Clinical benefits of single vs repeated courses of mesenchymal stem cell therapy in epilepsy patients.

Purpose: Epilepsy is defined as "drug-resistant" when existing anti-epileptic drugs (AED) are found to have minimal to no effect on patient's condition. Therefore the search and testing of new treatment strategies is warranted. This study focuses on the effects of autologous mesenchymal stem cells (MSC) in drug-resistant epilepsy patients within a Phase I/II open-label registered clinical trial NCT02497443.

Treatment of refractory epilepsy patients with autologous mesenchymal stem cells reduces seizure frequency: An open label study.

Purpose: Existing anti-epileptic drugs (AED) have limited efficiency in many patients, necessitating the search for alternative approaches such as stem cell therapy. We report the use of autologous patient-derived mesenchymal stem cells (MSC) as a therapeutic agent in symptomatic drug-resistant epilepsy in a Phase I open label clinical trial (registered as NCT02497443).

Patients And Methods: The patients received either standard treatment with AED (control group), or AED supplemented with single intravenous administration of undifferentiated autologous MSC (target dose of 1×10cells/kg), followed by a single intrathecal injection of neurally induced autologous MSC (target dose of 0.

Autologous mesenchymal stromal cells as a therapeutic in ALS and epilepsy patients: Treatment modalities and ex vivo neural differentiation.

Stem cell therapy for incurable central nervous system disorders has long been viewed as a promising therapeutic option. In this review, we discuss the existing data and approaches on cell transplantation in the context of the neural differentiation potential of adult autologous stem cells, focusing on those of mesenchymal origin as easily accessible and well studied. Mesenchymal stromal cells (MSCs) are a heterogeneous cell population with a remarkable therapeutic plasticity, demonstrated by their ability to dampen inflammation, inhibit pathogenic immune responses and secrete neuroprotective factors.

The incidence of T-cell receptor gene rearrangements in childhood B-lineage acute lymphoblastic leukemia is related to immunophenotype and fusion oncogene expression.

Immunoglobulin (Ig) and T-cell receptor (TCR) gene rearrangement is conventionally used for assessment of lymphoid malignant cells. TCR genes rearrangements were reported to occur at high frequency in B-lineage acute lymphoblastic leukemia (ALL). Therefore, we have analyzed 83 children with acute B-lineage ALL (67 de novo patients and 19 relapses) by PCR analysis for clonal IgH, incomplete TCRD (Vdelta2-Ddelta3 and Ddelta2-Ddelta3) and TCRG rearrangements.

Aberrant expression of tumor suppressor genes and their association with chimeric oncogenes in pediatric acute lymphoblastic leukemia.

Aberrant expression of tumor suppressor genes WT 1, RB 1, p53, homozygous deletion of p16 gene and their relationship with expression of oncogenes BCR-ABL, TEL-AML 1, MLL-AF 4, E2A-PBX 1, SIL-TAL 1 were determined in bone marrow samples of children with de novo B-lineage (n=170) and T-lineage (n=25) acute lymphoblastic leukemia (ALL). In contrast to expression of chimeric oncogenes alterations in p16, WT 1, RB 1 and p53 expression were T/B-lineage-unrestricted. Significant association between expression of MLL-AF 4 and WT 1, E2A-PBX 1 and p53; SIL-TAL 1 and homozygous deletion of p16 has been demonstrated.

Accumulation of chlorine e6 derivatives in cells with different level of expression and function activity of multidrug resistance protein P-gp 170.

Aim: This work deals with studying the influence of overexpression and function activity of multidrug transporter protein P-gp 170 on the intracellular accumulation of several porphyrin sensitizers, including chlorin e6 (Chl e6), di- (DME) and trimethyl esters (TME) of Chl e6.

Methods: A parental IM9 cell line and two IM9 drug-resistant IM9 sublines were used. With flow cytometry technique the rates of chlorines accumulation in different IM9 cells and values were related to the extent of multidrug resistance (MDR) phenotype.

Whole body hyperthermia in adjuvant therapy of children with renal cell carcinoma.

Whole body hyperthermia (WBH) in combination with chemotherapy has been proven to be effective in some patients with advanced malignancies. However, only limited experience exists regarding the application of WBH with chemotherapy in children. We present the results of applying WBH and chemotherapy in five children with advanced renal cell carcinoma (RCC).

Enhancement of antitumor response to sarcoma 45 in rats by combination of whole-body hyperthermia and interleukin-2.

Aim: To evaluate the summarized effect of hyperthermia and interleukin-2 (IL-2) administration on antitumor defense in tumor-bearing rats.

Methods: Nonbred rats after subcutaneous inoculation of sarcoma 45 cells were treated with whole-body hyperthermia (WBH, +42.5 degrees C, 60 min) and interleukin-2 (IL-2, 10,000 U/kg of body weight).

Significance of serum immunoglobulin G for leukocytosis and prognosis in childhood B-lineage acute lymphoblastic leukemia.

Background: This study was conducted to evaluate the significance of serum level of immunoglobulins (Igs) and particularly IgG for leukemic cell persistence in peripheral blood (PB) and prognosis for childhood acute lymphoblastic leukemia (ALL).

Procedure: Human sera were obtained from 68 children with primary B-lineage ALL at diagnosis and 46 healthy children (control). Serum level of IgM, IgG, IgA, IgG1, IgG2, IgG3, IgG4, antitumor antibody, homogeneous IgG were quantified by turbidimetric or enzyme-linked immunosorbent assays.

Comparative measurement of spontaneous apoptosis in pediatric acute leukemia by different techniques.

Background: To distinguish between subgroups of patients with acute leukemia, the rate of spontaneous (culture-induced) apoptosis of leukemic cells was evaluated using five methods.

Methods: Leukemic cells (cells) from the bone marrow of children with acute lymphoblastic leukemia (ALL, n = 112) and acute myeloid leukemia (AML, n = 30) were cultured for 20 h in vitro. The level of apoptosis was detected by fluorescent microscopy after staining with acridine orange (AO) or by flow cytometry after staining using PI, JC-1, the APO-BRDU kit, or the AnnexinV-FITC kit.