Jui-Wei Lin’s research while affiliated with Chang Gung Memorial Hospital and other places

Chordoid meningiomas (CM) account for approximately 0.5% to 1.0% of intracranial meningiomas. This tumor has a strong risk of recurrence and aggressive growth (World Health Organization grade II). His-tological analysis of CM tumors shows that the tissue is often dominated by chordoid morphology; however , the exact relationship between the percentage of the chordoid component and other clinicopathological features is unknown. We collected 26 surgical specimens from 17 patients who had a histological diagnosis of CM between January 1986 and June 2010. The chordoid elements constituted 30% to 98% of the area of the tumor. In 12 of 17 (70.6%) primary tumors, over 50% of the area displayed the chordoid pattern. Recurrence was noted in nine of these patients and five underwent a second operation. These five patients showed a histopathological progression of aggressive features. The proportion of chordoid elements in each recurrent tumor also increased. Thus, the chordoid proportion in CM is associated with a greater likelihood of recurrence.

Purpose This study aimed to investigate the feasibility of diffusion tensor imaging (DTI) and T2-mapping to assess temporal renal damage in deoxycorticosterone acetate–salt (DOCA-salt) hypertensive rats and compare the results with histopathologic and immunohistochemical findings. Procedures After baseline renal magnetic resonance imaging (MRI), 24 out of 30 uninephrectomized Sprague-Dawley rats with DOCA-salt-induced hypertension were divided equally into four groups. Group 1 had renal MRI at weeks 2, 4, 6, and 8, and groups 2, 3, and 4 had MRI at weeks 2, 4, and 6, respectively. The remaining 6 rats were used as sham controls. The renal cortex and outer and inner stripes of the outer medulla were examined over time using fractional anisotropy (FA), apparent diffusion coefficient (ADC), and T2-mapping, and the results were compared with baseline values. The degree of glomerular and tubular injury, endothelial cell thickening, hyaline arteriolosclerosis, macrophage infiltration, microcyst formation, and fibrosis in different zones at different time points in the DOCA-salt rats were compared with controls. Results Compared with baseline values, DOCA-salt rats demonstrated a significant decrease in renal cortical FA from week 4 to week 8 (0.244 ± 0.015 vs 0.172 ± 0.014–0.150 ± 0.016, P = 0.018–0.002), corresponding to significantly more glomerular damage, arteriolosclerosis, macrophage infiltration, and fibrosis. The DOCA-salt rats had significantly increased cortical ADC and T2 values at weeks 6 and 8 (1.778 ± 0.051 × 10⁻³ mm²/s vs 1.872 ± 0.058–1.917 ± 0.066 × 10⁻³ mm²/s; 93.7 ± 4.9 ms vs 98.0 ± 2.9–100.7 ± 4.0 ms, respectively, all P < 0.05), consistent with excessively fluid-filled microcysts (aquaporin-2+). Despite DOCA-salt rats harbored markedly increased fibrosis in outer and inner stripes of the outer medulla at weeks 6 and 8, only nonsignificant decreases in FA were observed in comparison with the controls suggesting that only limited microstructural changes were present. Conclusions Renal cortical FA is useful for the early detection and monitoring of renal damage in DOCA-salt hypertensive rats.

The aim of this study was to investigate the hyperacute and acute changes in apparent diffusion coefficient (ADC), T1, and T2 mapping in rat kidneys after severe bilateral renal ischemic-reperfusion injury (IRI). After baseline MRI, 24 Spraque-Dawley rats with renal IRI were divided equally as group 1 (post-IRI MRI at 6 hours, days 1, 3, and 7) and groups 2, 3, and 4 (post-IRI MRI at 6 hours; 6 hours and day 1; 6 hours, days 1 and 3, respectively), while six other rats without IRI (group 5) were used as sham control. ADC, T1, and T2 values of the cortex and outer and inner stripes of outer medulla (OSOM and ISOM), and immunohistochemical studies assessing monocyte chemoattractant protein-1 (MCP-1), CD68+ cells, tubular cast formation, and collagen deposition in three zones at different time points were evaluated. Significantly reduced ADCs in OSOM and ISOM are noninvasive biomarkers denoting hyperacute damages after IRI. Linear regression analysis revealed a significant inverse correlation between 6-hour/baseline ADC ratios and MCP-1 staining (P < 0.001, r² = 0.738). ADC, T1, and T2 values are useful for assessing variable IRI changes in different layers depending on underlying microstructural and histopathological changes at different time points.

Acute epididymo-orchitis (AEO)-related global testicular infarction (GTI) is rare. We report herein the clinical and ultrasound findings of 6 patients with AEO-related GTI. Seventeen patients with torsion-related GTI were also reviewed and compared. The echotexture of AEO-related GTI ranged from mildly inhomogeneous to diffuse heteroechoic, depending on the severity of testicular necrotic changes. All of the patients showed a juxta-epididymal string-of-bead pattern on color Doppler ultrasound, which was ascribed to patent arteries (5/6, 87%) and collateral vessels (1/6, 13%) in the tunica albuginea. There were no significant differences in age, laterality, leukocyte count, testicular volume ratio (infarcted/normal), frequencies of heteroechoic testicular parenchyma, scrotal skin thickening, and hydrocele between the 2 groups. However, the left testis was predominantly affected in both groups. Compared with torsion-related GTI, patients with AEO-related GTI had significantly longer duration from scrotal pain onset to surgery (13.5 ± 5.2 vs 2.6 ± 2.0 days, P < 0.001), a higher level of serum C-reactive protein (110.0 ± 82.0 vs 41.2 ± 35.9 mg/dL, P = 0.013), a higher frequency of the juxta-epididymal string-of-bead sign (100% vs 12%, P < 0.001), and a lower frequency of the whirlpool/knot sign (0% vs 88%, P = 0.002). Although the testis in AEO-related GTI may appear variable from mildly to extensively heteroechoic on gray-scale ultrasound, this unusual disease can be characterized by an avascular testis with a juxta-epididymal string-of-bead sign on color Doppler ultrasound.

Aims: Prolonged seizure activity may result in mitochondrial dysfunction and lead to cell death in the hippocampus. Mitochondrial fission may occur in an early stage of neuronal cell death. This study examined the role of the mitochondrial fission protein dynamin-related protein 1 (Drp1) in the hippocampus following status epilepticus. Methods: Kainic acid (KA) was microinjected unilaterally into the hippocampal CA3 area in Sprague Dawley rats to induce prolonged seizure activity. Biochemical analysis, electron microscopy, and immunofluorescence staining were performed to evaluate the subsequent molecular and cellular events. The effects of pretreatment with a mitochondrial fission protein inhibitor, Mdivi-1 (2 nmol), were also evaluated. Results: Phosphorylation of Drp1 at serine 616 (p-Drp1(Ser616)) was elevated from 1 to 24 h after the elicited seizure activity. Pretreatment with Mdivi-1 decreased the Drp1 phosphorylation at Ser616 and limited the mitochondrial fission. Mdivi-1 rescued the Complex I dysfunction, decreased the levels of oxidized proteins, decreased the activation of cytochrome c/caspase-3 signaling, and blunted cell death in CA3 neurons. Conclusion: Our findings suggest that activation of p-Drp1(Ser616) is related to seizure-induced neuronal damage. Modulation of p-Drp1(Ser616) expression is accompanied by decreases in mitochondrial fission, mitochondrial dysfunction, and oxidation, providing a neuroprotective effect against seizure-induced hippocampal neuronal damage.

Purpose: This study aimed to test the hypothesis that lung cancer patient-derived circulating microparticles (LCC-MPs) enhance metastatic lung tumors in a rat model. Procedures: The controls (n = 6) and LCC-MP-treated rats (n = 6) with N1S1-induced pulmonary metastatic hepatocellular carcinoma (HCC) underwent dual-source CT (DSCT) on days 10, 15, and 20. Cellular and molecular studies were performed subsequently. Results: DSCT revealed slow progression of metastatic lung tumors in the controls. Compared with the controls, the LCC-MP-treated rats exhibited significantly more and larger metastatic tumors on days 15 and 20 on DSCT, enhanced angiogenesis with higher microvessel count (CD34+), more CXCR4+ and VEGF+ cells in immunohistofluorescence studies, and higher protein expression levels of eNOS, angiopoietin, vascular endothelial growth factor, and CD31 on western blotting (Mann-Whitney test, all P < 0.05). Conclusions: LCC-MPs can elicit oncogenic stimulation and accelerate metastatic HCC growth in rat lung as demonstrated on DSCT and enhanced tumoral angiogenesis as confirmed in cellular and molecular studies.

We sought to evaluate the effects of adipose-derived mesenchymal stem cells (ADMSCs) exosomes on hepatocellular carcinoma (HCC) in rats using apparent diffusion coefficient (ADC), natural killer T-cell (NKT-cell) responses, and histopathological features. ADMSC-derived exosomes appeared as nanoparticles (30–90 nm) on electron microscopy and were positive for CD63, tumor susceptibility gene-101, and β -catenin on western blotting. The control ( n = 8 ) and exosome-treated ( n = 8 ) rats with N1S1-induced HCC underwent baseline and posttreatment day 10 and day 20 magnetic resonance imaging and measurement of ADC. Magnetic resonance imaging showed rapidly enlarged HCCs with low ADCs in the controls. The exosome-treated rats showed partial but nonsignificant tumor reduction, and significant ADC and ADC ratio increases on day 10. On day 20, the exosome-treated rats harbored significantly smaller tumors and volume ratios, higher ADC and ADC ratios, more circulating and intratumoral NKT-cells, and low-grade HCC ( P < 0.05 for all comparisons) compared to the controls. The ADC and volume ratios exhibited significant inverse correlations ( P < 0.001 , R 2 = 0.679 ). ADMSC-derived exosomes promoted NKT-cell antitumor responses in rats, thereby facilitating HCC suppression, early ADC increase, and low-grade tumor differentiation. ADC may be an early biomarker of treatment response.

We report a literature review and detailed evaluation of a rare case of posterior choroidal leiomyoma to emphasize the importance of differentiating this from other choroidal tumors. A 30-year-old male presented with variable blurred vision in his right eye secondary to a choroidal tumor. Clinical examinations were performed including fundus photography, optical coherence tomography, B scans, fluorescein and indocyanine green angiography, computed tomography, and magnetic resonance imaging. Preoperative examination revealed a suspected choroidal melanoma and enucleation was performed. However, a definitive diagnosis of choroidal leiomyoma was made following postoperative pathological light microscopy and immunohistochemical studies. Published case reports were collected and the common characteristics and distinctive features were compared with the current case. Posterior choroidal leiomyoma was summarized from the literature, and beneficial information for diagnosis and treatment was obtained. In conclusion, posterior choroidal leiomyoma is rare and should be differentiated from amelanotic melanomas. Despite the benign nature, an explanation regarding the rare incidence and difficult diagnosis of posterior choroidal leiomyoma must be provided to patients, prior to enucleation or detrimental treatment. © 2015 APMIS. Published by John Wiley & Sons Ltd.

Ganglioglioma (GG) is an uncommon brain parenchymal neoplasm. Although most cases have indolent clinical behaviour, a subgroup of GGs does recur, especially in patients with unresectable disease. O6-methylguanine DNA methyltransferase (MGMT) is a DNA repair protein that removes mutagenic and cytotoxic adducts from O6-guanine in DNA. Lack of MGMT protein expression immunohistochemically is related to drug responses in patients with malignant glioma treated with alkylating agents. Furthermore, MGMT promoter methylation has also been investigated as an independent favourable prognostic factor for glioblastoma. The primary management is surgical resection for GGs and gross total resection is recommended. Despite infrequent use of chemotherapy for low-grade GGs, it was still introduced to a subset of patients, especially those who had unresectable disease. We assessed clinicopathological features of nine cases of low-grade GG to further elucidate the relationship between the status of the MGMT protein expression and the prognosis. This series included four men and five women with a mean age of 21.6 years at the first surgery. The mean postoperative follow-up period was 6 years. Only two patients had recurrent disease after 1.7 and 3.2 years of the first surgery. Immunohistochemically, 11.1% exhibited 3+ nuclear staining for MGMT protein, 11.1% exhibited 2+ staining, 33.3% exhibited 1+ staining, and 44.4% exhibited 0 staining. Tumours with more intensive MGMT protein expression (2+~3+ immunostaining) tended to recur more frequently (p < 0.05), corresponding to the worse prognostic predictive value of intensive MGMT staining.

Idiopathic azygos vein aneurysm (AVA) is rare. This retrospective study evaluated the imaging features and outcomes in 10 cases of idiopathic AVA. We retrospectively evaluated 10 patients with surgically proven or typical imaging features of idiopathic AVA encountered in our institution between 1990 and 2012. Chest roentgenography and computed tomography (CT) were performed in all 10 patients, and magnetic resonance imaging (MRI) was performed in 4 of these patients. The clinical features, AVA morphologic characteristics, and outcomes were analyzed. Chest roentgenograms showed a right paratracheal nodule or mediastinal mass in 7 cases. CT and MRI disclosed 4 thrombosed saccular AVAs (short axis, 3-6 cm; mean, 4.7 cm) and 6 fusiform AVAs (short axis, 2.2-3 cm; mean 2.7 cm). Two large saccular AVAs that presented with chest tightness were resected shortly after diagnosis. One saccular AVA manifested as a pulmonary embolism, whereas the remaining AVA was asymptomatic; they showed 25% to 40% short-axis growth in a 3- to 5-year interval before subsequent AVA resection. Conversely, all 6 fusiform AVAs were asymptomatic and found incidentally, remaining rather stable with less than 8% short-axis growth during 3 to 8 years of follow-up. Compared with fusiform AVAs, saccular AVAs were larger and had a greater frequency of AVA-related symptoms, intralesional thromboses, and greater than 20% short-axis growth during the follow-up period. Saccular AVAs are larger than fusiform aneurysms, presenting with greater frequency of chest symptoms, intralesional thrombosis, considerable lesion growth, and need for surgical intervention. In contrast, fusiform AVAs are asymptomatic and rather stable in long-term follow-up.