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BACKGROUND Acute myocarditis is an acute myocardium injury that manifests as arrhythmia, dyspnea, and elevated cardiac enzymes. Acute myocarditis is usually caused by a viral infection but can sometimes be caused by autoimmunity. Graves’ disease is an autoimmune disease that is a rare etiology of acute myocarditis. Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults. CASE SUMMARY A rare case of new-onset Graves’ disease combined with acute myocarditis and thyrotoxic periodic paralysis is reported. The patient was a 25-year-old young man who suddenly became paralyzed and felt palpitations and dyspnea. He was then sent to our emergency department (ED). Upon arrival, electrocardiography revealed an accelerated junctional rhythm and ST-segment depression in all leads, and laboratory findings showed extreme hypokalemia and elevated troponin I, with the troponin I level being 0.32 ng/mL (reference range, 0-0.06 ng/mL). Coronary computer tomography angiography was performed, and there were no abnormal findings in the coronary arteries. Subsequently, the patient was admitted to the ED ward, where further testing revealed Graves’ disease, along with continued elevated cardiac enzyme levels and B-type natriuretic peptide (BNP) levels. The troponin I level was 0.24 ng/mL after admission. All of the echocardiography results were normal: Left atrium 35 mm, left ventricle 48 mm, end-diastolic volume 102 mL, right atrium 39 mm × 47 mm, right ventricle 25 mm, and ejection fraction 60%. Cardiac magnetic resonance was performed on the fifth day of admission, revealing myocardial edema in the lateral wall and intramyocardial and subepicardial late gadolinium enhancement in the lateral apex, anterior lateral, and inferior lateral segments of the ventricle. The patient refused to undergo an endomyocardial biopsy. After 6 d, the patient’s cardiac enzymes, BNP, potassium, and electrocardiography returned to normal. After the patient’s symptoms were relieved, he was discharged from the hospital. During a 6-mo follow-up, the patient was asymptomatic and subjected to thyroid function, liver function, kidney function, troponin I, and electrocardiograph routine tests for medicine adjustments. The hyperthyroid state was controlled. CONCLUSION Acute myocarditis is a rare manifestation of Graves’ disease. Accelerated junctional rhythm is also a rare manifestation of acute myocarditis in adults. When the reason for hypokalemia and elevated cardiac enzymes in patients is unknown, cardiologists should consider Graves’ disease and also pay attention to accelerated junctional rhythm.

BACKGROUND Colchicine has been widely used as an anti-gout medication over the past decades. However, it is less commonly used due to its narrow therapeutic range, meaning that its lethal dose is close to its therapeutic dose. The lethal dose of colchicine is considered to be 0.8 mg/kg. As chronic colchicine poisoning has multiple manifestations, it poses a challenge in the clinician’s differential diagnosis. Historically, the drug was important in treating gout; however, clinical studies are currently underway regarding the use of colchicine in patients with coronavirus disease 2019 as well as its use in coronary artery disease, making this drug more important in clinical practice. CASE SUMMARY A 61-year-old male with a history of gout and chronic colchicine intake was admitted to our Emergency Department due to numbness and weakness of the lower limbs. The patient reported a history of colchicine intake for 23 years. After thorough examination, he was diagnosed with colchicine poisoning, manifesting as neuromyopathy, multiple gastric ulcers and myelosuppression. We advised him to stop taking colchicine and drinking alcohol. We also provided a prescription of lansoprazole and mecobalamin, and then asked him to return to the clinic for re-examination. The patient was followed up for 3-mo during which time his gout symptoms were controlled to the point where he was asymptomatic. CONCLUSION Colchicine overdose can mimic the clinical manifestations of several conditions. Physicians easily pay attention to the disease while ignoring the cause of the disease. Thus, the patient’s medication history should never be ignored.

Single micro-light emitting diodes(LEDs) with different sizes and array micro-LED are designed and prepared, where the sizes of the single micro-LEDs are in a range of 40−100 μm, their electrodes are all co-N electrodes, P electrode is drawn out alone; the number of array pixels is \begin{document}$ 8\times8 $\end{document}, which is a passively driving structure with a pixel size of 60 μm. In the process of device preparation, N electrode and P electrode are fabricated by the sputtering & stripping method. The electrode thickness is 2.4 μm. Thick photoresist 5120 is used as a mask, and N GaN is etched to the substrate by using the ICP dry etching to form an isolation trench. The PECVD technique is used to deposit an SiO2 insulating layer with a thickness of 10000 Å. By optimizing the electrode structure and thickness, the reliability of the P electrode at the slope of the isolation trench is improved, and the SiO2 insulating layer has good encapsulation; field programmable gate array (FPGA) is used to drive and display the micro-LED passive array. The single micro-LEDs of different sizes are tested and analyzed in the aspects of electrics, photics and thermotics and the results of which show that the current density corresponding to the peak radiation flux of 80 μm micro-LED is 1869.2 A/cm2, which is 57.1% higher than that of 100 μm micro-LED, indicating that the current density corresponding to the peak radiation flux of micro-LED increases as the size decreases; compared with the ordinary blue LED, the micro-LED has a large k factor, and with the size decreases, the value of the k factor increases, indicating that the micro-LED series resistance is larger, and the thermal stability is not so good as the traditional blue LED. Finally, the field programmable gate array (FPGA) can achieve a good drive for the micro-LED passive array. The driving principle is passive scanning driving, which is carried out in a row-by-row lighting mode. The FPGA clock is 50 MHz, and 320 ns is required for the circuit to scan all rows.