Download Free Close To The Bone Book in PDF and EPUB Free Download. You can read online Close To The Bone and write the review.

This is a book for any person who is living with a life-threatening illness and for anyone who is caring for and/or loves a person who is ill. Bolen affirms that the price of going into the scary places, of feeling like a piece of green meat on a hook, is high, but worth it. We have no choice. We will all face health crises--our own and others. We can try to bury our heads in the sand. Or we can travel to the underworld. We can probe. We can listen. We can connect to what we know in our bones. In the ten years since the original publication of Close to the Bone, Jean Bolen has continued to explore the impact and the possibilities for finding purpose that confronting a serious illness and possible death present us. This expanded edition includes a new section about forming circles in the time of crises, plus more stories that support the process of hope and the desire to live and change as well as a very personal passage in which Dr. Bolen tells the story of the death of her son. This book is meant to help and heal, to make people less afraid, and to encourage them to trust the wisdom they have inside--what they know in their bones. * 10th Anniversary revised edition, with a guide for those who want to form support circles.
Close to the Bone scouts the territories of sex, the family, loneliness, the city, addiction, and AIDS, but these are not passive tales of victimization. Rather, these writers speak in voices that are unflinching, unerring, and filled with revelation.
The treatment of painful musculoskeletal disorders with acupuncture and other forms of Chinese medicine. It contains a substantial amount of new material, an increased emphasis on diagnosis and updated treatment recommendations.
"A must-read for fans of Cornwell and Grafton" Booklist “Taut suspense, a brave and likable heroine, a clever plot, and a slam-bang ending add up to a high-water mark for this popular series” Booklist on Close to the Bone Forensic scientist Theresa MacLean stumbles across a murder rather too close for comfort when she returns to the Medical Examiner’s office following a late-night call to find one deskman missing and the other beaten to death. Written in blood above the dead man’s head is a single word: ‘Confess’. It’s the first time a homicide has taken place actually within the ME’s office. Medical Examiner Stone works on how to spin the news while Theresa works the scene. When a second victim is discovered, Theresa uncovers a link to the death of another co-worker, records secretary Diane Allman, who was murdered in her own home ten years before. As she painstakingly pieces the clues together, Theresa realizes that she has become an integral part of a ruthless killer’s murderous agenda. And if she is to survive, she must find out what really happened to Diane all those years ago.
A fellow lawyer disappears from his boat, and Brady suspects foul play Although alleged criminals are considered innocent until proven guilty, acquittal doesn’t make them saints. Boston lawyer Brady Coyne knows this all too well, but believes firmly enough in the right to counsel that he doesn’t let it keep him up at night. His friend Paul Cizek, however, is another story. A rising young defense lawyer, Paul has made a name defending repugnant clients: hit men, child molesters, unrepentant drunk drivers. He’s good at what he does—so good that it’s eating him alive. After an emotional confession to Brady, Paul takes his boat out onto the Merrimack River in the middle of a storm. When the coast guard finds the vessel, the lawyer has vanished. Did he die in an accident, or did the stress of his work convince him to end it all? Brady suspects murder, and he will do whatever it takes to understand how his friend died.
Osteoporosis is a metabolic skeletal disease characterized by low bone mass, depleted micro-architecture and reduced strength. The public health costs of osteoporosis relate almost entirely to the fractures that are the clinical manifestation of the disease and it presents a significant cause of morbidity in today's ageing population. Oestrogen deficiency during the menopause is the primary causative factor for postmenopausal osteoporosis and although much is known about the pathophysiology of the disease, including dysregulated bone cell function whereby more bone is digested than is formed; the underlying mechanisms involved have not yet been delineated. Recent studies have suggested that although overall strength is decreased following osteoporotic bone loss, the remaining bone tissue is stronger and stiffer, suggesting an alteration in bone tissue composition. Bisphosphonates are among drug treatments administered to tackle bone loss, however the incidence of osteoporotic fractures still remains high. Furthermore, the precise effect of drug treatment on bone tissue mineralisation is unknown. The global aim of this thesis is to discern the alterations in the quantity and distribution of bone mineral during osteoporosis. Specifically, it is sought to test the hypotheses that bone mineral distribution is altered at a tissue level following oestrogen deficiency and bisphosphonate treatment and that oestrogen depletion alters normal mineralisation and mechano-responsiveness of bone cells. Quantitative backscattered imaging (qBEI) on a scanning electron microscope was used to examine individual bone trabeculae from the proximal femur of ovariectomised sheep (oestrogen deficient state), aged matched control sheep and sheep treated with the bisphosphonate Zoledronic acid. It was found that oestrogen deficiency caused significantly higher mineral heterogeneity within trabeculae (site speficic within the femur) and along a common osteoporotic fracture line. Bone mineralisation was diminished with prolonged oestrogen deficiency and conversely was higher in older healthy sheep compared to younger control sheep. Furthermore, significantly lower mineral heterogeneity was found in OVX sheep treated with Zoledronic acid compared to untreated OVX sheep. These results indicate that changes in bone tissue mineralisation during oestrogen deficiency may be a contributing factor for reduced mechanical strength during osteoporosis, while drug induced increased homogeneity may contribute to the ability of Zoledronic acid to prevent fracture occurrence during oestrogen deficiency. The next study aimed to delineate the mechanisms responsible for such altered mineral distribution. Osteoblast and osteocyte cells were pre-treated with oestrogen and the effects of oestrogen deficiency were evaluated by subsequently withdrawing oestrogen from cells, or blocking oestrogen receptors using an oestrogen antagonist, fulvestrant. Specifically, alkaline phosphatase expression was investigated using p-nitrophenyl phosphate (pNPP), proliferation by assessing DNA content, calcium production using alizarin red assay and apoptosis by measuring for caspase 3/7 activity. Although mineral production was significantly increased by oestrogen pre-treatment, a further increase in mineral production and apoptosis were observed following oestrogen withdrawal from cells. These observations increase our understanding of the mechanisms controlling bone formation and bone cell death and may aid in the development of enhanced therapeutics for the treatment of osteoporosis. The final study of this thesis aimed to determine if the mechano-biological response of osteoblasts is impaired during oestrogen deficiency and whether changes in bone mineralisation may be related to altered bone formation in response to mechanical stimulation. Osteoblasts were pre-treated with oestrogen and subsequently oestrogen was withdrawn from cell cultures and their responses under fluid shear stress were evaluated. Firstly, daily loading cycles, using an orbital rotator, were applied to cells and mineralisation and cell viability (using alamar blue assay) were assessed after 7 and 14 days. In a separate experiment, following 2 and 7 days of oestrogen withdrawal, osteoblasts were exposed to 2 hours of shear stress in a custom designed parallel plate bioreactor. PGE2 was quantified in cell culture conditioned media using an immunoassay kit. It was found that orbital fluid flow induced shear stress significantly increased mineral production by bone cells and that under an applied shear stress, mineral production was decreased during oestrogen withdrawal. It was also observed that mechanical loading and oestrogen are required in unison to promote mineral production. PGE2 release was significantly increased with applied laminar flow, but was decreased by oestrogen withdrawal. Together, these studies provide evidence that bone cells become accustomed to levels of circulating oestrogen and that diminished oestrogen causes osteocyte apoptosis, increased osteoblast mineralisation and altered mechano-sensitivity. These changes might explain the decreased mean concentrations of mineral, together with increased mineral heterogeneity, from our earlier in vivo studies. Therefore, the results of the thesis provide a unique insight into why the tightly coupled mechanisms of matching bone's structure and composition to the loads it experiences are disrupted when levels of circulating oestrogen are depleted.

Best Books