Biomedical subjects
Publications and source records attributed to C White.
The research committee of the RACGP has urged authorities in each State to introduce sentinel practice schemes in order to provide information on selected conditions not normally notifiable to public health agencies. To date not all States have taken up the request. In this article the history and role of such schemes are examined. Special attention is paid to the sentinel system that has operated in South Australia since 1983.
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We describe for the first time a case report documenting a chronic myelogenous leukemia (CML) patient who developed a blast crisis of natural killer (NK) lymphocytes. Many of the blasts exhibited large granular lymphocytic (LGL) morphology. Single parameter immunophenotyping results determined that the granulated as well as the agranulated blast cells were NK lymphocytes (CD45, NKH1, CD2, LEU 17, and CD16 positive; CD3, CD8, and LEU 7 negative). Dual parameter flow cytometric testing also determined that some of the blasts expressed the CD11b and CD11c markers as reported for some types of NK lymphocytes. Approximately 10% of the cells were in the S phase of the cell cycle as determined by a modified Vindelov DNA content analysis test and may theoretically reflect some of those cells expressing CD11b and CD11c. The cells did not express in vitro NK lymphocyte functional activity against a K562 target and therefore similar to other reported cases of presumably immature NK lymphocytic leukemias. The NK lymphocyte blast crisis was successfully treated with vincristine and prednisone. The patient's disease eventually relapsed and transformed to a progenitor stem cell before she died (CD45, 13, CD38, and CD34 positive). The flow cytometric immunophenotyping results contributed significantly as an important adjunct in determining the appropriate diagnosis, helping to select the type of therapy, and monitoring the patient with this unusual type of blast crisis.
The role of the physician and written educational material were assessed for effectiveness in increasing the regular performance of monthly testicular self-examination (TSE) by male college students. Of 633 students from three New England colleges, 4.7% (n = 30) performed monthly TSE. These respondents then received written material or written material plus a physician's lecture on testicular cancer and TSE. In follow-up, 18% of the students that received written material alone (n = 24 of 130) reported performing monthly TSE. Of the students that also received a physician's lecture, 36% (n = 58 of 163) reported performing monthly TSE, a statistically significant increase in performance. Still the majority of the students followed did NOT adopt the practice of monthly TSE. Although the physician appears to be able to make a significant difference in the group's performance of TSE, a search for more effective methods to increase this population's practice of TSE should be sought.
When Saccharomyces cerevisiae was cultured in the presence of thorium, the element was accumulated by the cells and was visible in electron micrographs as electron dense granules. When thorium was present during exponential growth, these granules were located mainly in the vacuole, with some present in the cytosol. Where thorium was present only during the stationary phase, there appeared to be greater thorium deposition in the cell wall than during exponential growth and some vacuolar deposits were also evident. Thorium uptake by exponential-phase cells was not stimulated by glucose and was thus independent of metabolic energy.
The KDI Quik test is a rapid qualitative method for detecting narcotics, cocaine, PCP, and amphetamines in urine. The accuracy of this test was evaluated by testing 106 clinical toxicology urine specimens. Three investigators independently reviewed the test results and compared them to results of standard toxicological analyses. Of 83 samples found positive by the reference technique, only 70 were correctly identified as positive on the Quik test; only nine of 23 truly negative controls were correctly identified as negative by the Quik test. The overall sensitivity of the test was 84.7% while the specificity was 39.1%. As inaccuracies of this degree could result in frequent clinical error, use of the Quik test is not recommended.
Three cases of injection of human saliva are presented, all of which occurred among incarcerated men. Although no previous cases have been described, we believe that this entity is not uncommon in the prison population.
Sulfation of organic compounds requires activation of inorganic sulfate via formation of adenosine 3'-phosphate 5'-phosphosulfate (PAPS). Inorganic sulfate can be formed by sulfoxidation of cysteine, which can be derived from GSH. Thus, a decrease in hepatic GSH may impair formation of inorganic sulfate, the synthesis of PAPS, and the sulfation of chemicals. This hypothesis was tested by investigating the effect of GSH depletion on the levels of inorganic sulfate in serum and of PAPS in liver, and on the capacity to form the sulfate conjugate of harmol in rats. Phorone (2 mmol/kg, i.p.) decreased hepatic GSH (97%), serum inorganic sulfate (63%), and hepatic PAPS (48%). Diethyl maleate and vinylidene chloride (6 mmol/kg, each, i.p.) were less effective than phorone in decreasing GSH in liver and inorganic sulfate in serum, and they did not alter hepatic PAPS levels. Three hours after phorone treatment, the nadir of hepatic PAPS concentration, harmol was injected in order to assess sulfation in vivo. After administration of harmol (100 and 300 mumol/kg, i.v.), less harmol sulfate and more harmol glucuronide were found in the serum of phorone-treated rats as compared to control rats. At the higher dosage of harmol, phorone reduced the biliary excretion of harmol sulfate while increasing the biliary excretion of harmol glucuronide. These results indicate that severe GSH depletion decreases PAPS formation and sulfation of chemicals. However, an increase in glucuronidation may compensate for the impaired sulfation.
We studied the in vitro secretion of macrophage-derived growth factor (MDGF) activity by peritoneal macrophages from fertile and infertile women. Peritoneal fluid was obtained from 55 women undergoing laparoscopy for evaluation and treatment of infertility or for tubal sterilization. Isolated macrophages were plated in tissue culture wells and incubated in Dulbecco's Modified Eagle's Medium plus 0.2% lactalbumin hydrolyzate at 37 C for 24 h. Medium MDGF activity was assayed by determining the ability of medium to stimulate [3H] thymidine incorporation in BALB-c 3T3 fibroblasts. Macrophages from 23 women released significant MDGF activity in vitro; the release was linear for up to 72 h. Among the 55 women, macrophages from 10 of 36 (28%) women with normal pelvic anatomy or tubal occlusion/pelvic adhesions released significant MDGF activity. In contrast, macrophages from 13 of 19 (68%) women with endometriosis, a significantly higher proportion (P less than 0.02), released MDGF. The finding that endometriosis is associated with in vivo primed peritoneal macrophages that produce MDGF in vitro may help to explain the proliferation or maintenance of endometrial tissue in the peritoneal cavity.
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Fibronectin, a known growth factor for fibroblasts, is produced by alveolar macrophages from patients with interstitial pulmonary fibrosis. Because peritoneal macrophages have been implicated in the disease process of endometriosis, we measured the production of fibronectin by peritoneal macrophages in vitro and the concentration of fibronectin in peritoneal fluid samples. Twenty-nine patients had a normal pelvis, 22 had endometriosis, and 14 had tubal occlusion and/or adhesions. Human peritoneal macrophages demonstrated de novo synthesis of fibronectin. The peritoneal macrophage fibronectin was detected by an enzyme-linked immunosorbent assay for serum fibronectin. Peritoneal macrophages from patients with endometriosis produced approximately three times the amount of fibronectin as normal patients or patients with tubal occlusion and/or adhesions (P less than or equal to .01 and P less than or equal to .02, respectively). The mean peritoneal fluid concentration of fibronectin, however, was about 30% lower in patients with endometriosis than in normal patients (P less than or equal to .02). We suggest that increased peritoneal macrophage fibronectin production in patients with endometriosis may contribute to the adhesion formation and associated reactive fibrosis seen in this disease, and may also influence the implantation of endometrial cells and their subsequent growth in the pelvis.
A combined in vivo/in vitro model of galactosamine hepatotoxicity was employed to test whether previously reported cytoprotective actions of cystamine administration on galactosamine-induced hepatic injury in vivo could be attributed to a direct action of cystamine on toxicant-challenged hepatocytes. In this model, male Sprague-Dawley rats received a 400 mg/kg galactosamine challenge via intraperitoneal injection 1 hr prior to portal vein cannulation for hepatocyte isolation. Isolated cells are established in monolayer culture and galactosamine-induced cellular injury is then expressed over the ensuing 24-48 hr in culture. Consistent with the biochemical basis of galactosamine-induced hepatocellular injury in vivo, cytotoxicity could be prevented by in vitro uridine treatments within 3 hr of the in vivo galactosamine challenge, but not when added 12 hr later. Cystamine, in contrast, exhibited a cytoprotective effect even when added to cultures 12 hr after the in vivo toxicant challenge. Post-toxicant cytoprotection by cystamine in vitro was concentration dependent and did not produce an alteration of hepatocyte nonprotein sulfhydryl content. Post-toxicant cytoprotection by uridine and cystamine in this in vivo/in vitro model of toxicity were fully consistent with in vivo protection from galactosamine-induced necrosis by these agents. This model eliminates potential "extrahepatic" mechanisms for cystamine's hepatoprotective effect and demonstrates a direct cytoprotective action on galactosamine-challenged hepatocytes.
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From the study of HLA, complement, and glyoxalase I alleles in 82 Venezuelan individuals belonging to 19 families of mixed ethnic origin having 20 affected newborns with salt-wasting congenital adrenal hyperplasia due to 21-hydroxylase (21-OH) deficiency, a total of 38 disease haplotypes and 53 nondisease haplotypes were found. Of the pathological haplotypes 47% were found to share the HLA-B39 or -Bw62 specificities, 55% of them in combination with the BFS, C2C, C4A4, C4B2 (SC42) complotype. The frequencies of HLA-B39 and -Bw62 among the affected haplotypes were 29 and 18% as compared with 6 and 0% among the nondisease haplotypes of the same families. Statistical associations (P less than 0.01) with salt-wasting adrenal hyperplasia were found with the SC42 complotype and with the combination SC42, HLA-B39. These results are markedly different from those reported in the literature which show an "association" at the population level among many Caucasoid samples of HLA-Bw47 and the extended haplotype (HLA-Bw47, DR7,FC91,0) with the salt-wasting form of the disease. Furthermore, four of the unrelated patients reported here were homozygous for all the major histocompatibility complex loci tested, while three others were homozygous for at least two HLA loci. Analysis of the geographical origin of the grandparents indicated clustering of the deficiency carrier HLA haplotypes. This observation, together with the fact that there is an excess of homozygotes among the patients in Venezuela, strongly suggests that salt-wasting 21-OH deficiency congenital adrenal hyperplasia is mostly the result of a founder effect of relatively hyperplasia is mostly the result of a founder effect identity by descent of a few abnormal alleles at the 21-OHB locus in most cases. The mutation marked by HLA-Bw47 was not observed in this population.
A Biostatistical Monitoring Committee was established to review periodically the procedures and performance of the data coordinating center of the National Cooperative Gallstone Study. The functions of this committee, the types of data coordinating center activities reviewed, the manner in which monitoring of these activities was carried out, and an assessment of the value of this committee to the study are discussed in this article.
Thyrotropin receptor antibodies (TRAb) were measured in serum from 49 patients with active and inactive juvenile Graves disease, and the results were compared with values from control subjects and patients with Hashimoto disease. With a thyrotropin binding inhibition immunoglobulin (TBII) assay, TRAb were found in serum from 25 (93%) of 27 patients with untreated, active Graves disease. The TRAb values remained positive in 20 (72%) of 29 patients during the first 6 months of antithyroid therapy and in 13 (54%) of 24 patients during the second 6 months. After discontinuation of antithyroid therapy, 15 patients experienced 18 episodes of relapse of thyrotoxicosis; during relapse TRAb values were positive in all but one patient. Among 19 patients who remained clinically and biochemically euthyroid after cessation of antithyroid therapy, TRAb were not detected in 28 (78%) of 36 serum specimens. Of the eight positive values from six patients, no antiidiotypic antibodies were found, and thyroid stimulating immunoglobulins (TSI) were not detected in four specimens. The TRAb determination correctly predicted the subsequent clinical course in 26 (72%) of 36 patients. Furthermore, TRAb values and results of triiodothyronine suppression tests were in agreement in 27 of 36 patients, or 75% of the time. TSI were present in serum from only 19 (73%) of 26 patients with active disease; however, TSI were negative in all patients with inactive Graves disease. During the management of Graves disease, TRAb measurements by TBII determinations are valuable in the diagnosis of active disease, assist in the decision to discontinue antithyroid drug therapy, and are useful as the T3 suppression test to predict the clinical course of the disease. The TSI measurement is most useful to determine the activity of the disease when TRAb values are positive in a euthyroid patient.
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Bilateral palmar skin conductance and heart rate were measured throughout a series of psychological tests and during both sitting and ambulant social interactions in 14 right-handed men with chronic schizophrenic disorder and 12 healthy volunteers matched for age and handedness. Miniature radio telemetry equipment was used to collect the physiological data. The schizophrenic group was effectively unresponsive to 70-dB auditory stimuli, while all but one of the control group responded and habituated to a nil response by the tenth tone in sequence. The schizophrenic group showed some evidence of increased skin conductance activity at rest, and in socially demanding conditions skin conductance level and variability were increased in the right hand. The present group of electrodermal 'non-responders' was not in general autonomically under-active. Asymmetry of skin conductance activity during social interaction may be a characteristic of chronic schizophrenic disorder.