In particular, artificial synapses are the core parts of neuromorphic systems because they perform information processing like pattern recognition, output prediction, and learning and store memory by regulating synaptic weight in response to presynaptic signals. [3] In these operations, the operation accuracy differs based on synaptic characteristics such as the symmetry and linearity of synaptic weight change, ratio of maximum to minimum conductance, and number of synaptic weights. [4,5] To accomplish high operation accuracy of neuromorphic systems, which are analogous to the human brain, variety sort of 2-terminal and 3-terminal devices as artificial synapsesThe ORCID identification number(s) for the author(s) of this article can be found under
BackgroundUnder certain conditions, exertional headaches may reflect coronary ischemia.Case ReportA 44-year-old woman developed intermittent exercise-induced headaches with chest tightness over a period of 10 months. Cardiac catheterization followed by acetylcholine provocation demonstrated a right coronary artery spasm with chest tightness, headache, and ischemic effect of continuous electrocardiography changes. The patient's headache disappeared following intra-arterial nitroglycerine injection.ConclusionsA coronary angiogram with provocation study revealed variant angina and cardiac cephalalgia, as per the International Classification of Headache Disorders (code 10.6). We report herein a patient with cardiac cephalalgia that manifested as reversible coronary vasospasm following an acetylcholine provocation test.
Background: The purpose of this study was to investigate whether brain AT1 receptor stimulation contributes as a hypertensive mechanism to deoxycorticosterone acetate (DOCA)-salt hypertension. Methods: 1) Acute injection: Losartan (1 mg/4 uL) or artificial cerebrospinal fluid (aCSF) was injected into the lateral cerebral ventricle (icv) of conscious control uninephrectomized Wistar rats or rats with DOCA-salt at 2 or 4 weeks, and mean arterial pressure (MAP) and heart rates (HR) were recorded. 2) Chronic injection: Using osmotic minipump, losartan (1 mg/kg/d) or aCSF was injected to a sham group or three DOCA-salt rat groups [icv-aCSF, icv-losartan, sc-losartan (subcutaneous) groups] for 4 weeks, after which the MAP and HR were recorded in addition to the weights of the left (LV) and right ventricles (RV) and kidneys. Results: 1) Acute injection: In rats treated with DOCA-salt, resting MAP significantly increased compared to the control group [144±6 mmHg (2 weeks), 170± 5 mmHg (4 weeks) vs 115-120 mmHg (controls)]. MAP decreased significantly (2 weeks, 4 weeks) at 4, 8, 24 hours after icv injection of losartan to the level of the control group. 2) Chronic injection: The general trend showed that MAP decreased more in the icv-losartan group than in the icv-aCSF group (127±15.2 mmHg vs 141.1±5.5 mmHg, p=0.0578). In all DOCA-salt groups, no differences in RV weight were found. In the icv-aCSF and sclosartan groups, the kidney weight increased compared to the control group, but there was no difference in LV and kidney weight between the icv-losartan group and the control group. Conclusions: Normalization of MAP after acute or chronic icv administration of the AT 1 receptor antagonist suggests that the stimulation of the brain AT 1 receptor plays a significant role in the development and maintenance of hypertension in the DOCAsalt hypertensive rat model. Losartan icv injection appeared to have a protective effect on the heart and kidney.
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