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Biomedical subjects

A Boucher

Publications and source records attributed to A Boucher.

At least 55 records · Page 3Linked to original sources
PubMed1992

A viroid from Nematanthus wettsteinii plants closely related to the Columnea latent viroid.

A viroid was isolated from symptomless Nematanthus wettsteinii plants using the return-PAGE method for analysis of low M(r) nucleic acids. The RNA was transmitted to tomato, three cultivars of potato, and Scopolia sinensis plants by mechanical inoculation or by grafting. Infected solanaceous plants developed symptoms similar to those caused by potato spindle tuber viroid (PSTVd). The Nematanthus viroid consists of 372 nucleotides, 214 G+C, 158 A+U, with a G+C/A+U ratio of 1.35. One of seven cDNA clones showed a sequence heterogeneity (G to A) at position 73. The most stable secondary structure of this viroid has 78 G:C, 37 A:U and 11 G:U base pairs with a minimum free energy of -456.9 kJ. The viroid is closely related to the 370 nucleotide Columnea latent viroid. The Nematanthus viroid possesses regions of 100% sequence identity with six viroids belonging to the PSTVd and apple scar skin viroid groups. The viroid also replicated in tomato plants when mixed with PSTVd. Tomato plants were cross-protected against PSTVd when preinfected with the viroid from N. wettsteinii.

Base Sequence↗
PubMed1992

Antibodies in the serum of patients with autoimmune thyroid disorders react with a recombinant 98 amino acid fragment of a full length 64 kDa eye muscle membrane protein which is also expressed in the thyroid.

We have tested sera from patients with autoimmune thyroid disorders with or without ophthalmopathy for immunoreactivity, in a dot blot assay, against a recombinant 98 amino acid fragment of a cloned 64 kDa protein, D1, which is expressed in human eye muscle and thyroid, in the form of a Lac Z fusion protein. Tests were positive in 19 out of 40 patients with established thyroid-associated ophthalmopathy (TAO), in 12 out of 21 patients with Graves' hyperthyroidism (GH) without clinically evident ophthalmopathy, in 5 out of 10 patients with thyroid autoimmunity and lid retraction but no other signs of ophthalmopathy, in 4 out of 23 patients with Hashimoto's thyroiditis (HT) without evident ophthalmopathy and in 2 out of 18 patients with benign adenoma or multinodular goitre, but in only 2 out of 37 normal subjects tested. SDS-polyacrylamide gel electrophoresis and Western blotting for an antibody reactive with a 64 kDa antigen in pig eye muscle membranes was also carried out on sera from patients with TAO and GH. While immunoblotting for antibodies reactive with a 64 kDa protein was more often positive in patients with TAO, in whom 58% had serum antibodies which reacted with a 64 kDa protein, this was not the case in patients with GH without eye signs in whom the prevalence of positive immunoblot tests was 35%. Overall there was a fairly close correlation between the two tests although there were many exceptions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Nature and significance of orbital autoantigens and their corresponding autoantibodies in thyroid-associated ophthalmopathy.

There is now considerable evidence that the pathogenesis of thyroid-associated ophthalmopathy is closely linked to the presence of a shared autoantigen(s) in the thyroid and the eye muscle, against which cytotoxic mechanisms are directed. Although the orbital connective tissue is certainly involved in the orbital inflammatory process, a 64 kDa membrane protein expressed by both the eye muscle and the thyroid and recognized consistently by antibodies in the sera of TAO patients, seems to be the most likely target candidate. While its presence in non ocular skeletal muscle is not as well established, more recent data tend to suggest the existence of a 64 kDa molecule in the three tissues. The availability of a cDNA encoding a 572 amino acid protein corresponding to a MW of 63-64 kDa, which may be the same molecule, will allow us to determine more clearly the structural characteristics of the different molecules proposed as targets. The role of the corresponding autoantibodies in the pathogenesis of the eye disease is far less well defined. Whether they play a role in the induction of the ophthalmopathy or only represent helpful markers remains to be clarified.

Autoantibodies↗
PubMed1991

Thyroid-associated ophthalmopathy--a model for the association of organ-specific autoimmune disorders.

The development of a characteristic ophthalmopathy is a feature of autoimmune diseases of the thyroid. The link between the conditions has not yet been discovered, but here Jack Wall and colleagues develop the theory that an autoimmune response to a 64 kDa antigen expressed on both thyroid and eye muscle membranes is responsible for this thyroid-associated ophthalmopathy.

Autoantigens↗
PubMed1991

[Longitudinal study of histocompatibility antigen expression in renal transplants followed for 10 years].

Using monoclonal antibodies against class I and class II (DR antigen) major histocompatibility complex antigens, 65 renal transplant biopsies from 21 recipients whose renal transplants survived ten years or more were studied. Seven biopsies were performed while acute rejection of the renal transplant was under way. The other biopsies were carried out on a routine basis, 6 months (10 biopsies), 2 years (15 biopsies), 4 years (12 biopsies), and 10 years (21 biopsies) after transplantation. Semiquantitative evaluation of fibrous tubulointerstitial lesions was carried out on the biopsies taken after ten years. During episodes of acute rejection, strong expression of class I and class II HLA molecules by transplant tubule epithelial cells was found. When there was no acute rejection, tubule expression of class I and class II HLA molecules was more common in earlier biopsies as compared with later biopsies. In the long-term, persistence of DR antigen in tubule epithelium was associated with increased severity of fibrous tubulointerstitial lesions. A last remarkable finding in some patients was loss of expression of class I antigens in tubule cells from transplants with the longest survivals.

Adolescent↗
PubMed1989

Estrogen replacement decreases the set point of parathyroid hormone stimulation by calcium in normal postmenopausal women.

Estrogens decrease serum total and ionized calcium (Ca) concentrations in postmenopausal women with or without primary hyperparathyroidism, but cause little or no increase in serum PTH suggesting a modification of the relationship between the two. In order to define this relationship, we studied the effect of conjugated estrogens on total and ionized serum Ca and serum PTH concentrations in five normal postmenopausal women, before and after 3, 11, and 23 weeks of therapy. Dynamic tests of parathyroid gland function, based on 2-h iv infusions of CaCl2 and NaEDTA, were performed at each time. Total and ionized serum Ca and carboxylterminal PTH were measured every 15 min during the infusions, and parathyroid function was evaluated by a nonlinear 4-parameter mathematical model. Estrogen therapy caused decreases in serum total [2.36 +/- 0.04 (SD) mmol/L, baseline vs. 2.19 +/- 0.05 mmol/L, 23 weeks, P less than 0.005) and ionized calcium (1.27 +/- 0.01 mmol/L, baseline vs. 1.21 +/- 0.02 mmol/L, 23 weeks, P less than 0.005]; the decreases were evident at 3 weeks and persisted for the duration of the study. Serum PTH concentrations did not change (8.94 +/- 1.84 pmol/L, baseline vs. 8.98 +/- 2.38 pmol/L, 23 weeks). Three parameters of the parathyroid function, the maximal response to hypocalcemic stimulation, the nonsuppressible fraction of circulating PTH, and the slope of PTH on calcium at the set point were not affected by estrogen treatment. The fourth parameter, the set point of PTH stimulation by serum total calcium (2.16 +/- 0.04 mmol/L, baseline vs. 1.97 +/- 0.07 mmol/L, 23 weeks, P less than 0.0166) or by serum ionized Ca (1.19 +/- 0.04 mmol/L, baseline vs. 1.12 +/- 0.03 mmol/L, 23 weeks, P less than 0.01), was decreased by estrogen treatment. This was evident at the earliest time point studied and persisted thereafter. The decrease in ionized Ca set point only explained 40% of the decrease in total calcium set point, the remaining 60% being related to hemodilution of plasma protein during therapy. We conclude that estrogen replacement can influence parathyroid function in postmenopausal women by resetting the set point of PTH stimulation by ionized Ca. This in turn could contribute to the estrogen-induced changes in their Ca balance.

Calcium↗
PubMed1989

Suppression of T4 secretion in a metastatic follicular carcinoma.

Despite total thyroidectomy, a patient with metastatic follicular carcinoma of the thyroid remained biologically euthyroid three months after stopping thyroxine (T4) therapy. Thyroid hormone production was investigated by means of a modified tri-iodothyronine (T3) suppression test, in which serum T4 was used as a suppression marker. After three weeks of oral T3 (Cytomel) therapy (50 micrograms/day), the serum T4 decreased from normal (108 nmol/L) to undetectable values. However, even though suppressive therapy was effective in preventing TSH dependent hormone secretion by the tumor, it did not prevent tumor growth and the eventual death of the patient.

Adenocarcinoma↗
PubMed1988

Androgen priming and chemotherapy in advanced prostate cancer: evaluation of determinants of clinical outcome.

We conducted a randomized clinical trial in men with stage D2 prostate cancer to test whether androgen priming potentiates the efficacy of cytotoxic chemotherapy. Eighty-five men with progressive prostate cancer refractory to orchiectomy were treated continuously with aminoglutethimide and hydrocortisone to lower adrenal androgen secretion and were administered cyclic intravenous (IV) chemotherapy. The patients were randomized to receive either androgen priming or no additional treatment for three days before and on the day of chemotherapy. Median duration of follow-up was 43 months. Response rate (remission plus disease stabilization) was not significantly different between the stimulation and control arm when the analysis was restricted to evaluable patients (79% v 73%, respectively) or when it was extended to all patients (46% v 61%). Median duration of response was similar for the stimulation and control arm (9 and 10 months, respectively). Median survival was 10 months in the stimulation and 15 months in the control group (P = .0047). The androgen sensitivity of the tumors was supported by the greater toxicity in the stimulation arm associated with androgen administration. Factors found to be independently associated with improved clinical outcome included a high Karnofsky score and hematocrit, long duration of response to the initial castration, and normalization of an elevated serum acid phosphatase on treatment. We conclude that in this group of patients with advanced disease, androgen priming does not potentiate the efficacy of chemotherapy and is actually associated with a worse outcome. Furthermore, our data emphasize the heterogeneity of biologic behavior of prostate cancer.

Acid Phosphatase↗
PubMed1988

Clinical performance of a parathyrin immunoassay with dynamically determined reference values.

We compared the clinical performance of a carboxyl-terminal radioimmunoassay for human parathyroid hormone (iPTH), using either a dynamic reference interval (95% confidence limits of serum iPTH concentrations observed in 11 normal individuals during intravenous infusions of Na2EDTA and CaCl2) or a gaussian (2 SD) reference interval derived from 233 normocalcemic individuals. The 2 SD ranges were 3.5 to 9.8 pmol/L for serum iPTH and 2.19 to 2.53 mmol/L for total calcium. The iPTH dynamic interval was lower for calcium concentrations greater than 2.50 mmol/L; it was higher, wider, and continued to increase for calcium values less than or equal to 2.25 mmol/L. Use of the dynamic reference interval increased the clinical sensitivity of our assay from 81% and 61% to 100%, respectively, in primary hyperparathyroidism (n = 47) and hypoparathyroidism (n = 18). Test specificity was maintained at 100% in hypocalcemic disorders but fell to 93% (62/67) in hypercalcemic disorders. Overall, use of the dynamic reference interval improved the assay performance.

Adult↗
PubMed1987

Relationship between the integrity of Bowman's capsule and the composition of cellular crescents in human crescentic glomerulonephritis.

Cell constituents of glomerular crescents still remain controversial. We examined cellular crescents in ten cases of crescentic glomerulonephritis (GN) using indirect immunoperoxidase technique and monoclonal antibodies against T cells (OKT3) and subsets: T helper/inducer cell (T4), T suppressor/cytotoxic cell (OKT8), T activated cell (IoT14 and IoT15); B cells (B1, B4, OKB2 and IoB3) and subsets (B2 and IoB1); monocytes/macrophages (LeuM3); DR Ag (I2) and renal native cells: podocytes (IoT5), Bowman's capsule (BC) parietal epithelial cell (OKB2, IoB3). Studied cases were 2 anti-glomerular basement membrane (GBM) GN, 4 immune complex GN, 3 vasculitis and 1 idiopathic GN. When the BC continuity was preserved almost all crescent cells were identified; they originated in majority from the BC parietal epithelium and ranged from 55 to 95 per cent. The other main constituents which represented 15 to 35 per cent of the crescent cells were monocytes (LeuM3+) and T-activated cells (IoT15+). In the interstitial infiltrate, which was mostly periglomerular, LeuM3+ cells and IoT15+ cells accounted for more than 70 per cent of the cell population. On the other hand, when BC were ruptured, mononuclear inflammatory cells, mainly LeuM3+ and IoT15+ cells accompanied by significant number of T4+ and T8+ cells, constituted the glomerular crescents. At this time, BC parietal epithelial cells were rarely identified (15 per cent). These findings strongly support the importance of BC integrity to discriminate the nature of crescent cells.

Antibodies, Monoclonal↗
PubMed1986

Characterization of mononuclear cell subsets in renal cellular interstitial infiltrates.

Indirect immunoperoxidase analysis using monoclonal antibodies (Mo Ab) was performed in 33 renal biopsies with interstitial cellular infiltration obtained from non-transplanted patients. We reviewed four acute interstitial nephritis (IN), three chronic IN, four granulomatous IN, four acute tubular necrosis, four vasculitis, seven primary glomerulonephritis and seven active lupus nephritis (LN). We used Mo Ab recognizing T and B cell markers [OKT3, OKT8, T4, B1, IOT14 (IL2 receptor)], HLA-DR related antigen (I2) and monocytes/macrophages (LeuM3). In all cases the interstitial cellular infiltrates were predominantly T cells, whereas the B cell population accounted for less than 20% of the infiltrate. LeuM3+ cells were present in 28 of 32 cases, usually in a lesser proportion than T cells. IOT14+ cells were exceptional. T4+/T8+ cells were clearly greater than one in three acute IN, three granulomatous IN, two LN and two vasculitis. The T8+ cell population predominated in one case of chronic IN related to a non-steroidal anti-inflammatory drug. In all the remaining cases T4+ and T8+ cells were equally present. Aberrant strong HLA-DR expression within tubular cells was noted in nine cases (4 LN) irrespective of the presence of tubular lesions. On the basis of the phenotypic analysis, our data do not support a specific pattern of the infiltrate in regard to a given etiology and thus cannot be used as a diagnostic tool. However, such analysis may aid in understanding the mechanisms of tissue injury.

Adult↗
PubMed1984

Clinical effect of aminoglutethimide, medical adrenalectomy, in treatment of 43 patients with advanced prostatic carcinoma.

The initial treatment of patients with Stage D prostatic carcinoma with orchiectomy or estrogens is successful in giving objective and subjective improvement for variable periods of time. However, after initial endocrine treatment patients generally relapse, and go on to further progression of their disease. However, a subgroup of approximately 22% of these Stage D prostatic cancer patients respond to either surgical adrenalectomy or hypophysectomy, indicating some degree of continued hormonal responsiveness. Forty-three previously castrated patients with Stage D prostatic carcinoma were treated with 1000 mg of aminoglutethimide and 40 mg of hydrocortisone daily and have been evaluated using the criteria of the National Prostatic Cancer Project. Progression of disease after initial hormonal therapy has varied from 3 to 25 months. One patient has had a complete response, and continues in remission after 290 weeks of therapy. Partial objective responses have been observed in 6 patients, and 10 patients have remained objectively stable for an average of 35 weeks in this latter group.

Adenocarcinoma↗