Egg transmission after infection of hens with Salmonella enteritidis phage type 4.
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Biomedical subjects
Publications and source records attributed to R C Baker.
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A case of reversible indomethacin-induced oligohydramnios is presented. This case suggests a relationship between the dose of indomethacin and the quantity of amniotic fluid.
The activity of protein kinase C (PKC) in whole brain and brain areas of mice selectively bred for resistance (short sleep, SS) or sensitivity (long sleep, LS) to the acute ataxic effect of ethanol has been investigated. The cytosolic and membrane fractions of whole brain PKC activities are significantly less in LS mice than in SS mice. There are significant differences in PKC activity between brain areas in both the SS and LS lines. Ethanol given in ataxic doses results in significantly increased amounts in PKC activity in whole brain cytosolic fractions and in some brain areas but equally in both SS and LS mice. Ethanol added in vitro reduced enzyme activity slightly in SS brain membranes, suggesting that the mechanism of the increase in PKC activity seen after in vivo administration is indirect. These results indicate that PKC is not involved in the mechanism whereby LS and SS mice differ in alcohol sensitivity. Direct intracerebroventricular (ICV) injection of phorbol myristate acetate (PMA), an activator of PKC, resulted in increased sleep times in both SS and LS mice. ICV injection of PMA also caused a more marked decrease in body temperature in LS than in SS mice. The half-life of PMA in brain was determined to be 9.6 hr and no metabolites could be detected. At limiting calcium concentrations, PMA added in vitro activated PKC equally well in both lines. However, PMA given ICV did not alter the level of PKC as determined in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
The interaction between ethanol and 1-0-alkyl-2-acetyl-sn-glycerol-3-phosphocholine (platelet activating factor, PAF) was addressed using platelets obtained from normal nonalcoholic volunteers. Ethanol at concentrations of 20 to 100 mM inhibited PAF activation of human platelets. Ethanol inhibited prominently the second or arachidonic acid metabolite dependent wave of platelet aggregation, which occurs with human platelets in citrated plasma. It also inhibited serotonin release and thromboxane A2 formation associated with this secondary phase of aggregation. Ethanol did not readily inhibit the primary wave of PAF-induced aggregation. The incorporation of PAF into platelets or metabolism of PAF was not influenced by up to 100 mM ethanol. Since ethanol inhibited only the secondary response, a direct interaction between PAF, ethanol, and a platelet PAF receptor is unlikely. The effect of ethanol on PAF-induced platelet aggregation shows a selectivity similar to that demonstrated by other investigators for epinephrine and adenosine diphosphate.
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A prospective study of patients with fever and petechiae was performed. Of 190 patients enrolled in the 1-year study, 13 (7%) had meningococcal disease. The most common bacterial association was Streptococcus pyogenes (19 patients). Viral infections were documented in 28 patients. Patients with invasive bacterial disease (group I) appeared more sick, were more likely to have signs of meningeal irritation, and were more likely to have petechiae on the lower extremities than those with less serious, nonbacteremic disease (group II). No patient in group I had petechiae only above the nipple line. Patients in group I had a significantly higher peripheral white blood cell count and absolute band form count. Although no laboratory test or physical finding was sufficiently sensitive to detect all patients with serious disease, the patient with abnormal cerebrospinal fluid, elevated white blood cell count, or elevated absolute band form count was at increased risk for invasive, bacterial disease. Conversely, the risk of serious disease was small if all of these values were in the normal range in the nonill-appearing child or if sore throat and clinical pharyngitis were present in the patient older than 3 years of age.
A prospective study of the effects of fever reduction on the clinical appearance of infants at risk for occult bacteremia was undertaken to study the hypothesis that infants with bacteremic illness fail to improve clinically following defervescence compared with infants with benign viral illness. A total of 154 children were enrolled in the study, including 19 with bacteremia: 13 with occult Streptococcus pneumoniae bacteremia, two with occult Haemophilus influenzae, type b bacteremia, and four with Haemophilus meningitis and bacteremia. There were no differences in degree of temperature reduction with acetaminophen between the bacteremic and nonbacteremic groups of infants. Among infants with bacteremia but without meningitis, differences from nonbacteremic children were detected in clinical appearance prior to fever reduction but not following defervescence. All patients with meningitis appeared seriously ill before and after defervescence. It was concluded that clinical improvement with defervescence is not a reliable indicator of the presence of occult bacteremia. Lack of clinical improvement with defervescence may be a reliable indicator for the presence of meningitis. Because there were differences in clinical appearance prior to fever reduction, routine administration of acetaminophen may interfere with the clinical evaluation by the physician.
Eicosanoids have been implicated in the pathogenesis of autoimmune diseases. In this study, peritoneal macrophages from autoimmune-prone mice were examined for their capacity to produce proinflammatory 5-lipoxygenase metabolites. The results indicate that enhanced production of leukotriene C4 is a common feature of murine autoimmunity and suggest further that aberrations in 5-lipoxygenase activity may play a role in the development of lupus.
There are variations of ascorbic acid levels in different brain areas of mice and rats. However, there are no differences in ascorbic acid levels between lines of mice selectively bred for differences in ethanol sensitivity for 25 generations. Thus, it is unlikely that brain ascorbic acid plays a significant role in the acute sedative effects of ethanol in these mice. Studies with inbred strains of mice known to differ in ethanol preference, acute sensitivity and withdrawal sensitivity also failed to reveal any differences in brain ascorbic acid levels. There were differences in ascorbic acid content between selectively bred lines of rats in various brain areas at generation five of selection.
The effects of chronic ethanol administration on striatal and cerebellar adenylate cyclase systems were investigated in the rat. The chronic ethanol treatment resulted in behavioral tolerance, but no difference in the sensitivity of adenylate cyclase to in vitro ethanol was observed. In one set of experiments using 173-195 g rats, GTP-, dopamine- and NaF-stimulated adenylate cyclase activities in the striatum were higher in rats chronically treated with ethanol when compared to animals pair-fed the liquid diet. However, no difference in adenylate cyclase activity was observed in cerebellar or striatal tissues when larger rats (280-385 g) were used. In conclusion, an adaptive change in activation of adenylate cyclase by in vitro ethanol does not occur after chronic ethanol treatment. The observed changes in enzyme activity measured in the absence of in vitro ethanol do not appear to be a simple, direct effect of chronic ethanol treatment.
The response of the soft-tissue profile to retraction of the maxillary incisors is still a matter of controversy. The purpose of this study was to improve the clinician's ability to predict the soft-tissue profile changes caused by retraction of the maxillary incisors by quantifying the profile changes, and identifying and quantifying the contribution of the most significant factors responsible for these changes. The cephalometric records of 80 Class II, Division 1 treated female subjects and 53 untreated female subjects were digitized and analyzed by means of a stepwise multiple regression analysis. The statistical assessment of the data suggested the following conclusions: In general, growth was associated with only minimal changes in the soft-tissue profile in a period not exceeding 36 months. The three clinically significant soft-tissue changes occurring in response to orthodontic treatment that included a mean upper incisor retraction of 6.7 mm were the retraction of the upper lip, the increase in the lower lip length, and the increase in the nasolabial angle. Other soft-tissue changes, which were of little clinical significance, included the retraction of the lower lip, the reduction of the interlabial gap, the increase in the thickness of both the upper and lower lips, the increase in the soft-tissue lower facial height and the lower soft-tissue component, which is the distance between lower stomion and soft-tissue menton. The length of the upper lip did not increase with either growth or orthodontic treatment. In general, changes in the lower lip in response to orthodontic tooth movement were more predictable than those of the upper lip. The low degree of predictability associated with the upper lip response to orthodontic tooth movement may be caused by the complex anatomy and/or dynamics of the upper lip, which could not be evaluated by the presently available cephalometric techniques.
Long sleep (LS) and short sleep (SS) lines of mice were derived from a heterogeneous stock of mice (HS) and have been selectively bred on the basis of the time the animals were devoid of the righting reflex (sleep time) following acute ethanol administration. We have tested a large group of the HS mice for sleep time response to ethanol. Animals were then selected from the extremes of the HS sleep time response and designated short sleep (HS-SS) or long sleep (HS-LS). The ED50 value for loss of righting reflex was compared between these mice (HS-SS and HS-LS) and animals that had undergone 25 generations of selection (SS and LS mice). The ED50 value was not significantly different for the HS-LS (1.9 g/kg) and LS (2.17 g/kg) mice but was markedly different between HS-SS (3.02 g/kg) and SS (4.21 g/kg) mice. The ED50 values for the eight inbred strains that constituted the HS stock ranged only from 2.33 to 2.78 g/kg. The value for LD50 one hour after ethanol administration was found to be 9.03 g/kg and for SS mice 6.94 g/kg for LS mice, in contrast to our previous findings of no difference in LD50 values between SS and LS mice when ascertained 24 hr after the ethanol dose. Since the two lines were selected only for a sleep time difference, a differential sensitivity to other consequences of acute ethanol exposure, such as the lethal dose, would not be expected unless the effects shared a common genetic mechanism of action with ethanol sleep time.(ABSTRACT TRUNCATED AT 250 WORDS)
Gangliosides appear to be factors in CNS membrane responses to ethanol. Responses of membranes to ethanol might be influenced by the membrane concentration of gangliosides, the distribution of ganglioside molecular species, or the surface orientation of gangliosides at the plasma membrane surface. To determine the importance of these influences to the acute effect of ethanol, we have chosen to study them in long sleep (LS) and short sleep (SS) mice. This report presents our findings on the composition of gangliosides from LS and SS mouse cerebellum and hippocampus, the composition of gangliosides from synaptosomal plasma membranes (SPM) of LS and SS mice, and the molecular species of cerebellar gangliosides from the two lines. It has been found that GM1 is elevated in the cerebellum and in cerebellar SPM of LS mice compared to SS mice, but that there is no difference between the GM1 concentration in the whole hippocampus of the two lines. Further, there are no differences in the molecular species of the cerebellar gangliosides of LS and SS mice.
The presence of Campylobacter jejuni was tested for but not isolated from any of 276 eggs sampled from 23 egg farms in New York State. The presence of C. jejuni was evaluated in broilers, kosher broilers, spent layers, Peking ducks, and turkeys. Four of five poultry dressing plants tested showed positive growth of C. jejuni on the 25-carcass samples at various stages of processing. Twenty to 100% of live birds sampled contained C. jejuni on the skin but 90 to 100% were contaminated after scalding and defeathering operations from contaminated birds and equipment. A three to four-fold increase in carcass contamination was observed after evisceration. The number of C. jejuni on the carcasses decreased after washing and chilling. The organisms did not survive the salting, rinsing, and chilling operations in a kosher processing plant. Several pieces of equipment, i.e., shackles, eviscerating troughs, and cooling tanks were contaminated with C. jejuni. This study illustrates how C. jejuni may be transmitted from the live bird to the final poultry product.
The relationship between genetically determined acute ethanol sensitivity and cerebellar phospholipid composition was investigated. Cerebellar phospholipid composition was compared in two lines of mice that have been selected for differential sensitivity to the acute hypnotic actions of ethanol. The relative ethanol sensitivity of the long sleep (LS) and ethanol resistance of short sleep (SS) mice is well established, and was observed in this study. Cerebellar phospholipid and cholesterol concentrations were found to be identical in the two lines. No differences were found in the total cerebellar or synaptosomal plasma membrane phospholipid fatty acid composition between the two lines. Additionally, there was no change in phospholipid composition or cholesterol concentration in the cerebellum of either SS or LS mice following chronic alcohol treatment. This study suggests that neither total cerebellar nor synaptosomal phospholipid composition is a major determinant of the differential response to acute ethanol in the ethanol sensitive and resistant mouse lines.
Three pediatric patients presenting with fever and petechiae with unexpected rapid development of shock are reported. Clinical and laboratory parameters which may identify patients at risk for rapid deterioration are presented. The pathophysiology of meningococcal disease is discussed with emphasis on the possible implications in management. Patients identified at increased risk should be monitored closely; cardiovascular decompensation should be treated aggressively with fluids, pressors, and steroids in an attempt to reverse this process.
The effect of 80% CO2 (balance air) on the survival and growth of microorganisms most often associated with spoilage and foodborne disease in poultry carcasses was compared to air at 2, 7, and 13 C. The CO2 atmosphere substantially retarded the growth of the total bacterial load in uninoculated ground chicken meat and parts at all temperatures when compared to air; however, temperature had a larger overall effect than atmosphere. Ground chicken meat and synthetic broth were inoculated (greater than 10(4) cells/ml or g) with Pseudomonas fragi, Salmonella typhimurium, Staphylococcus aureus, or Clostridium sporogenes and the influence of 80% CO2 and incubation temperature studied. With the exception of Cl. sporogenes, 80% CO2 was inhibitory when compared to air at any given temperature. In most cases, CO2 was more inhibitory at 2 C than at 7 or 13 C. The Cl. sporogenes inoculum failed to grow above initial inoculum levels in any combination of temperature and atmosphere, but samples packed in 80% CO2 had higher numbers of colony forming units than air-packaged samples. This study does not indicate that modified atmosphere packaging of refrigerated poultry in elevated CO2 atmospheres increases the microbial hazards when compared to air at the same temperature.