Journal of Yeungnam medical science最新文献

Myofascial pain syndrome (MPS) is a common musculoskeletal disorder characterized by muscle pain, tenderness, and trigger points. Ultrasonography has emerged as a key tool for diagnosing and treating MPS owing to its ability to provide precise, minimally invasive guidance. This review discusses the use of ultrasonography in various approaches to evaluate and manage MPS. Studies have shown that shear-wave sonoelastography can effectively assess muscle elasticity and offer insights into trapezius stiffness in patients with MPS. Ultrasound-guided interfascial hydrodissection, especially with visual feedback, has demonstrated effectiveness in treating trapezius MPS. Similarly, ultrasound-guided rhomboid interfascial plane blocks and perimysium dissection for posterior shoulder MPS have significantly reduced pain and improved quality of life. The combination of extracorporeal shockwave therapy with ultrasound-guided lidocaine injections has been particularly successful in reducing pain and stiffness in trapezius MPS. Research regarding various guided injections, including dry needling, interfascial plane blocks, and fascial hydrodissection, emphasizes the importance of ultrasonography for accuracy and safety. Additionally, ultrasound-guided delivery of local anesthetics and steroids to the quadratus lumborum muscle has shown lasting pain relief over a 6-month period. Overall, these findings highlight the pivotal role of ultrasonography in the assessment and treatment of MPS.

The prevalence of childhood and adolescent obesity has increased and exacerbated during the coronavirus disease 2019 pandemic, both in Korea and globally. Childhood and adolescent obesity poses significant risks for premature morbidity and mortality. The development of serious comorbidities depends not only on the duration of obesity but also on the age of onset. Obesity in children and adolescents affects almost all organ systems, including the endocrine, cardiovascular, gastrointestinal, reproductive, nervous, and immune systems. Obesity in children and adolescents affects growth, cognitive function, and psychosocial interactions during development, in addition to aggravating known adult comorbidities such as type 2 diabetes mellitus, hypertension, dyslipidemia, nonalcoholic fatty liver disease, obstructive sleep apnea, and cancer. Childhood and adolescent obesity are highly associated with increased cardiometabolic risk factors and prevalence of metabolic syndrome. The risk of cardiovascular and metabolic diseases in later life can be considerably decreased by even a small weight loss before the onset of puberty. Childhood and adolescent obesity is a disease that requires treatment and is associated with many comorbidities and disease burdens. Therefore, early detection and therapeutic intervention are crucial.

Background: Electrodiagnostic testing (EDX) is important in the diagnosis and follow-up of neuropathic and myopathic diseases. This study aimed to demonstrate the compatibility between clinical prediagnosis and electrophysiological findings.

Methods: EDX results from 2004 to 2020 at the physical medicine and rehabilitation (PM&R) clinic were screened. Tests with missing data, reevaluation studies, and cases of peripheral facial paralysis were excluded. The clinical prediagnosis and EDX results were recorded, and their compatibility was evaluated.

Results: A total of 2,153 tests were included in this study. The mean age was 49.0±13.9 years and 1,533 of them (71.2%) were female. The most frequently referred clinic was the PM&R clinic (90.0%). Numbness (73.6%) was the most common complaint, followed by pain (15.3%) and weakness (13.9%). The most common prediagnosis was entrapment neuropathy (55.3%), radiculopathy (16.1%), and polyneuropathy (15.7%). Carpal tunnel syndrome was the most frequently identified type of entrapment neuropathy (78.3%). Six hundred and seventy EDX results (31.1%) were within normal limits. While the EDX results were consistent with the prediagnosis in 1,328 patients (61.7%), a pathology different from the prediagnosis was detected in 155 patients (7.2%). In the discrepancy group, the most common pathologies were entrapment neuropathy (51.7%), polyneuropathy (17.3%), and radiculopathy (15.1%). The most common neuropathy type was carpal tunnel syndrome (79.3%).

Conclusion: After adequate anamnesis and physical and neurological examinations, requesting further appropriate tests will increase the prediagnosis accuracy and prevent unnecessary expenditure of time and labor.

Aortic dissection in pregnant patients results in an inpatient mortality rate of 8.6%. Owing to the pronounced mortality rate and speed at which aortic dissections progress, efficient early detection methods are crucial. Here, we highlight the importance of early chest computed tomography (CT) for differentiating aortic dissection from pulmonary embolism in pregnant patients with dyspnea. We present the unique case of a 38-year-old pregnant woman with elevated D-dimer and N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, initially suspected of having a pulmonary embolism. Initial transthoracic echocardiography did not indicate aortic dissection. Surprisingly, after an emergency cesarean section, a chest CT scan revealed a DeBakey type I aortic dissection, indicating a diagnostic error. Our findings emphasize the need for early chest CT in pregnant patients with dyspnea and elevated D-dimer and NT-proBNP levels. This case report highlights the critical importance of considering both aortic dissection and pulmonary embolism in the differential diagnosis of such cases, which will inform future clinical practice.

Background: Nonalcoholic fatty liver disease (NAFLD) is characterized by an increase in hepatic triglyceride content and increased inflammatory macrophage infiltration through the C-C motif chemokine receptor (CCR) 5 pathway in the liver. DA-6034 (7-carboxymethyloxy-3',4',5-trimethoxy flavone), is a synthetic derivative of eupatilin that exhibits anti-inflammatory activity in inflammatory bowel disease. However, the effect of DA-6034 on the inflammatory response in NAFLD is not well elucidated. Therefore, we aimed to determine the effect of DA-6034 on hepatic steatosis and inflammation.

Methods: Forty male C57BL/6J mice were divided into the following four groups: (1) regular diet (RD), (2) RD with DA-6034, (3) high fat diet (HFD), and (4) HFD with DA-6034. All mice were sacrificed 12 weeks after the start of the experiment. The effects of DA-6034 on macrophages were assessed using RAW264.7 cells.

Results: DA-6034 not only reduced hepatic triglyceride levels and lipid accumulation but also macrophage infiltration and proinflammatory cytokines in HFD-fed mice. According to fluorescence-activated cell sorter analysis, DA-6034 reduced the CD8+ T cell fraction in the liver of HFD-fed mice. DA-6034 also reduced CCR5 expression and the migration of liver macrophages in HFD-fed mice and inhibited CCR2 ligand and CCR4 ligand, which stimulated the migration of macrophages.

Conclusion: Overall, DA-6034 attenuates hepatic steatosis and inflammation in obesity by regulating CCR5 expression in macrophages.

Acute kidney ischemia-reperfusion (IR) injury is a life-threatening condition that predisposes individuals to chronic kidney disease. Since the kidney is one of the most energy-demanding organs in the human body and mitochondria are the powerhouse of cells, mitochondrial dysfunction plays a central role in the pathogenesis of IR-induced acute kidney injury. Mitochondrial dysfunction causes a reduction in adenosine triphosphate production, loss of mitochondrial dynamics (represented by persistent fragmentation), and impaired mitophagy. Furthermore, the pathological accumulation of succinate resulting from fumarate reduction under oxygen deprivation (ischemia) in the reverse flux of the Krebs cycle can eventually lead to a burst of reactive oxygen species driven by reverse electron transfer during the reperfusion phase. Accumulating evidence indicates that improving mitochondrial function, biogenesis, and dynamics, and normalizing metabolic reprogramming within the mitochondria have the potential to preserve kidney function during IR injury and prevent progression to chronic kidney disease. In this review, we summarize recent advances in understanding the detrimental role of metabolic reprogramming and mitochondrial dysfunction in IR injury and explore potential therapeutic strategies for treating kidney IR injury.