Academic literature on the topic 'Mice Mice Tretinoin'

Tretinoin has an important role in wound healing process include improve fibroplasia and collagen synthesis, maintening humoral immunity, and neutralize steroid effect.Epithelization and fibroblast proliferation were very important event in wound healing process. The aims of this study were studying epithelization and fibroblas proliferation on incision wound healing process using pre treatment of Tretinoin 0,1% topically on mice. This research used 24 male mice, 3 month of age, with 150 -180 gram of body weight. The mice were divided into 2 groups, control group (K) and treatment group (P). The control group was a group of mice with an incision wound, while the treatment group was a group of mice with an incision wound that received a pretreatment of Tretionin of 0.1% topically. Each group was divided into 2 sub groups K4, K7, P4, P7 based on time of samples collecting. K4 and P4 were examined at day 4, while K7 and P7 were examined at day 7. Epithelialization was observed by measuring the length of the epithelial incision area, whereas fibroblast proliferation was performed by counting the number of fibroblasts in five field of view on histopathologic skin preparations processed by HE staining.In this study,pretreatment of Tretinoin 0,1% topically can increase epithelialization and number of fibroblast significantly (p<0,05).This increase may be due to 1% Tretinoin in the tissues to induce keratinocyte basal proliferation including its migration to the skin surface via retinoic acid receptors ( RARδ)Pretreatment of Tretinoin 0,1% topically can increased epithelialization and number of fibroblast on incision wound healing process of albino rats

Recently topical use of 2% Ketoconazole solution has been reported to have a therapeutic effect on androgenic alopecia. Minoxidil is a vasodilatory medication used primarily as antihypertensive drug. It was discovered to have the side effect of hair growth and reversing baldness. Tretinoin is commonly used topically for acne treatment and in the treatment of photoaging. It is used by some as hair loss treatment. Objective. To compare the stimulatory effect of Ketoconazole, Minoxidil, and Minoxidil with Tretinoin on hair growth in a mouse model. Materials and Methods. Coat hairs on the dorsal skin of seven weeks old male mice were gently clipped and then stained by using commercial dye. These mice were divided into four groups each of five treated with topical application of ethanol 95%, Ketoconazole solution 2%, Minoxidil solution 5%, and Minoxidil with Tretinoin solution 0.1%, respectively. The drugs were applied once daily for three weeks, the clipped area was photographed, and the ratio of regrown coat area was calculated. Results. The results demonstrated that Ketoconazole, Minoxidil, and Minoxidil with Tretinoin had a significant stimulatory effect on hair growth compared with the control group and Minoxidil was the most effective drug among them.

Aim: Multicompartmental lipid–protein nanohybrids (MLPNs) were developed for combined delivery of the anticancer drugs tretinoin (TRE) and genistein (GEN) as synergistic therapy of lung cancer. Materials & methods: The GEN-loaded lipid core was first prepared and then coated with TRE-loaded zein shell via nanoprecipitation. Results: TRE/GEN-MLPNs demonstrated a size of 154.5 nm. In situ ion pair formation between anionic TRE and the cationic stearyl amine improved the drug encapsulation with enhanced stability of MLPNs. TRE/GEN-coloaded MLPNs were more cytotoxic against A549 cancer cells compared with combined free GEN/TRE. In vivo, lung cancer bearing mice treated with TRE/GEN-MLPNs displayed higher apoptotic caspase activation compared with mice-treated free combined GEN/TRE. Conclusion: TRE/GEN-MLPNs might serve as a promising parenteral nanovehicles for lung cancer therapy.

Abstract Acute myeloid leukemia (AML) is characterized by an early failure of healthy hematopoiesis and a high relapse rate, caused by persistent leukemia initiating cells in the bone marrow niche. The hematopoietic stem cell niche in myeloid malignancies shows severe structural and functional alterations with an inflammatory response upon leukemia infiltration and impaired immunosurveillance. CD38 is a glycoprotein that is expressed on various immunoregulatory cells and commonly on AML blasts. Targeting CD38 by using the monoclonal antibody daratumumab showed high efficacy in multiple myeloma which is mediated by both cell-autonomous as well as immunomodulatory mechanisms. In this study we have investigated the anti-leukemic efficacy of daratumumab as well as its underlying mechanisms in AML. Using an in vitro co-culture model with different human AML cell lines together with a fibroblast cell line (MS-5) or human umbilical vein endothelial cells (HUVEC) revealed a significant reduction in AML cell growth upon daratumumab treatment in 5 of 8 AML cell lines. Interestingly, anti-leukemic activity of daratumumab was more pronounced when co-cultured with MS-5 stroma cells and to lower extent with HUVECs as compared to mono-cultured AML cells (mean cell reduction in MS-5 co-culture, range from 12.9 to 31%; in HUVEC co-culture, range from 1.9 to 24.1% and in mono-culture, range from 9.9 to 18%). To validate the anti-leukemic activity of daratumumab in human AML and to elaborate the microenvironment-mediated effects we created a 3D invitro model with HUVECs and human mesenchymal spheres cultured with primary AML or normal donor cells. We could demonstrate that this triple-culture model led to an increased growth support for both AML as well as normal donor samples as compared to mono-cultured cells. Adding daratumumab to mono-cultured AML cells reduced cell growth by only 7.2% (p<0.01), whereas the anti-leukemic efficacy increased to 35.6% in triple-cultured AML samples (p<0.05; n=10 replicates). Of note, daratumumab did not show any significant cytotoxicity in normal donor samples at any culture condition. The anti-leukemic efficacy of daratumumab in AML appeared to depend on the level of CD38 expression. Addition of tretinoin (ATRA) induced a ~4-fold increase of CD38 expression in AML blasts and to a lower extent in normal donor cells. In fact, combination of tretinoin and daratumumab led to an enhanced anti-leukemic activity in AML. As daratumumab has been shown to exert diverse effects in myeloma we next assessed the underlying mechanisms in AML. Upon daratumumab treatment there were no significant differences in blast proliferation and apoptosis as assessed by BrdU and Annexin V assays, nor did we observe any induction of differentiation. Given the strong immunological reactions induced by daratumumab we next performed effector function assays. While there was no increase in antibody dependent cellular cytotoxicity (ADCC) or complement dependent cytotoxicity (CDC), we observed a significant induction of antibody dependent phagocytosis (ADCP) with daratumumab compared to IgG1 control. Human macrophages showed a ~1.7-fold increase in phagocytosis of AML cell lines and primary human AML cells after daratumumab treatment. To prove the anti-leukemic activity of daratumumab in AML in vivo we intravenously transplanted primary human AML cells into immunodeficient NOD scid gamma (NSG) mice. Leukemic mice were treated with ATRA over 4 weeks and once weekly with either daratumumab or IgG1 control. Preliminary results show a reduction in circulating blasts with a significant decrease of leukemia burden in peripheral blood by ~42% (p=0.0354), while there were no significant changes in bone marrow infiltration (n=5-6 mice per group). Ongoing experiments will further elucidate the anti-leukemic efficacy of daratumumab in combination with low-dose cytarabine. In summary, we found that targeting CD38 shows promising anti-leukemic activity with both cell-autonomous and microenvironment-mediated effects in AML. Together with tretinoin und putatively low-dose chemotherapy the efficacy of daratumumab in AML could be increased. This combination of well tolerated drugs could present a new option of niche-targeted therapies in AML. Disclosures Duehrsen: Janssen: Honoraria; Gilead: Consultancy, Honoraria; AbbVie: Consultancy, Honoraria; Roche: Honoraria, Research Funding; Celgene: Honoraria, Research Funding; Amgen: Research Funding.

The splotch (sp) mutation has been identified as a mutation in the paired box gene, Pax-3. Heterozygous mice carrying this mutation are phenotypically normal, with the exception of a white spot on their bellies. Homozygous embryos do not live to birth, and suffer from a wide range of developmental defects, all of which result from delayed neural tube closure, or inadequate neural crest cell migration. Most notably, homozygotes have an increased rate of spina bifida with or without exencephaly. Retinoic acid (RA), which has been shown to be very important in the development of a number of systems, was shown to cause a selective mortality of the homozygous splotch embryos when administered maternally at day 9 p.c. (Moase and Trasler, 1987). Since cellular retinoic acid binding protein (CRABP) is localized to the tissues which are affected by both the splotch gene, and retinoic acid teratogenesis, its expression patterns in the developing splotch embryo were examined. It was found that the distribution of CRABP mRNA is normal, but its expression levels are excessive in splotch homozygous day 9 mouse embryos.

Lee, Man Yuen.<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 2011.<br>Includes bibliographical references (leaves 191-215).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Abstract also in Chinese.

As exogenously administered RA suppressed the expression of the RA synthesizing enzymes, further investigation on whether this would lead to deficiency in endogenous RA concentrations was conducted. Results showed that exogenously administered RA significantly reduced the endogenous RA level in the head region with C57 embryos showing a greater reduction than ICR embryos.<br>In addition, detailed morphological and histological studies were conducted to determine if RA treatment caused early embryonic changes with strain difference. When compared with ICR embryos, C57 embryos exhibited more pronounced responses to RA, including developmental retardation, underdevelopment of the anterior neural plate and absence of or smaller optic pit/optic vesicle formation. However, RA treatment did not cause abnormal apoptosis in the early stages in both strains.<br>Since the teratogenic effect of RA is highly developmental stage-dependent, it is possible that there is a difference in the developmental stage between these 2 mouse strains at the time of RA injection. Indeed, it was found that the developmental stage of ICR embryos was approximately 6 hours ahead of C57 embryos. However, the role that this factor plays in the differential strain susceptibility to RA can be excluded since C57 fetuses were still 3 times more susceptible to developing anophthalmia/microphthalmia than ICR fetuses that were subject to RA treatment at equivalent developmental stages. Comparison of susceptibility to RA-induced anophthalmia/microphthalmia was also made among heterozygous fetuses obtained from reciprocal matings between C57 and ICR male and female mice, and those in homozygous ICR and C57 fetuses. Results showed that the C57 strain has conferred both genetic predisposition and maternal effects in increasing the embryo's susceptibility to RA-induced ocular defects.<br>Since the type of RA-induced ocular defects mimic those that developed in Raldh2 null mutant embryos, the effect of RA treatment on the expression of RA synthesizing enzymes, Raldh2 and Raldh3, and the RA-inducible gene Cyp26a1, as well as some early eye development genes were examined. Exogenously administered RA reduced the mRNA expression levels of Raldh2, Raldh3 and Cyp26a1 in the head region, with C57 embryos showing a greater reduction than ICR embryos.<br>Taken together, results of this thesis suggest that there is a strain difference in susceptibility to RA-induced ocular defects in which exogenously applied RA suppresses the expression of RA synthesizing enzymes and leads to endogenous RA deficiency. This finding may shed light on understanding why both excess and deficiency of RA can lead to similar types of ocular defects.<br>To determine if there are strain differences in the susceptibility to RA-induced ocular defects, two mouse strains were used. They are C57BL/6J (C57), mice that spontaneously develop ocular defects and ICR mice, which are not prone to developing ocular defects. Detailed time and dose response studies were conducted and eye defects were examined in near-term fetuses. C57 fetuses were found to be significantly more susceptible to RA-induced anophthalmia/microphthalmia than ICR fetuses.<br>Vitamin A (retinol) and its most active metabolite, all- trans retinoic acid (RA) is essential for vision in the adult and for eye development in the embryo. It is well documented that in humans, excess intake or deficiency of vitamin A or RA is associated with congenital ocular defects such as microphthalmia. However, the underlying mechanism remains unclear. The aim of this study is to examine the pathogenic mechanism of RA-induced developmental ocular defects.<br>Lau, Wing Sze Josephine.<br>Source: Dissertation Abstracts International, Volume: 71-01, Section: B, page: 0240.<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 2009.<br>Includes bibliographical references (leaves 186-211).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Abstracts in English and Chinese.