Personalized and Precision Medicine Journal

Abstract Myeloproliferative neoplasm (MPN) is a neoplasm with three categories; essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF) and it usually is diagnosed through mutation analysis in several essential genes; JAK2, MPL, CALR. The mutations of mentioned genes in 50 patients with MPN and 50 healthy volunteers were determined via allele-specific PCR and sequencing. Based on the results, MPN and its subtypes have significant relation with mutations (p<0.05). JAK2 (exon 14) mutation was related to MPN and its subtypes except for ET and CALR (exon 9) type 1 was merely related to ET, but CALR (exon 9) type 2 mutation was more prevalent in MPN and PV (p<0.05). None of the mutations co-occurred simultaneously. There was no evidence of mutation in JAK2 (exon 12) and MPL (exon 9 and 10) in our study, so they are unsuitable diagnostic candidates. So, mutations in JAK2 (exon 14), and CALR (exon 9) type 1 and 2 are essential in MPN diagnosis in Iranians.

Abstract Background: Lots of people die from heart failure (HF) because of fibrosis formation. As injured myocytes deregulated MMP-2, MMP-4, TIMP-2, Ang, plasma renin activity  (PRA), and ACE leading to fibrosis, their regulation can improve HF. One of the most effective treatments for heart failure is the use of hAMSCs-CM, which has been shown to improve heart function and reduce symptoms. The study innovation was the investigation of the in vivo mode of action of hAMSCs-CM on HF fibrosis focusing on the mentioned proteins for the first time. We expected that this study partly fill the scientific gap in HF treatment.
Methods: Frothy rats were divided into 4 groups; Control, HF, culture medium, and CM. To induce HF, isoproterenol (ISO) was injected into all animals except for the control. CM were injected into the CM group and the culture medium group received culture medium. Then, cardiac functions were measured using echocardiography and serum fibrosis was evaluated by ELISA.
Results: HF model showed decreased MMP-2, MMP-4, Ang, PRA, and ACE and increased TIMP-2, whereas hAMSCs-CM therapy reversed them compared with controls.
Conclusion: Our result has partially filled the HF treatment’s gap as hAMSCs-CM improved cardiac function and reduced cardiac fibrosis and the serum fibrogenic proteins.

Abstract Background: A lot of patients are suffering from asthma. For decreasing the asthma symptoms, we studied the effects of conditioned medium (CM) of human amniotic membrane mesenchymal stem cells (hAM-MSCs) as a source of anti-inflammatory cytokines on splenocyte and lung tissue of asthmatic Balb/c mice.
Methods: Forty mice were categorized into four groups; ovalbumin (OVA)-induced asthma, CM-treated asthma, DMEM (Dulbecco's Modified Eagle Medium)-treated asthma, and saline control. Each group received related treatment. The lung alpha-smooth muscle actin (α-SMA)  and splenocyte inflammatory cytokines and IgE were examined through Western blot analysis.
Results: Western blot showed α-SMA overexpression in the OVA and DMEM groups compared with the saline group. CM therapy could significantly reverse it compared with OVA and OVA+DMEM categories by elevating IL-10 and IFN-γ and reducing IL-4, IgE, and TGF-β .
Conclusion: CM treatment could improve asthma symptoms by adjusting α-SMA in lung tissue and pro-inflammatory cytokines and IgE in splenocytes.