The ecology of Colorado tick fever in Rocky Mountain National Park in 1974. II. Infection in small mammals

Field studies of Colorado tick fever (CTF) in small mammals in Rocky Mountain National Park (RMNP) in 1974 established that Eutamias minimus and Spermophilus lateralis were the most important hosts for CTF virus and were the source of virus for immature stages of the tick vector, Dermacentor andersoni. Other species (Peromyscus maniculatus, Spermophilus richardsonii, Eutamias umbrinus) are secondary hosts. The intensity of viral activity in rodents varied greatly from locality to locality. Highest rodent infection rates were found to occur in the Moraine Park area of RMNP. Lowest infection rates occurred above 3,290 meters in altitude at Rainbow Curve and on the tundra. The prevalence of infection in rodents was constant from April--July (5--6% of animals captured were viremic) and then declined to 1.7--2.5% in August and September coincident with a decline in nymphal tick ectoparasitism. Many animals were captured which were simultaneously viremic and antibody-positive. Under field conditions, neutralizing antibody seroconversion does not always occur.     

Similar relative risks of seizures following measles containing vaccination in children born preterm compared to full-term without previous seizures or seizure-related disorders

Background

Febrile seizures are associated with the first dose of measles-containing vaccines and the risk increases with chronologic age during the second year of life. We used the Vaccine Safety Datalink (VSD) to determine if the relative increase in risk of seizures following receipt of measles-containing vaccine differs by gestational age at birth.

The discovery of (2S,3S)-cis-2-(diphenylmethyl)-N-[(2-methoxyphenyl)methyl]-1- azabicyclo[2.2.2]-octan-3-amine as a novel, nonpeptide substance P antagonisst.

We describe the structure-activity relationship development of a series of quinuclidines which culminated in the first potent, selective, nonpeptide substance P (SP) antagonist, (2S,3S)-cis-2-(diphenylmethyl)-N-[(2-methoxy-phenyl)methyl]-1- azabicyclo[2.2.2]octan-3-amine, 3 (CP-96,345). Compound 3 is a potent displacer of [3H]SP binding in human IM-9 cells and blocks SP-induced and capsaicin-induced plasma extravasation, as well as SP-induced salivation in the rat in vivo. This compound may both help to further our understanding of the interactions of small molecules with peptide receptors and serve to evaluate the therapeutic potential of a SP antagonist.     

Immunohistologic properties of benign and malignant mixed tumor of the lacrimal gland.

We studied the immunohistopathologic features of normal lacrimal gland, benign mixed tumor, and malignant mixed tumor of the lacrimal gland. Primary antisera were to keratin, muscle-specific actin, vimentin, and glial fibrillary acid protein. Keratin stained in occasional myoepithelial cells in normal gland, ductal epithelium in normal gland and the tumors, and occasional stromal epithelioid cells in the tumors. Muscle-specific actin stained in myoepithelium and vascular smooth muscle in normal gland and the tumors, and occasional spindle-shaped and clusters of stromal cells in the tumors. Vimentin staining was nonspecific. Glial fibrillary acid protein stained in occasional myoepithelial cells in normal gland and polyhedral stromal cells in benign mixed tumor. Our findings indicate that ductal epithelium develops into the epithelial component, and some cells in the stroma and myoepithelium develop into some cells in the stroma of benign and malignant mixed tumor of the lacrimal gland.     

Paget's disease of the breast: What the radiologist may expect to find

Paget's disease of the nipple is characterized by the presence of Paget's cells in the epidermis of the nipple or areola. Two case reports of Paget's disease are described and used to highlight unusual features of the disease. The literature on the radiographic and pathologic findings of this disease is reviewed.     

Regional distribution of protease-resistant prion protein in fatal familial insomnia

Protease-resistant prion protein, total prion protein, and glial fibrillary acidic protein were measured in various brain regions from 9 subjects with fatal familial insomnia. Six were homozygotes methionine/methionine at codon 129 (mean duration, 10.7 ± 4 months) and 3 were heterozygotes methionine/valine (mean duration, 23 ± 11 months). In all subjects, protease-resistant prion protein was detected in gray matter but not in white matter and peripheral organs. Its distribution was more widespread than that of the histopathological lesions, which were observed only in the presence of a critical amount of the abnormal protein. In the mediodorsal thalamic nucleus, however, a severe neuronal loss and astrogliosis were associated with relatively moderate amounts of protease-resistant prion protein, suggesting a higher vulnerability. There was no overall correlation between amount of protease-resistant prion protein and either glial fibrillary acidic protein or total prion protein. While protease-resistant prion protein was virtually limited to subcortical areas and showed a selective pattern of distribution in the subjects with disease of the shortest duration, it was more widespread in the subjects with a longer clinical course, indicating that with time the disease process spreads within the brain. The kinetics of the accumulation of protease-resistant prion protein varied among different brain regions: While in the neocortex and to a lesser extent in the limbic lobe and in the caudate nucleus, the amount increased with disease duration, in the mediodorsal thalamic nucleus and in the brainstem it was present in comparable amounts in all subjects regardless of the disease duration. These findings indicate that in fatal familial insomnia, the pathological phenotype is the result of the variability, in different brain regions, of the (1) timing and rate of accumulation of protease-resistant prion protein, and (2) vulnerability to the presence of protease-resistant prion protein.     

General practice and teaching hospital use of barium meal examinations in the City and Hackney Health District

The value of barium meal examination in the management of younger patients with dyspepsia has been seriously questioned as diagnostic yield is reported to be low with only minor abnormalities detected. Our 9 month survey of general practice and hospital out-patient use of barium meal examination in the City and Hackney Health District during 1983-84 shows that 51% of patients investigated were less than 50 years and 20% less than 30 years of age, suggesting that clinicians have not heeded these warnings. However, 30% of the younger patients had barium meal mucosal abnormalities. Over all age groups abnormalities were more prevalent in men and in general practice rather than hospital out-patient referrals (59% vs 45%; P less than 0.02). Previous studies may therefore have underestimated the prevalence of barium meal abnormalities in younger patients, and continued use of this examination in such patients may indicate that clinicians have found the results helpful in patient management.     

Interaction between oral hydralazine and propranolol. II. Assessment of altered splanchnic blood flow as the determinant of altered presystemic extraction

Coadministration of p.o. hydralazine and d-propranolol or dl-propranolol in six conscious dogs caused a significant increase in peak plasma concentration and area under the p.o. plasma concentration-time curve of propranolol (P less than .01, P less than .01, peak plasma concentration; P less than .01 and P less than .05, area under the plasma concentration-time curve; d-propranolol and dl-propranolol, respectively). Coadministration of p.o. hydralazine with p.o. dl-propranolol resulted in a small trend toward an increase in systemic clearance of i.v. dl-[3H]propranolol; however, this did not reach statistical significance (P less than .2, P less than .1, d-propranolol and dl-propranolol, respectively). When a mixture of d-propranolol and 14C-labeled dl-propranolol was administered into the jejunum of seven anesthetised dogs, the absorption into portal vein of the 14C-labeled dl-propranolol paralleled closely that of d-propranolol both in terms of time to peak and absorption as measured by a percentage of total area under the plasma concentration-time curve at an arbitrary time (10 min) postdose. Assessment of hepatic extraction (E) showed similar close parallels (d-propranolol, E = 0.85 +/- 0.02; dl-[14C]propranolol, E = 0.86 +/- 0.03: mean +/- S.E.M., n = 5, P less than .70). Hepatic extraction of propranolol and blood flow in mesenteric artery and hepatic artery were measured in 23 anesthetised dogs given a constant infusion of d-propranolol into portal vein (11 micrograms/kg/min), made up to 6 control and 17 hydralazine-treated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)