Teaching students to use medical notes.
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Confidentiality↗
Biomedical subjects
C Jamieson
Publications and source records attributed to C Jamieson.
Capecitabine (Xeloda) improves medical resource use compared with 5-fluorouracil plus leucovorin in a phase III trial conducted in patients with advanced colorectal carcinoma.
Standard therapy for advanced or metastatic colorectal cancer consists of 5-fluorouracil plus leucovorin (5-FU/LV) administered intravenously (i.v.). Capecitabine (Xeloda), an oral fluoropyrimidine carbamate which is preferentially activated by thymidine phosphorylase in tumour cells, mimics continuous 5-FU and is a recently developed alternative to i.v. 5-FU/LV. The choice of oral rather than intravenous treatment may affect medical resource use because the two regimens do not require the same intensity of medical intervention for drug administration, and have different toxicity profiles. Here we examine medical resource use in the first-line treatment of colorectal cancer patients with capecitabine compared with those receiving the Mayo Clinic regimen of 5-FU/LV. In a prospective, randomised phase III clinical trial, 602 patients with advanced or metastatic colorectal cancer recruited from 59 centres worldwide were randomised to treatment with either capecitabine or the Mayo regimen of 5-FU/LV. In addition to clinical efficacy and safety endpoints, data were collected on hospital visits required for drug administration, hospital admissions, and drugs and unscheduled consultations with physicians required for the treatment of adverse events. Capecitabine treatment in comparison to 5-FU/LV in advanced colorectal carcinoma resulted in superior response rates (26.6% versus 17.9%, P=0.013) and improved safety including less stomatitis and myelosuppression. Capecitabine patients required substantially fewer hospital visits for drug administration than 5-FU/LV patients. Medical resource use analysis showed that patients treated with capecitabine spent fewer days in hospital for the management of treatment related adverse events than did patients treated with 5-FU/LV. In addition, capecitabine reduced the requirement for expensive drugs, in particular antimicrobials fluconazole and 5-HT3-antagonists to manage adverse events. As anticipated with an oral home-based therapy patients receiving capecitabine needed more frequent unscheduled home, day care, office and telephone consultations with physicians. In the light of clinical results from the phase III trial demonstrating increased efficacy in terms of response rate, equivalent time to progression (TTP) and survival (OS), and a superior safety profile, the results from this medical resource assessment indicate that capecitabine treatment of colorectal cancer patients results in a substantial resource use saving relative to the Mayo Clinic regimen of 5-FU/LV. This benefit is derived principally from the avoidance of hospital visits for i.v. drug administration, less expensive drug therapy for the treatment of toxic side-effects, and fewer treatment-related hospitalisations required during the course of therapy for adverse drug reactions in comparison to patients treated with 5-FU/LV.
Adult↗
Ambulatory blood pressure in heart failure.
Ambulatory blood-pressure monitoring (ABPM) is accepted in the evaluation and management of hypertension. The use of ABPM in heart failure has received considerably less attention. Many patients with advanced heart failure experience disabling fatigue, orthostatic dizziness and symptoms of coronary and cerebrovascular insufficiency that may relate to periods of hypotension. These may be exacerbated by vasodilator drug therapy and may be difficult to evaluate by casual clinic recordings. ABPM in heart failure may help in the following: (i) evaluating time-dependent pharmacodynamic drug effects, such as peak and end-of-dose phenomena, tolerance and rebound; (ii) titrating ACE inhibitors and other drugs to highest-tolerated doses; and (iii) correlating circadian blood-pressure profiles with symptoms, quality of life, severity of heart failure, progression of ventricular and renal dysfunction, risks of stroke and myocardial infarction, and life expectancy. Devices for ABPM have been beset by problems of inaccuracy and unreliability. Standards for their manufacture and sale (including bench tests of accuracy against sphygmomanometry and intra-arterial recordings, and field tests of reliability) have been devised independently by several agencies, including the British Hypertension Society (BHS) and US Association for the Advancement of Medical Instrumentation (AAMI). A joint BHS/AAMI set of guidelines is in preparation. These guidelines emphasize the suitability of ABPM devices for hypertensive patients and those under general anesthesia, and may not be applicable to ambulant individuals with heart failure and blood pressures at or below the lower end of the evaluated ranges. Prospective studies of the accuracy and reliability of ABPM devices, their clinical utility and research potential should be undertaken in patients with heart failure before their informal and uncontrolled use in this population becomes widespread.
Blood Pressure Monitoring, Ambulatory↗
Inhibition of the ubiquitin-proteasome system in Alzheimer's disease.
Alzheimer's disease is the most common cause of dementia in the elderly. Although several genetic defects have been identified in patients with a family history of this disease, the majority of cases involve individuals with no known genetic predisposition. A mutant form of ubiquitin, termed Ub(+1), has been selectively observed in the brains of Alzheimer's patients, including those with nonfamilial Alzheimer's disease, but it has been unclear why Ub(+1) expression should be deleterious. Here we show that Ub(+1) is an efficient substrate for polyubiquitination in vitro and in transfected human cells. The resulting polyubiquitin chains are refractory to disassembly by deubiquitinating enzymes and potently inhibit the degradation of a polyubiquitinated substrate by purified 26S proteasomes. Thus, expression of Ub(+1) in aging brain could result in dominant inhibition of the Ub-proteasome system, leading to neuropathologic consequences.
Alzheimer Disease↗
Gene dosage effects of steroidogenic factor 1 (SF-1) in adrenal development and the stress.
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Adrenal Glands↗
A new model for recognizing and rewarding the educational accomplishments of surgery faculty.
Faculty members' educational endeavors have generally not received adequate recognition. The Association for Surgical Education in 1993 established a task force to determine the magnitude of this problem and to create a model to address the challenges and opportunities identified. To obtain baseline information, the task force reviewed information from national sources and the literature on recognizing and rewarding faculty members for educational accomplishments. The group also developed and mailed to surgery departments at all U.S. and Canadian medical schools a questionnaire asking about the educational endeavors of the surgery faculty and their recognition for such activities. The response rate after two mailings was only 56%, but the responses reaffirmed the inadequacy of systems for rewarding and recognizing surgeon-teachers and surgeon-educators, and confirmed that the distinction between the roles of teacher and educator was rarely made. The task force created a four-tier hierarchical model based on the designations teacher, master teacher, educator, and master educator as a framework to offer appropriate recognition and rewards to the faculty, and endorsed a broad definition of educational scholarship. Criteria for various levels of achievement, ways to demonstrate and document educational contributions, appropriate support and recognition, and suggested faculty ranks were defined for these levels. The task force recommended that each surgery department have within its faculty ranks a cadre of trained teachers, a few master teachers, and at least one educator. Departments with a major commitment to education should consider supporting a master educator to serve as a resource not only for the department but also for the department's medical school and other medical schools. Although this model was created for surgery departments, it is generalizable to other disciplines.
Academic Medical Centers↗
Human long-term bone marrow culture.
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Bone Marrow Cells↗
In vitro clonal culture of human hematopoietic progenitor cells.
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Cell Culture Techniques↗
Thyroid xenografts from patients with Graves' disease in severe combined immunodeficient mice and NIH-beige-nude-xid mice.
OBJECTIVE: To compare human thyroid xenografts from patients with Graves' disease in severe combined immunodeficient (SCID) mice and triple immunodeficient NIH-beige-nude-xid (NIH-3) mice to obtain an improved animal model for studying these xenografts. DESIGN: Animal study. PARTICIPANTS AND ANIMALS: Patients with Graves' disease; SCID and NIH-3 mice. INTERVENTIONS: Thyroid tissue from six patients with Graves' disease was xenografted to SCID and NIH-3 mice; in addition, peripheral blood mononuclear cells (PBMC) from 12 patients with Graves' disease were grafted intraperitoneally to separate SCID and NIH-3 mice. OUTCOME MEASURES: Levels of human immunoglobulin (IgG), thyroperoxidase antibodies (TPO-Ab), thyroglobulin (Tg-Ab), and expression of thyrocyte intercellular adhesion molecule-1 (ICAM-1) and histocompatibility leukocyte antigen (HLA-DR) in mice after xenografting. RESULTS: IgG was detected in all mice grafted with Graves' thyroid tissue and some mice grafted with PBMC; levels of human IgG peaked 6 to 10 weeks after xenografting. Human IgG levels reached a mean of 500 mg/L (standard error of the mean [SEM] 150 mg/L) in the NIH-3 mice with thyroid xenografts. This was similar to results in SCID mice with thyroid xenografts, which had a mean level of human IgG of 640 mg/L (SEM 230 mg/L). PBMC xenografting resulted in a mean IgG level of 1200 mg/L (SEM 250 mg/L) in NIH-3 mice, which was similar to the mean level of 1000 mg/L (SEM 280 mg/L) in SCID mice. The rate of rise in human IgG in the sera of the NIH-3 mice with thyroid xenografts was similar to that in the SCID mice. TPO-Ab were also detected in some mice with Graves' thyroid grafts and in a few mice injected with PBMC, with levels peaking 4 to 6 weeks after xenografting. TPO-Ab levels reached a mean 109.3 U/mL (SEM 57.2 U/mL) in the NIH mice with thyroid xenografts, which were similar to the mean level of 91.7 U/mL (SEM 34.2 U/mL) in the SCID mice. There were no significant differences in the Tg-Ab levels in each type of mice (13.9 [SEM 12.1] U/mL v. 17.9 [SEM 7.9] U/mL). Eight weeks after xenografting into mice, the expression of xenograft thyrocyte ICAM-1 decreased significantly in both the SCID and NIH-3 mice (from 43.4%, SEM 4.9%, to 35.9%, SEM 4.6%, in the NIH-3 mice, p < 0.05, and from 43.4%. SEM 4.9%, to 32.5%, SEM 5.2%, in the SCID mice, p < 0.05). However, the expression of thyrocyte HLA-DR did not change significantly in the NIH-3 mice (from 11.5%, SEM 3.3%, to 10.8%, SEM 3.3%), whereas it decreased significantly in the SCID mice (from 11.5%, SEM 3.3%, to 4.2%, SEM 2.0%, p < 0.02). CONCLUSIONS: Not only SCID mice but also NIH-3 mice may be useful as animal models for xenografted thyroid tissue, which will help us elucidate the pathogenesis of autoimmune thyroid disease. NIH-3 mice are superior to SCID mice in maintaining the expression of thyrocyte HLA-DR in Graves' thyroid xenografts at levels as high as those before xenografting; this maintenance of expression may be due to the lack of natural killer cells in NIH-3 mice.
Animals↗
Teaching effectiveness of surgeons.
BACKGROUND: Evaluation of clinical teaching is essential for feedback to teachers, and for reliable and valid data for the purpose of promotion and tenure. METHODS: The teaching effectiveness of 43 surgeons was evaluated continuously over a 9-year period. Stability of Teaching Effectiveness Scores (TES) over the 9-year period, correlation with age, and the changes after academic promotion were analyzed. RESULTS: A total of 3,750 evaluations were completed. The average of 10 evaluations per surgeon per year gave an intraclass correlation of 0.65. The mean TES did not show any significant change over the 9 years. The majority of the "good" and "average" surgeons maintained their TES ratings, and most of the "poor" group improved their TES. The age of the surgeon was not a factor. Most surgeons had a decrease in their TES after academic promotion. CONCLUSIONS: A reliable system of teaching evaluation was achieved. Teaching scores were stable over time for good and average teachers, whereas the poor teachers tended to improve their scores.
Adult↗
Selective elimination of malignant stem cells using photosensitizers followed by light treatment.
The pros and cons of purging of either bone marrow or peripheral blood stem cell preparations for autologous transplantation for cancer has been debated strongly over the past decade. Recent data implicating the role of minimal residual disease in autografted marrow in cancer relapse have renewed interest in this question. There is a considerable body of literature supporting the possibility that photosensitizer molecules in combination with light might provide a therapeutic window permitting selective elimination of malignant stem cells while sparing those of normal lineage. Molecules of this class are known to be taken up more actively by most malignant cells, and intracellular concentrations are critical in their cytotoxic effect when they are activated by light at an appropriate wavelength. The present paper reviews the observations made over the past decade on a variety of photosensitizers and their effects on hemopoietic progenitors.
Bone Marrow Purging↗
Expression of intercellular adhesion molecule-1 on human thyroid cells from patients with autoimmune thyroid disease: study of thyroid xenografts in nude and severe combined immunodeficient mice and treatment with FK-506.
It has been suggested that intercellular adhesion molecule-1 (ICAM-1) may play an important role in the initiation, localization, and perpetuation of autoimmune thyroid diseases (AITD). In an effort to clarify its role, we have investigated the expression of ICAM-1 on thyroid epithelial cells (TEC) of patients with AITD, patients with nontoxic goiter (NTG), and normal subjects (PN) by flow cytometric analysis under basal conditions and after modulation with cytokines, before and after 8 weeks of thyroid tissue xenotransplantation in nude athymic mice (which lyses all passenger lymphocytes), and in severe combined immunodeficient (SCID) mice where these cells survive. Before xenografting, ICAM-1 was expressed on 56% of TEC from Hashimoto's thyroiditis (n = 5), 54% of Graves' disease (n = 6), 15% of NTG (n = 5), and 12% of PN TEC. After the xenografts had been 8 weeks in nude mice, ICAM-1 expression decreased markedly in AITD TEC [from 56% to 10% in Hashimoto's thyroiditis (P < 0.001) and from 54% to 8% in Graves' disease (P < 0.01)], but did not change significantly in NTG or PN. After the xenografts had been 8 weeks in SCID mice, the expression of ICAM-1 was significantly higher on TEC of AITD compared with the same tissue in nude mice. When the SCID mice engrafted with AITD tissue were treated with the anti-CD4+ T (helper) cell agent FK-506, the expression of ICAM-1 was reduced significantly compared with that in the original tissue or that in nontreated mice engrafted with the same tissue. The proportion of TEC that were ICAM-1 positive was up-regulated in all cases by certain cytokines (e.g. interferon-gamma and tumor necrosis factor-alpha applied alone or in combination). We also detected the presence of ICAM-1 in AITD frozen tissues using an immunohistochemical technique. These data suggest a role for ICAM-1 in human AITD. However, the expression of ICAM-1 appears to be a secondary phenomenon in response to the immune assault, rather than a primary event. Our results support the idea that TEC may act as passive captives to immunological events in human AITD.
Animals↗
Studies of human thyroid xenografts from Hashimoto's thyroiditis in severe combined immunodeficient (SCID) mice: detection of thyroid stimulation-blocking antibody.
Human thyroid xenografts from 7 patients with Hashimoto's thyroiditis (HT) and 3 normal persons (N) were xenografted into severe combined immunodeficient (SCID) mice to study the intrathyroidal lymphocytes that were expected to survive in these animals. Human IgG was detected in all mice engrafted with HT thyroid tissue peaking at 6-10 weeks after xenografting. Thyroperoxidase-antibody (TPO-Ab) was also detected in all mice with HT thyroid grafts peaking at 4-6 weeks after xenografting, reaching up to 44% of donors' original concentrations. In contrast, maximal thyroglobulin (Tg)-Ab production in some SCID mice with HT thyroid grafts was higher than the donors' original level, and was detectable in mice with thyroid grafts from Tg-Ab-negative HT donors. Thyroid stimulation-blocking antibody (TSBAb) was found in 2 mice with thyroid xenografts from 1 HT patient whose original serum TSBAb and thyrotropin-binding inhibitor immunoglobulin (TBII) had been positive; the maximal TSBAb level in SCID mice exceeded the donor's original level. TSBAb production in SCID mice reached its peak at 10 weeks after xenografting, i.e., later than that of thyroid-stimulating antibody (TSAb) observed in our recent report, suggesting the existence of distinct intrathyroidal B cell autoreactive clones of different life span responsible for secreting TSAb or TSBAb. When autologous peripheral blood mononuclear cells (PBMC) were engrafted alone (without thyroid tissue), TSBAb was undetectable.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effect of FK-506 on xenografted human Graves' thyroid tissue is severe combined immunodeficient mice.
OBJECTIVE: We studied the macrolide antibiotic FK-506, an immunosuppressive agent, in an attempt to ameliorate the lesion of autoimmune thyroid disease in human thyroid tissue xenografted into severe combined immunodeficient (SCID) mice. It was not felt appropriate to employ this agent directly in patients with autoimmune thyroid disease because adequate therapeutic modalities are available and the introduction of new, experimental agents could not be justified. Moreover, the study of the tissue before and after treatment could not have been undertaken directly in patients. DESIGN: Human thyroid xenografts from four patients with Graves' disease and two normal persons were xenografted into SCID mice. Two weeks after xenografting, human immunoglobulin G (IgG) was detectable in all SCID mice xenografted with Graves' thyroid tissue. Mice were divided into two groups with human IgG levels similar to each other. Mice in the first group were treated with FK-506 daily for 6 weeks; mice in the second (similar) group were given phosphate-buffered saline (PBS) only (control group). MEASUREMENTS: Blood samples were taken every 2 weeks from the tail veins for human IgG, thyroid stimulating antibody, thyroperoxidase antibodies, thyroglobulin antibodies, and interferon-gamma (IFN-gamma). After 8 weeks treatment, animals were sacrificed; thyroid tissue was examined histologically and for thyrocyte HLA-DR expression. FK-506 was also added to thyrocytes in in-vitro tissue culture conditions. RESULTS: After 4-6 weeks of FK-506 therapy, human IgG, all thyroid antibodies and IFN-gamma were suppressed, while the levels remained elevated in the control group. Lymphocytic infiltration virtually disappeared in the human thyroid tissue of the FK-506-treated mice and thyrocyte HLA-DR expression markedly declined; in the control mice, lymphocytic infiltration remained heavy and HLA-DR expression remained high. On the other hand, FK-506 added directly to thyrocytes in vitro (without lymphocytes) did not reduce thyrocyte HLA-DR expression. CONCLUSIONS: FK-506 appears to suppress the activation of intrathyroidal lymphocytes, but not thyrocytes. From these observations, it is concluded that this agent, by its action on intrathyroidal lymphocytes, is able to ameliorate the immunologically mediated histological and serological disturbance in human autoimmune thyroid disease, at least under these circumstances.
Animals↗
Effect of removing human Graves' thyroid xenografts after eight weeks in nude mice and rexenografting them into SCID mice.
Human thyroid xenografts from four patients with Graves' disease (GD) and two normal persons were initially xenografted into nude mice. Eight weeks after xenografting, the thyroid tissue appeared normal; indeed, thyroid infiltrating lymphocytes in the GD xenograft could no longer be identified when analyzed histologically. Thus, human immunoglobulin G (IgG), thyroperoxidase (TPO)-antibodies (Abs), thyroglobulin (Tg)-Abs, thyroid-stimulating antibodies (TSAb), and thyrocyte histocompatibility leucocyte antigen (HLA)-DR expression were undetectable. These same tissues were retrieved from the nude mouse and rexenografted into severe combined immunodeficient (SCID) mice (with no prior xenograft); autologous peripheral blood mononuclear cells (PBMC) or CD8-depleted PBMC (non-CD8 cells) were simultaneously injected into some of these SCID mice. Engraftment of a GD thyroid rexenograft (TH) alone did not cause IgG, TSAb, TPO-Ab, or Tg-Ab production, thyrocyte HLA-DR expression, or lymphocytic infiltration in thyroid grafts. Engraftment of GD PBMC or non-CD8 cells alone (i.e. without a thyroid xenograft) caused human IgG to rise, but only minimal titers of thyroid antibodies appeared. When TSAb, TPO-Ab, and Tg-Ab were quantified, GD TH plus PBMC-engrafted SCID mice showed significantly higher production of each antibody than that of GD PBMC alone, and this phenomenon was further enhanced by the removal of CD8+ cells. GD thyrocytes showed marked HLA-DR expression at human surgery; however, after 8 weeks' sojourn in nude mice, DR expression disappeared. After a further 8 weeks following rexenografting into SCID mice, TH plus PBMC resulted in a reappearance of DR expression only in GD but not in grafts from normal persons, and this was enhanced by the depletion of CD8 cells. These results were also in parallel with histological findings inasmuch as the normal tissue remained normal with no thyroid antibodies appearing with PBMC or CD8-depleted cells. In experiments from two GD patients, autologous skeletal muscle as well as thyroid tissue were xenografted into nude mice. Eight weeks after xenografting, these were rexenografted into SCID mice that contained prior autologous primary GD thyroid xenografts. Histological findings showed new lymphocytic infiltration in rexenografted thyroid tissues in the SCID mice but not in autologous skeletal muscle. This signifies that the immune assault in GD is specifically targeted to the thyroid tissue.(ABSTRACT TRUNCATED AT 400 WORDS)
Adult↗
Relative sensitivity of leukemic (CML) and normal progenitor cells to treatment with the photosensitizer benzoporphyrin derivative and light.
Normal bone marrow and peripheral blood committed progenitor cells were found to be significantly more resistant to treatment with the photosensitizer benzoporphyrin derivative (BPD) and white fluorescent light (11 J/cm2) than were clonogenic cells from two cell lines (K562 and EM2) derived from nonremission patients with myelogenous leukemias. Bone marrow and peripheral blood committed progenitor cells from normal donors were also found to be more resistant to this treatment than were equivalent cells from patients with chronic myelogenous leukemia (CML). Normal bone marrow mononuclear cells grown in long-term marrow culture (LTMC) following treatment with BPD and light showed that no differences in stem cell productivity existed between control and treated samples. When bone marrow from CML patients was treated in the same manner, the numbers of progenitors detected in the nonadherent population during culture were greatly reduced compared to control material. Two rounds of PCR using nested primers to detect BCR-ABL mRNA showed that while this treatment significantly decreased the numbers of stem cells bearing the Philadelphia chromosome, it did not eliminate them.
Blood Cells↗
Reconstitution of severe combined immunodeficient mice with intrathyroidal lymphocytes of thyroid xenografts from patients with Hashimoto's thyroiditis.
Thyroid tissues from patients with Hashimoto's thyroiditis (HT) have been xenografted to both severe combined immunodeficiency (SCID) mice and nude mice to study the intrathyroidal lymphocytes which were expected to migrate from the xenografts in the SCID mice. Peripheral blood mononuclear cells from HT, Graves' disease, and normal donors have also been separately engrafted. SCID mice, but not nude mice with HT thyroid grafts produce human immunoglobulins. More immunoglobulin G (IgG), but less IgM and IgA is produced in SCID mice with HT thyroid grafts (SCID-TH), compared to SCID mice injected with peripheral blood mononuclear cells from patients with HT or normal donors (SCID-PB), suggesting that different B cell subpopulations were active in the SCID-PB vs. SCID-TH. Production of IgG by SCID-PB and SCID-TH was maintained 6 weeks after engraftment, and decreased thereafter. SCID mice but not nude mice grafted with HT thyroid tissue produce antibodies to thyroglobulin and thyroperoxidase. Lymphocytes within intact HT thyroid grafts persist in SCID mice, and migrate to the spleen, whereas human lymphocytes do not survive in the thyroid grafts or other tissues of the nude mouse. In 6 weeks, the xenografts in nude mice became histologically normal. In contrast, xenografts from SCID mice showed more marked inflammatory changes than in the original human lesion, although the ratio of T/B cells is unchanged. This worsening of the lesion may relate to the increase in activation of the T-lymphocytes.
Animals↗
Studies of thyroid xenografts from Graves' disease in severe combined immunodeficient mice.
Thyroid tissues from normal (paranodular) subjects and patients with Graves' disease (GD) and Hashimoto's thyroiditis (HT) were xenografted to severe combined immunodeficiency (SCID) mice, and the same tissues were engrafted into nude mice; in addition, peripheral blood mononuclear cells were engrafted to separate SCID mice (SCID-PB). Thyroglobulin (TG) and microsomal antibodies (Abs) became detectable with high titers by hemagglutination assays in SCID mice xenografted with thyroid tissues (SCID-TH) from GD and HT patients; moreover, TG Ab was detectable even in SCID-TH from TG Ab-negative GD and HT donors. On the other hand, only 2 of 10 SCID-PB had detectable Abs with low titers. TSH receptor (TSH-R) Ab was detectable in all sets of SCID-TH from GD. After peaking (3-7 weeks), their levels decreased despite the fact that immunoglobulin G levels increased. In addition, in 3 of 4 sets of SCID-PB from GD patients, TSH-R Ab was also detectable. SCID-TH from GD and HT patients showed transient hyperthyroxinemia, peaking at 2 weeks; these values were significantly higher [free T4, 6.48 +/- 0.90 and 5.50 +/- 0.77 pmol/L (mean +/- SE), respectively; P < 0.05] than SCID-TH from normal controls (2.5 +/- 0.24). Histologically, intrathyroidal infiltrating lymphocytes (ITL) survived in SCID mice, but not in nude mice after 8 weeks. The follicles of GD tissue in SCID mice were virtually destroyed with ITL, and their appearance was similar to that in HT. In conclusion, TSH-R Ab was clearly produced from ITL, and some peripheral blood mononuclear cells grafts could also produce TSH-R Ab. In spite of the presence of TSH-R Ab, SCID-TH from GD patients did not show persistent hyperthyroxinemia, presumably because destructive thyroiditis may be occurring in the grafted tissue, with decreasing levels of TSH-R Ab.
Animals↗