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Because the alveolar macrophage (AM) phenotype of horses with severe equine asthma (SEA) is unknown, the cytokines expressed by M1- and M2-polarized AM were determined and the hypothesis that natural hay/straw challenge (NC) induces divergent AM phenotypes in control horses and horses with SEA was tested. Macrophages from control horses were activated either with eIFNγ + lipolysaccharide (LPS) or eIL-4 to characterize M1- or M2-polarized AM gene expression, respectively and determine the response of polarized cells to pathogen-associated molecular patterns (PAMPS): LPS, zymosan, peptidoglycan and hay dust. Subsequently, gene expression was explored in AM of control horses and horses with SEA at pasture and after NC. M1 polarization increased expression of pro-inflammatory cytokines (TNFα, IL-8, IL-12p40), IL-10, and CD80. M2 polarization increased CD206 and down-regulated arginase-II and IL-10. Expression of pro-inflammatory cytokines and CD80 in response to PAMPS was further increased by M1 pre-polarization whereas M2 pre-polarization down-regulated expression of pro-inflammatory cytokines and IL-10 but increased CD206. In horses with SEA, AMs had elevated expression of IL-10 both at pasture and after NC, but only after NC in control horses. CD206 expression increased in both groups during NC. At pasture, stimulation by PAMPS augmented expression of IL-8 and IL-10 in horses with SEA compared to control horses. NC eliminated this difference by selectively increasing expression of IL-10 in control horses. A fundamental shift in the macrophage phenotype in SEA is supported by consistently elevated production of IL-10. A similar non-canonical phenotype develops temporarily in control horses upon NC suggesting that AMs in horses with SEA have lost the ability to respond dynamically to environmental cues.

Each year in the United States, nearly 500,000 infants a year are born prematurely. Babies born before 35 weeks gestation are often placed on ventilators and/or given supplemental oxygen. This increase in oxygen, while critical for survival, can cause long-term damage to lungs, retinas and brains. In particular, hyperoxia causes apoptosis in neurons and alters glial activity. Brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) are members of the neurotrophin family of proteins that function to promote the growth, differentiation and development of the nervous system. We hypothesized that hyperoxia can alter the regulation of these genes and by doing so adversely affect the development of the brain. We predicted that mice exposed to hyperoxic conditions would have differences in BDNF and GDNF mRNA expression and relative level of methylated promoter regions coinciding with differences in the relative levels of DNMT1 and DNMT3a mRNA expression. To test this hypothesis, newborn C57Bl/6 mice and their littermates were placed in hyperoxic or normoxic conditions from postnatal day 7 to 12. There were significant decreases in BDNF mRNA expression in the prefrontal cortex following hyperoxia, but a significant increase in the isocortex. GDNF mRNA expression was significantly increased in both the isocortex and prefrontal cortex following hyperoxia. DNMT1 mRNA expression was significantly decreased in the isocortex but significantly increased in the prefrontal following hyperoxia. Together these data suggest that short-term exposure to hyperoxic conditions can affect the regulation and expression of BDNF and GDNF potentially leading to alterations in neural development.

When tiling three gratings, with each individually exhibiting astigmatism and power due to holographic errors and coating stress, the resulting wavefront aberrations contain high-frequency components as well as the fundamental frequency, which is nearly three cycles across the aperture in the tiling direction. A deformable mirror (DM) that was designed to compensate for much slower errors (e.g., those arising from distortion in amplifier disks) is being used to compensate for this tiling-induced error. This investigation studies the effectiveness of compensating only the fundamental frequency of the tiled aberration, and shows that this provides a significant improvement that is adequate for a range of expected aberrations. Limitations of the DM correction technique are also studied.

Previous work in rhesus monkeys has shown that both acute or chronic subcutaneous (s.c.) administration of insulin-like growth factor (IGF)-I elevates serum concentrations of IGF binding protein (IGFBP)-3. In order to determine whether an analog of IGF-I, which has a reduced affinity for the IGFBPs, has similar effects, a series of studies using adolescent female rhesus monkeys were conducted. In the first study, an s.c. injection of IGF-I (110 mg/kg; n = 6) significantly elevated serum IGFBP-3 concentrations through 7 h following treatment. In contrast, serum IGFBP-3 decreased throughout the day following an injection of Long R 3 IGF-I (110 mg/kg, s.c., n = 5). However, this decrease was not due to the analog treatment as serum IGFBP-3 also declined in a similar fashion in untreated females ( n = 5) sampled on the same schedule. Serum GH levels were acutely suppressed by both IGFs but were not altered in untreated females. In the second study, serum IGFBP-3 were compared between untreated control females ( n = 6) and females treated continuously by s.c. infusion with either Long R 3 IGF-I (120 mg/kg/day, s.c.; n = 5) or IGF-I (120 mg/kg/day, s.c.; n = 5) or IGF-I s.c.; n = 4). Serum IGFBP-3 was consistently elevated by IGF-I infusion, whereas levels in analog-treated monkeys were similar to those in control females. Although acute or chronic administration of Long R 3 IGF-I did not elevate serum IGFBP-3, chronic administration of the analog did not block the acute facilitating effects of IGF-I on serum IGFBP-3. The increase in serum IGFBP-3 following an acute injection of IGF-I (110 mg/kg, s.c.) was not significantly different between untreated females and females receiving a constant s.c. infusion of Long R 3 IGF-I. These data indicate either acutely or chronically administered IGF-I but not its analog Long R 3 IGF-I can elevate serum concentrations of IGFBP-3. Although the analog fails to increase serum IGFBP-3, it does not block the facilitating effects of IGF-I on concentrations of this IGFBP. Taken together, these data suggest that the increase in serum IGFBP-3 by exogenous IGF-I may not be a receptor mediated event but may be the result of IGF-I binding to IGFBP-3 and forming the binary and ternary complex, slowing IGFBP-3 degradation.

Two studies were conducted to assess the potential for adverse physiologic and genotoxic effects of long-term fluoride ingestion in adults residing in three communities with varying water fluoride levels (0.2 ppm, 1.0 ppm, and 4.0 ppm). All were long-time (≥30 years) residents of their respective communities. Plasma and urine samples were collected for fluoride analyses. Additional plasma was collected to determine blood chemistry, and plasma lymphocytes were examined to determine the frequency of sister chromatid exchange. Significant differences in urine (P = 0.001) and plasma (P = 0.0001) fluoride levels were found in the three communities. Seven of the blood parameters were statistically different among the communities, although all were within the defined normal range of the pathology laboratory. Sister chromatid exchange frequency was statistically higher in the 4.0 ppm fluoride community ascompared to the other communities. Because of the higher SCE frequency in the 4.0 ppm fluoride community, a second study was performed to determine if the increased frequency was potentially related to the fluoride level of the communal water supply. Of the 58 adults recruited; 30 had used city water and 28 had used well water (≤0.3 ppm fluoride) as their principal water source for 30 years. Data analyses showed that the sister chromatid exchange frequency did not differ between the groups, indicating that the increased sister chromatid exchange frequency was not related to the fluoride level of the communal water. The investigation provided evidence that the long-term ingestion of water containing 4.0 ppm fluoride did not have any clinically important physiologic or genotoxic effects in healthy adults. Environ. Mol. Mutagen. 29:265-271, 1997 © 1997 Wiley-Liss, Inc.

The intercondylar fossa is believed to play an important role in the pathology of cranial cruciate ligament rupture and therefore has received considerable attention in the last decade. Accurate radiographic imaging of the intercondylar fossa requires that the central x-ray beam pass through the center of the intercondylar “tunnel”. The anatomy of the canine intercondylar fossa is similar to humans, however, the orientations of the intercondylar fossa's differ. Consequently, the positioning techniques described for humans are not appropriate for the dog. To pass through the center of the dog, intercondylar fossa, the central x-ray beam should be 12° (S.D. 1.7°) caudal from the femoral diaphysis in the sagittal plane and obliqued caudolateral to craniomedial 7° (S.D. 0.60°) (caudo78°proximo7° lateralcraniodistomedial oblique). Cross table positioning was used with the hip flexed and the radiograph cassette placed on the cranial surface of the stifle. However, superimposition of the tuber ischii and soft tissues caudal to the femur made 15° to 20° the best angle obtainable. There was not a significant difference (p = 0.17) in the notch width index between a 12° versus 20° angle of the central x-ray beam caudal to the femoral diaphysis, both with 7° of external rotation of the stifle. The notch width index of 0.252 obtained from radiographic measurements was not significantly different from measurements obtained grossly of 0.254 (n = 26; p = 0.69). Failure to oblique the central x-ray beam caused a significant (p = 0.0008) decrease in the apparent fossa width radiographically.

A prototype thin superconducting solenoid magnet has been developed to verify technical feasibility of an advanced thin superconducting solenoid magnet with a magnetic field of 2 T in a cylindrical volume of 3.4 m /spl phi//spl times/9 m and with a transparency of 1.2 radiation length (Xo). The magnet is required to have a stored energy/effective cold mass (E/M) ratio of 7.5 kJ/kg. The technical goal has been successfully achieved with realizing E/M=9.6 kJ/kg as a result of the prototype R&D. The prototype development and test results are presented. >

This study was conducted to test the hypothesis that physiological changes which occur during aging increase the biological impact of fluoride and reduce the threshold of safe fluoride exposure. Four groups of rats were fed a low-fluoride diet (< 1.2 ppm) ad libitum and received 0, 5,15, or 50 ppm fluoride in their drinking water. Animals were killed after three, six, 12, or 18 months of treatment. Blood and urine were monitored for biochemical markers of tissue function, and plasma, urine, feces, and representative tissues were analyzed for fluoride. In addition, bone marrow cells from animals killed after 18 months of treatment were examined for frequency of sister chromatid exchange (SCE), a marker of genetic damage. Study results indicated that, within treatment groups, fluoride intake, excretion, and retention did not change significantly between three and 18 months. Fluoride concentration in soft tissues did not change with treatment duration in the fluoride-treated animals. Mineralized tissue fluoride concentration and the total fluoride in the carcasses increased continually as the animals aged. In spite of significant, dose-related differences in tissue fluoride levels which occurred in all age groups in this study, there were no indications that increased fluoride in the tissues caused any adverse physiological or genotoxic effects. None of the monitored clinical "wellness" markers of tissue integrity and function was altered by fluoride in a clinically significant manner. Therefore, there was no evidence from this study that aging reduces the threshold of safe chronic fluoride exposure.

Adolescent growth is regulated by developmental increases in growth hormone (GH) secretion. Although the hypothalamic release of GH-releasing hormone (GHRH) stimulates and the release of SRIF inhibits GH secretion, it is not known how these regulatory mechanisms change developmentally. In addition, GH secretion is facilitated during maturation by increases in peripheral estradiol and may be inhibited, via a negative feedback mechanism, by insulin-like growth factor-I (IGF-I). It is not clear whether these act through the hypothalamic regulation of GHRH and somatostatin (SRIF). In order to further understand the regulation of GH secretion during development, the present study determined how estradiol and IGF-I altered SRIF mRNA in the hypothalamus in immature female rats. The working hypotheses were that estradiol would decrease SRIF mRNA accounting, in part, for its positive effect on GH release and IGF-I would increase SRIF mRNA representing a negative feedback mechanism regulating GH secretion. Preprosomatostatin (ppSRIF) mRNA levels within the periventricular nucleus (PeVN) were measured with in situ hybridization in ovariectomized female rat pups (n = 5 per group). Infusions were delivered sc via either a Silastic capsule (oil, 10 or 60 μg/ml estradiol) or an osmotic minipump (acetic acid, 120 or 240 μg IGF-I/day). Following ovariectomy on Day 21, animals were treated for either 1 or 7 days beginning on Day 24 of age. A total of 18 treatment groups were evaluated, including control, estradiol alone, IGF-I alone, and estradiol and IGF-I combined at both doses and treatment durations. Quantification of the area, density, and integrated density for ppSRIF mRNA within the PeVN revealed that treatments for only 1 day had no effect on the expression of ppSRIF mRNA, while those lasting 7 days significantly altered ppSRIF mRNA grain area and density. Both estradiol and IGF-I treatment at either dose significantly lowered ppSRIF mRNA and the decrease was exacerbated when estradiol and IGF-I were given in combination at either dose. Serum levels of rGH were not affected by any treatment. These data are consistent with the hypothesis that estradiol facilitates GH secretion during development, in part, by diminishing the inhibitory tone of SRIF via a decrease in ppSRIF mRNA. These data also suggest that any negative feedback action of peripheral increase in IGF-I on GH secretion is not mediated through regulation of SRIF mRNA in prepubertal rats.

Wilson disease (WND) is an autosomal recessive condition that results in accumulation of copper in the liver and brain when a membrane bound copper transporter, ATP7B, is defective. ATP7B is expressed in hepatic, brain and kidney cells, and a defect can lead to liver, neurological and renal damage in WND patients. Presentation is variable with a broad range of age of onset and symptoms, and not all biochemical signs used in diagnosis are found in every patient. Therefore, diagnosis by mutation analysis is particularly important. To date, there are approximately 380 probable disease-causing variants in ATP7B, 33 of which are splice site variants that are predicted to affect splicing, based on their location. Few of these splice site variants have been analyzed in vivo. Some exonic variations also have the potential to affect splicing. The aim of this project was to use minigenes for transcript analysis. We have chosen exon 8 as our focus and have cloned a wild-type three-exon minigene into a mammalian expression vector. After transfection, extracted RNA was analyzed by reverse transcription PCR and accurate splicing was detected. This minigene will facilitate the analysis of the numerous potential splice variants identified in exon 8 of ATP7B, with the advantage that patient cell lines are not required for each variant.

Summary A questionnaire sent to 109 anaesthetists in the South West Region has revealed that there is a problem with dissemination of information relating to hazards with equipment. Thirty-four per cent of consultants, and 67% of junior anaesthetists were only slightly or not at all confident that they see the Hazard Notices and Safety Action Bulletins relating to the equipment they use. The study has also demonstrated the large amount of new equipment coming into circulation and has highlighted deficiencies in the reading of equipment manuals. Some suggestions are made as to how the current system may be improved.

Ingested fluoride is incorporated into bone apatite and can affect the structural integrity of bone. Fluoride absorption in the gut and incorporation into bone is affected by the presence of other ions, including calcium. We hypothesized that a low calcium phosphate diet combined with high fluoride intake would have independent detrimental effects on vertebral bone strength. We measured the vertebral biomechanical properties and bone histology for rats given controlled diets with varied fluoride and calcium phosphate intakes for either 16 or 48 weeks. Diets were designed to produce mild calcium deficiency while keeping Ca:P ratio constant. Hence calcium deficiency was accompanied by a proportional phosphate deficiency. Calcium phosphate deficiency (25% of normal) significantly diminished vertebral strength only in younger rats. As the rats grew older, the effects of calcium phosphate deficiency were mitigated. Calcium phosphate deficiency reduced vertebral strength in young rats primarily by reducing the trabecular bone volume. The highest fluoride intake (50 mg/L) significantly diminished vertebral strength, but there was no effect of lower fluoride intakes on bone strength. In contrast to calcium phosphate deficiency, high fluoride intake had no effect on trabecular bone volume but instead increased the amount of unmineralized osteoid, particularly in older rats. This impairment of mineralization by fluoride appeared to be the primary cause of the diminished vertebral strength. The detrimental effects of fluoride on vertebral bone strength were not amplified by calcium phosphate deficiency.

Irreversible damage caused by cold shock has been assumed to occur when boar semen is exposed to temperatures below 15 degrees C. Identification of the lower critical temperature at which extended boar semen undergoes cold shock, however, has yet to be defined. The aims of this study were to 1) identify the cold-shock critical temperature and time on extended boar semen as assessed by sperm motility and morphology, and 2) determine the effects on fertility of using extended porcine semen exposed to this critical temperature and time. For Objective 1, ejaculates from 18 boars were collected, analyzed and extended in Androhep to 50 x 10(6) sperm/mL. Doses (4 x 10(9) sperm) from each ejaculate were exposed to 5 storage temperatures (8, 10, 12, 14 and 17 degrees C). Sperm motility and morphology (including acrosomes) were assessed following collection and at 12-h intervals for 48-h. Decreases in sperm motility occurred within the first 12-h at all temperatures. Sample motility dropped below 70% within 12-h in the 8 degrees C group and by 48-h in the 10 degrees C group. Sample motility was > 75% in the 12, 14 and 17 degrees C (control) groups throughout the trial. The percentage of morphologically abnormal sperm cells, including acrosomes, did not change within or between treatment groups over the 48-h storage period. In Objective 2, boar ejaculates (n = 9) were handled as in the first objective and were equally divided into treated (12 degrees C for < or = 60-h) and control (17 degrees C for < or = 60-h) groups. Using a timed, double insemination technique, 135 sows were bred by AI using either 12 degrees C (n = 74) or 17 degrees C (n = 61) extended, stored semen. No differences were observed in the farrowing rate (93 vs 95%), total offspring born (11.58 vs 11.61) or number live born (10.68 vs 10.63) between 12 and 17 degrees C groups, respectively. The results demonstrate that acceptable fertility can be obtained with Androhep extended boar semen exposed to temperatures as low as 12 degrees C for up to 60-h, and that cold shock appears to occur in vitro when extended boar semen is exposed to storage temperatures below 12 degrees C.

On the basis of observations that endemic fluorosis occurs more often in malnourished populations, a series of studies tested the hypothesis that deficient dietary intake of calcium, protein or energy affects fluoride metabolism so that the margin of safe fluoride exposure may be reduced. The objective of the investigation was to determine whether changes in fluoride metabolism in nutritionally deficient rats resulted in manifestation of any extraskeletal toxic fluoride effects not observed in healthy animals. This investigation included two studies, one that monitored the effect of calcium deficiency on the effects of chronic fluoride exposure, and a second study that observed fluoride effects in rats that were deficient either in protein or in energy and total nutrient intake. Control and experimental rats received drinking water containing 0, 0.26 (5), 0.79 (15) or 2.63 (50) mmol fluoride/L (mg/L) for 16 or 48 wk. Control rats were fed optimal diets and experimental rats were fed diets deficient in calcium (Study 1) or protein (Study 2). An additional group of experimental rats (Study 2) was provided with a restricted amount of diet; thus these rats were deficient in energy and total nutrient intake. The intake, excretion and retention of fluoride were monitored; after the rats were killed, tissue fluoride levels and biochemical markers of tissue function were analyzed. Bone marrow cells were harvested from some of the rats, after 48 wk of treatment, for determining the frequency of sister chromatid exchange, a marker of genetic damage. Although there were significant differences among fluoride treatment groups in fluoride excretion and retention that resulted in significantly greater fluoride levels in tissues of the experimental rats, we were unable to detect any harmful, extraskeletal biochemical, physiologic or genetic effects of fluoride in the nutritionally deficient rats.

This study was conducted to test the hypothesis that the margin of safe fluoride exposure is narrowed in rats that are physiologically compromised by renal dysfunction. The study objective was to determine whether increases in fluoride retention and tissue fluoride levels in rats with surgically induced renal insufficiency result in toxic fluoride effects not ordinarily observed in healthy animals. Uremic and sham-operated control rats received 0 µg/ml, 5 (0.26 mmol/l), 15 (0.79), or 50 µg/ml (2.63 mmol/l) of fluoride in their drinking water for 3 or 6 months. Fluoride retention was monitored, and, following euthanasia, tissue fluoride and biochemical markers of tissue function were analyzed. Selected tissues were saved for histology, and bone marrow cells were harvested for determining the frequency of sister chromatid exchange, a marker of genetic damage. In spite of significantly higher levels of fluoride in the tissues of the animals with renal insufficiency, there were no clinically adverse, fluoride-induced, extraskeletal physiological, biochemical, or genetic effects of chronic exposure to common levels of fluoride in these rats.

This study is part of a comprehensive programme to investigate fluoride toxicity and the hypothesis that fluoride ingested by "medically compromised' animals will result in altered physiological function. Its objectives were to monitor fluoride retention, tissue fluoride concentrations and genetic variables in diabetic and control rats chronically exposed to fluoride, and to determine whether or not adverse effects occurred. Male, Zucker fatty diabetic rats and Zucker age-matched lean controls were fed a low-fluoride diet ( < 1.2 parts/10(6) F-) ad libitum and received 0, 5, 15 or 50 parts/10(6) fluoride in their drinking water for 3 or 6 months. Fluoride metabolic balance was determined for 4 days before the end of each study phase. Plasma and urine were analysed for biochemical markers of tissue function, and plasma, urine, faeces and tissues were analysed for fluoride. Bone marrow cells from animals killed after 6 months of treatment were examined for frequency of sister chromatid exchange, a marker of genetic damage. The diabetic rats consumed, excreted and retained significantly greater amounts of fluoride than the controls (p < 0.05). There were dose-related increases in fluoride excretion, retention and tissue concentrations in both classes of animals, which were significantly greater in the diabetic rats. In spite of greater amounts of fluoride in the tissues of diabetic animals, there was no evidence, under these experimental conditions, that any of the fluoride exposures tested caused measurable adverse effects on the physiological, biochemical or genetic variables that were monitored.

The conditions for emergency tracheal intubation of patients with cervical spine injury were simulated in 157 patients during induction of anaesthesia for routine surgery. The view of the larynx obtained during laryngoscopy with the head in the optimum intubating position was compared with that obtained when manual in-line stabilisation of the cervical spine and cricoid pressure were used. During laryngoscopy with cervical stabilisation, the view of the larynx was reduced in 45% of patients, and in 22% of patients nothing was visible beyond the epiglottis. To assess the ease of intubation with the neck stabilised and with cricoid pressure applied, patients were randomised to either direct visual intubation (n = 79), or intubation aided by a gum elastic bougie (n = 78). The median time taken for visual intubation was 20 s, but in six patients intubation took over 45 s. In addition, five patients in this group could not be directly intubated. Using the gum elastic bougie all patients, including the failures from the visual group, were intubated within 45 s (median 25 s). We recommend the gum elastic bougie as an aid to intubating the patient with suspected cervical spine injury, particularly when the glottis is not immediately visible.

A simple graphical method is described that allows the assessment of a student's progress while learning intravenous cannulation and tracheal intubation. Thirty-four students were studied during their initial training; 91% of those students who obtained a sufficient number of trials to allow a final assessment to be made met the criterion of 80% success for cannulation and 95% achieved similar success in intubation. Thirty-one ambulance staff who returned for a 3-day refresher course were also assessed; 44% (for intravenous cannulation) and 61% (for tracheal intubation) met the 80% success criterion.

Eikenella corrodens is a facultatively anaerobic Gram-negative bacterium which is among the predominant cultivable microflora of periodontal lesions characterized by loss of attachment level. In the present study, we examined the potential role of complement-mediated killing in host defense against this periodontopathic organism. Seven clinical isolates obtained from human subgingival plaque and one reference strain of E. corrodens were characterized with respect to (a) susceptibility to the bactericidal properties of pooled human serum and (b) the role of the classical and/or alternative pathway(s) of complement in effecting killing of sensitive strains. Six strains, including the reference strain, were found to be variably serum-sensitive, exhibiting 1-12.5% survival after two hr of incubation in the presence of 20% pooled human serum. The remaining two isolates were serum-resistant. Both serum-resistant and serum-sensitive strains consumed complement via the classical pathway in normal but not in hypogammaglobulinemic serum, thus ruling out an antibody-independent mechanism of classical pathway activation. Four of six serum-sensitive strains exhibited little or no loss of viability following incubation with serum depleted of the classical pathway component Clq. One strain which was resistant to killing by normal human serum was, nevertheless, highly susceptible to complement-mediated killing in the presence of rabbit immune serum. Two additional serum-sensitive strains were killed, albeit to a lesser extent, in Clq-depleted serum, indicative of a role of the alternative pathway in killing of some serum-sensitive strains. These results indicate a potential role for complement-mediated killing in host defense against Gram-negative periodontal bacteria such as E. corrodens. However, the ultimate contribution of this immune defense mechanism may be defined, at least in part, by the presence of a humoral response to key bacterial membrane constituents.

The diurnal lemurs Propithecus verreauxi verreauxi and Lemur catta at Berenty in southern Madagascar, have been studied for the last 30 years. The August 1981 census indicates that the population size of L. catta remains stable at 150 adults but that P. v. verreauxi troops have become fragmented and scattered and the population is apparently increasing. Eight different vegetation types were classified within the reserve and their influence on the distribution of L. catta and P. v. verreauxi investigated. Behavioural data obtained shows the niche separation between these two, potentially competitive, sympatric lemurs.

Effects of estradiol benzoate and prostaglandin F(2alpha) (PGF(2alpha)) on concentrations of progesterone and estrogen in serum and the percentage of live births were determined in 21 gilts treated with exogenous progesterone in late gestation. All gilts received progesterone (25mg s.c. four times daily) from Days 108 through 113 of gestation. Gilts receiving no other treatments (controls) had elevated levels of progesterone through 1800 h on Day 114 (29.2 +/- 11.4 ng/ml) and farrowed at 115.6 +/- 0.3 d of gestation with a relatively low percentage of live births (66.8 +/- 17.3). Gilts treated with PGF(2alpha) administered at 0600 h on Day 114 had less (P0.01) progesterone by 1800 h (7.0 +/- 1.3 ng/ml) relative to that of the controls, but they had similar gestation lengths (115.5 +/- 0.3) and percentages of live births (50.0 +/- 16.2). Administration of estradiol benzoate (10 mg) to gilts at 0600 h on Day 114 did not reduce progesterone on Day 114 or the gestation length relative to that of the control gilts, but it did increase (P0.05) the percentage of live births (100%).

The incidence of placental malaria at parturition and its effects on the conceptus have been investigated in The Gambia, West Africa. Malarious placentae occurred in 1300 (20.2%) of 6427 singleton births, in 32 (18.6%) of 172 sets of twins and in none of six sets of triplets. Plasmodium falciparum infections predominated; P. malariae or P. ovale infections were found in only nine instances. In the large group of single births placental malaria occurred less frequently (12.0%) in residents of urban than of other, more rural, communities (27.1%). In the former group incidence showed no clear change with season; in the latter group it was highest in the trimester following the end of the rains and lowest in the second half of the dry season. In both residential groups it was more frequent in primiparae (urban 16.1%; other 46.9%) than in multiparae (urban 8.9%; other 20.3%). The sex of the child did not influence malaria incidence. Dense placental infections were more frequent in primiparae. Stillbirth rates of singleton infants were significantly higher for males than for females, but no clear and consistent relationship between stillbirth and placental malaria was detected. Mean singleton birthweights were depressed by about 170 g in the presence of malaria; the deficits were statistically significant only among first born infants and tended to diminish progressively with increasing maternal parity. No distinct gradient linking birthweight with ascending density of placental parasitaemia was observed. Singleton birthweights of 2.5 kg or less occurred more frequently in association with malarious than non-malarious placentae and the association was more marked among first born than later birth rank infants. Differences between the weights of malarious and non-malarious placentae were small and not significant. The findings of the study are discussed in relation to the widely prevalent view that pregnancy exacerbates maternal malaria by attenuating acquired immunity.

The chemical composition of regenerating mouse liver was examined over a 28-day period subsequent to partial hepatectomy. The following chemical constituents were measured: lipides (including phospholipide, neutral fat, and total cholesterol); moisture; nitrogen (total and protein); phosphorus compounds (with special reference to DNA and PNA); and the enzymes, succinoxidase, liver esterase, and acid and alkaline phosphomonoesterases. For purposes of achieving maximum evaluation, the results were computed in most instances on the basis of total regenerated liver, nuclear counts, and nitrogen. All measured chemical constituents were restored to normal or nearly normal levels within the investigated time intervals. A persistent incomplete restoration of cell numbers was found to be a characteristic feature of the regenerated organ, resulting in the presence of a smaller number of cells containing correspondingly greater amounts of chemical constituents.

Publisher Summary This chapter discusses the number of characteristics in the fields of automation and control engineering which are slowly being rectified. Consideration of the new concepts and evaluation of human factors in industry still tended to come too late in the planning process. There was insufficient dialog and inadequate cooperation between control engineers and social scientists about human affairs in general, and about the needs and potential contributions of employees of all kinds. The significance of inadequate skill level in operative jobs to provide for those who wished it a degree of challenge and of the job satisfaction associated with this. A first consideration in the humanization of work was the provision of the opportunity to earn and work for this purpose.

Summary Reports of anaesthetic misadventures were regularly collected in the Anaesthetic Department of a district general hospital, to identify recurring problems. Eighty-one misadventures, none of which had serious outcome, were reported during a 6-month period, in which 8312 anaesthetics were administered. Human error was more frequently responsible than equipment failure, and failure to perform a normal check was the factor most frequently associated. Local hazard warnings were circulated when necessary to members of the Department, and the reports formed the basis of departmental discussion and teaching.

Summary Anaesthetists lacking special paediatric experience were asked to calculate the dose of some anaesthetic drugs for children of various weights and ages. Using their own routine method of calculation the doses varied considerably. A nomogram resulted in quicker and more accurate predictions.

Five kinds of malarial antigens were characterized in extracts of infected human placental blood. Their storage properties were investigated. L-antigens were labile to heating at 55°C and La1-antigens could be selectively destroyed in this way. In contrast, S-antigens and some normal serum glycoproteins remained in solution after boiling. The antigenicity, electrophoretic mobility and microheterogeneity of boiled S-antigens was intact. The various antigens were poorly separated on Sephadex G—200 but one was separated from the others by DEAE cellulose chromatography. La1-antigen appeared to aggregate under conditions of low ionic strength and was fractionated by differential ultra-centrifugation.

Stereotaxic lesions made in the MGB lead to the finding of Nauta-stained degeneration in the anterior, middle and posterior ectosylvian gyri, i.e., areas AI, AII, Ea, Ep, SF and I-T. Degeneration was not found in SII except in 2 brains in which the ventrobasal complex was probably involved in the lesion. There was no significant projection from the MGB to the marginal gyrus, suprasylvian gyrus or precuciate gyrus. Small lesions in MGB produced continous distributions of cortical degeneration, and no evidence was found for multiple discrete projections. There was some indication that the more rostral parts of MGB project more rostrally on the ectosylvian gyrus. The more medial lesions in the MGB affecting the magnocellular nucleus caused a spread of degeneration further towards the temporal pole and insulotemporal area than the more lateral lesions.

Summary The distribution of the terminals of the corpus callosum within the visual areas of the rabbit were studied by removing the occipital cortex on one side and looking for Nauta degeneration in the other hemisphere. The degeneration was found as a narrow band running rostrocaudally over the occipital cortex. In other rabbits an electrophysiological map of the visual field was produced by recording, with tungsten electrodes, the response to a small flash of light. The map consisted of 2 visual area I medial to visual area II. When these maps of the visual field were compared with the distribution of the callosal degeneration, it was found that the band of degeneration coincided with the junction between the 2 visual areas. The significance of these results is discussed.