Occupational contact dermatitis from vitamin B12.
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Biomedical subjects
Publications and source records attributed to A Rodriguez.
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Esterified cholesterol (EC) accumulation was induced in THP-1 macrophages after exposure to acetylated LDL (acLDL), and the extent of accumulation was dependent on cell density. EC mass was 5-fold greater in cells plated at 1.0 x 10(6) cells/35 mm dish compared to cells plated at density 4.0 x 10(6) cells/dish. In addition, [14C]oleate incorporation into EC also increased with decreasing cell number, with 4-fold greater incorporation (6 h: 177 +/- 0.014 vs. 45 +/- 0.001 pmol/mg cell protein, P < 0.001; 24 h: 515 +/- 0.037 vs. 120 +/- 0.012 pmol/mg, P < 0.001) in cells plated less densely compared to cells plated at a higher density. The rate of 125I-labeled acLDL degradation was about 2-fold greater in cells plated at the lower density (105 vs. 60 ng/h per mg cell protein). Northern analysis showed a 2-fold reduction in the expression of human scavenger receptor mRNA in density plated cells, and immunoprecipitation also demonstrated a 2-fold decrease in scavenger receptor protein. Conditioned media did not differentially affect EC formation at either cell density. Fatty acid supplementation increased EC formation and the proportion of esterified sterol content only in cell plated at the higher density. The fatty acid effect was also seen when cells were exposed to beta-VLDL, which induced comparable levels of EC accumulation by non-scavenger receptor-mediated processes in densely plated cells. Foam cell formation in THP-1 macrophages may depend on cell density, which appears to affect both scavenger and non-scavenger receptor activity.
PURPOSE: To examine the effects of modification of immune effector cells, including macrophages, in the pathogenesis of herpes simplex virus retinitis in BALB/c mice. METHODS: Two intravitreal injections (2 microliters each) of anti-CD11b monoclonal antibody (mAb) [13 micrograms/microliters] were administered to the contralateral eyes of 10 BALB/c mice on days 6 and 8 after HSV inoculation into the right anterior chamber (AC) with HSV-1. A control group consisted of mice injected with anti-HLA-DR mAb in the same fashion. Specific macrophage depletion was performed in an additional group of 12 BALB/c mice by intravenous (i.v.) injection of dichloromethylene diphosphonate (Cl2MDP)-liposomes 7 days before AC HSV-1 inoculation into the eye. Control group consisted of mice receiving i.v. PBS-liposomes. Mice were clinically observed for 14 days postinfection, and the incidence of chorioretinal disease was confirmed by histopathologic studies. RESULTS: Intravitreal injections of anti-CD11b mAb produced a dramatic suppression of the contralateral retinal necrosis (2 of 10 mice) compared to 9 of 10 controls receiving an irrelevant antibody therapy (P < 0.05). Mice treated with i.v. Cl2MDP-liposomes also showed a significant inhibition of the development of contralateral chorioretinitis, with only 3 of 12 mice developing retinal disease compared to 9 of 12 mice from the control group (P < 0.05). FACS analysis performed on peripheral blood and spleen cells showed a significant depletion of Mac-1+ cells of Cl2MDP-liposome-treated but not of PBS-liposome-treated mice (controls). CONCLUSION: Intravitreal anti-CD11b mAb therapy, a broadly directed depletion strategy against many effector cells (macrophages, granulocytes, natural killer cells, and even cytotoxic T-cells) was most efficient in suppressing the HSV-1 induced contralateral disease. A more specific technique (i.v. Cl2MDP-liposome therapy) to deplete macrophages also produced a significant inhibition of HSV-1 induced contralateral chorioretinitis. These findings suggest that macrophages are important participants in the effector phase of the destructive inflammatory immune response induced by HSV-1 in the eye.
A multicentre evaluation of the new analyser, Hitachi 911, is reported for three different classes of homogeneous immunoassays (latex assays, immunoprecipitation assays, and CEDIA assays). The evaluation protocol follows ECCLS, IFCC and NCCLS guidelines. Using patient samples and commercial controls, within run and between run coefficients of variation were less than 3% in most cases, but as high as 9.7% for some CEDIA and latex assays. All the assays were linear, either in the reference or the therapeutic range of the analytes. No interference by haemolysis, lipaemia or icterus was observed. The methods were compared with other commercial methods. Coefficients of correlation were higher than 0.94 for all the methods. However, there were differences of slope and intercept for rheumatoid factor, apolipoprotein A-I and apolipoprotein B. On the Hitachi 911, all of the eight methods give precise and accurate results, and compare well with other established methods on immunoassay dedicated analysers. The discrepancies observed could be ascribed to current problems of immunoassay standardization.
Although obesity and trauma both are common in the general population, discussion of the care of the critically injured obese patient has been relatively absent. Obesity is associated with significant clinical and occult multisystem disease. Because host factors are key determinants of post-traumatic course and outcome, obesity appears to be a marker of high risk. Obesity should be considered with age, pregnancy, cardiopulmonary disease, and substance abuse as a host factor that has significant post-traumatic ramifications. Only by employing a comprehensive, multidisciplinary approach to the critical care management of such patients will post-traumatic complications be prevented and treated effectively.
The records of 92 patients with flail chest injury treated at a Level I trauma center were analyzed retrospectively. Associated intrathoracic injuries included pulmonary contusion (46 percent) and pneumothorax or hemothorax, or both (70 percent). The incidence of great vessel, tracheobronchial and diaphragmatic injuries was no different from that of a control population with simple rib fractures. Adult respiratory distress syndrome developed in 27 percent of patients with flail chest; 69 percent of all patients required ventilation (mean duration, 22 days). Mean length of hospital stay was 24 days. The mortality rate was 33 percent. We conclude that flail chest serves as a marker of significant intrathoracic injury, highly associated with pulmonary contusion, but even more so with pneumothorax or hemothorax. Flail chest does not seem to be a marker for great vessel, tracheobronchial, or diaphragmatic injuries. The majority of patients (more than two-thirds) will require mechanical ventilation for prolonged periods. Of paramount importance is the recognition of flail chest as a marker of high kinetic energy absorption, resulting in life-threatening thoracic as well as nonthoracic injuries.
Corneal infection of susceptible mice with HSV-1 causes herpetic stromal keratitis (HSK), which serves as a model of human HSK. To study the properties of the T lymphocytes involved in HSK, susceptible mice were immunized with the synthetic peptide corresponding to the amino terminal of HSV-1-associated glycoprotein D (gD 5-23). A CD4+ long-term T cell line and a clone bearing V beta 8.2 TCR were derived from peptide-primed lymph node cells. These T cells recognize gD 5-23 peptide in the context of I-Ed and require CD4 and LFA-1 for Ag-specific proliferation. Significantly, a truncated peptide gD 15-23 induced vigorous proliferation, indicating that these 9 amino acids constitute an epitope recognized by these T cells. The gD-specific T cells produced IL-4 and used it as the autocrine growth factor and hence belong to the Th2 subtype. Adoptive transfer of gD-specific Th2 cells into susceptible mice increased both the onset and severity of HSK after corneal HSV-1 infection. Injection of gD-specific Th2 cells without HSV-1 infection failed to cause eye damage. In addition, an irrelevant Ag-specific Th2 clone failed to induce similar tissue damage when the corresponding Ag was applied to the eye. These data indicate that the T cell-mediated exacerbation of HSK in these studies is dependent on the specific recognition of gD after corneal HSV-1 infection. Finally, gD-specific Th2 cell transfer also rendered HSK-resistant mice susceptible for HSK, suggesting that the freedom from HSK in resistant mice may primarily be due to their inability to produce the pathogenic Th2 cells. The data collectively implicate an important role for Th2 cells in the induction of HSV-mediated keratitis in mice.
Eighty-eight patients underwent serial coronary arteriography before, immediately after, 24 hours after and 7 +/- 2 months after successful percutaneous transluminal coronary angioplasty (PTCA) of 102 lesions. Severity of coronary obstruction was measured using quantitative digital angiography. Three groups of lesions were defined when comparing angiograms recorded immediately after and 24 hours after PTCA: group I--lesions with either no change or < or = 10% increase in arterial diameter stenosis after PTCA (n = 71); group II--lesions with > 10% increase in diameter stenosis after PTCA (n = 19); and group III--patients with total occlusion (n = 12). There were no significant differences in the severity of stenosis before or immediately after PTCA among the 3 groups of lesions. Twenty-four hours after PTCA the diameter stenosis was 14.2 +/- 6.3% in group I, 34.7 +/- 8.1% in group II and 100 in group III (p < 0.0001). At 7.1 +/- 2 months after PTCA the diameter stenosis was 21.2 +/- 16.8% in group I, 61.3 +/- 1.1% in group II, and 98.5 +/- 1.3% in group III (p < 0.0001). Restenosis (> or = 50% stenosis diameter) at follow-up per lesion was significantly greater in group II than in group I (73.6 vs 9.8%) (p < 0.0001). Thus, early angiographic study after successful PTCA stratifies lesions into angiographic subsets with low (group I) and high (group II) risk of coronary restenosis.
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OBJECTIVE: To analyze clinical fluids for the presence of Borrelia burgdorferi DNA using the polymerase chain reaction (PCR). METHODS: We utilized a modified, nested PCR to detect the presence of Borrelia DNA in 99 samples of serum, urine, cerebrospinal fluid (CSF), or synovial fluid obtained from 44 patients with various stages of Lyme disease and 47 control subjects. Primer specificity was corroborated by examining 2 DNA data banks, testing against DNA from other organisms, and confirming results with a second set of nested primers. RESULTS: Nested PCR was capable of detecting DNA from fewer than 10 organisms in 1 ml of fluid. The specificity of this technique was 96.4%, with a sensitivity of 76.7%. Although the specificity was uniformly high, the sensitivity was dependent upon the body fluid being tested: CSF 100%, urine 100%, synovial fluid 80%, and serum 59%. The rate of false-positive results was 3.6%. CONCLUSION: These data demonstrate the potential utility of PCR in confirming the clinical diagnosis of Lyme disease as well as providing insight into the pathogenesis of various stages of this disorder.
Five patients: three children, one adolescent, and one young adult, examined in an emergency room setting were diagnosed with post-traumatic transient cortical blindness. This syndrome is characterized by transient visual loss, normal pupillary response and normal funduscopic examination following minor head trauma. In each case, vision returned to normal within minutes to hours following injury, leaving no neurological sequelae. Headache, confusion, irritability, anxiety, nausea and vomiting were the most common related symptoms. While the mechanism responsible for the transient blindness is unknown, most authors propose an abnormal vascular response to trauma with resultant transient hypoxia and cerebral dysfunction. The similarity between the symptoms accompanying this syndrome and those seen during a classic migraine attack has led many investigators to suggest a common underlying pathophysiology. The purpose of this report is to highlight the salient clinical features and diagnostic approaches to this syndrome, thereby providing ophthalmologists and emergency room physicians a heightened awareness of this entity and the means to detect it.
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Good health is an integral component of the quality of human life, a prerequisite for developing human potential and an important determinant of economic development. When a person is ill from a tropical disease in an agricultural economy, a complex interaction between the individual's welfare and the family's welfare is set in motion. So complex are these interactions that few empirical studies exist on this subject and even where they do, empirical quantification of these interactions and economic losses places the analyst in the minefield of valuing time, ability and contribution to economic welfare. Placing monetary values on these commodities is always a little unsatisfactory since dollar values do not adequately reflect the nature of the losses. Secondly, the ill person's struggle to minimize the economic effects of disease on family income will mask its true impact; thirdly, tropical diseases disproportionately affect low-income groups and therefore measuring the income effects of disease amongst these groups will only reach at the earnings effect, and underestimate the economic implications of tropical disease control. Despite these difficulties, quantification of the economic impact of disease is important from a public health point of view. This study is an attempt at such a task, and focuses on the intra-familial struggle to minimize economic losses due to malaria. Using a case-control approach, time-losses and labour reallocations within the household are examined in an attempt to understand the economic consequences of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: This study was designed to compare freedom from combined cardiac events (death, angina, myocardial infarction) at 1-, 3- and 5-year follow-up in patients with multivessel disease randomized to either percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery. BACKGROUND: Percutaneous transluminal coronary angioplasty has been an effective approach in patients with coronary artery disease, but its role in patients with multivessel coronary artery disease is still controversial. METHODS: One-hundred twenty-seven patients with multivessel disease and lesions suitable for either form of therapy were randomized to either coronary artery bypass grafting (n = 64) or coronary angioplasty (n = 63). In this study we report the immediate results and freedom from combined cardiac events at 1-year follow-up. RESULTS: Demographic, clinical and angiographic characteristics were similar in both groups. There were no differences in in-hospital deaths, frequency of periprocedure myocardial infarction or need for emergency revascularization procedures between the two groups. At 1-year follow-up, there were no differences in mortality or in the incidence of myocardial infarction between the groups. However, patients treated with coronary artery bypass grafting were more frequently free of angina, reinterventions and combined cardiac events than were patients treated with coronary angioplasty (83.5% vs. 63.7%, p < 0.005). In-hospital cost and cumulative cost at 1-year follow-up were greater for the coronary artery bypass grafting than for the coronary angioplasty group. CONCLUSIONS: No significant differences were found in major in-hospital complications between patients treated with coronary artery bypass grafting or coronary angioplasty. Although at 1-year follow-up there were no differences in survival and freedom from myocardial infarction, patients in the coronary artery bypass grafting group were more frequently free from angina, reinterventions and combined events than were patients in the coronary angioplasty group.
Extraction, washout and chemical integrity of technetium(I) hexakis (2-carbomethoxy-2-isocyano propane), (99mTc-CPI) were evaluated in isolated contractile rat atrial tissue. 99mTc-CPI accumulated linearly over time at 32 degrees C with uptakes that were both concentration dependent and temperature sensitive. Uptake rates also increased with contractile strength, indicating a dependence of retention on metabolic status of the tissue. Retention indices showed that percent washout of 99mTc-CPI was much slower than control studies with 99mTcO4. HPLC analysis of retained radioactive products in atrial tissue showed most of the activity present as the 99mTc-CPI complex (75%). These observations in isolated rat atrial tissue help explain the interspecies differences in biodistribution of 99mTc-CPI and support the membrane potential dependent model for uptake and retention of technetium isonitrile complexes.
Since right blunt traumatic diaphragmatic rupture (BTDR) is reported with increasing frequency, BTDR may be a disease in evolution. Data were collected on 59 left, 16 right, and five bilateral BTDRs at a level 1 trauma center. Patients with right BTDR had lower Glasgow Coma Scale (GCS) scores (p < 0.05), were more likely to be initially in hypovolemic shock, and were admitted directly from the field (p < 0.01). Left and right BTDRs were diagnosed from chest films in 37% and 0% of cases, respectively (p < 0.05). Diagnostic peritoneal lavage results were negative in 16% of left and left of 0% of right BTDRs. For right BTDRs, the liver was more likely to be injured (p < 0.001). The mortality rates were similar and ICU and hospital stays, complications, and duration of mechanical ventilation were similar for early survivors with right and left BTDRs. The clinical signs and symptoms, diagnosis, and surgical findings associated with right and left BTDR are different.
Although there has been recent comparison of the Canadian and American health care systems, the issue of trauma has received little attention. Data were collected on all adult motor vehicle crash (MVC) victims admitted to the Sunnybrook Trauma Unit (CAN), Toronto, Canada, and the R Adams Cowley Shock Trauma Center (USA), Baltimore, Maryland from July 1986 through July 1990. Similar MVC victims at CAN and USA had equivalent mortality rates with similar discharge dispositions (p = NS), but patients at USA were twice as likely to be admitted to the ICU and had longer ICU stays (p < 0.01). The hospital-based cost for an average MVC patient at CAN was significantly less than for an average patient at USA and professional charges were at least five times greater at USA. This study provides some insight into the differences in trauma care between Canada and the United States.
OBJECTIVE--To test the hypothesis that the complement system may be activated in patients with type II diabetes and CAD. RESEARCH DESIGN AND METHODS--The plasma C3d concentration was measured in 106 type II diabetic patients and 25 nondiabetic control subjects. The patient group was subdivided according to AER, and the groups were adjusted for age, sex, and known duration of diabetes. For the assignment to a given subgroup, normoalbuminuria was defined as AER < 15 microns/min, microalbuminuria as AER 16-250 micrograms/min, and macroalbuminuria as AER > 250 micrograms/min. The presence or absence of coronary disease was assessed through clinical examination, ECG, and coronary angiography. An RIA system was used for measurement of urinary albumin levels, and the plasma C3d concentrations were measured by ELISA. RESULTS--Within each of the AER-defined subgroups, the plasma C3d levels were significantly higher in patients with IHD than in those without. Thus, in the normoalbuminuric group, plasma C3d levels were 16.3 AU/ml (95% CI 13.9-19) in patients with IHD vs. 11.6 AU/ml (95% CI 10.5-12.7) in those without (P < 0.001). The corresponding data for the microalbuminuric and macroalbuminuric groups were 21.8 (95% CI 18.1-26.3) vs. 13.6 (95% CI 12.3-15.1) and 31.6 (95% CI 24.9-40) vs. 17.5 (13.6-22.6) AU/ml (P < 0.01), respectively. Patients with IHD also had significantly higher plasma C3d levels than normal control subjects, regardless of AER subgroup. A multiple logistic regression analysis demonstrated an association between the plasma C3d concentration and IHD and AER. CONCLUSIONS--Activation of the complement system may play a role in the development of macrovascular disease in type II diabetes.