. Previously, we have indicated the low dose of ethanol that could not influence on the survival of neurons and neural stem cell (NSC) suppress differentiation to neurons but glias through activation of neuron-restrictive silencing factor/repressor element-1 silencing transcription factor (NRSF/REST). We revealed the endoplasmic reticulum function and trophic factor signaling change implicated in this mechanism of ethanol action on NSC differentiation change. The analysis of potentials of psychotropic drugs on the ethanol-induced NSC function change may reveal the possible biological way of neural network impairment and its repair. Furthermore, the approach of using stem cells such as intravenous NSC transplantation can be a useful method to clarify the neural network reconstruction damaged by ethanol. The importance of interactive analysis of in vitro to in vivo should be documented for the pathophysiological understanding and new therapy development against alcohol-induced brain damage.

[Neural network abnormalities caused by alcohol: approach for repair using neural stem cells].

Recent clinical neuroimaging studies have revealed the possible relation between morphological brain changes, and memory, cognitive impairment in the course of alcoholism and depression. In the previous studies, we have been analyzing the mechanism of neural network disruption by ethanol using postmortem human brain and cultured cells, and identified the sensitive effect of ethanol on the neural stem cell (NSC) differentiation rather than the influence on neuronal cell survival. Furthermore, to develop a novel method for reconstruction of the neural network damaged by ethanol, we tried to analyze the usefulness of intravenous NSC transplantation in fetal alcohol syndrome spectrum disorder (FASD) model rats. In the in vitro studies, we have found the suppressive effect of ethanol on NSC differentiation to neurons, through alteration of transcription factor, CREB and NRSF/REST activities, by the cellular signaling cascade changes including trophic factors and endoplasmic reticulum (ER) function. In the in vivo studies, we have shown the effective migration of labeled NSCs into the brain of FASD model rats, and revealed the therapeutic potential of this transplantation for the treatment of anxiety/cognitive dysfunction and behavioral abnormalities in alcohol-induced brain neural network damage. We are going to the next step for analysis of transplanted NSC dynamics in the brain, which must play a pivotal role in the effective induction of behavioral recoveries.

Implementation of a quantum controlled-SWAP gate with photonic circuits.

Quantum information science addresses how the processing and transmission of information are affected by uniquely quantum mechanical phenomena. Combination of two-qubit gates has been used to realize quantum circuits, however, scalability is becoming a critical problem. The use of three-qubit gates may simplify the structure of quantum circuits dramatically. Among them, the controlled-SWAP (Fredkin) gates are essential since they can be directly applied to important protocols, e.g., error correction, fingerprinting, and optimal cloning. Here we report a realization of the Fredkin gate for photonic qubits. We achieve a fidelity of 0.85 in the computational basis and an output state fidelity of 0.81 for a 3-photon Greenberger-Horne-Zeilinger state. The estimated process fidelity of 0.77 indicates that our Fredkin gate can be applied to various quantum tasks.

An entanglement-enhanced microscope.

Among the applications of optical phase measurement, the differential interference contrast microscope is widely used for the evaluation of opaque materials or biological tissues. However, the signal-to-noise ratio for a given light intensity is limited by the standard quantum limit, which is critical for measurements where the probe light intensity is limited to avoid damaging the sample. The standard quantum limit can only be beaten by using N quantum correlated particles, with an improvement factor of √N. Here we report the demonstration of an entanglement-enhanced microscope, which is a confocal-type differential interference contrast microscope where an entangled photon pair (N=2) source is used for illumination. An image of a Q shape carved in relief on the glass surface is obtained with better visibility than with a classical light source. The signal-to-noise ratio is 1.35±0.12 times better than that limited by the standard quantum limit.

The role of neural stem cells for in vitro models of schizophrenia: neuroprotection via Akt/ERK signal regulation.

Recent neuroimaging studies have revealed progressive morphological brain changes during the course of schizophrenia, and the neurotrophic and neurogenetic effects of atypical antipsychotics are believed to prevent or retard these brain volume reductions. In addition to drug-induced neural stem cell (NSC) activation, transplantation of exogenous NSCs has been proposed as a possible approach to repair the damaged brain in psychiatric disease. NSC transplantation embraces not only neuron replacement but also enhanced neuroprotection of existing neurons with the goal of restoring the impaired brain. However, little is known about the cell-cell interactions of exogenous NSCs with existing neurons, or about their neuroprotective actions especially in psychiatric diseases. In the present study, we used cortical neuron cultures to examine the neurotrophism and neuroprotection of exogenous NSCs against the neuronal damage induced by exposure to the NMDA receptor antagonist, MK-801. We also investigated their role in serum/nutrient deprivation stress. The exogenous NSCs exerted neuroprotective effects against both types of apoptotic injuries considered as in vitro schizophrenic disease models. Exogenous NSCs also altered cellular survival signaling in injured neurons by indirect cell-cell contact in an injury-dependent manner. In MK-801 exposure, NSCs increased phosphorylated Akt (p-Akt) and ERK (p-ERK), both of which were reduced by this stress. While, in serum/nutrient deprivation, NSCs increased p-Akt, but decreased p-ERK which was increased by this damage. Our results demonstrate that exogenous NSCs have anti-apoptotic activities and can rescue cortical neurons by directing cellular survival signaling of neurons into the proper direction, without cell contact.

Effect of antidepressants on brain-derived neurotrophic factor (BDNF) release from platelets in the rats.

Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family, and enhances the growth and maintenance of several neuronal systems. In addition, BDNF may promote neurogenesis and protect against hippocampal volume loss in depressive disorders. Although first detected in brain, BDNF also exists in peripheral tissues and is mainly stored in platelets and circulates in blood. Recent reports indicate that serum BDNF levels in depressive patients are lower than in control subjects, and antidepressant treatment increases serum BDNF levels in responders. A single report suggests that decreased serum BDNF in major depression is related to mechanisms of platelet BDNF release; however, the mechanisms of changes in BDNF blood levels are still poorly understood. In the present study, we investigated the direct influence of antidepressants on BDNF release from platelets and their effects on serum levels. We used samples of washed platelets prepared from rat blood, and investigated the platelet BDNF release and serum BDNF concentration changes in response to adding antidepressants. We found that BDNF was dose-dependently released from platelets by direct treatment with various kinds of antidepressants in vitro, and serum BDNF concentration was also increased by intravenous antidepressant treatment. These results confirm that BDNF release from platelets is affected by antidepressants, which may relate to the circulating BDNF level change in peripheral blood. The response of BDNF release differs depending on the type and amount of antidepressants, making BDNF a serious candidate as a predictor of antidepressant treatment response.