Purpose: To report a case of paraneoplastic autoimmune retinopathy in a patient with a history of testicular cancer.Case summary: A 29-year-old man presented with photopsia and floaters. Initial fundus examination revealed no abnormal findings. However, he returned 1 month later with complaints of visual field defects. Fundus examination revealed diffuse white spots in the macula and midperipheral retina and fundus autofluorescence demonstrated hyper-autofluorescence. Optical coherence tomography showed disruption of the ellipsoid zone sparing the fovea. Visual field examination revealed peripheral visual field defects and an electroretinogram showed reduced rod and cone cell responses. Considering his history of testicular cancer, serum paraneoplastic autoantibody panel testing was performed which revealed borderline levels of anti-recoverin antibody leading to a diagnosis of paraneoplastic autoimmune retinopathy. The patient was treated with oral steroids and mycophenolate mofetil for 1 year. However, there was no improvement in the subjective symptoms or ophthalmologic findings. Conclusions This case of paraneoplastic autoimmune retinopathy in a young man with a history of testicular cancer highlights an early clinical presentation of the disease. It is crucial to recognize that the initial clinical presentation of autoimmune retinopathy can be nonspecific.

Purpose: To report a case of paraneoplastic autoimmune retinopathy in a patient with a history of testicular cancer.Case summary: A 29-year-old man presented with photopsia and floaters. Initial fundus examination revealed no abnormal findings. However, he returned 1 month later with complaints of visual field defects. Fundus examination revealed diffuse white spots in the macula and midperipheral retina and fundus autofluorescence demonstrated hyper-autofluorescence. Optical coherence tomography showed disruption of the ellipsoid zone sparing the fovea. Visual field examination revealed peripheral visual field defects and an electroretinogram showed reduced rod and cone cell responses. Considering his history of testicular cancer, serum paraneoplastic autoantibody panel testing was performed which revealed borderline levels of anti-recoverin antibody leading to a diagnosis of paraneoplastic autoimmune retinopathy. The patient was treated with oral steroids and mycophenolate mofetil for 1 year. However, there was no improvement in the subjective symptoms or ophthalmologic findings. Conclusions This case of paraneoplastic autoimmune retinopathy in a young man with a history of testicular cancer highlights an early clinical presentation of the disease. It is crucial to recognize that the initial clinical presentation of autoimmune retinopathy can be nonspecific.

Purpose: To report a case of paraneoplastic autoimmune retinopathy in a patient with a history of testicular cancer.Case summary: A 29-year-old man presented with photopsia and floaters. Initial fundus examination revealed no abnormal findings. However, he returned 1 month later with complaints of visual field defects. Fundus examination revealed diffuse white spots in the macula and midperipheral retina and fundus autofluorescence demonstrated hyper-autofluorescence. Optical coherence tomography showed disruption of the ellipsoid zone sparing the fovea. Visual field examination revealed peripheral visual field defects and an electroretinogram showed reduced rod and cone cell responses. Considering his history of testicular cancer, serum paraneoplastic autoantibody panel testing was performed which revealed borderline levels of anti-recoverin antibody leading to a diagnosis of paraneoplastic autoimmune retinopathy. The patient was treated with oral steroids and mycophenolate mofetil for 1 year. However, there was no improvement in the subjective symptoms or ophthalmologic findings. Conclusions This case of paraneoplastic autoimmune retinopathy in a young man with a history of testicular cancer highlights an early clinical presentation of the disease. It is crucial to recognize that the initial clinical presentation of autoimmune retinopathy can be nonspecific.

Purpose: To compare the effectiveness of warm saline and anti-fog solution for preventing fogging of a non-contact wide-field viewing system during vitrectomy. Methods: Five liters of water at 36°C were placed in a transparent container. The fogging areas of wide-field lenses were microscopically measured. We created three groups: lenses soaked in normal saline at 25°C for 1 minute (control), lenses soaked in normal saline at 50°C for 1 minute (warm saline), and lenses that were wiped with a sponge soaked in anti-fog solution (ULTRASTOP pro med. Solution, Sigmapharm, Vienna, Austria) after prior soaking in normal saline at 25°C for 1 minute (anti-fog). Images of fogged areas were acquired at 10 seconds and 1, 3, and 5 minutes. Extent of fogged areas and central lens invasion were determined. All experiments were repeated 10 times. Results: In the control group, the entire areas were always completely fogged. The average fog coverage values were 4.34 ± 1.28, 6.30 ± 1.38, 56.00 ± 25.01, and 93.81 ± 5.88% at 10 seconds and 1, 3, and 5 minutes in the warm saline group and 4.74 ± 0.57, 7.35 ± 0.96, 10.13 ± 1.09, and 11.74 ± 1.74% in the anti-fog group, respectively. There were significant differences at 3 and 5 minutes (p = 0.029, p = 0.012). Fogging of the central lens was detected in 8 tests after 3 minutes and all 10 tests after 5 minutes in the warm saline group, but no fogging was detected in the anti-fog group. Conclusions Application of an anti-fog solution to a wide-field viewing lens prevents lens fogging during vitrectomy.

Ultraviolet (UV) irradiation is a relevant environment factor to induce cellular senescence and photoaging. Both autophagy- and silent information regulator T1 (SIRT1)-dependent pathways are critical cellular processes of not only maintaining normal cellular functions, but also protecting cellular senescence in skin exposed to UV irradiation. In the present studies, we investigated whether modulation of autophagy induction using a novel synthetic SIRT1 activator, heptasodium hexacarboxymethyl dipeptide-12 (named as Aquatide), suppresses the UVB irradiation-induced skin aging. Treatment with Aquatide directly activates SIRT1 and stimulates autophagy induction in cultured human dermal fibroblasts. Next, we found that Aquatide-mediated activation of SIRT1 increases autophagy induction via deacetylation of forkhead box class O (FOXO) 1. Finally, UVB irradiation-induced cellular senescence measured by SA-β-gal staining was significantly decreased in cells treated with Aquatide in parallel to occurring SIRT1 activation-dependent autophagy. Together, Aquatide modulates autophagy through SIRT1 activation, contributing to suppression of skin aging caused by UV irradiation.
Autophagy ; Cell Aging* ; Fibroblasts ; Humans ; Skin ; Skin Aging

A 43-year-old male presented with effort angina. Ammonia positron emission tomography (PET) revealed reversible perfusion defect in left anterior descending artery (LAD) and left circumflex artery (LCX) territories with decreased coronary flow reserve. Coronary angiogram showed significant stenosis in proximal LAD and intermediate diffuse stenosis in LCX and right coronary artery (RCA). Fractional flow reserve (FFR) showed similar results with ammonia PET. After percutaneous coronary intervention for LAD and LCX, flow and pressure checked by PET and FFR showed improvement. Simultaneously use of ammonia PET and FFR could be useful for determining ischemia-inducible lesion especially in diffuse intermediate lesion with discrepancy between functional studies.
Adult ; Ammonia ; Arteries ; Constriction, Pathologic ; Coronary Artery Disease ; Coronary Vessels ; Humans ; Male ; Percutaneous Coronary Intervention* ; Perfusion ; Positron-Emission Tomography*

Stent thrombosis is a fatal complication in patients who have undergone percutaneous coronary intervention, and discontinuation of anti-platelet agent is a major risk factor of stent thrombosis. We report a rare case of very late stent thrombosis (VLST) following discontinuation of anti-platelet agents in a patient who experienced acute myocardial infarction and essential thrombocytosis. She had undergone implantation of a drug eluting stent (DES) and a bare metal stent (BMS) two and half years prior to her presentation. VLST developed in DES, not in BMS, following interruption of anti-platelet therapy.
Drug-Eluting Stents ; Humans ; Myocardial Infarction ; Percutaneous Coronary Intervention ; Risk Factors ; Stents ; Thrombocythemia, Essential ; Thrombocytosis ; Thrombosis

BACKGROUND AND OBJECTIVES: It is well known that atherosclerosis is characterized by chronic inflammation of an injured intima and the pathological processes are initiated by an accumulation of morphologically distinct, modified forms of low density lipoprotein (LDL)-cholesterol. However, it is not well known whether the level of modified LDL-cholesterol has clinical significance for the patients who underwent percutaneous coronary intervention (PCI). SUBJECTS AND METHODS: Eighty seven patients (mean age: 63.0 +/- 11.1 years, 58 men) who underwent PCI were enrolled. The patients with stable or unstable angina pectoris were classified as group I (n=44, mean age: 62.4 +/- 9.3 years), and the patients with acute myocardial infarction were classified as group II (n=43, mean age: 63.6 +/- 12.7 years). Modified LDL-cholesterol was expressed semiquantitatively by agarose gel electrophoresis with using the charge modification frequency (CMF). The clinical and coronary angiographic data was analyzed. RESULTS: The clinical diagnosis was stable angina in 13 patients, unstable angina in 31 patients, non-ST elevation myocardial infarction in 5 patients and ST elevation myocardial infarction in 38 patients. There were no significant differences of the CMF between two groups (3.0 +/- 7.9 vs. 2.1 +/- 10.9, respectively, p=0.671). The diameter stenosis was severe in the patients with a CMF greater than 10 (84.0 +/- 10.4% vs. 78.6 +/- 13.7%, respectively, p=0.047). The six-month major adverse cardio-vascular events (MACEs) had no relationship with the CMF in group I. However, in group II, the 6-month MACEs developed more frequently in the patients with a CMF higher than 10 {2 (28%) for group ll vs. 2 (5%) for group 1, p=0.031}. The patients with acute myocardial infarction and whose CMF was higher than 10 had in-stent restenosis observed on their follow-up coronary angiography (p=0.003). CONCLUSION: A higher level of modified LDL-cholesterol is associated with severe angiographic findings and a poor prognosis for patients with acute myocardial infarction.
Acute Coronary Syndrome ; Angina, Stable ; Angina, Unstable ; Atherosclerosis ; Constriction, Pathologic ; Coronary Angiography ; Electrophoresis, Agar Gel ; Fees and Charges ; Follow-Up Studies ; Humans ; Inflammation ; Lipoproteins ; Myocardial Infarction ; Pathologic Processes ; Percutaneous Coronary Intervention ; Prognosis

The aim of this study was to examine the anti-inflammatory effect of abciximab-coated stent in a porcine coronary overstretch restenosis model. Ten abciximab-coated stents, ten sirolimus-eluting stents (SES), and ten paclitaxel-eluting stents (PES) were deployed with oversizing (stent/artery ratio 1.3:1) in porcine coronary arteries, and histopathologic analysis was done at 28 days after stenting. There were no significant differences in the neointima area normalized to injury score and inflammation score among the three stent groups (1.58+/-0.43 mm2, 1.57+/-0.39 mm2 in abciximab-coated stent group vs. 1.69+/-0.57 mm2, 1.72+/-0.49 mm2 in the SES group vs. 1.92+/-0.86 mm2, 1.79+/-0.87 mm2 in the PES group, respectively). In the neointima, most inflammatory cells were lymphohistiocytes. Significant positive correlations were found between the extent of inflammatory reaction and the neointima area (r=0.567, p<0.001) and percent area stenosis (r=0.587, p<0.001). Significant correlations were found between the injury score and neointimal area (r=0.645, p<0.001), between the injury score and the inflammation score (r=0.837, p<0.001), and between the inflammation score and neointimal area (r=0.536, p=0.001). There was no significant difference in the inflammatory cell counts normalized to injury score among the three stent groups (75.5+/-23.1/microliter in abciximabcoated stent group vs. 78.8+/-33.2/microliter in the SES group vs. 130.3+/-46.9/microliter in the PES group). Abciximab-coated stent showed comparable inhibition of inflammatory cell infiltration and neointimal hyperplasia with other drug-eluting stents in a porcine coronary restenosis model.
Animals ; Anti-Bacterial Agents/administration & dosage ; Anti-Inflammatory Agents/*pharmacology ; Antibodies, Monoclonal/administration & dosage/*pharmacology ; Arteries/injuries/pathology ; Constriction, Pathologic ; Coronary Restenosis/*therapy ; Disease Models, Animal ; *Drug-Eluting Stents ; Female ; Hyperplasia ; Immunoglobulin Fab Fragments/administration & dosage/*pharmacology ; Inflammation ; Paclitaxel/administration & dosage ; Sirolimus/administration & dosage ; Swine ; Tunica Intima/pathology

BACKGROUND AND OBJECTIVES: Endothelial dysfunction and increased vascular inflammation may be associated with variant angina (VA). However, their exact roles remain to be clarified. The aim of the presents study is to investigate whether the level of inflammation markers and the flow-mediated dilation (FMD) are related to VA. SUBJECTS AND METHODS: The study included 46 patients (VA group: 53.9+/-12.0 years, 20 males) with positive spasm provocation tests and they were without significant coronary stenosis, and 14 patients (control group: 46.6+/-13.5 years, 7 males) with negative spasm provocation tests and they were without significant coronary stenosis. The clinical characteristics and inflammatory markers, including the high sensitive C-reactive protein (hsCRP) level, the monocyte count and the von Willebrand factor (vWF) level, and the FMD were compared between the two groups. The FMD and inflammatory markers were measured in the morning before performing the ergonovine provocation coronary angiogram. RESULTS: The level of vWF was significantly higher in the VA group than in the control group (166.5+/-41.9% vs. 118.0+/-65.3%, respectively, p=0.029). The FMD was significantly decreased in the VA group compared with the control group (9.2+/-4.3% vs. 12.4+/-4.2%, respectively, p=0.021). Nitrate-mediated dilation did not differ between the two groups. The levels of the monocyte count, hs-CRP and homocysteine were higher in the VA group than in the control group (554.7+/-261.0/mm3 vs. 440.7+/-136.0/mm3, respectively, p=0.039; 0.3+/-0.4 mg/dL vs. 0.1+/-0.1 mg/dL, respectively, p=0.029; 7.54+/-4.0micronmol/L vs. 5.92+/-1.6micronmol/L, respectively, p=0.033). CONCLUSION: The results of this study suggested that increased inflammatory markers and endothelial dysfunction may be associated with variant angina.
Angina Pectoris ; C-Reactive Protein ; Coronary Stenosis ; Endothelium ; Ergonovine ; Homocysteine ; Humans ; Inflammation ; Monocytes ; Spasm ; von Willebrand Factor