Internal circulation

Luận án này tập trung mô phỏng quá trình tuần hoàn nội (khí kéo nước) để xác định: Lượng nước (QN) được kéo lên bởi mỗi lượng khí (QK); và khả năng khuấy trộn của khí sinh ra và nước tuần hoàn. Từ đó, tính toán cơ cấu tuần hoàn trong hệ IC. Trong luận án cũng trình bày kết quả thử nghiệm chế tạo mô hình hệ IC quy mô phòng thí nghiệm nhằm xác định năng lực xử lý của hệ IC khi vận hành hệ thống với nước thải chăn nuôi lợn.

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This thesis focuses on simulating the internal circulation process (gas pulling water) to determine: The amount of water (QN) was pulled up by the amount of gas (QK); and mixing ability of generated gas and circulating water flow, from which to calculate the periodic structure in the IC system.

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Luận án này tập trung mô phỏng quá trình tuần hoàn nội (khí kéo nước) để xác định: Lượng nước (QN) được kéo lên bởi mỗi lượng khí (QK); và khả năng khuấy trộn của khí sinh ra và nước tuần hoàn. Từ đó, tính toán cơ cấu tuần hoàn trong hệ IC. Trong luận án cũng trình bày kết quả thử nghiệm chế tạo mô hình hệ IC quy mô phòng thí nghiệm nhằm xác định năng lực xử lý của hệ IC khi vận hành hệ thống với nước thải chăn nuôi lợn.

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von Willebrand Disease vWD is the most common inherited bleeding disorder. Estimates from laboratory data suggest a prevalence of approximately 1%, but data based on symptomatic individuals suggest that it is closer to 0.1% of the population. vWF serves two roles: (1) as the major adhesion molecule that tethers the platelet to the exposed subendothelium; and (2) as the binding protein for FVIII, resulting in significant prolongation of the FVIII half-life in circulation.

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Patients with type 2 vWD have functional defects; thus, the vWF antigen measurement is significantly higher than the test of function. For types 2A, 2B, and 2M, vWF activity is decreased, measured as ristocetin cofactor or collagen binding activity. In type 2A vWD, the impaired function is due either to increased susceptibility to cleavage by ADAMTS13, resulting in loss of intermediate- and high-molecular weight (M.W.) multimers, or to decreased secretion of these multimers by the cell.

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B Cell Chronic Lymphoid Leukemia/Small Lymphocytic Lymphoma: Treatment Patients whose presentation is typical B cell CLL with no manifestations of the disease other than bone marrow involvement and lymphocytosis (i.e., Rai stage O and Binet stage A; Table 105-7) can be followed without specific therapy for their malignancy. These patients have a median survival 10 years, and some will never require therapy for this disorder.

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Chronic lymphocytic leukemia. The peripheral white blood cell count is high due to increased numbers of small, well-differentiated, normal-appearing lymphocytes. The leukemia lymphocytes are fragile, and substantial numbers of broken, smudged cells are usually also present on the blood smear. If the primary presentation is lymphadenopathy and a lymph node biopsy is performed, pathologists usually have little difficulty in making the diagnosis of small lymphocytic lymphoma based on morphologic findings and immunophenotype.

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Internal iron exchange. Normally about 80% of iron passing through the plasma transferrin pool is recycled from broken-down red cells. Absorption of about 1 mg/d is required from the diet in men, 1.4 mg/d in women to maintain homeostasis. As long as transferrin saturation is maintained between 20–60% and erythropoiesis is not increased, iron stores are not required. However, in the event of blood loss, dietary iron deficiency, or inadequate iron absorption, up to 40 mg/d of iron can be mobilized from stores. RE, reticuloendothelial.

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Etiology Humoral hypercalcemia of malignancy (HHM) occurs in up to 20% of patients with cancer. HHM is most common in cancers of the lung, head and neck, skin, esophagus, breast, genitourinary tract, and in multiple myeloma and lymphomas. Several distinct humoral causes of HHM occur, most commonly overproduction of PTHrP. In addition to acting as a circulating humoral factor, bone metastases (e.g., breast, multiple myeloma) may produce PTHrP, leading to local osteolysis and hypercalcemia.

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Tumor angiogenesis is a complex process involving many different cell types that must proliferate, migrate, invade, and differentiate in response to signals from the tumor microenvironment. Endothelial cells (ECs) sprout from host vessels in response to VEGF, bFGF, Ang2, and other proangiogenic stimuli. Sprouting is stimulated by VEGF/VEGFR2, Ang2/Tie-2, and integrin/extracellular matrix (ECM) interactions.

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Assessment of Circulating (Visceral) Proteins The serum proteins most used to assess nutritional status include albumin, total iron-binding capacity (or transferrin), thyroxine-binding prealbumin (or transthyretin), and retinol-binding protein. Because they have differing synthesis rates and half-lives—the half-life of serum albumin is about 21 days whereas those of prealbumin and retinol-binding protein are about 2 days and 12 h, respectively—some of these proteins reflect changes in nutritional status more quickly than others.

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Harrison's Internal Medicine Chapter 67. Applications of Stem Cell Biology in Clinical Medicine Applications of Stem Cell Biology in Clinical Medicine: Introduction Organ damage and the resultant inflammatory responses initiate a series of repair processes, including stem cell proliferation, migration, and differentiation, often in combination with angiogenesis and remodeling of the extracellular matrix. Endogenous stem cells in tissues such as liver and skin have a remarkable ability to regenerate the organs, whereas heart and brain have a much more limited capability for self-repair.

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Most patients with trichotillomania, pressure-induced alopecia. The most common causes of nonscarring alopecia include telogen effluvium, androgenetic alopecia, alopecia areata, tinea capitis, and some cases of traumatic alopecia (Table 54-5). In women with androgenetic alopecia, an elevation in circulating levels of androgens may be seen as a result of ovarian or adrenal gland dysfunction. When there are signs of virilization, such as a deepened voice and enlarged clitoris, the possibility of an ovarian or adrenal gland tumor should be considered.

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Drug-induced erythroderma (exfoliative dermatitis) may begin as an exanthematous (morbilliform) eruption (Chap. 56) or may arise as diffuse erythema. A number of drugs can produce an erythroderma, including penicillins, sulfonamides, carbamazepine, phenytoin, gold, allopurinol, and zalcitabine. Fever and peripheral eosinophilia often accompany the eruption, and there may also be facial swelling, hepatitis, and allergic interstitial nephritis; this constellation is frequently referred to as drug reaction with eosinophilia and systemic symptoms (DRESS).

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Hormonal Evaluation Androgens are secreted by the ovaries and adrenal glands in response to their respective tropic hormones, luteinizing hormone (LH) and adrenocorticotropic hormone (ACTH). The principal circulating steroids involved in the etiology of hirsutism are testosterone, androstenedione, and dehydroepiandrosterone (DHEA) and its sulfated form (DHEAS). The ovaries and adrenal glands normally contribute about equally to testosterone production.

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Hyponatremia in the setting of ECF volume expansion is usually associated with edematous states, such as congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome. These disorders all have in common a decreased effective circulating arterial volume, leading to increased thirst and increased AVP levels. Additional factors impairing the excretion of solute-free water include a reduced GFR, decreased delivery of ultrafiltrate to the diluting site (due to increased proximal fractional reabsorption of Na+ and water), and diuretic therapy.

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Diagnosis (Fig. 46-1) Hyponatremia is not a disease but a manifestation of a variety of disorders. The underlying cause can often be ascertained from an accurate history and physical examination, including an assessment of ECF volume status and effective circulating arterial volume. The differential diagnosis of hyponatremia, an expanded ECF volume, and decreased effective circulating volume includes congestive heart failure, hepatic cirrhosis, and the nephrotic syndrome.

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Endophthalmitis This occurs from bacterial, viral, fungal, or parasitic infection of the internal structures of the eye. It is usually acquired by hematogenous seeding from a remote site. Chronically ill, diabetic, or immunosuppressed patients, especially those with a history of indwelling IV catheters or positive blood cultures, are at greatest risk for endogenous endophthalmitis. Although most patients have ocular pain and injection, visual loss is sometimes the only symptom.

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Differential Diagnosis Nausea and vomiting are caused by conditions within and outside the gut as well as by drugs and circulating toxins (Table 39-1).

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Endothelin This potent peptide vasoconstrictor is released by endothelial cells; its concentration is elevated in heart failure and contributes to renal vasoconstriction, Na+ retention, and edema in heart failure. Natriuretic Peptides Atrial distention and/or a Na+ load cause release into the circulation of atrial natriuretic peptide (ANP), a polypeptide; a high-molecular-weight precursor of ANP is stored in secretory granules within atrial myocytes.

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