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Background Rheumatoid arthritis (RA) is a known debilitating autoimmune disease. Immune-suppressants that are used for disease treatment have serious side effects, therefore, trivalent chromium (Cr (III)); which has shown evidence of its influences on some inflammatory pathways and cytokines; was used in this study for the first time to be assessed for its therapeutic effect in RA rat model and was compared to prednisolone in a trial to find a treatment with lesser side effects. Methods Adult male albino rats were randomly divided into four groups: normal, untreated RA, prednisolone treated RA (1.25 mg/kg/day) and Cr (III) treated RA groups (80 μg/kg/day), induction of RA was done by subcutaneous complete Freund adjuvant injection. Study duration was 4 weeks throughout which arthritis scoring and weight measurement were pursued. Histopathological examination and immunohistochemical FOXP3 assessment were done for joint biopsies. Serum inflammatory markers (interleukin 17, interleukin 10, CRP) and synovial erosive arthritis marker (Cathepsin G) were measured. HDL and non-HDL cholesterol were estimated as well. Results Cr (III) treatment showed marked clinical and histopathological improvement, also astonishing anti-inflammatory effects (increase in FOXP3 expression and interleukin 10, with decrease in interleukin 17, CRP and synovial Cathepsin G) to the extent that Cr (III) effects on inflammation abolishment were comparable to that of prednisolone and even better at some aspects. Moreover, Cr (III) was protective from side effects, i.e., weight gain and dyslipidemia that were seen with prednisolone treatment. Conclusions Cr (III) is promising in treating RA and it lacks some side effects of accustomed immune-modulatory agents including prednisolone. Further experimental studies and clinical trials should be held to see the efficacy of Cr (III) in different doses and to assess its long term side effects when used for rheumatoid arthritis and other autoimmune diseases treatment.

Introduction: Triple negative breast cancer (TNBC), defined as lacking the expression of estrogen receptor alpha (ERα), progesterone receptor and human epidermal growth factor receptor is an aggressive breast cancer subtype for which there is a need to identify new therapeutic targets. About 50-80% of TNBC express Estrogen Receptor Beta (ERβ). Given its slight differences from ERα in terms of structure, signaling and its anti-proliferative effects on breast cancer cells, ERβ may be a possible therapeutic target. This study sought to assess the presence of ERβ and its correlation with the clinico-pathological features among the Egyptian females with TNBC. Material and Methods: The study was a retrospective analysis. The following data was retrieved from patient’s files and recorded: age, tumor size, lymph nodes metastasis, and stage. Paraffin blocks for patients confirmed by IHC to be TNBC were subjected to immunohistochemical staining for ERβ, CK5/6, and Ki 67. Results: ERβ was positive in 80% of cases (n=32/40). ERβ significantly correlated with Age (rs = -0.473, P = 0.002, n = 40), Tumor size (rs = -0.471, P = 0.007, n = 40), Lymph nodes (rs = -0.365, P = 0.021, n =40), and Stage (rs = -0.468, P = 0.002, n = 40). There was no correlation between ERβ with Ki-67 and CK5/6 a marker of the basal phenotype. All 8 patients without ERβ had an aggressive disease. 4 received neoadjuvant chemotherapy with minimum or no pathologic complete response in the axillary lymph nodes, 2 presented with upfront metastatic disease while the other 2 were cases of local recurrence with a change in the molecular phenotype of the tumor from luminal subtype to TNBC. Conclusion: This study shows ERβ expression occurs in TNBC. It may have the potential to become a therapeutic target for TNBC.

The transcriptomic regulation induced by isotretinoin (13-cis retinoic acid) is still a matter of debate as short-term exposures of immortalized sebocytes with isotretinoin produced conflicting results. Based on translational evidence, it has been hypothesized that oral isotretinoin treatment upregulates the expression of the transcription factor p53. Twenty-five patients suffering from acne vulgaris were treated with isotretinoin (0.6 mg/kg body weight) for 6 weeks. Biopsies from back skin were taken before and after isotretinoin treatment for the determination of p53 expression by immunohistochemical staining, quantification of p53 protein concentration by enzyme-linked immunosorbent assay and TP53 gene expression by quantitative reverse transcription real time PCR. Fifteen socio-demographically cross-matched healthy volunteers served as controls. Isotretinoin treatment significantly increased the nuclear expression of p53 in sebaceous glands of treated patients compared to pre-treatment levels and p53 levels of untreated controls. Furthermore, the p53 protein and gene expression significantly increased in the skin after treatment. The magnitude of p53 expression showed an inverse correlation to acne severity score and body mass index. Under clinical conditions, isotretinoin induced the expression of p53, which controls multiple transcription factors involved in the pathogenesis of acne vulgaris including FoxO1, androgen receptor and critical genes involved in the induction of autophagy and apoptosis. Increased p53-FoxO1 signalling enhanced by systemic isotretinoin treatment explains the underlying transcriptomic changes causing sebum suppression but also the adverse effects associated with systemic isotretinoin therapy.