No abstract available.

No abstract available.
Female ; Pregnancy ; Pregnancy, Ectopic*

We report a case of pneumonia in 36 year-old male patient who presented acute respiratory failure and associated radiologic findings of bilateral ground-glass opacity with focal cystic changes, showing rapidly aggravating course and was diagnosed as concomitant Pneumocystis carinii and Cytomegalovirus pneumonia accompanied by acquired immunodeficiency syndrome through antemortem open lung biopsy.
Acquired Immunodeficiency Syndrome ; Biopsy ; Cytomegalovirus ; Humans ; Lung ; Male ; Pneumocystis carinii ; Pneumonia ; Respiratory Insufficiency*

The latest recommendations for the diagnosis and management of crystal-induced arthritis, such as gout and calcium pyrophosphate dihydrate (CPPD) deposition disease, recognize the diagnostic potential of musculoskeletal ultrasonography (MSUS). MSUS allows rapid, highly sensitive, non-invasive detection of microcrystal aggregates in multiple anatomic areas, and can be used as a safe, reliable guide for aspiration of articular and periarticular specimens suitable for microscopic analysis. MSUS can also be used to monitor disease after treatment. Ultrasonographic differentiation between gout and CPPD deposition disease is based on the characteristics of crystal aggregates and their preferential localization in different anatomical areas. This rapid assessment may profoundly affect the clinical process, avoiding expensive, time-consuming diagnostic procedures. This article reviews the current status of and recent advances in MSUS imaging in crystal-induced arthritis.
Arthritis* ; Calcium Pyrophosphate ; Chondrocalcinosis ; Diagnosis ; Gout ; Ultrasonography

While glutamate, a key neurotransmitter in the central nervous system, is fundamental to neuronal viability and normal brain function, its excessive accumulation leads to oxidative stress, contributing to neuronal damage and neurodegenerative diseases. In this study, we investigated the effect of β-lapachone (β-Lap), a naturally occurring naphthoquinone, on glutamate-induced injury in HT22 cells and explored the underlying mechanism involved. Our results show that β-Lap significantly improved cell viability in a dose-dependent manner. Additionally, β-Lap exhibited a significant antioxidant activity, reducing intracellular reactive oxygen species levels and restoring glutathione levels. The antioxidant capacity of β-Lap was further demonstrated through 2,2-Diphenyl-1-picrylhydrazyl (DPPH) and 2,2’-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging assays. Western blot analysis revealed that β-Lap upregulated brain-derived neurotrophic factor (BDNF) and promoted the phosphorylation of tropomyosin receptor kinase B (TrkB), extracellular signal-regulated kinase (ERK), and cAMP response elementbinding protein (CREB), which were downregulated by glutamate. Furthermore, β-Lap enhanced the cellular antioxidant molecules, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). In conclusion, β-Lap can protect HT22 cells against glutamate-induced injury by activating the BDNF/TrkB/ERK/CREB and ERK/Nrf2/HO-1 signaling pathways, suggesting its therapeutic potential for neurodegenerative diseases.

While glutamate, a key neurotransmitter in the central nervous system, is fundamental to neuronal viability and normal brain function, its excessive accumulation leads to oxidative stress, contributing to neuronal damage and neurodegenerative diseases. In this study, we investigated the effect of β-lapachone (β-Lap), a naturally occurring naphthoquinone, on glutamate-induced injury in HT22 cells and explored the underlying mechanism involved. Our results show that β-Lap significantly improved cell viability in a dose-dependent manner. Additionally, β-Lap exhibited a significant antioxidant activity, reducing intracellular reactive oxygen species levels and restoring glutathione levels. The antioxidant capacity of β-Lap was further demonstrated through 2,2-Diphenyl-1-picrylhydrazyl (DPPH) and 2,2’-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging assays. Western blot analysis revealed that β-Lap upregulated brain-derived neurotrophic factor (BDNF) and promoted the phosphorylation of tropomyosin receptor kinase B (TrkB), extracellular signal-regulated kinase (ERK), and cAMP response elementbinding protein (CREB), which were downregulated by glutamate. Furthermore, β-Lap enhanced the cellular antioxidant molecules, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). In conclusion, β-Lap can protect HT22 cells against glutamate-induced injury by activating the BDNF/TrkB/ERK/CREB and ERK/Nrf2/HO-1 signaling pathways, suggesting its therapeutic potential for neurodegenerative diseases.

While glutamate, a key neurotransmitter in the central nervous system, is fundamental to neuronal viability and normal brain function, its excessive accumulation leads to oxidative stress, contributing to neuronal damage and neurodegenerative diseases. In this study, we investigated the effect of β-lapachone (β-Lap), a naturally occurring naphthoquinone, on glutamate-induced injury in HT22 cells and explored the underlying mechanism involved. Our results show that β-Lap significantly improved cell viability in a dose-dependent manner. Additionally, β-Lap exhibited a significant antioxidant activity, reducing intracellular reactive oxygen species levels and restoring glutathione levels. The antioxidant capacity of β-Lap was further demonstrated through 2,2-Diphenyl-1-picrylhydrazyl (DPPH) and 2,2’-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) radical scavenging assays. Western blot analysis revealed that β-Lap upregulated brain-derived neurotrophic factor (BDNF) and promoted the phosphorylation of tropomyosin receptor kinase B (TrkB), extracellular signal-regulated kinase (ERK), and cAMP response elementbinding protein (CREB), which were downregulated by glutamate. Furthermore, β-Lap enhanced the cellular antioxidant molecules, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). In conclusion, β-Lap can protect HT22 cells against glutamate-induced injury by activating the BDNF/TrkB/ERK/CREB and ERK/Nrf2/HO-1 signaling pathways, suggesting its therapeutic potential for neurodegenerative diseases.

BACKGROUND: Reperfusion of ischemic myocardium is clinically encountered during thrombolytic therapy of acute myocardial infarction, percutaneous transluminal coronary angioplasty(PTCA), and coronary artery bypass graft(CABG). Reperfusion results in endothelial dysfunction characterized by a reduced release of endothelium-derived relaxing factor(EDRF) in animal studies. Studies with experimental animals have emphasized the role of oxygen free radicals and lipid peroxidation in pathophysiology of reperfusion injury and myocardial stunning. The object of this study is to determine whether endothelial dysfunction was developed after open heart surgery and to evaluated the role of oxygen free radical and lipid peroxidation in reperfusion injury. METHODS: The study group was comprised 13 patients who underwent open heart surgery(male/female : 2/11, mean age : 43+/-4 year, Atrial septal defect in 4, Ventricular septal defect in 1, Mitral regurgitation in 2, Tetralogy of Fallot in 1, and Aortic stenosis and Regurgitation with Mitral stenosis in 5 patients). The endothelial function was evaluated with the vasomotor response to acetylcholine and nitroglycerin by change of arterial diameter during the continous infusion of acetylcholin, from 10(-9) to 10(-6) molar concentration to the coronary artery and intracoronary injection of 200microg nitroglycerin after acetylcholine infusion. The infusion study was performed before and 10 days after surgery. For analysis of the role of oxygen free radical and lipid peroxidation in reperfusion injury, blood samples for malondialdehyde and neutrophil respiratory burst test(hydrogen peroxide amount of neutrophils) were obtained in pre-declamping of aorta and 5 min, 10 min, and 20 min after declamping of aorta from coronary sinus. RESULTS: 1) The vasoconstrictor response to acetylcholine, 10(-9) to 10(-6)M concentration, at proximal and distal left anterior descending coronary artery, were increased significantly in post-operation infusion study but there was no singnificant difference in vasodilator response to nitroglycerin. 2) The mean absorbance value of malondialdehyde(MDA) in pre-declamping and 5min, 10min, and 20min after reperfusion were 96+/-12, 73+/-12, 89+/-11 and 77+/-12, respectively. There was no significant difference in plasma MDA level and hydrogen peroxide amount of neutrophils after reperfusion(aortic declamping). CONCLUSION: These data suggest that endothelium dependent vascular relaxation is impaired in patients with open heart surgery and post-ischemic reperfusion injury may be responsible for the abnormal response. But we did not determine the role of lipid peroxidation and oxygen free radical in reperfusion injury.
Acetylcholine ; Animals ; Aorta ; Aortic Valve Stenosis ; Coronary Artery Bypass ; Coronary Sinus ; Coronary Vessels ; Endothelium ; Free Radicals ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Hydrogen Peroxide ; Lipid Peroxidation* ; Malondialdehyde ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Molar ; Myocardial Infarction ; Myocardial Stunning ; Myocardium ; Neutrophils ; Nitroglycerin ; Oxygen* ; Plasma ; Relaxation ; Reperfusion Injury* ; Reperfusion* ; Respiratory Burst ; Tetralogy of Fallot ; Thoracic Surgery* ; Thrombolytic Therapy

BACKGROUND: Reperfusion of ischemic myocardium is clinically encountered during thrombolytic therapy of acute myocardial infarction, percutaneous transluminal coronary angioplasty(PTCA), and coronary artery bypass graft(CABG). Reperfusion results in endothelial dysfunction characterized by a reduced release of endothelium-derived relaxing factor(EDRF) in animal studies. Studies with experimental animals have emphasized the role of oxygen free radicals and lipid peroxidation in pathophysiology of reperfusion injury and myocardial stunning. The object of this study is to determine whether endothelial dysfunction was developed after open heart surgery and to evaluated the role of oxygen free radical and lipid peroxidation in reperfusion injury. METHODS: The study group was comprised 13 patients who underwent open heart surgery(male/female : 2/11, mean age : 43+/-4 year, Atrial septal defect in 4, Ventricular septal defect in 1, Mitral regurgitation in 2, Tetralogy of Fallot in 1, and Aortic stenosis and Regurgitation with Mitral stenosis in 5 patients). The endothelial function was evaluated with the vasomotor response to acetylcholine and nitroglycerin by change of arterial diameter during the continous infusion of acetylcholin, from 10(-9) to 10(-6) molar concentration to the coronary artery and intracoronary injection of 200microg nitroglycerin after acetylcholine infusion. The infusion study was performed before and 10 days after surgery. For analysis of the role of oxygen free radical and lipid peroxidation in reperfusion injury, blood samples for malondialdehyde and neutrophil respiratory burst test(hydrogen peroxide amount of neutrophils) were obtained in pre-declamping of aorta and 5 min, 10 min, and 20 min after declamping of aorta from coronary sinus. RESULTS: 1) The vasoconstrictor response to acetylcholine, 10(-9) to 10(-6)M concentration, at proximal and distal left anterior descending coronary artery, were increased significantly in post-operation infusion study but there was no singnificant difference in vasodilator response to nitroglycerin. 2) The mean absorbance value of malondialdehyde(MDA) in pre-declamping and 5min, 10min, and 20min after reperfusion were 96+/-12, 73+/-12, 89+/-11 and 77+/-12, respectively. There was no significant difference in plasma MDA level and hydrogen peroxide amount of neutrophils after reperfusion(aortic declamping). CONCLUSION: These data suggest that endothelium dependent vascular relaxation is impaired in patients with open heart surgery and post-ischemic reperfusion injury may be responsible for the abnormal response. But we did not determine the role of lipid peroxidation and oxygen free radical in reperfusion injury.
Acetylcholine ; Animals ; Aorta ; Aortic Valve Stenosis ; Coronary Artery Bypass ; Coronary Sinus ; Coronary Vessels ; Endothelium ; Free Radicals ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Hydrogen Peroxide ; Lipid Peroxidation* ; Malondialdehyde ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Molar ; Myocardial Infarction ; Myocardial Stunning ; Myocardium ; Neutrophils ; Nitroglycerin ; Oxygen* ; Plasma ; Relaxation ; Reperfusion Injury* ; Reperfusion* ; Respiratory Burst ; Tetralogy of Fallot ; Thoracic Surgery* ; Thrombolytic Therapy

Pulmonary embolism is one of the most common acute pulmonary disease in the adult general hospital populalion. However, the disease is still frequenfly unsuspected and underdiagnosed due to the nonspecifieity of both clinical findings and laboratory tests. The chest radiography in a patient suspected acute pulmonary embolism do not provide adequate information to establish or exclude the diagnosis of pulmonary embolism. Even in the case of infarction, there is no pathognomonic clues on the chest film. Rarely infarction presents unusual roentgenologic manifestation such as lobar consolidation, coin lesion, multinodular opacity, or massive pleural effusion. Especially, lobar consolidation in pulmonary embolism might mislead into the diagnosis of pneumonia. We experienced a case of pulmonary embolism presenting lobar consolidation in a 62 years old woman, originated from deep vein thrombosis. She took a compression stocking and underwent anticoagulant therapy with excellent outcome.
Adult ; Diagnosis ; Female ; Hospitals, General ; Humans ; Infarction ; Lung Diseases ; Middle Aged ; Numismatics ; Pleural Effusion ; Pneumonia ; Pulmonary Embolism ; Radiography ; Respiratory Insufficiency* ; Stockings, Compression ; Thorax ; Venous Thrombosis