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Biomedical subjects

K Johnson

Publications and source records attributed to K Johnson.

At least 181 records · Page 10Linked to original sources
PubMed1997

Tuberculin skin testing of hospitalized patients.

OBJECTIVES: We sought to define the prevalence of tuberculin skin test (TST) positivity in a group of newly hospitalized patients, to identify risk factors for positive tests, and to examine the impact of testing on infection control practices. DESIGN: Unblinded cohort study over 5 days in July 1992. SETTING: A 1,000-bed university-affiliated hospital. PATIENTS: All patients admitted (excluding obstetric patients and newborns) were interviewed. Patients without a history of tuberculosis (TB) or a positive TST were offered a TST with Candida and tetanus controls. RESULTS: Of 346 patients offered the test, 21 (6%) had a prior history of TB or a positive TST, and 36 (10%) declined to participate; 279 of the remaining 289 completed the study. Anergy was demonstrated in 94 (33.7%) of 279 patients. New positive TSTs were identified in 19 (10.3%) of 185 nonanergic patients. Of the 19 TST-positive patients, 6 (32%) had infiltrates on chest radiographs and were evaluated for active TB. One patient was treated empirically for active TB, and five received isoniazid prophylaxis. Risk factors for a new positive TST included age (odds ratio [OR], 1.56 per decade of life; P = .021), African American race (OR, 4.81; P = .008), alcohol abuse (OR, 5.53; P = .005), and peptic ulcer disease (OR, 4.53; P = .017). Risk factors for anergy included admission to a surgical service (OR, 2.1; P = .006), current use of steroids (OR, 2.65; P = .005), and human immunodeficiency virus (HIV) infection (OR, undefined; P = .034). CONCLUSIONS: Despite a high rate of anergy, routine tuberculin skin testing identified a substantial number of patients with TB infection who might otherwise have gone unrecognized.

Adolescent↗
PubMed1997

Somatic instability of the myotonic dystrophy (CTG)n repeat during human fetal development.

Myotonic dystrophy is characterised by the striking level of somatic heterogeneity seen between and within tissues of the same patient, which probably accounts for a significant proportion of the pleiotropy associated with this disorder. The congenital form of the disease is associated with the largest (CTG)n repeat expansions. We have investigated the timing of instability of myotonic dystrophy (CTG)n repeats in a series of congenitally affected fetuses and neonates. We find that during the first trimester the repeat is apparently stable and that instability only becomes detectable during the second and third trimesters. In our series repeat instability is apparent only after 13 weeks gestational age and before 16 weeks. The appearance of heterogeneity shows some tissue specificity, with heart most commonly having the largest expansion. The degree of heterogeneity is not correlated with initial expansion size as gauged by chorionic villus and blood (CTG)n repeat sizes.

Embryonic and Fetal Development↗
PubMed1997

Superficial necrolytic dermatitis and a pancreatic endocrine tumour in a dog.

A 13-year-old dog was referred for a severe dermatological problem of 12 months duration. Skin biopsy results were compatible with superficial necrolytic dermatitis. The only laboratory abnormalities were hyperglycaemia and hyperglucagonaemia. These findings suggested a pancreatic endocrine tumour in association with superficial necrolytic dermatitis. Abdominal ultrasound examination was unremarkable. The dog was euthanased due to the lack of clinical improvement following symptomatic therapy. Postmortem examination revealed a pancreatic endocrine tumour with liver metastases. Pancreatic endocrine tumour cells were immunoreactive for glucagon, insulin and islet amyloid polypeptide.

Amyloid↗
PubMed1997

Hyperoxia exacerbates microvascular lung injury following acid aspiration.

OBJECTIVES: To examine the effects of an increase in ambient oxygen (O2) concentrations on the extent of inflammatory pulmonary damage following acid aspiration. DESIGN: Prospective, controlled laboratory study. SETTINGS: University-affiliated animal research facility. SUBJECTS: Male, Long Evans rats weighing 250 to 300 g. INTERVENTION: Rats were injured by instillation of 1.2 mL/kg normal saline solution/HCl, pH= 1.25 (acid), into the lungs via a tracheotomy. Animals were allowed to awaken and were exposed to 21%, 50%, or 98% O2 for 0 to 5 h (n/group > or = 10). In a separate set of experiments, injured rats exposed to 98% O2 were treated with different doses of deferoxamine, just prior to injury. Uninjured rats and rats injured with normal saline solution, pH = 5.3, were used as the control group. MEASUREMENTS: Injury was determined by assessing lung function (lung compliance and arterial blood gases) and alveolar-capillary wall integrity (wet/dry weight, lung albumin permeability index [PI], and intrapulmonary hemorrhage [HI]). RESULTS: Intrapulmonary instillation of acid increased PI, HI, and decreased static lung compliance compared to uninjured control animals. Increased ambient oxygen following acid aspiration decreased lung compliance, 1.06+/-0.03 mL/kg/cm H2O, in oxygen-exposed lungs when compared to the lungs exposed to air, 1.26+/-0.04, following a low pH aspirate (p<0.05). An increase in protein leakage into the lung tissue was noted in oxygen-exposed animals, PI=1.33+/-0.10, vs air-exposed rats, 0.89+/-0.07 (p<0.05). The hyperoxia-induced increase in lung injury was prevented by 30 mg/kg or higher deferoxamine treatment, 0.78+/-0.05 (p<0.05). Exposure of animals to 98% O2 for 2 h was sufficient to produce the same increase in microvascular protein leakage as 5-h exposure to O2 following low pH aspirate. CONCLUSION: Hyperoxia increases acid aspiration-induced inflammatory microvascular lung injury. This appears to be mediated by production of reactive species of O2.

Animals↗
PubMed1997

Harlequin ichthyosis (ichq): a juvenile lethal mouse mutation with ichthyosiform dermatitis.

The harlequin ichthyosis (ichq) mouse mutation arose spontaneously in 1989 in a colony of BALB/cJ mice at The Jackson Laboratory. Affected mice developed thick skin due to formation of compact, orthokeratotic scales that fractured over articular surfaces, secondary to bending. Harlequin ichthyosis mice on the inbred BALB/cJ background died between 9 and 12 days of age. Onset of the clinical phenotype corresponded with emergence of hair fibers from follicles at 5 days of age. There was marked proliferation of the root sheaths of anagen hair follicles, limited to the region within the dermis. Sebaceous glands were present but small compared with those of littermate controls. Emerging hair fibers were surrounded by a thick, compact sheath of cornified cells. Mutant skin contained large mitochondria with lamellar-shaped, electron-dense structures at the ultrastructural level. Keratohyalin granules were smaller and less pleomorphic than those in control mice. Lamellar bodies were not evident in either mutant or littermate control mice. Using a panel of antibodies to evaluate changes in keratinocyte differentiation, mouse-specific keratin 6 was overexpressed in the suprabasilar, hyperplastic epidermis. Loricrin expression, within the cytoplasm of cells in the stratum granulosum, decreased rapidly postmortem, unlike that in normal mice where it was stable for over 24 hours postmortem. Filaggrin expression, within granules of cells in the stratum granulosum, was prominent, corresponding to hypergranulosis evident by light microscopy in mutant mouse skin. Skin grafts from harlequin ichthyosis mice grafted onto immunodeficient nude mice maintained the phenotype for the 10-week observation period. The mutant gene locus mapped to the proximal end of mouse chromosome 19 and is inherited as a fully penetrant autosomal recessive gene. The harlequin ichthyosis mouse mutation is very similar to human type 2 harlequin ichthyosis for which it may be a good model.

Animals↗
PubMed1996

Stability of levofloxacin in intravenous solutions in polyvinyl chloride bags.

The stability of levofloxacin in 10 commonly used infusion fluids was studied. Levofloxacin 25-mg/mL injection was diluted to 0.5 and 5 mg/mL in each of the following i.v. infusion fluids: 0.9% sodium chloride injection, 5% dextrose injection, 5% dextrose and 0.9% sodium chloride injection, 5% dextrose and lactated Ringer's injection, 5% sodium bicarbonate injection, Plasma-Lyte 56 and 5% dextrose injection, 5% dextrose and 0.45% sodium chloride and 0.15% potassium chloride injection, 1/6 M sodium lactate injection, sterile water for injection, and 20% mannitol injection. Ten polyvinyl chloride bags were prepared for each solution; two were stored for 3 days at 25 degrees C, two for 7 days at 5 degrees C, two for 14 days at 5 degrees C, two for 13 weeks at -20 degrees C followed by 14 days at 5 degrees C, and two for 26 weeks at -20 degrees C, all in the dark. The solutions were visually examined, tested for turbidity and particulate matter, and subjected to stability-indicating high-performance liquid chromatography; solution pH was determined. Levofloxacin was stable in and compatible with all but two of the diluents tested. Precipitation occurred under all conditions in 20% mannitol injection for the 0.5-mg/mL levofloxacin concentration and after storage for 13 weeks at -20 degrees C for the 5-mg/mL concentration. Levofloxacin 0.5 mg/mL in 5% sodium bicarbonate injection formed a precipitate when stored at -20 degrees C for 13 weeks and beyond. Levofloxacin 0.5 and 5 mg/mL was compatible with and stable in 8 of the 10 infusion fluids studied.

Anti-Infective Agents↗
PubMed1996

Mechanisms of drug-induced lupus. II. T cells overexpressing lymphocyte function-associated antigen 1 become autoreactive and cause a lupuslike disease in syngeneic mice.

Current theories propose that systemic lupus erythematosus develops when genetically predisposed individuals are exposed to certain environmental agents, although how these agents trigger lupus is uncertain. Some of these agents, such as procainamide, hydralazine, and UV-light inhibit T cell DNA methylation, increase lymphocyte function-associated antigen 1 (LFA-1) (CD11a/CD18) expression, and induce autoreactivity in vitro, and adoptive transfer of T cells that are made autoreactive by this mechanism causes a lupuslike disease. The mechanism by which these cells cause autoimmunity is unknown. In this report, we present evidence that LFA-1 overexpression is sufficient to induce autoimmunity. LFA-1 overexpression was induced on cloned murine Th2 cells by transfection, resulting in autoreactivity. Adoptive transfer of the transfected, autoreactive cells into syngeneic recipients caused a lupuslike disease with anti-DNA antibodies, an immune complex glomerulonephritis and pulmonary alveolitis, similar to that caused by cells treated with procainamide. These results indicate that agents or events which modify T cell DNA methylation may induce autoimmunity by causing T cell LFA-1 overexpression. Since T cells from patients with active lupus have hypomethylated DNA and overexpressed LFA-1, this mechanism could be important in the development of human autoimmunity.

Animals↗
PubMed1996

The proinflammatory cytokine response to coagulation and endotoxin in whole blood.

Acute inflammatory illnesses, including the sepsis syndrome, often include a component of coagulation. A human whole blood culture system was developed so that the relationship between coagulation activation and cytokine responses in the presence or absence of lipopolysaccharide (LPS) could be evaluated. In the absence of LPS stimulation, coagulation activation resulted in a novel pattern of cytokine production. During a 4-hour culture of coagulating blood, significant production of interleukin-8 (IL-8; >2,000 pg/mL) was observed, whereas other proinflammatory cytokines including IL-1 beta, IL-6, or tumor necrosis factor a were undetectable or less than 35 pg/mL. The cytokine profile was distinct from that of fully anticoagulated, LPS-stimulated blood, which showed levels of all the indicated proinflammatory cytokines > or = 2,000 pg/mL over the same time period. Over 24 to 48 hours, the coagulation-induced cytokine response was characterized by marked and sustained IL-8 production, limited IL-6 generation (with kinetics delayed relative to IL-8), and minimal or undetectable tumor necrosis factor alpha levels. The magnitude of the whole blood IL-8 response correlated with the level of coagulation activation as determined by measurement of thrombin-antithrombin III complex formation. The combined stimuli of coagulation activation and LPS challenge induced a synergistic enhancement of IL-8 production but not of IL-6. Coagulation-induced cytokine production and the synergistic production of IL-8 by coagulation and LPS could be attenuated by hirudin or tissue factor pathway inhibitor (TFPI). Studies to elucidate mechanisms implicated (1) the TFPI third Kunitz and carboxy-terminus as important structural components for TFPI regulation of coagulation activation and (2) thrombin as a candidate mediator of the mononuclear cell cytokine response to coagulation activation. In summary, a unique aspect of the crosstalk between the coagulation and cytokine cascades in whole blood is shown with the identification of IL-8 as a key proinflammatory participant.

Blood Coagulation↗