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By following up on the effect of rubber, which has recently been widely used as a direct additive to the asphalt binder or to the concrete mix as a percentage of the weight of the aggregate. The success of the effect of this type of admixture on improving the modified asphalt binder in addition to the modified concrete mix has been investigated. As it was noted the importance of following the asphalt properties due to the increasing use of crumb rubber modifiers in asphalt mixtures, there is a more position to check their rheological and physical properties comprehensively. In general, the performance of the asphalt rubber binder is affected by the rubber crumb content and mixing conditions. This research used 40/50 asphalt grade and Crumb Rubber additives with contents (5, 10, 15, and 20%). The main objectives of this study were to investigate the physical and rheological properties of rubber-modified asphalt binder and mixture. These purposes were achieved by testing HMA samples using the Marshall test approach to determine (Marshall stability and flow and void properties) and measuring the retained Marshall stability and DSR and Viscosity test. Sample testing showed that when recycled rubber was used as modifiers for asphalt mixes, the mixture became more stable, had a higher bulk specific gravity, and had less flow value and air voids. This infers that using recycled rubber can enhance the rutting resistance of bituminous mix.

Neurotoxic side effects of chemotherapy are second in frequency to hematological toxicity. Unlike hematological side effects that can be treated with hematopoietic growth factors, neuropathies cannot be treated and protective treatment strategies have not been effective. The mechanism underlying chemotherapy-induced peripheral neuropathy (CIPN) is unknown. Metabolic changes resulting from the accumulation of the drug in the dorsal root ganglia cells, mitochondrial-mediated disregulation of Ca++ homeostasis and dis-regulation of neurotrophins may contribute to the pathogenesis of CIPN.For the neurologist, the diagnosis of a chemotherapy-induced peripheral neuropathy though is primarily based on case history and clinical presentation, the electrophysiological study; nerve conduction study (NCS) and electromyography (EMG) represent a valuable, useful and helpful test in the neurological evaluation of the types and grading of the severity of the neuropathy. Our objective is to evaluate role of neurophysiological test in the diagnosis of peripheral neuropathy in patient receiving chemotherapy. NCS was performed on 40 patients receiving chemotherapy with clinical diagnosis of peripheral neuropathy and 40 healthy controls. The result revealed a statistically significant prolongation in latency, reducing amplitude and slowing of conduction velocity in addition to EMG finding of spontaneous activity and large MUAPs for patient group (P <0.05). NCS plays an important role in the evaluation of chemotherapy induced peripheral neuropathy by determining the pathology and the distribution of the nerve fiber damage. [ABSTRACT FROM AUTHOR]

Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype, and it exhibits resistance to common breast cancer therapies. Immune checkpoint inhibitors (ICIs) targeting programmed cell death 1 (PD-1) and its ligand, PD-L1, have been approved to treat various cancers. However, the therapeutic efficacy of targeting PD-1/PD-L1 axis in breast cancer is under clinical investigation. In addition, the mechanisms of action of drugs targeting PD-1 and PD-L1 have not been fully elucidated. In this study, we investigated the effect of human TNBC cell lines, MDA-MB-231 and MDA-MB-468, and the non-TNBC cell line, MCF-7, on the expression of immune checkpoints (ICs) on CD4+ T cell subsets, including regulatory T cells (Tregs), using a co-culture system. We also examined the effect of blocking PD-1 or PD-L1 separately and in combination on IC expression by CD4+ T cell subsets. We found that breast cancer cells upregulate the expression of ICs including PD-1, cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) and lymphocyte activation gene-3 (LAG-3) in CD4+ T cell subsets. We also found that the co-blockade of PD-1 and PD-L1 further upregulates the co-expression of TIM-3 and LAG-3 on CD4+CD25+ T cells and CD4+CD25+FoxP3+Helios+ Tregs in the presence of TNBC cells, but not in non-TNBC cells. Our results indicate the emergence of compensatory inhibitory mechanisms, most likely mediated by Tregs and activated non-Tregs, which could lead to the development of TNBC resistance against PD-1/PD-L1 blockade. [ABSTRACT FROM AUTHOR]

: Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype, and it exhibits resistance to common breast cancer therapies. Immune checkpoint inhibitors (ICIs) targeting programmed cell death 1 (PD-1) and its ligand, PD-L1, have been approved to treat various cancers. However, the therapeutic efficacy of targeting PD-1/PD-L1 axis in breast cancer is under clinical investigation. In addition, the mechanisms of action of drugs targeting PD-1 and PD-L1 have not been fully elucidated. In this study, we investigated the effect of human TNBC cell lines, MDA-MB-231 and MDA-MB-468, and the non-TNBC cell line, MCF-7, on the expression of immune checkpoints (ICs) on CD4 + T cell subsets, including regulatory T cells (Tregs), using a co-culture system. We also examined the effect of blocking PD-1 or PD-L1 separately and in combination on IC expression by CD4 + T cell subsets. We found that breast cancer cells upregulate the expression of ICs including PD-1, cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), T cell immunoglobulin and mucin domain-containing protein 3 (TIM-3) and lymphocyte activation gene-3 (LAG-3) in CD4 + T cell subsets. We also found that the co-blockade of PD-1 and PD-L1 further upregulates the co-expression of TIM-3 and LAG-3 on CD4 + CD25 + T cells and CD4 + CD25 + FoxP3 + Helios + Tregs in the presence of TNBC cells, but not in non-TNBC cells. Our results indicate the emergence of compensatory inhibitory mechanisms, most likely mediated by Tregs and activated non-Tregs, which could lead to the development of TNBC resistance against PD-1/PD-L1 blockade.