Adipose tissue is a readily available and plentiful source of multipotent mesenchymal stromal/stem cells (AT-MSC). The immunomodulatory properties of AT-MSC are being introduced in type 2 diabetes (T2D) cell-based therapy. The study aimed to uncover the impact of T2D, on the interplay between AT-MSC and immune cells to develop an effective and safe AT-MSC immunotherapeutic modality. Thus, a direct allogenic co-culture of healthy AT-MSC (nAT-MSC) and peripheral blood mononuclear cells (PBMC), from healthy (nPBMC) or T2D (dPBMC) donors, and stimulated with anti-CD3/CD28, was established in vitro. PBMC proliferation was evaluated by measuring 5-bromo-20-deoxyuridine (Brdu) incorporation in the DNA of proliferating cells in a colorimetric ELISA assay. Expression levels of CD3 + T cell activation surface markers (CD25 and HLA-DR) were detected using a flow cytometer. As well, the anti-proliferative effect of naïve and interferon gamma (IFN-ɤ) -primed AT-MSC, isolated from T2D patients (dAT-MSC), on autologous PBMC was explored using the Brdu proliferation assay. In the applied co-culture setting, the diabetic milieu does not significantly impact the potential of nAT-MSC to suppress stimulated PBMC proliferation. However, it significantly compromises nAT-MSC ability to modulate the activation markers expression, making them less potent to suppress CD25 and HLA-DR expression. Moreover, the dAT-MSC have attenuated ability to suppress the proliferation of autologous stimulated dPBMC, nevertheless, priming of dAT-MSC with IFN-ɤ, might improve such defect. The results suggest that T2D might affect the immunosuppressive potential of AT-MSC and pre-conditioning of dAT-MSC with a pro-inflammatory stimulus could enhance their therapeutic effect.

Fluorescence in situ hybridization (FISH) depends on the complementary nature of the labeled probe and its targeted chromosomal segment. FISH technique allows the detection of numerical chromosomal aneuploidy by using the centromeric probes. Numerical aberrations represent a significant percentage of chromosomal abnormalities and is a main cause of pregnancy loses and cancer. The present study aimed to produce in-house FISH centromeric probes that help in the identification of numerical chromosomal aberrations (copy number variants) and can be used as a control probe. In this study, the probes were produced from human genomic DNA using Polymerase Chain Reaction (PCR) with specific primers. PCR was used for amplification and labeling of alpha satellite centromeric probes of chromosomes 1 and 7. The alpha satellite centromeric probes allow us to identify the numerical abnormalities of its corresponding chromosome. All the produced probes were sensitive and specific for the detection of chromosomal copy number variants. To our knowledge this is the first time to produce FISH probes in Egypt; our next plan is to produce double color probes for specific locus.

The success of etoposide for the treatment of testicular cancer is limited by its undesirable side effects on reproductive system, which is generally ascribed to inflammation and oxidative stress. In the current study, the protective effects of montelukast and curcumin on etoposide-induced reproductive toxicity were investigated. Rats were divided into four groups; group 1 was kept as control. In group 2, etoposide was administered at a dose of (20 mg/kg/day, i.p) for 5 days, while in groups 3; montelukast was given at a dose of (10mg/kg/day, p.o) and in group 4; curcumin was given at a dose of (20mg/kg/day, p.o) respectively for 21 days in both groups, during that i.p. injection of etoposide (20 mg/kg/day, i.p) was injected from day 8 through day 12 in both groups. Etoposide induced oxidative stress via significant increase in MDA level and significant decrease in GSH level as well as SOD and CAT activities. Montelukast and curcumin prevented these effects through antioxidant properties. In addition, the deleterious effects of etoposide on spermatogenesis, serum testosterone level, oxidative stress, ATP, mtDNA and nDNA damage as well as histopathological changes were eliminated by montelukast or curcumin treatment, notably curcumin could normalized some of these parameters. The present study showed that montelukast and curcumin can reverse toxic effects of etoposide on the reproductive system that can be contributed due to anti-oxidant, antiinflammatory and antiapoptotic potential.

Synthetic cannabinoids (SCs) abuse is a serious social problem worldwide. It can cause severe toxicity, including seizures and even death. This study aims to examine the role of sub-chronic administration of AMB-FUBINACA SC in the induction of brain injury. 32 Male adult rats divided into four groups (8 rats per cage) were used, Control group: Intraperitoneally (IP) injected with 0.5 ml of the vehicle, and the others each one of them IP injected with 0.5 ml of the three different doses of AMB-FUBINACA as following: Group1: 1mg/kg, Group 2: 3mg/kg and Group 3: 4mg/kg. The drug was injected once a day for six consecutive days. Tremors were observed 30 minutes following drug injection especially with 3 and 4 mg/kg examined doses followed by depressant effect. Then rats became hyperactive and aggressive. The drug administration induced a significant disturbance in the redox status of brain and significantly increased tumor necrosis factor-α (TNF-α), interlukin-6 (IL-6) and the soluble calcium binding protein B (S100B) serum levels. In addition, the mRNA expression levels of nuclear factor kappa B (NF-𝜅B), mitogen activated protein kinase p38 (MAPK p38) and Caspase-3 were significantly up-regulated. Meanwhile, the mRNA expression levels of Cannabinoid receptors (CB1R, CB2R) and brain derived neurotrophic factor (BDNF) were significantly downregulated. The obtained results demonstrated that, AMB-FUBINACA harmful effects increase with the dose, which was supported by the brain histopathological examination. We concluded that, AMB-FUBINACA has a functional and structural deleterious central nervous system (CNS) effects with sub chronic exposure in adult male rats. The induced brain injury and seizures that accompanied with the synthetic cannabinoids abuse might be mediated through the generation of oxidative stress, activating inflammatory cellular signaling mechanism and neural cell death via apoptosis.