RESUMO
Objective: This study aims to investigate the clinical application value of high-frequency ultrasound technology in diagnosing subcutaneous lipohypertrophy at insulin injection sites in diabetes patients. Methods: All diabetes patients treated in our hospital from January 2022 to January 2023 were selected as the study subjects. The incidence of subcutaneous lipohypertrophy was calculated at the end of the study period. All patients were screened, and those meeting the inclusion criteria were registered, and basic data were collected. Patients were screened for subcutaneous lipohypertrophy using conventional clinical examination (control group) and high-frequency ultrasound technology (study group). Results: The study found that the incidence of subcutaneous lipohypertrophy in diabetes patients receiving insulin injections in our hospital from January 2022 to January 2023 was 80.99%. The average longitudinal diameter of subcutaneous lipohypertrophy in these patients was 11.66 (7.56, 21.44) mm, the transverse diameter was 12.04 (8.96, 18.29) mm, depth was (5.62±2.17) mm, and the area was 188.79 (76.85, 331.78) mm². The clinical detection rate in the study group was higher than that in the control group (P<0.05). The quantity of detected sites was greater in the study group compared to the control group (P<0.05). Conclusion: The incidence of subcutaneous lipohypertrophy in diabetes patients receiving insulin injections is relatively high clinically, and high-frequency ultrasound technology demonstrates significant potential in diagnosis. By providing high-resolution imaging and quantitative data, it effectively improves the clinical detection rate and clarifies symptoms. This technology is likely to become an important auxiliary tool in future diabetes treatment, providing more precise treatment plans for patients.
RESUMO
LncRNA UCA1 plays a vital role in cardiovascular diseases. Endothelial cell dysfunction is a prerequisite for atherosclerosis (AS) development. However, the pathophysiological role of UCA1 in endothelial cell dysfunction induced by ox-LDL remains obscure. Here, we observed that UCA1 was upregulated in the sera of patients with AS and ox-LDL-treated endothelial cells. UCA1 knockdown dramatically reduced the cell apoptosis induced by ox-LDL and the production of pro-inflammatory cytokines and ROS in endothelial cells. Mechanistically, we found that UCA1 directly targeted miR-873-5p. UCA1 knockdown increased, while UCA1 overexpression decreased the expression of miR-873-5p. Further, we found that mitogen-activated protein kinase 8 (MAPK8) was a downstream target gene of miR-873-5p. MAPK8 overexpression or miR-873-5p knockdown reduced the enhancement of ox-LDL-induced cell apoptosis, oxidative stress, and pro-inflammatory cytokine production conferred by UCA1 knockdown. In conclusion, UCA1 can protect Human Umbilical Vein Endothelial Cells from ox-LDL-induced injury via the miR-873-5p/MAPK8 axis.
