Investigations into the relationship of the PPVT-R and the WISC-R with incarcerated delinquents

Examined the relationship between the Peabody Picture Vocabulary Test-Revised (PPVT-R), the Peabody Picture Vocabulary Test (PPVT), and the Wechsler Intelligence Scale for Children-Revised (WISC-R) with 35 incarcerated delinquents between the ages of 13–10 and 16–10. Mean scaled scores were computed across all measures. A statistically significant difference (p <. 01) between the PPVT-R mean scaled score and all other measures was obtained. The PPVT-R correlated significantly (p <. 0001) with the WISC-R VIQ (r = 0.87), PIQ (r = 0.78), FSIQ (r = 0.86) and the PPVT (r = 0.80), whereas the original PPVT demonstrated significant yet lower correlations with the WISC-R VIQ (r = 0.78), PIQ (r = 0.77) and FSIQ (r = 0.80). The clinical significance of utilizing the PPVT-R as a measure of receptive vocabulary and its practical relationship to the PPVT and WISC-R with a juvenile delinquent population was discussed.     

Efficacy of tilt training in the treatment of neurally mediated syncope. A randomized study.

Recurrent neurally mediated syncope represents a common clinical event and a therapeutic challenge. Recently tilt training has been proposed for the treatment of recurrent neurally mediated syncope. To evaluate the efficacy of tilt training in preventing tilt-induced syncope and its feasibility, this controlled, randomized study was undertaken. Sixty-eight consenting patients (25 males and 43 females, mean age 40 +/- 19) with recurrent neurally mediated syncope and 2 consecutive positive nitroglycerin-potentiated head-up tilt tests were randomized to tilt training (35 patients) or no treatment (controls, 33 patients). The tilt training programme consisted of daily 30-min sessions of upright standing against a vertical wall 6 days a week for at least 3 weeks, until a reevaluation tilt test (3 patients of both groups dropped out). On this third head-up tilt test, 19 (59%) of 32 tilt trained patients and 18 (60%) of 30 controls still had a positive test. Treated patients performed a mean number of 15 +/- 7 sessions (median 16) and only 11 patients (34%) did all the programmed sessions. Only 1 patient (3%) discontinued treatment because of intolerance, while all other patients did not perform tilt training adequately, because of poor compliance. Thus, in our study tilt training was not effective in reducing tilt testing positivity rate in patients with neurally mediated syncope. Because of poor compliance, tilt training appears to be a feasible treatment only for highly motivated patients, but not for the majority of patients with recurrent neurally mediated syncope.     

uPAR Controls Vasculogenic Mimicry Ability Expressed by Drug-Resistant Melanoma Cells

Malignant melanoma is a highly aggressive skin cancer characterized by an elevated grade of tumor cell plasticity. Such plasticity allows adaptation of melanoma cells to different hostile conditions and guarantees tumor survival and disease progression, including aggressive features such as drug resistance. Indeed, almost 50% of melanoma rapidly develop resistance to the BRAFV600E inhibitor vemurafenib, with fast tumor dissemination, a devastating consequence for patients’ outcomes. Vasculogenic mimicry (VM), the ability of cancer cells to organize themselves in perfused vascular-like channels, might sustain tumor spread by providing vemurafenibresistant cancer cells with supplementary ways to enter into circulation and disseminate. Thus, this research aims to determine if vemurafenib resistance goes with the acquisition of VM ability by aggressive melanoma cells, and identify a driving molecule for both vemurafenib resistance and VM. We used two independent experimental models of drug-resistant melanoma cells, the first one represented by a chronic adaptation of melanoma cells to extracellular acidosis, known to drive a particularly aggressive and vemurafenib-resistant phenotype, the second one generated with chronic vemurafenib exposure. By performing in vitro tube formation assay and evaluating the expression levels of the VM markers EphA2 and VE-cadherin by Western blotting and flow cytometer analyses, we demonstrated that vemurafenib-resistant cells obtained by both models are characterized by an increased ability to perform VM. Moreover, by exploiting the CRISPR-Cas9 technique and using the urokinase plasminogen activator receptor (uPAR) inhibitor M25, we identified uPAR as a driver of VM expressed by vemurafenib-resistant melanoma cells. Thus, uPAR targeting may be successfully leveraged as a new complementary therapy to inhibit VM in drug-resistant melanoma patients, to counteract the rapid progression and dissemination of the disease.     

Th17 lymphocyte-dependent degradation of joint cartilage by synovial fibroblasts in a humanized mouse model of arthritis and reversal by secukinumab

How T-helper (Th) lymphocyte subpopulations identified in synovial fluid from patients with juvenile idiopathic arthritis (JIA) (Th17, classic Th1, or nonclassic Th1) drive joint damage is of great interest for the possible use of biological drugs that inhibit the specific cytokines. Our objective was to clarify the role of such Th subpopulations in the pathogenesis of articular cartilage destruction by synovial fibroblasts (SFbs), and the effect of Th17 blockage in an animal model. SFbs were isolated from healthy subjects and patients with JIA, and peripheral blood Th lymphocytes subsets were obtained from healthy subjects. Fragments of human cartilage from healthy subjects in a collagen matrix containing JIA or normal SFbs grafted underskin in SCID mice were used to measure cartilage degradation under the effects of Th supernatants. JIA SFbs overexpress MMP9 and MMP2 and Th17 induce both MMPs in normal SFbs, while nonclassic Th1 upregulate urokinase plasminogen activator (uPA) activity. In vitro invasive phenotype of normal SFbs is stimulated with conditioned medium of Th17 and nonclassic-Th1. In the in vivo “inverse wrap” model, normal SFbs stimulated with supernatants of Th17-lymphocytes and nonclassic Th1 produced a cartilage invasion and degradation similar to JIA SFbs. Secukinumab inhibits the cartilage damage triggered by factors produced by Th17.     

A two-stage hepatectomy procedure combined with portal vein embolization to achieve curative resection for initially unresectable multiple and bilobar colorectal liver metastases

OBJECTIVE: To assess outcome after a 2-stage hepatectomy procedure (TSHP) combined with portal vein embolization (PVE) in the treatment of patients with unresectable multiple and bilobar colorectal liver metastases (MBCLM). BACKGROUND: Patients with MBCLM are often considered for palliative chemotherapy only, due to too small future remnant liver (FRL). Recently, right hepatectomy with simultaneous left liver wedge resections after previous right PVE has been reported in a curative intent. However, the growth of metastatic nodules in FRL after PVE can be more rapid than that of the nontumoral remnant hepatic parenchyma. Therefore, metastases located in the FRL should be ideally resected before PVE. Then, a right (or extended right) hepatectomy can be safely performed during a second-stage hepatectomy. Therefore, we analyzed our experience with the use of TSHP combined with PVE in treatment of MBCLM. PATIENTS AND METHODS: Between December 1996 and April 2003, 33 patients with unresectable MBCLM were selected for a TSHP. A right or an extended right hepatectomy was planned after treatment of left FRL metastases to achieve a curative resection. The first-stage hepatectomy consisted in a clearance of the left hemiliver by resection or radiofrequency destruction of metastases of the left FRL. Subsequently, a right PVE was performed to induce atrophy of the right hemiliver and hypertrophy of the left hemiliver. Finally, a second-stage hepatectomy was planned to resect the right liver metastases. RESULTS: There was no operative mortality. Post-PVE morbidity was 18.1%; postoperative morbidity was 15.1% and 56.0% after first- and second-stage hepatectomy, respectively. TSHP could be achieved in 25 of 33 patients (75.7%). The 1- and 3-year survival rates were 70.0% and 54.4%, respectively, in the 25 patients in whom the TSHP was completed. CONCLUSIONS: In selected patients with initially unresectable MBCLM, a TSHP combined with PVE can be achieved safely with long-term survival similar to that observed in patients with initially resectable liver metastases.     

Diluted magnetic semiconductor properties in TM doped ZnO nanoparticles

The hydrothermal method was used to create dilute magnetic semiconductor nanoparticles of Zn_1−xCo_xO (x = 0, 0.01, 0.05, 0.09). The effect of cobalt doping on the microstructure, morphological and optical properties of Zn_1−xCo_xO was also studied and the Co doping to host ZnO was confirmed from XRD and EDX analysis. The structural analysis showed that doping of cobalt into ZnO decreased the crystallinity, but the preferred orientation didn''t change. SEM analysis revealed that the cobalt dopant did not have a strong influence on the shape of the synthesized nanoparticles. No defect-related absorption peaks were observed in the UV-Vis spectra. The crystallinity of the doped samples was improved by high growth temperature and long growth time. Ferromagnetic behavior above room temperature was detected in co-doped ZnO nanoparticles. The ferromagnetic behavior increased with increasing Co (up to x = 0.05) doping. The ferromagnetic behavior declined when the Co content was further increased. Related research shows that doped ZnO nanoparticles have better dielectric, electrical conductivity, and magnetic properties than pure ZnO. This high ferromagnetism is usually a response reported for dilute magnetic semiconductors. These semiconductor nanoparticles were further used to designed spintronic based applications.

The enlarged central part M–H loop shows for the Co = 0.09 doped ZnO sample, the ferromagnetic (FM) behavior increased, i.e., a M_r of 0.2412 emu g⁻¹ with a H_c of 85 Oe.     

Urokinase and its receptor in follicular and inflammatory cysts of the jaws

Oral Diseases (2010) 16 , 753–759 Objective: Proteases are considered critical in peri‐cystic tissue degradation required in jaw cyst expansion. We studied the expression of the plasminogen activation system (plasminogen activators; their inhibitor type‐1, PAI‐1; the receptor for the urokinase‐type plasminogen activator, uPAR) in follicular and inflammatory cysts of the jaw, to identify a possible role of this system in jaw cyst enlargement. Materials and Methods: Jaw cysts were collected by therapeutic enucleation. ELISA and casein zymography were used to measure and characterize plasminogen activators in cyst fluid. By immunohistochemistry we examined the presence of uPAR in cyst walls and inflammatory cells, and by Western blotting the molecular forms of uPAR within the cyst fluid. Results: Inflammatory cysts fluid contained higher amounts of plasminogen activators of the urinary‐type (uPA), and lower amounts of PAI‐1, when compared to follicular cysts fluid. Epithelial layers of both types of cysts and inflammatory cells expressed uPAR. Native 3‐domain uPAR was scarcely detectable within cysts, where its cleavage was accounted for by uPA. Conclusion: These data suggest a plasminogen activation‐dependent mechanism of cyst enlargement, where only the outward uPAR expressed on epithelial cells and on inflammatory cells direct the peri‐cystic protease cascade, in a way similar to tumor enlargement within tissues.