A case report of high cervical spinal infarction after stenting with severe stenosis at the beginning of left vertebral artery.

BACKGROUND: Spinal cord infarction is an uncommon nervous system disorder. We present a case of high cervical cord infarction caused by stenting of the origin of the left vertebral artery (VA). The incidence of spinal cord infarction is minimal, and it must be distinguished from a number of other disorders. The diagnosis is primarily based on imaging, clinical symptoms, and history. Currently, there is no focused treatment for spinal cord infarction. Thrombolysis, high-dose glucocorticoid shocks, tube dilatation to promote circulation, and nutritional neurotropic medicines given early in the course of the disease can all help to slow the disease's progression. There is no agreement on the etiology, diagnosis, or therapy options for these people. CASE PRESENTATION: On October 7, 2023, an 81-year-old man was admitted to the hospital primarily for recurrent chest tightness and pain that had persisted for more than 2 years and 1 month. Cerebral angiography upon admission revealed significant blockage of the right VA and stenosis of the left vertebral arterial origin. Six days following admission, a drug-eluting stenting procedure was carried out under local anesthesia to open the left VA origin via the femoral artery. Following the procedure, the patient experienced a progressive loss of muscle strength in all 4 limbs and paraplegia below the cervical 3 spinal cord. One week following the procedure, the patient was released from the hospital. After the procedure, the patient was released 1 week later. After the procedure, the patient's symptoms persisted for a month. CONCLUSION: High awareness for high cervical cord infarction is required when neck discomfort and limb weakness with progressive progression arises after surgery. Complications of high cervical cord infarction following stenting for stenosis of VA origin are uncommon in clinical settings. Patients' prognoses can be improved by prompt diagnosis and care.

Observation of phonon Stark effect.

Stark effect, the electric-field analogue of magnetic Zeeman effect, is one of the celebrated phenomena in modern physics and appealing for emergent applications in electronics, optoelectronics, as well as quantum technologies. While in condensed matter it has prospered only for excitons, whether other collective excitations can display Stark effect remains elusive. Here, we report the observation of phonon Stark effect in a two-dimensional quantum system of bilayer 2H-MoS2. The longitudinal acoustic phonon red-shifts linearly with applied electric fields and can be tuned over ~1 THz, evidencing giant Stark effect of phonons. Together with many-body ab initio calculations, we uncover that the observed phonon Stark effect originates fundamentally from the strong coupling between phonons and interlayer excitons (IXs). In addition, IX-mediated electro-phonon intensity modulation up to ~1200% is discovered for infrared-active phonon A2u. Our results unveil the exotic phonon Stark effect and effective phonon engineering by IX-mediated mechanism, promising for a plethora of exciting many-body physics and potential technological innovations.

Ultralow Power In-Sensor Neuronal Computing with Oscillatory Retinal Neurons for Frequency-Multiplexed, Parallel Machine Vision.

In-sensor and near-sensor computing architectures enable multiply accumulate operations to be carried out directly at the point of sensing. In-sensor architectures offer dramatic power and speed improvements over traditional von Neumann architectures by eliminating multiple analog-to-digital conversions, data storage, and data movement operations. Current in-sensor processing approaches rely on tunable sensors or additional weighting elements to perform linear functions such as multiply accumulate operations as the sensor acquires data. This work implements in-sensor computing with an oscillatory retinal neuron device that converts incident optical signals into voltage oscillations. A computing scheme is introduced based on the frequency shift of coupled oscillators that enables parallel, frequency multiplexed, nonlinear operations on the inputs. An experimentally implemented 3 × 3 focal plane array of coupled neurons shows that functions approximating edge detection, thresholding, and segmentation occur in parallel. An example of inference on handwritten digits from the MNIST database is also experimentally demonstrated with a 3 × 3 array of coupled neurons feeding into a single hidden layer neural network, approximating a liquid-state machine. Finally, the equivalent energy consumption to carry out image processing operations, including peripherals such as the Fourier transform circuits, is projected to be <20 fJ/OP, possibly reaching as low as 15 aJ/OP.

Cardiomyocyte-Specific Loss of Glutamyl-prolyl-tRNA Synthetase Leads to Disturbed Protein Homeostasis and Dilated Cardiomyopathy.

Glutamyl-prolyl-tRNA synthetase (EPRS1), an aminoacyl-tRNA synthetase (ARS) ligating glutamic acid and proline to their corresponding tRNAs, plays an essential role in decoding proline codons during translation elongation. The physiological function of EPRS1 in cardiomyocytes (CMs) and the potential effects of the CM-specific loss of Eprs1 remain unknown. Here, we found that heterozygous Eprs1 knockout in CMs does not cause any significant changes in CM hypertrophy induced by pressure overload, while homozygous knockout leads to dilated cardiomyopathy, heart failure, and lethality at around 1 month after Eprs1 deletion. The transcriptomic profiling of early-stage Eprs1 knockout hearts suggests a significantly decreased expression of multiple ion channel genes and an increased gene expression in proapoptotic pathways and integrated stress response. Proteomic analysis shows decreased protein expression in multi-aminoacyl-tRNA synthetase complex components, fatty acids, and branched-chain amino acid metabolic enzymes, as well as a compensatory increase in cytosolic translation machine-related proteins. Immunoblot analysis indicates that multiple proline-rich proteins were reduced at the early stage, which might contribute to the cardiac dysfunction of Eprs1 knockout mice. Taken together, this study demonstrates the physiological and molecular outcomes of loss-of-function of Eprs1 in vivo and provides valuable insights into the potential side effects on CMs, resulting from the EPRS1-targeting therapeutic approach.