Bone marrow aspirate concentrate - A novel approach to alter the course of temporomandibular joint osteoarthritis (a clinical study).

INTRODUCTION: TMJ OA is characterized by severe osteocartilaginous degradation of the joint structure resulting in severe deterioration of both joint function as well as joint structure. bone marrow aspirate concentrate (BMAC) gained wide acceptance as an auspicious addition for regenerative medicine as it is confirmed to be a rich source of pluripotent mesenchymal stem cells and growth factors that produce promising relief of clinical symptoms with significant repair of the joint structure. Thus, the study aims at assessing the efficacy of bone marrow aspirate concentrate (BMAC) as a treatment modality for TMJ osteoarthritis and compare its efficacy with that of hyaluronic acid (HA). METHODS: 24 patients were included in the present study and divided into 12 patients in each group. Joint arthrocentesis was performed to all patients followed by intra-articular BMAC injection in Group I. While Group II received HA acid injection RESULTS: A trend towards long term joint repair at 12 and 18 months follow up period was observed in the bone marrow aspirate concentrate (BMAC) group as a therapeutic modality for TMJ OA by providing necessary growth factors and anti-inflammatories that impedes the progression of the osteoarthritic degeneration. On the contrary to the viscosupplementary action of hyaluronic acid (HA) that showed relapse of patients conditions. CONCLUSION: Bone marrow aspirate concentrate (BMAC) is able to reverse the degenerative effects of TMJ OA however,further studies are mandatory with larger population and longer follow-up time.

Gene expression profiling of non-hodgkin lymphomas.

BACKGROUND: Chromosomal translocations are genetic aberrations associated with specific non-Hodgkin lymphoma (NHL) subtypes. This study investigated the differential gene expression profile of Egyptian NHL cases based on a microarray approach. MATERIALS AND METHODS: The study included tissue samples from 40 NHL patients and 20 normal lymph nodes used as controls. Total RNA was extracted and used for cDNA microarray assays. The quantitative real time polymerase chain reaction was used to identify the aberrantly expressed genes in cancer. RESULTS: Significant associations of 8 up-regulated and 4 down-regulated genes with NHL were observed. Aberrant expression of a new group of genes not reported previously was apparent, including down-regulated NAG14 protein, 3 beta hydroxy-delta 5-c27 steroid oxi-reductase, oxi-glutarate dehydrogenase (lipo-amide), immunoglobulin lambda like polypeptide 3, protein kinase x linked, Hmt1, and caveolin 2 Tetra protein. The up-regulated genes were Rb binding protein 5, DKFZP586J1624 protein, protein kinase inhibitor gamma, zinc finger protein 3, choline ethanolamine phospho-transferase CEPT1, protein phosphatase, and histone deacetylase-3. CONCLUSIONS: This study revealed that new differentially expressed genes that may be markers for NHL patients and individuals who are at high risk for cancer development.

Dynamic interplay between CXCL levels in chronic hepatitis C patients treated by interferon.

BACKGROUND: Combined pegylated interferon-α and ribavirin therapy has sustained virological response (SVR) rates of 54% to 61%. Pretreatment predictors of SVR to interferon therapy have not been fully investigated yet. The current study assesses a group of chemokines that may predict treatment response in Egyptian patients with chronic HCV infection. PATIENTS AND METHODS: CXCL5, CXCL9, CXCL11, CXCL12, CXCL 13, CXCL 16 chemokines and E-Cadherin were assayed in 57 chronic HCV patients' sera using quantitative ELISA plate method. All studied patients were scheduled for combined pegylated interferon alpha and ribavirin therapy (32 patients received pegylated interferon α 2b, and 25 patients received pegylated interferon α 2a). Quantitative hepatitis C virus RNA was done by real time RT-PCR and HCV genotyping by INNOLIPAII. RESULTS: There was no significant difference (p > 0.05) in baseline HCV RNA levels between responders and non-responders to interferon. A statistically significant difference in CXCL13 (p = 0.017) and E-Cadherin levels (P = 0.041) was reported between responders and nonresponders at week 12. Significant correlations were found between changes in the CXCL13 levels and CXCL9, CXCL16, E-cadherin levels as well as between changes in E-cadherin levels and both CXCL16 and ALT levels that were maintained during follow up. Also, significant changes have been found in the serum levels of CXCL5, CXCL13, and CXCL16 with time (before pegylated interferon α 2 a and α 2 b therapy, and at weeks 12 and 24) with no significant difference in relation to interferon type and response to treatment. CONCLUSION: Serum levels of CXCL13 and E-Cadherin could be used as surrogate markers to predict response of combined PEG IFN-α/RBV therapy, especially at week 12. However, an extended study including larger number of patients is needed for validation of these findings. CLINICAL TRIAL NO: NCT01758939.

Molecular prognostic profile of Egyptian HCC cases infected with hepatitis C virus.

BACKGROUND: Hepatocellular carcinoma (HCC) is a common and aggressive malignancy. Despite of the improvements in its treatment, HCC prognosis remains poor due to its recurrence after resection. This study provides complete genetic profile for Egyptian HCC. Genome-wide analyses were performed to identify the predictive signatures. PATIENTS AND METHODS: Liver tissue was collected from 31 patients with diagnosis of HCC and gene expression levels in the tumours and their adjacent non-neoplastic tissues samples were studied by analyzing changes by microarray then correlate these with the clinico-pathological parameters. Genes were validated in an independent set by qPCR. The genomic profile was associated with genetic disorders and cancer focused on gene expression, cell cycle and cell death. Molecular profile analysis revealed cell cycle progression and arrest at G2/M, but progression to mitosis; unregulated DNA damage check-points, and apoptosis. RESULT: Nine hundred fifty eight transcripts out of the 25,000 studied cDNAs were differentially expressed; 503 were up-regulated and 455 were down-regulated. A total of 19 pathways were up-regulated through 27 genes and 13 pathways were down-regulated through 19 genes. Thirty-seven genes showed significant differences in their expression between HCC cases with high and low Alpha Feto Protein (AFP≥600 IU/ml). The validation for the microarray was done by real time PCR assay in which PPP3CA, ATG-5, BACE genes showed down-regulation and ABCG2, RXRA, ELOVL2, CXR3 genes showed up-regulation. cDNA microarrays showed that among the major upregulated genes in HCC are sets. CONCLUSION: The identified genes could provide a panel of new diagnostic and prognostic aids for HCC.