Anatomical Popliteal Artery Entrapment Syndrome Caused by an Aberrant Plantaris Muscle

PURPOSE: We report on cases of anatomical popliteal artery entrapment syndrome (PAES) caused by an aberrant plantaris muscle and highlight the involvement of this muscle in PAES. MATERIALS AND METHODS: Seven symptomatic PAES legs in six patients treated at The Division of Vascular Surgery, Asan Medical Center, Seoul, Korea, between 1995 and 2011 were included in this study. We retrospectively analyzed patient records, magnetic resonance imaging (MRI) and/or computed tomography (CT) scans of the knee joint, Doppler pressure studies, CT angiographies, and conventional femoral arteriographies. RESULTS: Five males and one female patient with a median age of 32 (18-53) years old were enrolled in the study. All patients complained of intermittent claudication of the affected leg. All aberrant plantaris muscles were higher and more medially located than normal plantaris muscles, causing occlusion of the popliteal artery upon forced plantar flexion of the ankle. For arterial lesions, five occlusions of the popliteal artery and two patent popliteal arteries with positive provocation were noted. As for treatment, myotomy of the aberrant plantaris muscle was done for two non-occlusive PAES legs. For occlusive PAES legs, one thrombectomy, one saphenous vein graft interposition of the popliteal artery followed by myotomy, and two below-knee femoro-popliteal bypasses were performed. The median follow-up period was 88 (7-148) months. CONCLUSION: An aberrant plantaris muscle can cause anatomical PAES. Classification or diagnosis of PAES should be based on axial studies using CT scans or MRI using various reconstruction methods. Treatment, including myotomy of the plantaris muscle, should be individualized.

Mitochondrial Dynamics in the Heart as a Novel Therapeutic Target for Cardioprotection / 전남의대학술지

Traditionally, mitochondria have been regarded solely as energy generators for cells; however, accumulating data have demonstrated that these complex organelles play a variety of roles within the cardiomyocyte that extend beyond this classic function. Mitochondrial dynamics involves mitochondrial movements and morphologic alterations by tethering, fusion, and fission, which depend on cellular energy requirements and metabolic status. Many studies have indicated that mitochondrial dynamics may be a fundamental component of the maintenance of normal cellular homeostasis and cardiac function. Mitochondrial dynamics is controlled by the protein machinery responsible for mitochondrial fusion and fission, but cardiomyocytes are densely packed as part of an intricate cytoarchitecture for efficient and imbalanced contraction; thus, mitochondrial dynamics in the adult heart are restricted and occur more slowly than in other organs. Cardiac mitochondrial dynamics is important for cardiac physiology in diseased conditions such as ischemia-reperfusion (IR) injury. Changes in mitochondrial morphology through modulation of the expression of proteins regulating mitochondrial dynamics demonstrates the beneficial effects on cardiac performance after IR injury. Thus, accurately defining the roles of mitochondrial dynamics in the adult heart can guide the identification and development of novel therapeutic targets for cardioprotection. Further studies should be performed to establish the exact mechanisms of mitochondrial dynamics.

Mitochondrial Dynamics in the Heart as a Novel Therapeutic Target for Cardioprotection / 전남의대학술지

Traditionally, mitochondria have been regarded solely as energy generators for cells; however, accumulating data have demonstrated that these complex organelles play a variety of roles within the cardiomyocyte that extend beyond this classic function. Mitochondrial dynamics involves mitochondrial movements and morphologic alterations by tethering, fusion, and fission, which depend on cellular energy requirements and metabolic status. Many studies have indicated that mitochondrial dynamics may be a fundamental component of the maintenance of normal cellular homeostasis and cardiac function. Mitochondrial dynamics is controlled by the protein machinery responsible for mitochondrial fusion and fission, but cardiomyocytes are densely packed as part of an intricate cytoarchitecture for efficient and imbalanced contraction; thus, mitochondrial dynamics in the adult heart are restricted and occur more slowly than in other organs. Cardiac mitochondrial dynamics is important for cardiac physiology in diseased conditions such as ischemia-reperfusion (IR) injury. Changes in mitochondrial morphology through modulation of the expression of proteins regulating mitochondrial dynamics demonstrates the beneficial effects on cardiac performance after IR injury. Thus, accurately defining the roles of mitochondrial dynamics in the adult heart can guide the identification and development of novel therapeutic targets for cardioprotection. Further studies should be performed to establish the exact mechanisms of mitochondrial dynamics.

Retrospective Comparisons about Effects of Angiotensin II Receptor Blocker and/or Steroid on Proteinuria Reduction and Renal Protection in IgA Nephropathy Patients with Proteinuria less than 1 g/g / 대한신장학회지

PURPOSE: It remains controversial how to treat the IgA nephropathy (IgAN) patients with proteinuria <1g/day. We investigated effects of single or combined use of angiotensin II receptor blocker (ARB) and steroid on proteinuria reduction and renal protection in IgAN patients with normal renal function and urine protein/creatinine ratio (PCR) < or =1 g/g. METHODS: Oral prednisolone was given at an initial dose of 1 mg/kg every day for 2 months and then gradually tapered for 4 months. An ARB irbesartan or losartan or valsartan was given until the end of follow-up. RESULTS: Over a mean follow-up period of about 40 mo, the urine PCR decreased from 0.64+/-0.29 g/g to 0.32+/-0.31 g/g in the combination group (n=26) (p<0.05). But in ARB (n=17) and steroid groups (n=20), it decreased from 0.56+/-0.26 g/g to 0.54+/-0.45 g/g and from 0.50+/-0.26 g/g to 0.34+/-0.32 g/g, respectively, while there were no statistical significances. Serum creatinine decreased from 0.83+/-0.13 mg/dL to 0.73+/-0.14 mg/dL in steroid group (p<0.01), and from 0.92+/-0.17 mg/dL to 0.81+/-0.23 mg/dL in combination group (p<0.01). But in ARB group, no statistical significance was noticed. All patients achieved the BP goal < or =130/80 mmHg by adding anti-hypertensive drugs, if necessary. CONCLUSION: Our results indicate that (steroid or) combination therapy reduced proteinuria and improved renal function in the patients with proteinuria < or =1 g/g. Further prospective controlled studies are required to clarify the effect of steroid over the long term.

Primary Sjogren's Syndrome Associated with Membranous Glomerulonephritis / 대한신장학회잡지

Sjogren's syndrome is a chronic autoimmune disorder causing dry eye or dry mouth from the lymphocytic infiltration in the lacrimal gland and the salivary gland. Renal involvement is seen in about 20-40% of patients with primary Sjogren's syndrome. Tubulointerstitial nephritis is the most common renal complication in primary Sjogren's syndrome. However, glomerulonephritis such as membranoproliferative glomerulonephritis, membranous glomerulonephritis rarely may complicate primary Sjogren's syndrome. Sjogren's syndrome associated with glomerulonephritis hasn't been reproted yet in Korea. We report nephrotic syndrome associated with membranous glomerulonephritis in a case with primary Sjogren's syndrome. Nephrotic syndrome resolved after treatment with corticosteroid.

A Study on the Distribution of NADPH-Diaphorase and Neuropeptide Y Positive Neurons in the Cerebral Cortex of Apodemus Agrarius / 대한해부학회지

Apodemus agrarius has been using for experimental purpose to identifying the route of infection and pathogenesis of korean hemorrhagic fever. However, despite the increasing amount of information being published at present about the physiologic and ecologic characteristics of Apodemus, few data are availalle about the morphologic findings in the brain. The NADPH-diaphorase[NADPH-d] positive neurons, uniquely resistant to toxic insults and neurodegenerative diseases, have been colocalized with neurons in the brain and peripheral tissue containing nitric oxide synthase, which generates nitric oxide, a recently identified neuronal messenger molecule. In this study we used NADPH-d histochemistry to evaluate the distribution of neuropeptide Y-immunoreactive[NPY-IR] cells within neurons which contain nitric oxide synthase. In the cerebral cortex of Apodemus agrarius, NADPH-d positive and NPY-IR neurons were observed in all cortical layers, but they were concentrated in two bands layer II/III and V/VI extending into the subcortical white matter. Double labeling for NADPH-d and NPY showed colocalization of NPY with NADPH-d in numerous neurons of the cerebral cortex. The data obtained showed that about 74-79% of NPY-IR neurons contained NADPH-d in the neocortex and that 77-89% in the allocortex. The number of NPY-IR/NADPH-d positive neurons was about 10-13 per unit area [2,500,000 micrometer] in the neocortex and about 11-25 in the allocortex except retrosplenial cortex. In the retrosplenial cortex, the number of double labeled neurons was about 5 per unit area. NPY-IR and NADPH-d positive neurons were predominantly medium-sized with extended, multipolar or bipolar dendritic branches which belong to fusiform or stellate cell types. A moderately dense network of fine, varicose NADPH-d positive fibers was present throughout all cortical layers.