Margin status and histologic property both affect the prognosis of MFS. The former correlates with improved LRFS and translates into final survival benefits.

A nitridation treatment technology with a urea/ammonia complex nitrogen source improved resistive switching property in HfO2-based resistive random access memory (RRAM). The nitridation treatment produced a high performance and reliable device which results in superior endurance (more than 109 cycles) and a self-compliance effect. Thus, the current conduction mechanism changed due to defect passivation by nitrogen atoms in the HfO2 thin film. At a high resistance state (HRS), it transferred to Schottky emission from Poole-Frenkel in HfO2-based RRAM. At low resistance state (LRS), the current conduction mechanism was space charge limited current (SCLC) after the nitridation treatment, which suggests that the nitrogen atoms form Hf–N–Ox vacancy clusters (Vo +) which limit electron movement through the switching layer.

The biological brain has set a golden standard in computational efficiency, both due to its massive parallelism, and its ability to perform in-memory computing within the same ionic substrate. Ion-gated channels determine synaptic strength which is known to be a mechanism for memory storage, and the very same ions that pass through these gates encode data in the form of spikes. Communication, computation, and storage all occur within the same local medium. The brain's ability to perform in-memory processing within a unified ionic mechanism has driven many researchers to apply ion-driven non-volatile memories to emulate learning rules at the device-level. [1-12] The operating principles of resistive random access memory (RRAM) draw parallel with biological synapses. From a physical standpoint, the top electrode (TE) corresponds to a pre-synaptic terminal, the insulator layer acts as the substrate through which neurotransmitters are released, and the bottom electrode (BE) Biologically plausible computing systems require fine-grain tuning of analog synaptic characteristics. In this study, lithium-doped silicate resistive random access memory with a titanium nitride (TiN) electrode mimicking biological synapses is demonstrated. Biological plausibility of this RRAM device is thought to occur due to the low ionization energy of lithium ions, which enables controllable forming and filamentary retraction spontaneously or under an applied voltage. The TiN electrode can effectively store lithium ions, a principle widely adopted from battery construction, and allows state-dependent decay to be reliably achieved. As a result, this device offers multi-bit functionality and synaptic plasticity for simulating various strengths in neuronal connections. Both short-term memory and long-term memory are emulated across dynamical timescales. Spike-timing-dependent plasticity and paired-pulse facilitation are also demonstrated. These mechanisms are capable of self-pruning to generate efficient neural networks. Time-dependent resistance decay is observed for different conductance values, which mimics both biological and artificial memory pruning and conforms to the trend of the biological brain that prunes weak synaptic connections. By faithfully emulating learning rules that exist in human's higher cortical areas from STDP to synaptic pruning, the device has the capacity to drive forward the development of highly efficient neuromorphic computing systems.

Li P-C, Chen W-C, Chang L-C, Lin S-C. Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure. Am J Physiol Lung Cell Mol Physiol 294: L912-L920, 2008. First published March 7, 2008 doi:10.1152/ajplung.00443.2007.-This study aimed to 1) assess whether substance P (SP) acts via neurokinin (NK)-1 and NK-2 receptors to stimulate neurogenic inflammation (indicated by formation of ICAM-1 expression and oxidative stress) following oil smoke exposure (OSE) in rats; and 2) determine if pretreatment with antioxidants ameliorates the deleterious effects of OSE. Rats were pretreated with NK-1 receptor antagonist CP-96345, NK-2 receptor antagonist SR-48968, vitamin C, or catechins. OSE was for 30 -120 min. Rats were killed 0 -8 h later. Total lung resistance (RL), airway smooth muscle activity (ASMA), lung ICAM-1 expression, neurogenic plasma extravasation (via India ink and Evans blue dye), bronchoalveolar lavage fluid SP concentrations, and reactive oxygen species formation [via lucigenin-and luminalamplified chemiluminescence (CL)] were assessed. Lung histology was performed. SP concentrations increased significantly in nonpretreated rats following OSE in a dose-dependent manner. RL and total ASMA increased over time after OSE. Vitamin C and catechin pretreatments were associated with significantly reduced lucigenin CL 2 and 4 h after OSE. Pretreatment with catechins significantly reduced luminal CL counts 4 and 8 h after OSE. Evans blue levels were significantly reduced following 60 and 120 min of OSE in catechinand CP-96345-pretreated rats. ICAM-1 protein expression was significantly decreased in all pretreatment groups after OSE. Thickening of the alveolar capillary membrane, focal hemorrhaging, interstitial pneumonitis, and peribronchiolar inflammation were apparent in OSE lungs. These findings suggest that SP acts via the NK-1 receptor to provoke neurogenic inflammation, oxidative stress, and ICAM-1 expression after OSE in rats.reactive oxygen species; intracellular adhesion molecule-1; acute lung injury ACTIVATION OF NONMYELINATED bronchopulmonary C-fiber endings by various stimuli [including cigarette smoke (9), airway surface osmolality changes (14), and fire smoke (22)] causes the release of tachykinins and calcitonin gene-related peptide neuropeptides stored in the peripheral nerve terminals, eliciting both central nervous system (CNS) and local axon reflex responses (4). The CNS reflex consists of bronchoconstriction, expiratory apnea, rapid shallow breathing, cough, hypotension, and bradycardia, whereas the axon reflex response initiates local inflammation, increased mucous secretion, and bronchoconstriction. Substance P (SP), a tachykinin neuropeptide, induces a range of neuroimmunogenic effects on target smooth muscle or parasympathetic ganglia cells expressing neurokinin (NK)-1 or NK-2 receptors (1, 2). These effects, collectively termed neurogenic airway inflammation, comprise bronchoconstriction, microvasc...

Dilute ethanol (EtOH) is a widely used agent to remove the corneal epithelium during the modern refractive surgery. The application of EtOH may cause the underlying corneal fibroblasts to undergo apoptosis. This study was designed to investigate the protective effect and potential mechanism of the respiratory chain coenzyme Q10 (CoQ10), an electron transporter of the mitochondrial respiratory chain and a ubiquitous free radical scavenger, against EtOH-induced apoptosis of corneal fibroblasts. Corneal fibroblasts were pretreated with CoQ10 (10 µM) for 2 h, followed by exposure to different concentrations of EtOH (0.4, 2, 4, and 20%) for 20 s. After indicated incubation period (2–12 h), MTT assay was used to examine cell viability. Treated cells were further assessed by flow cytometry to identify apoptosis. Reactive oxygen species (ROS) and the change in mitochondrial membrane potential were assessed using dichlorodihydrofluorescein diacetate/2′,7′-dichlorofluorescein (DCFH-DA/DCF) assays and flow-cytometric analysis of JC-1 staining, respectively. The activity and expression of caspases 2, 3, 8, and 9 were evaluated with a colorimetric assay and western blot analysis. We found that EtOH treatment significantly decreased the viability of corneal fibroblasts characterized by a higher percentage of apoptotic cells. CoQ10 could antagonize the apoptosis inducing effect of EtOH. The inhibition of cell apoptosis by CoQ10 was significant at 8 and 12 h after EtOH exposure. In EtOH-exposed corneal fibroblasts, CoQ10 pretreatment significantly reduced mitochondrial depolarization and ROS production at 30, 60, 90, and 120 min and inhibited the activation and expression of caspases 2 and 3 at 2 h after EtOH exposure. In summary, pretreatment with CoQ10 can inhibit mitochondrial depolarization, caspase activation, and cell apoptosis. These findings support the proposition that CoQ10 plays an antiapoptotic role in corneal fibroblasts after ethanol exposure.

We present here the case of a 40-year-old woman with a greater than 10 year prior history of bilateral breast silicone injection and saline bag implantation. Bilateral palpable breast nodules were observed, but the ultrasound scan was suboptimal and the magnetic resonance imaging showed no gadolinium-enhanced tumor. The 18F-FDG PET/CT scan showed a hypermetabolic nodule in the left breast with a 30% increase of 18F-FDG uptake on the delayed imaging, and this mimicked breast cancer. She underwent a left partial mastectomy and the pathology demonstrated a siliconoma.

Acupuncture and its meridians are important components of traditional Chinese medicine, and numerous opinions have been previously expressed regarding these meridians. This study aims to explore the phenomenon of meridians from the perspective of electronic physics by studying these meridians for the response current affected by electrical pulse and acupuncture. In this study, acupuncture which applies an electrical pulse was used to research the physical properties of the meridians. Different kinds of pulses were applied to the human body to realize abnormal electrical signals. Comparing these electrical measurement results with the isothermal transient ionic current (ITIC) theory, we found that the transmission of meridian messages may be related to ion conduction. The movement of ions induced by acupuncture and electrical stimulation can lead to drift and diffusion currents through the meridians. The ionic conduction of meridian hypothesis is proved in that the substances delivered by meridians are in fact ions.

In this study, an Ag-Cu alloy was chosen as the electrode in conductive bridging random access memory (CBRAM), with results indicating a significant decrease in forming voltage. In addition, resistive switching characteristics as well as a retention test indicated better stability and a resistive switching window of at least an order. The switching time of the Ag-Cu alloy CBRAM is shorter than that of both Ag and Cu electrode CBRAMs under fast current-voltage (fast I-V). The experimental result indicated that the mechanism was dominated by the galvanic effect. Active atoms (Ag) captured electrons of inactive atoms (Cu) and generated metallic ions (Cu ions) in the alloy electrode. Cu ions drifted into the insulator and generated a conductive path when applying voltage bias. The use of this alloy as an electrode in CBRAM can significantly decrease forming voltage and enhance CBRAM characteristics.