The largest amount of latent heat of the martensitic transformation in nickel titanium shape memory alloy was explored. The measured amounts of heat in the alloys with different compositions between ...48.0 at.% Ni and 51.0 at.% Ni were compared. The largest amounts of
-
37.8 J/g in absorption and 34.8 J/g in emission were obtained as the averaged values of several samples with equiatomic composition. These magnitudes are close to those of novel heat storage ceramics, VO
2
(51 J/g) and Ti
3
O
5
(60 J/g), suggesting the NiTi alloy is potential candidate for heat storage material.
Graphical abstract
How are sensory representations in the brain influenced by the state of an animal? Here we use chronic two-photon calcium imaging to explore how wakefulness and experience shape odor representations ...in the mouse olfactory bulb. Comparing the awake and anesthetized state, we show that wakefulness greatly enhances the activity of inhibitory granule cells and makes principal mitral cell odor responses more sparse and temporally dynamic. In awake mice, brief repeated odor experience leads to a gradual and long-lasting (months) weakening of mitral cell odor representations. This mitral cell plasticity is odor specific, recovers gradually over months, and can be repeated with different odors. Furthermore, the expression of this experience-dependent plasticity is prevented by anesthesia. Together, our results demonstrate the dynamic nature of mitral cell odor representations in awake animals, which is constantly shaped by recent odor experience.
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► Wakefulness makes mitral cell odor representations sparser, dynamic, and efficient ► Wakefulness enhances inhibitory granule cell activity ► Odor experience causes months-long, odor-specific changes of mitral cell tuning ► The expression of mitral cell experience-dependent plasticity requires wakefulness
How are brain sensory representations influenced by the state of an animal? Kato et al. use chronic two-photon calcium imaging to show that in the awake mouse olfactory bulb, odor representations are sparse and dynamic due to increased interneuron activity and are shaped by recent experience.
Animals require the ability to ignore sensory stimuli that have no consequence yet respond to the same stimuli when they become useful. However, the brain circuits that govern this flexibility in ...sensory processing are not well understood. Here we show in mouse primary auditory cortex (A1) that daily passive sound exposure causes a long-lasting reduction in representations of the experienced sound by layer 2/3 pyramidal cells. This habituation arises locally in A1 and involves an enhancement in inhibition and selective upregulation in the activity of somatostatin-expressing inhibitory neurons (SOM cells). Furthermore, when mice engage in sound-guided behavior, pyramidal cell excitatory responses to habituated sounds are enhanced, whereas SOM cell responses are diminished. Together, our results demonstrate the bidirectional modulation of A1 sensory representations and suggest that SOM cells gate cortical information flow based on the behavioral relevance of the stimulus.
•Passive sound experience causes habituation of sensory representations in A1•Habituation involves an increase in inhibition of layer 2/3 pyramidal cells•Habituation reflects the selective upregulation of SOM interneuron activity•Sound-guided behavior decreases SOM cell activity and rapidly reverses habituation
Kato et al. demonstrate that daily sound experience upregulates SOM interneuron activity in A1 and causes “habituation” of sound representations. Sound-guided behavior reverses these effects, indicating that sensory representations are bidirectionally modified based on the behavioral relevance of sensory stimuli.
Lateral inhibition is a fundamental circuit operation that sharpens the tuning properties of cortical neurons. This operation is classically attributed to an increase in GABAergic synaptic input ...triggered by non-preferred stimuli. Here we use in vivo whole-cell recording and two-photon Ca2+ imaging in awake mice to show that lateral inhibition shapes frequency tuning in primary auditory cortex via an unconventional mechanism: non-preferred tones suppress both excitatory and inhibitory synaptic inputs onto layer 2/3 cells (“network suppression”). Moreover, optogenetic inactivation of inhibitory interneurons elicits a paradoxical increase in inhibitory synaptic input. These results indicate that GABAergic interneurons regulate cortical activity indirectly via the suppression of recurrent excitation. Furthermore, the network suppression underlying lateral inhibition was blocked by inactivation of somatostatin-expressing interneurons (SOM cells), but not parvalbumin-expressing interneurons (PV cells). Together, these findings reveal that SOM cells govern lateral inhibition and control cortical frequency tuning through the regulation of reverberating recurrent circuits.
•Frequency tuning in auditory cortex of mice is shaped by lateral inhibition•Lateral inhibition is due to the suppression of recurrent excitation•Somatostatin-expressing interneurons trigger network suppression•Auditory cortex operates as an inhibition-stabilized network (ISN)
Kato et al. show that lateral inhibition shapes frequency tuning in primary auditory cortex via an unconventional mechanism: non-preferred stimuli suppress recurrent excitation. Somatostatin-expressing interneurons are critical for triggering this indirect form of cortical inhibition.
Information flow in the sensory cortex has been described as a predominantly feedforward sequence with deep layers as the output structure. Although recurrent excitatory projections from layer 5 (L5) ...to superficial L2/3 have been identified by anatomical and physiological studies, their functional impact on sensory processing remains unclear. Here, we use layer-selective optogenetic manipulations in the primary auditory cortex to demonstrate that feedback inputs from L5 suppress the activity of superficial layers regardless of the arousal level, contrary to the prediction from their excitatory connectivity. This suppressive effect is predominantly mediated by translaminar circuitry through intratelencephalic neurons, with an additional contribution of subcortical projections by pyramidal tract neurons. Furthermore, L5 activation sharpened tone-evoked responses of superficial layers in both frequency and time domains, indicating its impact on cortical spectro-temporal integration. Together, our findings establish a translaminar inhibitory recurrence from deep layers that sharpens feature selectivity in superficial cortical layers.
Mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) is a disease that should be considered as a differential diagnosis to acute ischemic stroke taking into account ...its onset pattern and neurological symptoms, which are similar to those of an ischemic stroke. Technological advancements in neuroimaging modalities have greatly facilitated differential diagnosis between stroke and MELAS on diagnostic imaging. Stroke-like episodes in MELAS have the following features: (1) symptoms are neurolocalized according to lesion site; (2) epileptic seizures are often present; (3) lesion distribution is inconsistent with vascular territory; (4) lesions are common in the posterior brain regions; (5) lesions continuously develop in adjacent sites over several weeks or months; (6) neurological symptoms and stroke-like lesions tend to be reversible, as presented on magnetic resonance imaging; (7) the rate of recurrence is high; and; (8) brain dysfunction and atrophy are slowly progressive. The m.3243ANG mutation in the
MT-TL1
gene encoding the mitochondrial tRNA
Leu
(UUR) is most commonly associated with MELAS. Although the precise pathophysiology is still unclear, one possible hypothesis for these episodes is a neuronal hyperexcitability theory, including neuron–astrocyte uncoupling. Supplementation, such as with L-arginine or taurine, has been proposed as preventive treatments for stroke-like episodes. As this disease is still untreatable and devastating, numerous drugs are being tested, and new gene therapies hold great promise for the future. This article contributes to the understanding of MELAS and its implications for clinical practice, by deepening their insight into the latest pathophysiological hypotheses and therapeutic developments.
Treatments for esophageal cancer: a review Kato, Hiroyuki; Nakajima, Masanobu
General thoracic and cardiovascular surgery,
06/2013, Letnik:
61, Številka:
6
Journal Article
Recenzirano
Esophageal cancer is the eighth most common form of cancer worldwide. The treatments for esophageal cancer depend on its etiology. For mucosal cancer, endoscopic mucosal resection and endoscopic ...submucosal dissection are standard, while for locally advanced cancer, esophagectomy remains the mainstay. The three most common techniques for thoracic esophagectomy are the transhiatal approach, the Ivor Lewis esophagectomy (right thoracotomy and laparotomy), and the McKeown technique (right thoracotomy followed by laparotomy and neck incision with cervical anastomosis). Surgery for carcinoma of the cervical esophagus requires an extensive procedure with laryngectomy in many cases. When the tumor is more advanced, neoadjuvant chemotherapy or neoadjuvant chemoradiotherapy is added. The theoretical advantages of adding chemotherapy to the treatment of esophageal cancer are potential tumor down-staging prior to surgery, as well as targeting micrometastases and, thus, decreasing the risk of distant metastasis. Cisplatin- and 5-fluorouracil-based regimes are used worldwide. Chemoradiotherapy is the standard for unresectable esophageal cancer and could also be considered as an option for resectable tumors. For patients who are medically or technically inoperable, concurrent chemoradiotherapy should be the standard of care. Although neoadjuvant chemoradiotherapy followed by surgery or salvage surgery after definitive chemoradiotherapy is a practical treatment; judicious patient selection is crucial. It is important to have a thorough understanding of these therapeutic modalities to assist in this endeavor.
In the olfactory bulb, odor representations by principal mitral cells are modulated by local inhibitory circuits. While dendrodendritic synapses between mitral and granule cells are typically thought ...to be a major source of this modulation, the contributions of other inhibitory neurons remain unclear. Here we demonstrate the functional properties of olfactory bulb parvalbumin-expressing interneurons (PV cells) and identify their important role in odor coding. Using paired recordings, we find that PV cells form reciprocal connections with the majority of nearby mitral cells, in contrast to the sparse connectivity between mitral and granule cells. In vivo calcium imaging in awake mice reveals that PV cells are broadly tuned to odors. Furthermore, selective PV cell inactivation enhances mitral cell responses in a linear fashion while maintaining mitral cell odor preferences. Thus, dense connections between mitral and PV cells underlie an inhibitory circuit poised to modulate the gain of olfactory bulb output.
•PV cells form dense reciprocal connections with most neighboring principal cells•PV cells show much broader odor-tuning properties compared to mitral or granule cells•Increase in respiration even without odors is a strong driver of PV cell activity•Inactivation experiments suggest that PV cells linearly control olfactory bulb output
Functions of neural circuits rely on inhibition provided by diverse types of inhibitory neurons. Kato et al. use paired recordings and in vivo two-photon calcium imaging to show that parvalbumin-expressing interneurons linearly control the output of the olfactory bulb.
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