Laboratory diagnostic methods, applied for the diagnosis of Acanthamoeba Keratitis, were evaluated for their usefulness in 16 patients of suspicious Acanthamoeba keratitis. Wet smear, Acridine orange(AO) stain, Gram stain and culture on nonnuturent agar plate were routinely used in all patients, and among them, and used saline of 7 contact lens not ideal for the corneal scraping specimens. AO and Gram stains were very useful in the identification of acanthamoeba, and culture on nonnutrient agar plates was essential to confirm this infection. Light and electron microscopic examinations were also useful in patients with negative results of ordinary diagnostic techniques. Suspicion of Acanthamoeba infection in patients that are recalcitrant to antibiotic treatment or related to contact lens wear, is the mont important step for the diagnosis of Acanthamoeba Keratitis. And also examination of corneal specimens by experienced observer is prerequisite for the accurate diagnosis of Acanthamoeba keratitis.
Acanthamoeba ; Acanthamoeba Keratitis ; Agar ; Clinical Laboratory Techniques* ; Coloring Agents ; Diagnosis ; Humans ; Keratitis*

Hepatitis C virus (HCV) infection is remarkably efficient in establishing viral persistence, leading to the development of liver cirrhosis and hepatocellular carcinoma (HCC). Direct-acting antiviral agents (DAAs) are promising HCV therapies to clear the virus. However, recent reports indicate potential increased risk of HCC development among HCV patients with cirrhosis following DAA therapy. CD8+ T-cells participate in controlling HCV infection. However, in chronic hepatitis C patients, severe CD4+ and CD8+ T-cell dysfunctions have been observed. This suggests that HCV may employ mechanisms to counteract or suppress the host T-cell responses. The primary site of viral replication is within hepatocytes where infection can trigger the expression of costimulatory molecules and the secretion of immunoregulatory cytokines. Numerous studies indicate that HCV infection in hepatocytes impairs antiviral host immunity by modulating the expression of immunoregulatory molecules. Hepatocytes expressing whole HCV proteins upregulate the ligands of programmed cell death protein 1 (PD-1), programmed death-ligand 1 (PD-L1), and transforming growth factor β (TGF-β) synthesis compared to those in hepatocytes in the absence of the HCV genome. Importantly, HCV-infected hepatocytes are capable of inducing regulatory CD4+ T-cells, releasing exosomes displaying TGF-β on exosome surfaces, and generating follicular regulatory T-cells. Recent studies report that the expression profile of exosome microRNAs provides biomarkers of HCV infection and HCV-related chronic liver diseases. A better understanding of the immunoregulatory mechanisms and identification of biomarkers associated with HCV infection will provide insight into designing vaccine against HCV to bypass HCV-induced immune dysregulation and prevent development of HCV-associated chronic liver diseases.

The liver lies at the intersection of multiple metabolic pathways and consequently plays a central role in lipid metabolism. Pathological disturbances in hepatic lipid metabolism are characteristic of chronic metabolic diseases, such as obesity-mediated insulin resistance, which can result in nonalcoholic fatty liver disease (NAFLD). Tissue damage induced in NAFLD activates and recruits liver-resident and non-resident immune cells, resulting in nonalcoholic steatohepatitis (NASH). Importantly, NASH is associated with an increased risk of significant clinical sequelae such as cirrhosis, cardiovascular diseases, and malignancies. In this review, we describe the immunopathogenesis of NASH by defining the known functions of immune cells in the progression and resolution of disease.
Cardiovascular Diseases ; Fatty Liver ; Fibrosis ; Insulin Resistance ; Lipid Metabolism ; Liver ; Metabolic Diseases ; Metabolic Networks and Pathways ; Non-alcoholic Fatty Liver Disease*

Spindle-cell carcinoma of the esophagus is a rare malignant tumor composed of both carcinomatous and sarcomatous elements, and has generated many terminology problems. It is characterized by a bulky polypoid intraluminal mass with a lobulated surface located in the middle third of the esophagus. Local expansion of this organ is observed. The lesion may be pedunculated but despite its bulk, causes little obstruction. We report the imaging findings of a case of spindle-cell carcinoma arising in the upper esophagus.
Carcinoma* ; Esophagus*

BACKGROUND AND OBJECTIVES: We assessed plaque erosion of culprit lesions in patients with acute coronary syndrome in real world practice. SUBJECTS AND METHODS: Culprit lesion plaque rupture or plaque erosion was diagnosed with optical coherence tomography (OCT). Intravascular ultrasound (IVUS) was used to determine arterial remodeling. Positive remodeling was defined as a remodeling index (lesion/reference EEM [external elastic membrane area) >1.05. RESULTS: A total of 90 patients who had plaque rupture showing fibrous-cap discontinuity and ruptured cavity were enrolled. 36 patients showed definite OCT-plaque erosion, while 7 patients had probable OCT-plaque erosion. Overall, 26% (11/43) of definite/probable plaque erosion had non-ST elevation myocardial infarction (NSTEMI) while 35% (15/43) had ST elevation myocardial infarction (STEMI). Conversely, 14.5% (13/90) of plaque rupture had NSTEMI while 71% (64/90) had STEMI (p<0.0001). Among plaque erosion, white thrombus was seen in 55.8% (24/43) of patients and red thrombus in 27.9% (12/43) of patients. Compared to plaque erosion, plaque rupture more often showed positive remodeling (p=0.003) with a larger necrotic core area examined by virtual histology (VH)-IVUS, while negative remodeling was prominent in plaque erosion. Overall, 65% 28/43 of plaque erosions were located in the proximal 30 mm of a culprit vessel-similar to plaque ruptures (72%, 65/90, p=0.29). CONCLUSION: Although most of plaque erosions show nearly normal coronary angiogram, modest plaque burden with negative remodeling and an uncommon fibroatheroma might be the nature of plaque erosion. Multimodality intravascular imaging with OCT and VH-IVUS showed fundamentally different pathoanatomic substrates underlying plaque rupture and erosion.
Acute Coronary Syndrome* ; Humans ; Membranes ; Myocardial Infarction ; Plaque, Atherosclerotic ; Rupture* ; Thrombosis ; Tomography, Optical Coherence ; Ultrasonography

Infectious keratitis is the most common serious ocular infection, and may be caused by various bacteria, fungi, viruses and parasites. The authors performed prospectively an epidemiological study to identify risk factors and causative organisms, and to evaluate clinical manifestations, methods and results of treatment in infectious keratitis under the identical protocol from April 1995 to September 1997. Logistic regression analysis [univariate analysis and multivariate analysis] was used to evaluate possible risk factors. Six hundred sixty cases of infectious keratitis reported from 19 hospitals were studied. Two hundred eighty-three organisms[247 bacteria, 32 fungi, 4 acanthamoeba] were detected in 626 eyes with infectious keratitis excluding 34 pherpetic keratitis. The Pseudomonas aeruginosa, coagulase negative staphylococcus, Staphylococcus aureus and Serratia marcescens were the major orgnisms in bacterial keratitis. Aspergillus, Fusarium and Candida were the major isolates in fungal keratitis. Contact lens wear was a risk factor for bacterial keratitis. Female, age[less than 40 years] and occupation[student, house-wife, office worker, servise] were associated with bacterial keratitis. Risk factors in herpetic keratitis were age[between 40 and 59 years] and ocular adnexal diseases. Male was associated factor with herpetic keratitis.
Adnexal Diseases ; Aspergillus ; Bacteria ; Candida ; Coagulase ; Epidemiologic Studies ; Epidemiology* ; Eye Infections ; Female ; Fungi ; Fusarium ; Humans ; Keratitis ; Keratitis, Herpetic ; Logistic Models ; Male ; Parasites ; Prospective Studies ; Pseudomonas aeruginosa ; Risk Factors ; Serratia marcescens ; Staphylococcus ; Staphylococcus aureus

BACKGROUND AND PURPOSE: Intracranial atherosclerotic stenosis (ICAS) is considered as a major cause of stroke. The carotid intima-media thickness (CIMT), which accurately reflects the burden of generalized atherosclerosis, is also associated with stroke. The aim of this study was to determine the association between the CIMT and ICAS responses to medical treatment. METHODS: This study constituted part of the "Trial of cilostazol in symptomatic intracranial arterial stenosis"-2 that evaluated the ICAS response after randomized antiplatelet treatment. Magnetic resonance angiography and CIMT measurement were performed at baseline and after 7 months of treatment. CIMT was measured using semiautomated software, and was presented as maximum (CIMT-max) and average (CIMT-ave) values. The change in CIMT was compared relative to the ICAS response (i.e., progression, no-change, and regression). Ordinal logistic regression and analysis of covariance (ANCOVA) were used to analyze the association between the responses. RESULTS: Among the 101 enrolled patients, 85 underwent follow-up CIMT measurement. CIMT increased most in the ICAS progression group (CIMT-max: 0.09+/-0.23, CIMT-ave: 0.04+/-0.12), and to a lesser degree in the no-change group (CIMT-max: 0.02+/-0.16, CIMT-ave: 0.02+/-0.11), but decreased in patients with ICAS regression (CIMT-max: -0.04+/-0.11, CIMT-ave: -0.03+/-0.07; CIMT-max: p=0.010, CIMT-ave: p=0.015). Ordinal logistic regression analysis demonstrated that the change in CIMT-max was independently associated with the ICAS response (p=0.032). However, the ANCOVA revealed that the reverse was not true, in that the ICAS response was not independently associated with the change in CIMT after adjusting for confounding factors. CONCLUSIONS: The ICAS response may be associated with the CIMT response to medical treatment.
Atherosclerosis ; Carotid Intima-Media Thickness* ; Constriction, Pathologic ; Follow-Up Studies ; Humans ; Intracranial Arteriosclerosis* ; Logistic Models ; Magnetic Resonance Angiography ; Stroke ; Tetrazoles

BACKGROUND AND PURPOSE: The pathophysiology of post-stroke depression (PSD) is complex and may differ according to an individual’s mood immediately after stroke. Here, we compared the therapeutic response and clinical characteristics of PSD at a later stage between patients with and without depression immediately after stroke. METHODS: This study involved a post hoc analysis of data from EMOTION (ClinicalTrials.gov NCT01278498), a placebo-controlled, double-blind trial that examined the efficacy of escitalopram (10 mg/day) on PSD and other emotional disturbances among 478 patients with acute stroke. Participants were classified into the Baseline-Blue (patients with baseline depression at the time of randomization, defined per the Montgomery-Asberg Depression Rating Scale [MADRS] ≥8) or the Baseline-Pink groups (patients without baseline depression). We compared the efficacy of escitalopram and predictors of 3-month PSD (MADRS ≥8) between these groups. RESULTS: There were 203 Baseline-Pink and 275 Baseline-Blue patients. The efficacy of escitalopram in reducing PSD risk was more pronounced in the Baseline-Pink than in the Baseline-Blue group (p for interaction=0.058). Several risk factors differentially affected PSD development based on the presence of baseline depression (p for interaction < 0.10). Cognitive dysfunction was an independent predictor of PSD in the Baseline-Blue, but not in the Baseline-Pink group, whereas the non-use of escitalopram and being female were more strongly associated with PSD in the Baseline-Pink group. CONCLUSIONS: Responses to escitalopram and predictors of PSD 3 months following stroke differed based on the presence of baseline depression. Our data suggest that PSD pathophysiology is heterogeneous; therefore, different therapeutic strategies may be needed to prevent PSD emergence following stroke.
Affective Symptoms ; Anger ; Citalopram ; Depression* ; Female ; Humans ; Random Allocation ; Risk Factors ; Stroke