Identification and quantification of factors affecting neonatal immunological transfer in dairy calves in the UK.

The object of the study was to quantify the prevalence of failure of passive transfer in UK dairy farms and to identify variables that had a significant impact on the rate of immunological transfer. In a six-month study of 444 calvings from seven UK dairy farms, 26 per cent of calves failed to receive adequate immunoglobulin transfer as judged by a plasma total protein (pTP) concentration less than 5.6 g/dl. Colostrum immunoglobulin concentration, indirectly measured using Brix refractometry, showed wide variations with samples ranging from 10.3 to 34.7 Brix units. Thirty-seven per cent of samples were below the suggested cut-off Brix score for colostrum quality of 22 per cent. Potential associations between covariates and plasma protein concentration were investigated using multiple linear regression models. The covariate with the greatest impact on the pTP concentration was the farm on which the calf was born (P<0.05). A significant but small association was demonstrated between colostrum immunoglobulin concentration and calf pTP concentration (P<0.01). Multiple linear regression models suggested that the time of colostrum collection after calving, parity of the dam, and the individual farm were associated with the Brix measurements (P<0.05). This study suggested that veterinary review of colostrum protocols on farm with emphasis on prompt collection and dosing after calving remains a simple and effective measure to improve passive transfer and thus calf health on UK dairy farms.

Kisspeptin, c-Fos and CRFR type 2 co-expression in the hypothalamus after insulin-induced hypoglycaemia.

Normal reproductive function is dependent upon availability of glucose and insulin-induced hypoglycaemia is a metabolic stressor known to disrupt the ovine oestrous cycle. We have recently shown that IIH has the ability to delay the LH surge of intact ewes. In the present study, we examined brain tissue to determine: (i) which hypothalamic regions are activated with respect to IIH and (ii) the effect of IIH on kisspeptin cell activation and CRFR type 2 immunoreactivity, all of which may be involved in disruptive mechanisms. Follicular phases were synchronized with progesterone vaginal pessaries and at 28 h after progesterone withdrawal (PW), animals received saline (n = 6) or insulin (4 IU/kg; n = 5) and were subsequently killed at 31 h after PW (i.e., 3 h after insulin administration). Peripheral hormone concentrations were evaluated, and hypothalamic sections were immunostained for either kisspeptin and c-Fos (a marker of neuronal activation) or CRFR type 2. Within 3 h of treatment, cortisol concentrations had increased whereas plasma oestradiol concentrations decreased in peripheral plasma (p < 0.05 for both). In the arcuate nucleus (ARC), insulin-treated ewes had an increased expression of c-Fos. Furthermore, the percentage of kisspeptin cells co-expressing c-Fos increased in the ARC (from 11 to 51%; p < 0.05), but there was no change in the medial pre-optic area (mPOA; 14 vs 19%). CRFR type 2 expression in the lower part of the ARC and the median eminence was not altered by insulin treatment. Thus, disruption of the LH surge after IIH in the follicular phase is not associated with decreased kisspeptin cell activation or an increase in CRFR type 2 in the ARC but may involve other cell types located in the ARC nucleus which are activated in response to IIH.

Neuronal responses in the brainstem and hypothalamic nuclei following insulin treatment during the late follicular phase in the ewe.

The aim of this study was to determine the neuronal responses following insulin administration during the late follicular phase. Intact ewes were given either saline or insulin (5 IU/kg, i.v.) at 35 h after progesterone withdrawal and killed 3 h later. There was a marked increase in the number of Fos-positive noradrenergic neurones in the caudal brainstem of insulin-treated ewes. In the hypothalamic paraventricular nucleus, insulin treatment increased the presence of Fos-positive corticotrophin-releasing hormone neurones (from 2% to 98%) and Fos-positive arginine vasopressin parvocellular neurones (from 2% to 46%). Interestingly, after insulin treatment, despite a general increase in Fos-positive neurones in the arcuate nucleus (ARC), there was a marked reduction (from 47% to 1%) in Fos-positive ß-endorphin neurones. Similarly, colocalized Fos and oestradiol receptor (ER) α-positive neurones decreased in the ARC after insulin (from 7% to 3%). Conversely, in the ventromedial nucleus, ERα-positive neurones with Fos increased (from 7% to 22%) alongside a general increase in Fos-positive neurones. Overall, a complex system of neurones in brainstem and hypothalamus is activated following insulin administration during the late follicular phase.

Integration between different hypothalamic nuclei involved in stress and GnRH secretion in the ewe.

This study investigated possible integrated links in the neuroanatomical pathways through which the activity of neurones in the paraventricular nucleus and arcuate nucleus may modulate suppression of gonadotrophin-releasing hormone (GnRH) secretion during stressful situations. Double-label immunofluorescence and laser scanning confocal microscopy were used to examine the hypothalamic sections from the follicular phase ewes. Noradrenergic terminals were in close contact with 65.7 ± 6.1% corticotrophin-releasing hormone (CRH) and 84.6 ± 3.2% arginine vasopressin (AVP) cell bodies in the paraventricular nucleus but not with ß-endorphin cell bodies in the arcuate nucleus. Furthermore, γ-amino butyric acid (GABA) terminals were close to 80.9 ± 3.5% CRH but no AVP cell bodies in the paraventricular nucleus, as well as 60.8 ± 4.1%ß-endorphin cell bodies in the arcuate nucleus. Although CRH, AVP and ß-endorphin cell terminals were identified in the medial pre-optic area, no direct contacts with GnRH cell bodies were observed. Within the median eminence, abundant CRH but not AVP terminals were close to GnRH cell terminals in the external zone; whereas, ß-endorphin cells and terminals were in the internal zone. In conclusion, neuroanatomical evidence is provided for the ewe supporting the hypothesis that brainstem noradrenergic and hypothalamic GABA neurones are important in modulating the activity of CRH and AVP neurones in the paraventricular nucleus, as well as ß-endorphin neurones in the arcuate nucleus. These paraventricular and arcuate neurones may also involve interneurones to influence GnRH cell bodies in medial pre-optic area, whereas the median eminence may provide a major site for direct modulation of GnRH release by CRH terminals.

Noradrenergic control of GnRH release from the ewe hypothalamus in vitro: sensitivity to oestradiol.

The present study investigates the influence of alpha(1)-adrenoreceptors in GnRH release in vitro and determines whether oestradiol modulates alpha(1)-adrenoreceptor-GnRH interaction. Within 10 min after ewe sacrifice, saggital midline hypothalamic slices were dissected, placed in oxygenated Minimum Essential Media-alpha (MEM-alpha) at 4 degrees C and within 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 0.15 ml/min), either with or without oestradiol (24 pg/ml). After 4-h equilibration, 10-min fractions were collected for 4 h interposed with a 10-min exposure at 60 min to specific alpha(1)-adrenoreceptor agonist (methoxamine) or antagonist (thymoxamine) at various doses (0.1-10 mm). The alpha(1)-adrenoreceptor agonist (10 mm) increased (p < 0.05) GnRH release at 90 min both in presence and absence of oestradiol. However, in presence of oestradiol, alpha(1)-adrenoreceptor agonist (10 mm)-induced GnRH release remained elevated (p < 0.05) for at least 60 min. The bioactivity of the released GnRH was studied using a hypothalamus-pituitary sequential double-chamber perifusion. Only after exposure of hypothalamic slices to alpha(1)-adrenoreceptor agonist (10 mm), did the hypothalamic eluate stimulate LH release from pituitary fragments (n = 9, 7.8 +/- 12.3-36.2 +/- 21.6 ng/ml) confirming that the alpha(1)-adrenoreceptor agonist stimulated release of biologically active GnRH. In summary, GnRH release from the hypothalamus is under stimulatory noradrenergic control and this is potentiated in the presence of oestradiol.

GABA control of GnRH release from the ewe hypothalamus in vitro: sensitivity to oestradiol.

The present study examines the involvement of GABA(A or B) receptors in gonadotrophin-releasing hormone (GnRH) release in vitro and determines whether oestradiol modulates gamma-aminobutyric acid (GABA)-GnRH interaction. Within 10 min after ewe killing, hypothalamic slices were dissected and placed in oxygenated Minimum Essential Media (MEM)-alpha at 4 degrees C; within 2 h, slices were singly perifused at 37 degrees C with oxygenated MEM-alpha (0.15 ml/min), with or without oestradiol (24 pg/ml). After 4 h equilibration, fractions were collected for 4 h interposed with a 10 min exposure to specific GABA(A or B) receptor ligands (0.1-10 mM). The GABA(A or B) agonists (muscimol or baclofen) did not greatly influence GnRH release. However, GnRH increased (p < 0.05) after exposure to 10 mM GABA(A or B) antagonists (bicuculline or CGP52432, respectively). The GABA(A) antagonist stimulated greater sustained GnRH release (p < 0.05) in the absence of oestradiol than in its presence. The bioactivity of the released GnRH was studied using a hypothalamus-pituitary sequential double-chamber perifusion. Only after exposure of hypothalamic slices to the GABA(A) antagonist, did the hypothalamic eluate stimulate luteinizing hormone release from pituitary fragments (p < 0.05) confirming that the GABA(A) antagonist stimulated release of biologically active GnRH. In summary, GnRH release from the hypothalamus is predominantly under GABA(A) receptor inhibitory control and this is attenuated in the presence of oestradiol.

Noradrenergic control of arginine vasopressin release from the ewe hypothalamus in vitro: sensitivity to oestradiol.

The present study aims at ascertaining the influence of alpha(1)-adrenoreceptors on arginine vasopressin (AVP) release in vitro and determine whether E(2) modulates the alpha(1)-adrenoreceptor and AVP interaction. Ten minutes after ewe killing, sagittal midline hypothalamic slices (from the anterior preoptic area to the mediobasal hypothalamus with the median eminence, 2 mm thick, 2 per sheep) were dissected, placed in oxygenated minimum essential media-alpha (MEM-alpha) at 4 degrees C and within 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 0.15 ml/min), either with or without E(2) (24 pg/ml). After 4 h equilibration, 10 min fractions were collected for 4 h interposed with 10 min exposure at 60 min to a specific alpha(1)-adrenoreceptor agonist or antagonist at various doses (0.1-10 mm). At the end of all perifusions, slices responded to KCl (100 mm) with AVP efflux (p < 0.05). Release of AVP was enhanced (p < 0.05) by the alpha(1)-adrenoreceptor agonist (methoxamine 10 mm; no E(2), n = 7 perifusion chambers: from 14.3 +/- 2.7 to 20.9 +/- 3.9, with E(2), n = 10: from 10.7 +/- 1.2 to 18.4 +/- 3.4 pg/ml) or the antagonist (thymoxamine 10 mm; no E(2), n = 5: from 9.5 +/- 3.1 to 30.4 +/- 6.0, with E(2), n = 10: from 10.8 +/- 0.9 to 39.1 +/- 6.3 pg/ml). With the agonist, the response occurred only at 80 min (p < 0.05) both in the presence and absence of E(2). Whereas, after the antagonist, values were higher (p < 0.05) throughout the post-treatment period (80-170 min) without E(2), but declined by 150 min in the presence of E(2). Furthermore, the response to the alpha(1)-adrenoreceptor antagonist was greater (p < 0.05; 90-140 min) than the agonist only in the presence of E(2). In conclusion, these results reveal direct alpha(1)-adrenoreceptor-mediated control of the hypothalamic AVP neuronal system which is modulated by E(2).

gamma-amino butyric acid control of arginine vasopressin release from the ewe hypothalamus in vitro: sensitivity to oestradiol.

The present study aims to ascertain the influence of gamma-amino butyric acid (GABA)(A or B) receptors on arginine vasopressin (AVP) release in vitro and determine whether E(2) modulates GABA-AVP interaction. Within 10 min of ewe killing, saggital midline hypothalamic slices (from the anterior preoptic area to the mediobasal hypothalamus along with the median eminence, 2-mm thick, two per ewe) were dissected, placed in oxygenated minimum essential media (MEM)-alpha at 4 degrees C and within 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 0.15 ml/min), either with or without E(2) (24 pg/ml). After 4-h equilibration, 10-min fractions were collected for 4 h interposed with a 10-min exposure at 60 min to a specific GABA(A or B) receptor agonist or antagonist at various doses (0.1-10 mm). GABA(A) (muscimol; no E(2), n = 7 perifusion chambers, with E(2), n = 11) or GABA(B) (baclofen; no E(2), n = 8, with E(2), n = 15) agonists (10 mm) did not influence AVP concentrations. However, AVP release increased (p < 0.05) 20-30 min after exposure to 10 mm GABA(A or B) antagonists (bicuculline, no E(2), n = 7: from 4.6 +/- 0.7 to 33.0 +/- 0.4, with E(2), n = 17: from 11.9 +/- 1.4 to 32.8 +/- 6.0; CGP52432, with E(2), n = 14: from 14.0 +/- 2.6 to 28.8 +/- 3.9 pg/ml). At the end of the collection period, hypothalamic slices responded to KCl (100 mm) with AVP efflux (p < 0.05). GABA(B) but not GABA(A) antagonist-stimulated AVP release was enhanced in the presence of E(2). In summary, AVP release is under the inhibitory influence of GABA input with further potentiation by E(2) through GABA(B) receptors in vitro.

Oestradiol stimulates the release of AVP and GnRH from the ewe hypothalamus in vitro.

Oestradiol (E(2)) sensitizes the stress and reproductive axes in vivo. Our current aim is to investigate whether E(2) directly influences hypothalamic AVP and GnRH release in vitro. Within 10 min of ewe killing, saggital midline hypothalamic slices (from the anterior preoptic area to mediobasal hypothalamus, 2 mm thick, two per sheep) were dissected, placed in oxygenated MEM-alpha at 4 degrees C and within next 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 150 microl/min) alone (vehicle; n = 15), with low (6 pg/ml; n = 14) or high E(2) (24 pg/ml; n = 13). After 5 h equilibration, 10 min fractions were collected for 3 h with exposure to 100 mm KCl for 10 min within the last hour. Concentrations of AVP and GnRH were measured by RIA. Baselines for AVP and GnRH were 7.0 +/- 1.1 and 17.4 +/- 0.8 pg/ml respectively. Basal values with low E(2) were similar to vehicle for AVP (7.5 +/- 1.2 pg/ml) and GnRH (17.5 +/- 1.1 pg/ml). However, high E(2) increased basal AVP (11.7 +/- 1.4 pg/ml; p < 0.05) and GnRH (23.7 +/- 1.4 pg/ml; p < 0.05). After KCl, AVP and GnRH respectively, increased (p < 0.05) to 25.6 +/- 7.5 and 38.2 +/- 5.6 (vehicle), 26.3 +/- 7.5 and 23.6 +/- 2.1 (low E(2)) and 24.1 +/- 5.4 and 41.3 +/- 6.6 pg/ml (high E(2)). After KCl, maximum values of AVP occurred at 20 and GnRH at 30 min. In conclusion, high E(2) concentration augments AVP and GnRH release by direct action on the ewe hypothalamus.

Hormonal interactions within the hypothalamus and pituitary with respect to stress and reproduction in sheep.

Endocrine systems may be used as indicators of stress in two ways. The primary role of a hormone may be as part of the homeostatic response to a stimulus (e.g., adrenaline, corticosteroids). The amplitude of hormone response may correlate with the severity of the stimulus and any change indicate that the body is responding. Alternatively, a hormone may have a key role in normal body function (e.g., reproduction) and stress may deleteriously alter the hormone signal prevent normal function. This demonstrates that the stimulus was sufficiently severe that homeostatic mechanisms were unable to maintain normal function. Stress may effect reproduction by reducing both LH pulse amplitude and frequency. The LH surge may also be delayed. Several mechanisms may account for these effects both at the hypothalamus and pituitary. Corticosteroids have a broad, yet fundamental, role in homeostasis and have been used as primary indicators of stress for many years. Excess corticosteroid can be detrimental so the concentration is controlled via the hypothalamus-pituitary-adrenal (HPA) axis by multi-level feedback mechanisms. Under field and experimental conditions, after an initial large response prolonged stimulation leads to a gradually reducing plasma corticosteroid concentrations. This has been interpreted as a reduction in perceived stimulus severity or habituation to the stimulus and the animal deemed "less stressed" and its welfare "better." However, this reduction may be due to the intrinsic control mechanisms designed to prevent prolonged increases in corticosteroid concentrations. The stress signal at higher brain levels may still be present and the animal may still be experiencing the stimulus as aversive. Thus, the welfare interpretation of a corticosteroid concentration may differ during the time course of a stress response. A greater understanding of the mechanisms controlling corticosteroid secretion at each level of the HPA is required to determine what is the correct interpretation at any time point. To address these issues, we have used mathematical modelling to produce representations of possible control mechanisms at each level of the HPA. The starting point was to measure AVP and CRH concentrations in hypophysial portal blood and ACTH and cortisol concentrations in jugular blood in conscious sheep during 2h road transport (a cognitive stimulus). Modelling identified the signal inputs that were most likely to explain the secretion rate of each hormone. Modelling suggested that the reduction in AVP and CRH secretion observed during transport was most likely due to a reduction in stimulus input, with a significant contribution from cortisol negative feedback only on AVP secretion. At the pituitary level, ACTH secretion was stimulated more by AVP than by CRH (ratio 2.3:1) and there was also a stimulatory effect related to cortisol concentration at the time of sampling. However, the responses to both stimuli were curtailed by cortisol negative feedback and an inhibitory effect of prior CRH concentration. These are complex effects, but the modelling does suggest that while "stress" inputs may reduce over time hormone negative feedback is a major factor reducing hormone responses. When interpreting hormone data for animal welfare purposes, it is important not to interpret a reduction in hormone concentration due to intrinsic hormone control mechanisms as a reduction due to a decrease in the stress stimulus.

Nutrient intakes during pregnancy: the influence of smoking status and age.

STUDY OBJECTIVE: To examine the relation of antioxidant and other nutrient intakes in pregnancy to smoking and sociodemographic variables. DESIGN: Cohort study. SETTING: St Mary's Maternity Hospital, Portsmouth. PARTICIPANTS: Pregnant nulliparous women, with no existing complications of pregnancy, were recruited from antenatal booking clinics. A total of 774 women completed seven day food diaries, and supplied detailed data on their use of nutrient supplements. MAIN RESULTS: Smokers had lower intakes of most micronutrients. After adjustment for the confounding effects of maternal age, height, and education, only vitamin C and carotenoid intakes remained significantly depressed. Age was strongly and significantly associated with the intake of most nutrients, including antioxidants, and this association was independent of other maternal factors. Antioxidant intake was therefore lowest in young women who smoked: for example smokers under 24 years had a mean vitamin C intake of 57 mg (SD 35) compared with 106 mg (SD 52) for non-smokers aged 28 and over (difference 49 mg, 95% CI 39, 59). The corresponding intakes of carotenoid equivalents were 1335 micrograms (SD 982) and 2093 micrograms (SD 1283) (difference 758 micrograms, 95% CI 496, 1020). CONCLUSIONS: The study has identified, for the first time, young pregnant women as a group at particular risk of low micronutrient intake. The health implications of poor nutrition now need to be evaluated, particularly for those women who smoke.

A comparative transcription map of the murine bare patches (Bpa) and striated (Str) critical regions and human Xq28.

The X-linked developmental mouse mutations bare patches (Bpa) and striated (Str) may be homologous to human X-linked dominant chondrodysplasia punctata (CDPX2) and incontinentia pigmenti (IP2), respectively, based on their genetic mapping and clinical phenotypes. Bpa and Str have been localized to an overlapping critical region of 600 kb that demonstrates conserved gene order with loci in human Xq28 between DXS1104 and DXS52. As part of efforts to isolate the genes involved in these disorders, we have begun to develop a comparative transcription map spanning this region in both species. Using techniques of cross-species conservation and hybridization, exon trapping, and cDNA selection we have identified four known genes or members of gene families--caltractin, a member of the gamma-aminobutyric acid (GABAA) receptor gene family, a member of the melanoma antigen gene (MAGE) family, and several members of the murine-specific, X-linked lymphocyte regulated gene (Xlr3) family. Trapped exons and, in some cases, longer cDNAs have been isolated for potentially 7-9 additional genes. One cDNA demonstrates highly significant homology with members of the Krüppel family of zinc finger transcription factors. A second novel cDNA demonstrates homology at the 3' end of the predicted amino acid sequence to a LIM domain consensus. Gene order appears conserved among those cDNAs determined to be present in both human and mouse. Three of the murine transcripts appear to be present in multiple copies within the Bpa/Str critical region and could be associated with a predisposition to genomic rearrangements. Reverse transcriptase PCR (RT-PCR) and Northern analysis demonstrate that several of the transcripts are expressed in mid-gestation murine embryos and neonatal skin, making them candidates for the Bpa and Str mutations and their respective homologous human disorders.

Stress and reproduction in farm animals.

Transport of post-partum cows or sheep before an oestradiol-induced LH surge delayed gonadotrophin secretion possibly by affecting hypothalamic activity but not via an opioid mediated mechanism as the effect could not be reversed by naloxone. In addition, reduced LH responses to GnRH were observed in cattle during transport. In sheep, adrenocorticotrophic hormone (ACTH) also diminished the LH response to GnRH, but only when GnRH was administered 3 h after ACTH, not after 0.5 h. This finding suggests that very early suppression of LH secretion by stressors is not mediated by ACTH action at the pituitary but that immediate activation of the sympathetic nervous system may be involved. In ewes during the breeding season, repeated exposure to GnRH at intervals of 2 h during transport resulted in lower LH responses to the second and third injections. When anoestrous ewes were treated with oestradiol and GnRH while being restrained and isolated, the onset of the LH surge was delayed. The effects of hypothalamus-pituitary-adrenal hyperactivity on LH release may involve suppression of GnRH receptor activity, a reduction in releasable LH, or both factors. Studies in vitro with perifused ovine pituitaries showed that ACTH or corticotrophin releasing hormone markedly suppressed LH secretion in response to the second of two exposures to GnRH. This occurred with pituitaries obtained from anoestrous ewes irrespective of prior treatment with oestradiol, suggesting that compounds from the hypothalamus-pituitary-adrenal do not exert effects on the oestradiol-sensitizing mechanisms on the pituitary. In conclusion, stressors affect reproductive function via actions at the hypothalamus as well as impairing pituitary LH release induced by GnRH.

Intraoperative autotransfusion in vascular surgery.

To determine the impact of intraoperative autotransfusion on vascular surgical care, data related to 304 major vascular surgical operations performed over a 42-month period were retrospectively analyzed. Procedures included abdominal aortic aneurysmectomy (N = 152), aortobilateral femoral bypass (N = 60), thoracoabdominal aortic aneurysmectomy (N = 20), and other vascular procedures (N = 68). Fifty percent of the transfusion requirement was met by autotransfusion for the average patient. The per patient average volumes (liters) autotransfused were as follows: elective abdominal aortic aneurysmectomy, 0.87 L and nonelective, 1.45 L; elective aortobilateral femoral bypass, 0.63 L; elective thoracoabdominal aortic aneurysmectomy, 2.47 L, and nonelective, 2.15 L; and elective other, 0.53 L and nonelective, 1.30 L. Results of immediate postoperative and hospital discharge hemoglobin, hematocrit, and coagulation studies (prothrombin time, partial thromboplastin time, and platelets) did not differ from results of preoperative studies in any group. Neither mortality nor morbidity was related to intraoperative autotransfusion. These data suggest that intraoperative autotransfusion is a safe blood replacement method during major vascular surgical operations.

Behavioral effects of prenatal exposure to lidocaine in the rat: effects of dosage and of gestational age at administration.

Pregnant Long-Evans hooded rats were dosed via injections into the gum with 3, 6, or 9 mg/kg lidocaine, or vehicle, or were uninjected, on gestational day 4 (GD4), GD11, or GD18. Offspring (8-11 litters/group) were tested on a variety of tests of behavioral development and adult behavior. No effects of any dose at any time of administration were found upon maternal weight gain in gestation, litter size, or initial birth weight or weight gain of the pups. Administration at GD4 produced few effects; only footshock sensitivity showed a significant effect of dosing, although there were trends toward dosing effects on spontaneous alternation. For administration on GD11, lidocaine was associated with slight but significant alterations in sex ratios, and a trend toward drug effects on development of spontaneous alternation. Vehicle administration at this age reduced barbiturate sleep time in offspring and slightly altered footshock sensitivity. Lidocaine dosing on GD18 was associated with a number of significant alterations of behavior, including visual discrimination, shuttlebox avoidance, tail flick, and water maze errors; there were also both vehicle and lidocaine effects on water maze latencies. These data reinforce our previous report that lidocaine may be a behavioral teratogen, and suggest that administration in later gestation in the rat may alter a broader range of behaviors than earlier in gestation.

Behavioral correlates of soman-induced neuropathology: deficits in DRL acquisition.

Rats (N = 45) pretrained to lever press for milk reinforcement on a continuous reinforcement (CRF) schedule were injected with 100-110 micrograms/kg of the anticholinesterase soman (N = 24) or saline (N = 21) SC. Subjects exposed to soman experienced moderate to severe acute symptoms of anticholinesterase intoxication. After a 3 week recovery period, all surviving subjects were retrained on CRF, then given 45 training sessions on a differential reinforcement of low rates (DRL) 20 sec schedule, followed by 10 sessions of extinction. Brains of all subjects were then examined for evidence of neuropathology. Subjects exposed to soman showed no improvement over sessions in the number of reinforcements earned on the DRL schedule due to an inefficient patterning of responses. There were no differences between groups in the number of total DRL responses or terminal extinction responses. Neuropathology was most evident in dorsal thalamic areas, primary olfactory/piriform cortex and amygdala of subjects exposed to soman. There were significant correlations between the severity of acute intoxication scores, degree of neuropathology, and deficits in DRL performance. The results demonstrate that exposure to high doses of this anticholinesterase agent can result in neural damage and persistent decrements in performance of certain operant tasks.

New aspects on the chemistry of tea and coffee. III.

The previous review for 1983/1984 is now continued with references to recent publications (1984/1985) and as before covers the chemistry and technology of tea (leaf, green and black) and coffee (raw, roasted and instant soluble), with particular reference to composition and changes during manufacture, extraction and storage. The effects of composition on the quality of the beverage, with mention of particular physiological properties, are included (210 references).

New aspects on the chemistry of tea and coffee. A short review.

Recent publications (1982/1983) on the chemistry and technology of tea (leaf, green and black) and coffee (raw, roasted and instant), in particular with respect of their composition and changes during manufacture and storage, and the effects of composition on the quality of the beverages, are reviewed (101 references).

New assay of protective activity of Rocky Mountain spotted fever vaccines.

Areas under the fever curves of guinea pigs inoculated with Rocky Mountain spotted fever vaccine over a restricted dose range and infected with a standardized dose of Rickettsia rickettsii varied linearly with log10 dose of vaccine. A calculator was programmed to plot fever curves and calculate the vaccine dose that reduced the fever of infected animals by 50%.