Stem Cell Institute Philippines

novel inductions for the future...

Stem Cell Treatment for Liver Disease is an Option at ASCI

 

Stem Cell Treatment for Liver Disease

Natural Killer Cells are isolated and grown to multiply their numbers. These Virus Fighting cells are then administered back to the patient to increase the patient's natural immunity.

Related Articles Bile acids promote diethylnitrosamine-induced hepatocellular carcinoma via increased inflammatory signaling. Am J Physiol Gastrointest Liver Physiol. 2016 Jul 01;311(1):G91-G104 Authors: Sun L, Beggs K, Borude P, Edwards G, Bhushan B, Walesky C, Roy N, Manley MW, Gunewardena S, O'Neil M, Li H, Apte U Abstract Hepatocellular carcinoma (HCC) is the most common hepatic malignancy and the third leading cause of cancer related deaths. Previous studies have implicated bile acids in pathogenesis of HCC, but the mechanisms are not known. We investigated the mechanisms of HCC tumor promotion by bile acids the diethylnitrosamine (DEN)-initiation-cholic acid (CA)-induced tumor promotion protocol in mice. The data show that 0.2% CA treatment resulted in threefold increase in number and size of DEN-induced liver tumors. All tumors observed in DEN-treated mice were well-differentiated HCCs. The HCCs observed in DEN-treated CA-fed mice exhibited extensive CD3-, CD20-, and CD45-positive inflammatory cell aggregates. Microarray-based global gene expression studies combined with Ingenuity Pathway Analysis revealed significant activation of NF-κB and Nanog in the DEN-treated 0.2% CA-fed livers. Further studies showed significantly higher TNF-α and IL-1β mRNA, a marked increase in total and phosphorylated-p65 and phosphorylated IκBα (degradation form) in livers of DEN-treated 0.2% CA-fed mice. Treatment of primary mouse hepatocytes with various bile acids showed significant induction of stemness genes including Nanog, KLF4, Sox2, and Oct4. Quantification of total and 20 specific bile acids in liver, and serum revealed a tumor-associated bile acid signature. Finally, quantification of total serum bile acids in normal, cirrhotic, and HCC human samples revealed increased bile acids in serum of cirrhotic and HCC patients. Taken together, these data indicate that bile acids are mechanistically involved pathogenesis of HCC and may promote HCC formation via activation of inflammatory signaling. PMID: 27151938 [PubMed - indexed for MEDLINE]
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Related Articles Equal distribution of mesenchymal stem cells after hepatic ischemia-reperfusion injury. J Surg Res. 2016 Jun 15;203(2):360-7 Authors: Isbambetov A, Baimakhanov Z, Soyama A, Hidaka M, Sakai Y, Takatsuki M, Kuroki T, Eguchi S Abstract BACKGROUND: Liver ischemia-reperfusion (I/R) injury is one of the major causes of hepatocellular injury-related mortality and morbidity after liver transplantation. Mesenchymal stem cells (MSCs) have been shown to reduce liver I/R injury and improve regeneration. The purpose of the present study was to investigate the difference in the distribution of systemically delivered MSCs in the recipient's liver between the ischemic injury area and nonischemic area. MATERIAL AND METHODS: Fishers' rats (7-8 week of age) were used as donors of MSCs and recipients. Bone marrow-derived MSCs were isolated from the donor's femur. Before systemic administration, MSCs were labeled with the fluorescent dye PKH26. The rats were divided into four groups: (1) I/R injury + MSC group, (2) MSC only, without I/R injury, (3) I/R injury + saline group, and (4) the Sham group. I/R injury was performed by clamping the inflow vascular structures of the left and middle lobes of the recipient's liver for 60 min. The right lobe was considered as a nonischemic part. Subsequently, 1.5 × 10(6) of MSCs or saline (NaCl, 0.9%) was administrated via the rat's tail vein. Thereafter, the rats were killed after days one, three, or seven for the analyses. RESULTS: A fluorescent microscopy assay for labeled MSCs showed positive cells in both ischemic and nonischemic parts of the recipient's liver. The number of cells was significantly higher in the I/R injury + MSC group compared with the only MSC, without I/R injury group. Immunohistochemical staining showed that there was no significant difference in the proliferation of Ki-67-positive cells between the I/R + MSCs and I/R + saline groups. In addition, the serum transaminase levels were not different between the I/R + MSCs and I/R + saline groups. CONCLUSIONS: After partial liver I/R injury, transplanted MSCs migrate equally to the ischemic and nonischemic parts of the recipient's liver. Considering the unique ability of the liver to regenerate, both parts of the liver presumably receive signals for regeneration. PMID: 27363644 [PubMed - indexed for MEDLINE]
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Related Articles Preterm infant gut microbiota affects intestinal epithelial development in a humanized microbiome gnotobiotic mouse model. Am J Physiol Gastrointest Liver Physiol. 2016 Sep 01;311(3):G521-32 Authors: Yu Y, Lu L, Sun J, Petrof EO, Claud EC Abstract Development of the infant small intestine is influenced by bacterial colonization. To promote establishment of optimal microbial communities in preterm infants, knowledge of the beneficial functions of the early gut microbiota on intestinal development is needed. The purpose of this study was to investigate the impact of early preterm infant microbiota on host gut development using a gnotobiotic mouse model. Histological assessment of intestinal development was performed. The differentiation of four epithelial cell lineages (enterocytes, goblet cells, Paneth cells, enteroendocrine cells) and tight junction (TJ) formation was examined. Using weight gain as a surrogate marker for health, we found that early microbiota from a preterm infant with normal weight gain (MPI-H) induced increased villus height and crypt depth, increased cell proliferation, increased numbers of goblet cells and Paneth cells, and enhanced TJs compared with the changes induced by early microbiota from a poor weight gain preterm infant (MPI-L). Laser capture microdissection (LCM) plus qRT-PCR further revealed, in MPI-H mice, a higher expression of stem cell marker Lgr5 and Paneth cell markers Lyz1 and Cryptdin5 in crypt populations, along with higher expression of the goblet cell and mature enterocyte marker Muc3 in villus populations. In contrast, MPI-L microbiota failed to induce the aforementioned changes and presented intestinal characteristics comparable to a germ-free host. Our data demonstrate that microbial communities have differential effects on intestinal development. Future studies to identify pioneer settlers in neonatal microbial communities necessary to induce maturation may provide new insights for preterm infant microbial ecosystem therapeutics. PMID: 27492329 [PubMed - indexed for MEDLINE]
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Related Articles Cost-effectiveness of the screening of blood donations for hepatitis E virus in the Netherlands. Transfusion. 2017 Feb;57(2):258-266 Authors: de Vos AS, Janssen MP, Zaaijer HL, Hogema BM Abstract BACKGROUND: The incidence of hepatitis E virus (HEV) has increased substantially in Europe recently, thereby threatening blood safety. A cost-effectiveness analysis for HEV screening of blood donations in the Netherlands was performed. STUDY DESIGN AND METHODS: A simulation model was developed to mimic the process of donation, infections in the donor population, donation testing, and transmission to transfusion recipients. The variability of viral loads among donors was modeled using observed loads. The number of (incurable) chronic HEV infections among organ and stem cell transplant patients and the costs avoided by implementing blood screening were estimated. RESULTS: HEV screening of whole blood donations in pools of 24 would prevent 4.52 of the 4.94 transfusion-associated chronic HEV infections expected annually, at approximately €310,000 per prevented chronic case. Per case not curable by ribavirin prevention, costs are approximately 10 times higher. Selective screening, if logistically feasible, could reduce screening costs by 85%. Sensitivity analyses show that uncertainty in the HEV transmissibility and the frequency of HEV clearing greatly impact the estimated cost-effectiveness. Of all HEV infections nationwide one in 700 is estimated to be due to blood transfusion, while for chronic infections this is one in 3.5. CONCLUSION: Despite uncertainties in our estimates, preventing HEV transmission by screening of blood donations appears not excessively expensive compared to other blood-screening measures in the Netherlands. However, the impact on HEV disease burden may be relatively small as only a minority of all HEV cases is transmitted by blood transfusion. PMID: 28144956 [PubMed - indexed for MEDLINE]
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