The most feared complication of left ventricular thrombus (LVT) is the occurrence of systemic thromboembolic events, especially in the brain. Herein, we report a patient with severe sepsis who suffered recurrent devastating embolic stroke. Transthoracic echocardiography revealed apical ballooning of the left ventricle with a huge LVT, which had not been observed in chest computed tomography before the stroke. This case emphasizes the importance of serial cardiac evaluation in patients with stroke and severe medical illness.
Brain ; Echocardiography ; Heart Ventricles ; Humans ; Sepsis ; Shock, Septic* ; Stroke* ; Thorax ; Thrombosis*

PURPOSE: To compare the efficacy of intravitreal dexamethasone implants according to previous response to bevacizumab treatment in patients with diabetic macular edema (DME).METHODS: Forty-nine eyes of 49 patients who received intravitreal dexamethasone implants for DME were reviewed retrospectively. Of these patients, 13 were treatment-naïve and 36 had previously received intravitreal injections of bevacizumab. Of the 36 previously treated patients, 24 comprised a refractory group showing no response to previous injections, and 12 comprised a responder group showing a response to previous treatments. The best-corrected visual acuity, central macular thickness (CMT), and retreatment percentages were assessed monthly for 6 months.RESULTS: After the intravitreal dexamethasone implants, visual acuity improved significantly over 6 months in the treatment-naïve group, while in the responder group, a significant improvement in visual acuity was seen at the 2-month follow-up. In the refractory group, there was no significant improvement in visual acuity during the follow-up period. The CMT showed a significant decrease in all three groups, and there was no significant difference in the CMT among the three groups at any time point. Five patients in the treatment-naive group (38.5%), 19 patients in the refractory group (79.2%), and nine patients in the responder group (75.0%) needed retreatment for recurrent macular edema, and there was a significant difference among the three groups in the rate of recurrence (p = 0.034).CONCLUSIONS: In DME patients, intravitreal dexamethasone implants were associated with a significant anatomical improvement irrespective of previous bevacizumab treatment response. However, the treatment-naïve and responder groups showed improvements in visual acuity, whereas the refractory group showed limited improvement.
Bevacizumab ; Dexamethasone ; Follow-Up Studies ; Humans ; Intravitreal Injections ; Macular Edema ; Recurrence ; Retreatment ; Retrospective Studies ; Visual Acuity

Purpose: We used optical coherence tomography angiography (OCTA) to investigate the correlation between retinal microvascular alteration and peripheral retinal ischemia (evaluated with the aid of ultra-widefield fluorescein angiography [UWFA]) in patients with branch retinal vein occlusion (BRVO). Methods: We retrospectively analyzed 23 eyes of 23 patients with BRVO. Vessel density (VD) and the foveal avascular zone area were measured using OCTA; UWFA was employed to measure the peripheral ischemic area and the ischemic indices (ISIs) of the entire retina and concentric retinal zones. We derived correlations between these factors. Receiver operating characteristic curves were used to predict ISI employing OCTA parameters. Results: The VDs of the superficial capillary plexus (SCP) correlated with the ischemic areas of all retinal zones, and the ISIs of all zones except the far-peripheral area (FPA). The VD of the deep capillary plexus (DCP) correlated significantly with the ischemic areas and ISIs of all retinal zones except those of the FPA. On multivariate linear regression analysis, the VD was significantly correlated with the ISI; when the VDs of the SCP and DCP decreased to 24.7 and 26.1% respectively, this raised a suspicion of severe ischemic conditions with ISI > 10%. Conclusions A decrease in the BRVO VD was associated with the severity of peripheral ischemia. Our findings may aid identification of high-risk patients who require invasive fluorescein angiography.

Purpose: Melanoma-associated antigen C2 (MAGEC2) is an oncogene associated with various types of cancers. However, the biological function of MAGEC2 in circulating tumor cells remains unclear. In this study, we investigated the role of MAGEC2 using adapted suspension cells (ASCs), which were previously developed to study circulating tumor cells (CTCs). Methods: Differential gene expression in adherent cells (ADs) and ASCs was examined using RNA-seq analysis. MAGEC2 expression was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR), immunoblotting, and ChIP-seq analysis. Depletion of MAGEC2 expression was performed using siRNA. MAGEC2-depleted ADs and ASCs were used to investigate changes in the proliferation rate and cell cycle. Then, the protein levels of signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3, and downstream of STAT3 were measured using control and MAGEC2-depleted ADs and ASCs. In ASCs, the direct effect of active STAT3 inhibition with Stattic, a STAT3 inhibitor, was assessed in terms of proliferation and apoptosis. Finally, an Annexin V/7-AAD assay was performed to determine the percentage of apoptotic cells in the Stattic-treated cells. Results: MAGEC2 was highly expressed in ASCs when compared with ADs. Depletion of MAGEC2 reduced the proliferation rate and viability of ASCs. To elucidate the underlying mechanism, the level of STAT3 was examined owing to its oncogenic properties. Tyrosinephosphorylated active STAT3 was highly expressed in ASCs and decreased in MAGEC2-depleted ASCs. Furthermore, on treating ASCs with Stattic, an active STAT3 inhibitor, the cells were markedly sensitive to intrinsic pathway-mediated apoptosis. Conclusions High MAGEC2 expression may play an important role in the survival of ASCs by maintaining the expression of activated STAT3 to prevent apoptotic cell death.

Purpose: Melanoma-associated antigen C2 (MAGEC2) is an oncogene associated with various types of cancers. However, the biological function of MAGEC2 in circulating tumor cells remains unclear. In this study, we investigated the role of MAGEC2 using adapted suspension cells (ASCs), which were previously developed to study circulating tumor cells (CTCs). Methods: Differential gene expression in adherent cells (ADs) and ASCs was examined using RNA-seq analysis. MAGEC2 expression was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR), immunoblotting, and ChIP-seq analysis. Depletion of MAGEC2 expression was performed using siRNA. MAGEC2-depleted ADs and ASCs were used to investigate changes in the proliferation rate and cell cycle. Then, the protein levels of signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3, and downstream of STAT3 were measured using control and MAGEC2-depleted ADs and ASCs. In ASCs, the direct effect of active STAT3 inhibition with Stattic, a STAT3 inhibitor, was assessed in terms of proliferation and apoptosis. Finally, an Annexin V/7-AAD assay was performed to determine the percentage of apoptotic cells in the Stattic-treated cells. Results: MAGEC2 was highly expressed in ASCs when compared with ADs. Depletion of MAGEC2 reduced the proliferation rate and viability of ASCs. To elucidate the underlying mechanism, the level of STAT3 was examined owing to its oncogenic properties. Tyrosinephosphorylated active STAT3 was highly expressed in ASCs and decreased in MAGEC2-depleted ASCs. Furthermore, on treating ASCs with Stattic, an active STAT3 inhibitor, the cells were markedly sensitive to intrinsic pathway-mediated apoptosis. Conclusions High MAGEC2 expression may play an important role in the survival of ASCs by maintaining the expression of activated STAT3 to prevent apoptotic cell death.

Acute myocardial infarction often evolves from a mild coronary lesion. Therefore, the evaluation and management of intermediate coronary stenosis are important to prevent cardiac events. However, the decision on how to treat these lesions is challenging. Here, we report acute myocardial infarction occurring at a preexisting intermediate coronary stenosis based on invasive coronary angiography performed 10 days before the event.
Coronary Angiography ; Coronary Stenosis* ; Coronary Vessels* ; Myocardial Infarction*

Objective: : Rapid dissolution of blood clots reduces vasospasm and hydrocephalus after subarachnoid hemorrhage (SAH), and locally administered fibrinolytic drugs (LAFDs) could facilitate the dissolution. However, the efficacy of LAFDs remains controversial. The aim of this meta-analysis was to determine the efficacy of LAFDs for vasospasm and hydrocephalus and in clinical outcomes. Methods: : From PubMed, EMBASE, and Cochrane database, data were extracted by two authors. Meta-analysis was performed using a random effect model. Inclusion criteria were patients who had LAFDs with urokinase-type or recombinant tissue-plasminogen activator after SAH in comparison with medically untreated patients with fibrinolytic drugs. We only included randomized controlled trials (RCTs) in this analysis. The outcomes of interest were vasospasm, hydrocephalus, mortality, and 90-day unfavorable functional outcome. Results: : Data from eight RCTs with 550 patients were included. Pooled-analysis revealed that the LAFDs were significantly associated with lower rates of vasospasm (LAFDs group vs. control group, 26.5% vs. 39.2%; odds ratio [OR], 0.48; 95% confidence interval [CI], 0.32–0.73); hydrocephalus (LAFDs group vs. control group, 26.0% vs. 31.6%; OR, 0.54; 95% CI, 0.32–0.91); and mortality (LAFDs group vs. control group, 10.5% vs. 15.7%; OR, 0.58; 95% CI, 0.34–0.99). The proportion of 90-day unfavorable outcomes was lower in the LAFDs group (LAFDs group vs. control group, 32.7% vs. 43.5%; OR, 0.55; 95% CI, 0.37–0.80). Conclusion : This meta-analysis with eight RCTs indicated that LAFDs were significantly associated with lower rates of vasospasm and hydrocephalus after SAH. Thus, LAFDs could consequently reduce mortality and improve clinical outcome after SAH.

Background: Alopecia areata (AA) is an autoimmune disease characterized by chronic inflammation, the pathogenesis of which is unknown. Stress is believed to play a role; however, evidence remains insufficient. A recent study showed that substance P (SP) damaged hair follicles by causing neurogenic inflammation, activating perifollicular mast cells, and inducing keratinocyte apoptosis. Objective: We aimed at studying the role of SP in AA pathogenesis. We investigated the SP levels in the lesional scalp tissues and serum. We also studied the effect of SP on the inflammatory response and hair growth in the outer root sheath (ORS) cells. Methods: We compared the serum levels of SP in 58 AA patients and 28 healthy subjects.Then, we checked the expression of SP and SP receptor, neurokinin-1 receptor (NK-1R) in the scalps of AA patients and healthy controls using immunohistochemical staining.Finally, we analyzed the mRNA expression of inflammatory cytokines and hair growthrelated factors in ORS cells. Results: SP and NK-1R expression were markedly higher in the hair follicles and interfollicular epidermis of the scalp lesions of AA patients. However, there was no statistically significant difference in serum SP levels between controls and patients, regardless of the type of alopecia. SP significantly increased the mRNA expression of inflammatory cytokines and decreased hair growth-related growth factors in ORS cells, but the results were not dramatic. Conclusion SP triggered a localized micro-inflammation in lesional hair follicles, provoked an inf lammatory response, and inhibited hair growth, thereby confirming the pathogenic role of SP in AA.