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  • Book
    Masaki Mandai, editor.
    Summary: This book thoroughly illustrates the designed and tailored medical approaches for tumors of the female reproductive organ. The chapters explore different cancer species such as ovarian cancer, endometrial cancer, cervical cancer, etc. Various treatment modalities such as immunotherapy and histotype-specific treatment are delivered, and it offers a chapter on how genome-wide analysis contributes to personalized treatment. It is essential to understand this concept because many molecular target drugs and the prevalence of genome-based analysis in clinical settings have enabled us to introduce valid precision medicine in the field of gynecologic oncology. Chapters explain the stream of transition from conventional standardized treatment to personalized treatment and address future perspectives. Personalization Gynecologic Oncology is a well-designed source for beginning to advanced oncologists, gynecologists, geneticists, genetic counselors, and nurses. Offering the latest treatment strategies, the Editor hopes the ideas presented here will be a foundation for further development in the field.

    Contents:
    1 Personalized treatment in ovarian cancer
    2 Carcinogenesis and personalization in hpv-associated precancer lesions of the cervix
    3 Personalized treatment for gestational trophoblastic tumor
    4 Personalized treatment in uterine sarcoma
    5 Clinical relevance of brca1/2 pathogenic variants and impaired dna repair pathways in ovarian carcinomas
    6 Personalized treatment in immunotherapy for gynecologic cancer
    7 Risk assessment and prevention strategies for hereditary gynecological cancers
    8 How genome-wide analysis contributes to personalized treatment in cancers including gynecologic cancers
    9 Personalized treatment of gynecological cancer according to age and symptom benefit.
    Digital Access Springer 2022
  • Article
    Järhult J, Holst JJ.
    Acta Physiol Scand. 1978 Oct;104(2):188-202.
    The effects of unloading of the carotid baroreceptors on arterial plasma glucose concentration as well as on portal plasma immunoreactive glucagon (IRG) and insulin (IRI) concentrations were studied in anestethized, vagotomized cats either by sectioning the sinus nerves or by lowering the pressure in the isolated carotid sinuses. Complete elimination of the carotid baroreceptor discharge by cutting the sinus nerves caused an increase in the arterial plasma glucose concentration by 100% and an increase in the portal IRG level by about 200%, whereas the portal IRI concentration decreased to 50% of its basal value. These baroreceptor-induced changes of the plasma IRG and IRI levels seemed to be graded in relation to the drop in carotid blood pressure and they were clearly detectable when the pressure was lowered from 120 to 90 mmHg in the isolated carotid sinus preparation. The described reflex hyperglycemia, hyperglucagonemia and hypoinsulinemia were mediated to the pancreas and liver mainly by the sympatho-adrenal system, since cutting the splanchnic nerves above the adrenal glands abolished the hyperglycemia and hypoinsulinemic responses and markedly depressed the magnitude of the hyperglucagonemic response. In adrenalectomized cats, complete unloading of the baroreceptors evoked both hyperglucagonemia and hypoinsulinemia although the magnitude of the hormonal responses was diminished. In animals where the pancreas and liver were sympathectomized but the adrenal glands left intact, cutting the sinus nerves evoked a doubling of the IRG level and a slight increase in plasma glucose, but no significant change of the IRI level. I.v. infusion of adrenaline (1 microgram/kg X min) or noradrenaline (5 microgram/kg X min) caused pronounced increases in IRG and plasma glucose and a clear-cut reduction of IRI. We conclude that the function of the endocrine pancreas in the cat can be influenced by variations in the blood pressure by means of a reflex control which originates from arterial baroreceptors. This reflex adjustment of the endocrine pancreas is mediated chiefly by two links of the sympatho-adrenal system, namely by catecholamine-release from the adrenal medulla and, more importantly, by a direct adrenergic nerve fibre influence on the alpha- and beta- cells.
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