Histamine H1- and H2-receptor vasodilation of canine intestinal circulation

Studies were conducted in anesthetized dogs to determine whether the mesenteric vasodilator response to histamine is mediated by H1 receptors alone or whether H2 receptors are also involved in the response. Evidence favoring a role for both receptors included: 1) the vasodilator response to histamine was inhibited by either the H1-receptor antagonist, tripelennamine, or the H2-receptor antagonist, metiamide; 2) both the H1 agonist, 2-methylhistamine, and the H2 agonist, 4-methylhistamine, induced dilator responses in the mesenteric circulation; and 3) two temporal patterns of vasodilation could be distinguished, namely a transient spike and subsequent fade of blood flow (seen with either the H1 agonist or with histamine after H2-receptor blockade) and a sustained and stable increase in flow (seen with either the H2 agonist or with histamine after H1 blockade). Metiamide appeared to be a potent inhibitor of the mesenteric vasodilator response to histamine at least equal to tripelennamine.     

Tuberculosis of the breast

Twenty-one cases of mammary tuberculosis are reported and the attendant clinical and histological difficulties described. It is probable that contemporary clinicians would now make the clinical diagnosis of breast abscess or carcinoma. Furthermore, the histological features (without demonstration or culture of the organism) may be confused with those granulomatous epithelloid reactions seen in mammary duct ectasia (comedo cell mastitis, plasma cell mastitis) and in traumatic fat necrosis.     

Occurrence of Gasterophilus intestinalis and some parasitic nematodes of horses in Sweden

The biological accuracy of a nonlinear compartmental model describing the in vivo kinetics of L-3,4-dihydroxy-6-[18F]fluorophenylalanine ([18F]FDOPA) metabolism was investigated. Tissue activities for [18F]FDOPA and its labeled metabolites 3-O-methyl-[18F]FDOPA ([18F]OMFD), 6-[18F]fluorodopamine ([18F]FDA), L-3,4-dihydroxy-6-[18F]fluorophenylacetic acid ([18F]FDOPAC), and 6-[18F]fluorohomovanillic acid ([18F]FHVA) were calculated using a plasma [18F]FDOPA input function, and kinetic constants estimated previously by chromatographic fractionation of 18F-labeled compounds in plasma and brain extracts from rat. Present data accurately reflected the measured radiochemical composition in rat brain for tracer circulation times past 10 min. We formulated the hypothesis that the discrepancy between calculated and measured fractions of [18F]FDOPA and the deaminated metabolite [18F]FDOPAC at times earlier than 10 min reflected storage of [18F]FDA in vesicles without monoamine oxidase. This hypothesis explained the initially rapid appearance of [18F]FDOPAC in striatum by delayed transfer of [18F]FDA from cytosol into vesicles. We conclude that the simpler model of [18F]FDOPA compartmentation is accurate when the cytosolic and vesicular fractions of [18F]FDA are at steady-state; the approach to equilibrium has a time constant of 15-30 min. The present model is valid for positron emission tomography studies of [18F]FDOPA metabolism in living brain.     

Production constraints on utterance-final consonant characteristics in babbling

In order to evaluate hypotheses regarding production constraints on final consonants in babbling, 721 utterance-final consonants produced by 6 infants in consonant-vowel-consonant (CVC) syllables were examined and compared with the preceding consonant in the CVC. Consistent with earlier studies, major patterns were observed for each of the three main consonantal properties--place and manner of articulation and voicing. These patterns included a strong tendency for final consonants to repeat the place of articulation of nonfinal consonants and a tendency for relatively more fricative, nasal and voiceless consonants to occur in final position than in nonfinal position. The high frequency with which final consonants shared place of articulation with the preceding consonant was considered to reflect 'frame dominance' or the tendency of a relatively constant mandibular cycle (the frame) to determine the structure of utterances with very little contribution from other active articulators. The manner and voicing effects were attributed to an overall terminal energy decrease in the vocal production system.     

Nonclinical model for assessing gastric effects of bisphosphonates

Mechanisms by which ketones potentiate manganese-bilirubin (Mn-BR)-induced cholestasis are unknown. The purpose of the present study was to investigate the effect of methyl isobutyl ketone (MiBK), a widely used ketonic solvent, at the level of the bile canalicular membrane (BCM) and to verify if altered membrane lipid dynamics could be involved in MiBK-potentiated Mn-BR cholestasis. Male Sprague-Dawley rats were exposed 4 hr/day for 3 days to MiBK vapors (200 or 600 ppm). Eighteen hours after the last exposure, manganese (Mn, 4.5 mg/kg) was given i.v. followed 15 min later by bilirubin (BR, 25 mg/kg). Rats were killed 30 min after BR; liver cell plasma membranes (bile canalicular and sinusoidal), microsomes, mitochondria, and cytosol were isolated by differential centrifugation. Lipids were extracted and cholesterol was measured in each fraction. After Mn-BR and MiBK exposure (600 ppm), results indicated a marked increase in BCM cholesterol content compared to rats exposed to air only. This increase was greater than that due to Mn-BR or MiBK given alone. Also, results indicated that cholesterol increased in a dose-related fashion in BCM after MiBK exposure, whereas PM cholesterol remained unaltered. To identify the source of the increased BCM cholesterol and to permit distinction between de novo cholesterol synthesis and subcellular shifts, the hepatic lipid pool was labeled in vivo with [3H]-cholesterol and [2-14C]-mevalonic acid, a cholesterol synthesis precursor. Results showed that after 600 ppm MiBK exposure, 14C-labeled cholesterol was greater than 3H-labeled cholesterol, indicating that the contribution of de novo cholesterol synthesis to the total cholesterol content of the various isolated hepatocellular fractions was more important than the contribution of intracellular pools. Therefore, increased BCM cholesterol content and enhanced accumulation of newly synthesized cholesterol appear to be involved in MiBK potentiation of Mn-BR-induced cholestasis.