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Biomedical subjects

J C English

Publications and source records attributed to J C English.

At least 55 records · Page 3Linked to original sources
PubMed1997

A new platelet-activating factor antagonist (CV-6209) in preservation of heart and lung for transplantation.

The objective of this experimental protocol was to evaluate the protective effect of a new, potent platelet-activating factor (PAF) antagonist CV-6209 and the use of this compound in combination with allopurinol on ischemia-reperfusion injury in a swine model of heart-lung transplantation. Forty-two swine were divided into three groups, with seven donors and seven recipients in each. In group A, the PAF antagonist CV-6209 was administered in a single dosage of 1 mg/kg by slow intravenous injection at 1 hour before crossclamping of the aorta in both donors and recipients. In group B the combination of allopurinol and the PAF antagonist CV-6209 was used. Allopurinol was administered as a pretreatment regime of 50 mg/kg/day for 3 days prior to ischemia. The PAF antagonist dosage and regime of administration were the same as in group A, and both donors and recipients were pretreated with this combination. Group C was the control in which heart-lung transplantations were performed without interventional therapies. Based on the comparison of pre- and post-transplantation assessments of cardiac and pulmonary functional integrity within groups, and post-transplantation among groups, animals in groups A and B were significantly (P < 0.05) better protected from ischemia-reperfusion injury than animals in group C. The difference between groups A and B, however, was insignificant at all times. Morphological findings are in agreement with measures of physiological variation among experimental groups. It is suggested that the new PAF antagonist CV-6209 is effective in the prevention of heart and lung ischemia-reperfusion injury with and without allopurinol pretreatment.

Animals↗
PubMed1997

Cutaneous hyperpigmentation and polyglandular autoimmune syndrome type II.

Primary adrenal insufficiency (Addison's disease) may initially present with cutaneous hyperpigmentation. Addison's disease, when associated with autoimmune thyroid disease and/or insulin-dependent diabetes mellitus, is referred to as polyglandular autoimmune syndrome type II. We present the case of a patient who initially was diagnosed as having Grave's disease and eventually Addison's disease due to persistent cutaneous hyperpigmentation, fatigue, weight loss, hypotension, hyponatremia, peripheral eosinophilia, and positive results of a synthetic corticotropin stimulation test. Addison's disease, polyglandular autoimmune syndrome type II, and cutaneous hyperpigmentation are reviewed.

Anti-Inflammatory Agents↗
PubMed1997

Right outflow tract obstruction by a pedunculated neurofibroma: case report and literature review.

Right outflow tract obstruction due to neurofibroma is rare, with only four cases identified in the world literature. Obstruction due to a pedunculated neurofibroma has never been reported. A 36-year-old woman with no known heart disease presenting with dyspnea, palpitations and chest pain was shown on echocardiogram to have a mobile right ventricular mass. Cardiac catheterization revealed normal coronary arteries and right ventricular outflow tract obstruction by a pedunculated mass, which was surgically removed and histologically proven to be a benign neurofibroma. Following surgery the patient's symptoms disappeared, with no recurrence three years postoperatively.

Adult↗
PubMed1997

Mees' lines in a patient with multiple parasitic infections.

Mees' lines, or transverse striate leukonychia, are classically associated with arsenic poisoning, but have been described in other cases of acute or chronic illness. Their pathogenesis is thought to be a disruption of nail plate keratinization secondary to systemic stress. Mees' lines are observed in a patient with helminthic and amebic infections and no history of arsenic exposure. This case demonstrates another clinical setting in which Mees' lines can appear, providing further evidence that Mees' lines may chronicle systemic disease.

Adult↗
PubMed1997

Autoimmune idiopathic thrombocytopenic purpura with the subsequent occurrence of systemic lupus erythematosus.

Cutaneous manifestations of petechiae, purpura, and ecchymosis can lead the physician to discover an underlying platelet abnormality. Autoimmune idiopathic thrombocytopenic purpura (AITP) is a diagnosis of exclusion, mediated by a destructive IgG antibody response to the platelets' membrane components. In addition to showing evidence of cutaneous and mucosal bleeding (ie, epistaxis, hematuria), patients with AITP are at an increased risk for systemic lupus erythematosus (SLE). Therefore, it is suggested that patients with AITP be closely monitored for SLE.

Adolescent↗
PubMed1996

Differences in the nephrotoxicity of hydroquinone among Fischer 344 and Sprague-Dawley rats and B6C3F1 mice.

The present studies indicate pronounced species-, sex-, and strain- related differences in the acute nephrotoxicity of hydroquinone (HQ) when administered by gavage to male and female Sprague-Dawley (SD) rats, Fischer 344 (F344) rats, and B6C3F1 mice. Following a single dose of 400 mg/kg, male and female F344 rats displayed pronounced enzymuria and glucosuria. In female F344 rats, urinary alkaline phosphatase and glucose were the most sensitive indicators of renal toxicity, reaching levels of, respectively, 157 times and 137 times control values within 24 h of dosing. HQ treatment of male F344 rats also resulted in significant enzymuria, although it was less marked than that seen in female F344 rats. Significant numbers of epithelial cells were also present in the urine from F344 rats at 200 (female) or 400 mg/kg (male and female). SD rats did not show evidence of elevated levels of urinary enzymes or increased blood urea nitrogen (BUN) after oral administration of HQ at a dose level of 400 mg/kg. Oral administration of HQ to male and female B6C3F1 mice at 350 mg/kg resulted in only slight but significant increases in BUN.

Animals↗
PubMed1996

Human exposure to naturally occurring hydroquinone.

Hydroquinone (HQ) is a nonvolatile chemical used in the photographic, rubber, chemical, and cosmetic industries. HQ is also known to occur in nature as the beta-D-glucopyranoside conjugate (arbutin), and free HQ is a known component of cigarette smoke. Low concentrations of HQ have been detected in the urine and plasma of humans with no occupational or other known exposure to HQ. The studies reported here investigate dietary and other potential sources of HQ and their contribution to HQ concentrations in the plasma and urine of human volunteers. Analysis of possible food sources of HQ by GC indicated significant amounts of arbutin in wheat products (1-10 ppm), pears (4-15 ppm), and coffee and tea (0.1 ppm). Free HQ was found in coffee (0.2 ppm), red wine (0.5 ppm), wheat cereals (0.2-0.4 ppm), and broccoli (0.1 ppm). After consuming a meal including arbutin- and HQ-containing foods, volunteers showed significant increases in plasma and urinary levels of HQ and its conjugated metabolites (total HQ). Mean plasma concentrations of total HQ peaked at 5 times background levels at 2 h after the completion of the meal, and mean urinary excretion rates of total HQ peaked at 12 times background at 2-3 h after the meal. Immediately after smoking four cigarettes in approximately 30 min, mean plasma concentrations of total HQ were maximally 1.5 times background levels; mean urinary excretion rates of total HQ peaked at 2.5 times background at 1-3 h after smoking. These data indicate that considerable human exposure to HQ can result from plant-derived dietary sources and, to a lesser extent, from cigarette smoke.

Acetaminophen↗
PubMed1996

A man with nevoid hyperkeratosis of the areola.

Nevoid hyperkeratosis of the nipple and areola is a unique clinical entity and a diagnosis of exclusion. The patient presenting with nipple/areolar hyperkeratosis must be examined carefully for other underlying cutaneous diseases such as epidermal nevi, ichthyosis, acanthosis nigricans, Darier's disease, cutaneous T-cell lymphoma, and other chronic skin dermatitides that may be responsible for the changes. If no other clinical findings are evident, the diagnosis can be made. Although the disorder is more common in women of childbearing age, men may show nevoid changes after estrogen therapy or idiopathically. The use of topical 12 percent lactic acid lotion (Lac-Hydrin) resolves the skin changes over a six-month period.

Biopsy↗
PubMed1996

Hepatitis C and porphyria cutanea tarda.

Porphyria cutanea tarda (PCT) is a clinical manifestation of decreased uroporphyrinogen decarboxylase (UPD) activity. Multiple endogenous and exogenous factors have been implicated in inducing PCT in genetically predisposed patients. The most recent is the RNA virus hepatitis C (HCV), which is transmitted via blood exposure. The mechanism of action in HCV-induced PCT is unknown but produces the same clinical, laboratory, and histopathologic changes seen in other forms of sporadic PCT. Therefore, patients presenting with PCT clinically should be tested serologically for antibodies against HCV and patients with HCV should be monitored for signs and symptoms of PCT.

Adult↗
PubMed1996

A pigmented scalp nodule: malignant blue nevus.

The malignant blue nevus is an aggressive dermal melanocytic neoplasm. The lesion occurs most frequently on the scalp of men in their fifth decade of life, often metastasizes to the regional lymph nodes, and commonly results in fatality. Controversy exists as to whether this lesion is a malignant melanoma in the dermis or a separate neoplasm arising in the architecture of a cellular blue nevus. The lesion is treated with wide local excision and close monitoring for the occurrence of metastatic disease.

Diagnosis, Differential↗
PubMed1996

Acrospiroma: a case report and review.

Acrospiromas are cutaneous tumors of sweat duct differentiation. They usually present as slowly enlarging 1 to 2 cm nodules in middle-aged or older adults without site predilection. On histologic examination they are multilobular dermal masses composed of a biphasic cell population. Acrospiromas are benign, and treatment consists of surgical excision.

Acrospiroma↗
PubMed1995

Analysis of studies related to tumorigenicity induced by hydroquinone.

Hydroquinone (HQ) produced renal adenomas in male F344 rats, and these tumors appeared to arise from areas of spontaneous progressive nephropathy; the nephropathy itself has been found to be enhanced by HQ. Other neoplasms were not confirmed to be causally related to HQ among the reported bioassays. In the male F344 rat, HQ administered alone was not DNA reactive. HQ produced enhanced proliferation of renal tubular epithelium, presumably through toxicity involving glutathione conjugate formation. In the kidney, bone marrow, and other tissues, HQ may induce toxicity by redox cycling and lipid peroxidation. In bone marrow, HQ may produce microtubulin dysfunction, which is a plausible explanation for positive cytogenetic tests, the only consistently positive genotoxicity effect reported for HQ. Although HQ is a metabolic product of benzene, several lines of evidence suggest that the effects of HQ exposure are significantly different from those of benzene. Based upon the plausible mechanisms by which HQ may produce kidney tumors in male rats, we have concluded that occupational exposure levels of HQ are not predicted to be a cancer risk for humans.

Adenoma↗
PubMed1994

Measurement of nuclear DNA modification by 32P-postlabeling in the kidneys of male and female Fischer 344 rats after multiple gavage doses of hydroquinone.

Oral administration of hydroquinone (HQ) to male Fischer 344 (F344) rats results in dose-related kidney toxicity beginning with mild enzymuria by 1 week, significant cell proliferation by 6 weeks, and nephropathy and an increase in the incidence of renal tubule adenomas after 2 years. Female F344 rats, B6C3F1 mice, Sprague-Dawley rats, dogs, and humans are resistant to the renal toxicity of HQ associated with repeated exposure. To determine the potential of HQ to induce covalent DNA adducts in the kidney, male and female F344 rats were given 0, 2.5, 25, or 50 mg/kg HQ by gavage for 6 weeks, and nuclear DNA isolated from kidneys was analyzed by the 32P-postlabeling assay. At 50 mg/kg, males, but not females, showed an increase in the rate of excretion of N-acetyl-beta-D-glucosaminidase, indicative of proximal tubular damage. Analysis of nuclear DNA preparations by the postlabeling assay showed that HQ does not produce covalent DNA adducts in the kidneys of male and female rats. The assay's lower limit of detection is 1 adduct in 10(9) to 10(10) DNA nucleotides. No treatment-related increases in background radioactivity levels on the chromatograms were seen at locations corresponding to the major in vitro adducts of HQ and p-benzoquinone. HQ treatment, however, resulted in the reduction of the levels of certain endogenous adducts (I-compounds), the biological significance of which is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗