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Filled with emotion and intensity, The Protector of Dunbar tells the story of how Queen Sara must safeguard her kingdom from endangerment. A secret is discovered that takes King Andrew away on a crucial mission, leaving Sara behind to protect Dunbar from wild animals, crop failures, and an external threat that puts the kingdom on the brink of extinction. An intense battle with a former foe shows Sara's true bravery and leads her back to Andrew. Life seems peaceful until a dark character brings chaos and destruction to Dunbar. Sara's wise intellect and tenacity will be put to the test. Does she have enough courage and faith to stand up to this mystery character? Or will the island's kingdoms be destroyed from within? Follow Sara and Andrew as they courageously battle for the survival of their people. The Protector of Dunbar is the sequel to The Adventures of Andrew Dunbar. It is a fictional story for young adults who are looking to be captivated in an exciting tale of fun, faith, and forgiveness.

Put Dat Work In is a motivational guide to beginners trying to find their way to accomplishing their fitness goals. You will find examples of mealplans and journals that will help beginners to find their "nitch" in the fitness world.

Diffuse Intrinsic Pontine Glioma (DIPG) is a near universally fatal pediatric brain tumor that occurs in the pons and other midline structures. These tumors are characterized by the presence of a unique histone mutation: H3 K27M. This mutation inhibits the polycomb repressive complex 2 (PRC2) and reduces the global H3 K27 trimethylation mark. DIPG is resistant to conventional therapies such as radiation and chemotherapy which contributes to the high mortality rate in DIPG patients. A major challenge to researching DIPG is a lack of tissue available for research models. Due to the sensitive location of DIPG tumors, these tumors cannot be removed by surgery. All current DIPG models are either generated from autopsies or genetically engineered from mice or human stem cells. Currently no drug developed from these research models have translated into a successful clinical therapy. In order to develop a model that more accurately represents to disease state, we developed a protocol to collect biopsies from DIPG patients prior to treatment. Using these treatment naive DIPG biopsy models, we observed similar resistance to radiation therapy compared to how the tumors behaved in the clinic. A key component of the resistance to radiation was the inability of DIPG cells to undergo apoptosis. We found that the pro-apoptotic protein BCL-2 associated X (BAX) was significantly reduced in DIPG compared to other pediatric brain tumors. When radiation sensitive cells were irradiated, they upregulated BAX but in DIPG this response was significantly reduced. In order to overcome the reduced levels of BAX, we inhibited the pro survival BCL-2 family proteins and found that the pan BCL-2, BCL-xl inhibitor navitoclax was able to sensitize DIPG cells to radiation. We measured the percent of pro-apoptotic cells and found the combination of navitoclax and radiation significantly increase the percent of pro-apoptotic cells in the combination treatment compared to either treatment individually. Future work will focus on why BAX is downregulated in DIPG compared to other pediatric brain tumors. We have identified several transcription factors and epigenetic regulators of BAX that are dysregulated in DIPG. This research has contributed to our understanding of how DIPG resists conventional therapy and may lead to targeted therapies which sensitize DIPG and improve the overall patient survival.