Effects of crude oil and ultraviolet radiation on immunity within mouse skin

Previous studies indicate that crude oil leads to increased pigmentation and erythema (sunburn) in response to sunlight in exposed individuals. However, no information is currently available concerning whether crude oil exposure might enhance the immunosuppressive effects of solar ultraviolet radiation (UVR) on the skin. In order to address this question, the back skin of shaved, female C3H/HeN mice was exposed to crude oil with or without subsequent treatment with medium-wavelength (UVB) (200 J/m2) or long-wavelength (UVA) (20,000 J/m2) UVR. Immune function was assessed in treated mice by measuring their ability to mount contact hypersensitivity responses to a hapten (2,4-dinitro-1-flyorobenzene, DNGFB) applied to the site of crude oil and UVR treatment as determined by ear swelling upon subsequent challenge. Since Langerhans cells represent an important component of immunity within the skin and because suppression of contact hypersensitivity following UVR treatment is often accompanied by disappearance of Langerhans cells from the epidermis, the impact of these agents on epidermal Langerhans cell density was also analyzed. This was accomplished by enumerating IA-positive cells within the epidermis of treated skin. In these studies, crude oil alone induced inhibition of contact hypersensitivity but had no effect on epidermal Langerhans cells. In contrast, combined treatment with crude oil and UVA led to suppression of contact hypersensitivity, which was accompanied by depletion of epidermal Langerhans cells.     

Immunoglobulin M Enzyme-Linked Immunosorbent Assay Using Recombinant Polypeptides for Diagnosis of Dengue

We demonstrate that a mixture of four recombinant dengue virus E polypeptides corresponding to the N-terminal region of the envelope protein from all serotypes substitutes for standard antigens in two immunoglobulin M enzyme-linked immunosorbent assay formats with 100% concordance, making these polypeptides a useful and accessible reagent for serological diagnosis of dengue in endemic countries.     

Rapid,simple identification of individual osteoblastic cells and their specific products by cell blotting assay

Biochemical and molecular biological studies of osteoblastic cell function and hormonal regulation are frequently confounded by the inherent cellular heterogeneity and phenotypic instability of existing in vitro and in vivo model systems. A new technique (derived from Western blotting or antibody-based detection of protein molecules bound to nitrocellulose paper) is described for identification of individual cells which synthesize osteoblast-specific gene products (bone Gla-protein, type I collagen, and alkaline phosphatase) or produce cAMP in response to parathyroid hormone (PTH) or isoproterenol. Dispersed primary neonatal rat calvariae or osteogenic sarcoma cells were “plated” on Immobilon-P (a hydrophobic transfer membrane with very high protein-binding capacity) for 30 minutes to several hours, followed by agonist treatment, formalin fixation, hematoxylin staining, and immunostaining with a battery of antibodies specific for osteoblastic products. Individual cells and their secretory zones were visualized by light microscopy and counted. Treatment with PTH with or without isoproterenol resulted in increases in the percentages of osteoblastic cells elaborating cAMP, as well as the intensity of immunostaining, but had no effects on MCF-7 cells, a nonosteoblastic breast carcinoma control line. The percentage of cells within each primary osteoblastic cell population isolated or rat osteogenic sarcoma cell clone (G2 or C12) that elaborated bone-specific proteins or that generated cAMP in response to PTH varied with time and the individual cellular preparation, reconfirming the cellular heterogeneity of these systems. This method, in conjunction with techniques such as in vitro hybridization, should prove useful in characterizing discrete osteoblastic bone cell subpopulations and in clarifying mechanisms of hormonal regulation by local and systemic agents.     

Effect of low dietary calcium on bone metabolism in the SENCAR mouse

The SENCAR (sensitive to carcinogenesis) mouse is a unique tool for investigating the interaction between a specific defect in intracellular signaling, dietary calcium, and metabolic bone disease. The SENCAR mouse was developed by selective breeding for enhanced sensitivity to two-stage carcinogenesis. Its major genetic defect, which renders it exquisitely sensitive to stimulation with diacylglycerol or phorbol esters, is in the regulatory domain of protein kinase C, one of the primary intracellular mediators of hormonal effects. At sexual maturity, SENCAR mice are large and have big bones, but our previous pharmacokinetic studies showed that they accumulate lesscalcium under normal conditions and lose more calcium under adverse conditions than do other, standard strains of mice. To histologically define the effect of low dietary calcium on bone metabolism, we performed histomorphometric analysis of tetracycline-labeled sections of femoral bone from male SENCAR mice maintained on calcium-sufficient and calcium-deficient diets during the critical period from 10 to 14 weeks of age. The bone volume, absolute osteoid volume, and mineral apposition rate were lower at 14 than at 10 weeks of age in SENCAR mice fed 0.02 or 0.6% calcium diets. Calcium deficiency increased the architectural disarray and the probability of observing focal discontinuities in the growth plate. Thus, characteristic features of impaired bone metabolism (low bone volume and apposition rate) develop early in SENCAR mice and are exacerbated by low dietary calcium. Detailed examinations of the histology and biochemistry of SENCAR mouse bone will provide insights into the mechanisms by which specific defects in the signal transduction of protein kinase C contribute to impaired bone metabolism.     

Methylmercury poisoning: Long-term clinical,radiological, toxicological,and pathological studies of an affected family

For 3 months in 1969 a family in the United States that included a pregnant mother consumed pork containing methylmercury. Children, aged 20, 13, and 8 years and a neonate, developed severe neurological signs. Twenty-two years later, the 2 oldest had cortical blindness or constricted visual fields, diminished hand proprioception, choreoathetosis, and atentional deficits. Magnetic resonance images showed tissue loss in the calcarine and parietal cortices and cerebellar folia. The youngest had quadriplegia, blindness, and severe mental retradation until their deaths. The brain of the 8-year-old who died at age 30 showed cortical atrophy, neuronal loss, and gliosis, most pronounced in the paracentral and parietooccipital regions. The total mercury level in formalin-fixed, left occipital cortex was 1,974 ng/gm as measured by atomic absorption. Regional brain mercury levels correlated with extent of brain damage. A control patient had 38.5 ng of mercury/gm in the occipital cortex. Systemic organs in the patient and a control subject had comparable mercury levels. In mercury-intoxicated rats, we found that only 5 to 10% of total brain mercury was lost by formalin fixation. Brain inorganic mercury in the patient ranged from 82 to 100%. Since inorganic mercury crosses the blood-brain barrier poorly, biotransformation of methyl to inorganic mercury may have occurred after methylmercury crossed the blood-brain barrier, accounting for its persistence in brain and causing part of the brain damage.     

Systemic necrotizing vasculitis associated with childhood sarcoidosis

Childhood sarcoidosis is a rare disorder with protean manifestations. The case of a child with prolonged fever, hepatosplenomegaly, pancytopenia, and systemic necrotizing vasculitis manifesting as fever, rash and skin infarctions, digital pregangrene, and foot drop is reported. This is the first case of systemic necrotizing vasculitis reported in sarcoidosis. The fulminant course of the disease required treatment with intravenous pulsed cyclophosphamide and high doses of corticosteroids. The spectrum of vasculitis in childhood and adult sarcoidosis is reviewed.     

Trabeculoretraction by argon laser. 5 and 8-year results]

To appreciate the current place of argon laser trabeculoplasty (ALT) in the therapeutic armamentarium of primary open-angle glaucoma (POAG), the first 211 photocoagulated phakic eyes were analysed. One hundred and fifty-nine eyes had a 5 year-follow-up and 147 eyes had a minimal 8 year-follow-up. These eyes came from an initial group of 151 patients: 76 women and 75 men with a mean age of 66 years. We decided, arbitrarily, to assess trabeculoplasty results according to three combined criteria of failure (insufficient or transient intraocular pressure drop (3 mmHg), progression in visual field loss and need for a filtrating surgery) and to various expected goals: prevent an increase of drugs with their subsequent side effects, taper a non tolerated medical treatment and, lastly, try to cease all medical treatment in non compliant patients. According to these criteria, during the first five years, the cumulative failure rate in the 159 eyes rose steadily from 19% (31 eyes) in the first year to 52% (82 eyes) in the fifth year. The initial mean intraocular pressure (27.22 mmHg) of 7 failures operated on during the first 2 months and that of all 27 operated on failures (24.41 mmHg) was higher than the initial mean intraocular pressure of the 77 successful cases (22.67 mmHg). In the 77 eyes still controlled at 5 years, the intraocular pressure drop was 6.57 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of intervention to improve breastfeeding technique on the frequency of exclusive breastfeeding and lactation-related problems.

This randomized clinical trial compared frequencies of exclusive breastfeeding and lactation-related problems during the first 30 days among 74 mothers who received a 30-minute counseling session on breastfeeding technique in the maternity ward, and 137 controls. The frequency of exclusive breastfeeding among mothers who had received intervention was similar to controls by 7 days (79.7% vs 82.5%, respectively) and 30 days (60.8% vs 53.3%). There was no difference between groups in the frequency of sore nipples at 7 and 30 days, in breast engorgement and mastitis, and in the quality of breastfeeding technique at 30 days. Therefore, a single intervention at maternity was not sufficient to improve breastfeeding technique, increase exclusive breastfeeding rates, and reduce the incidence of breastfeeding problems during the first month.