Temporal relationship between the onset of oestrus, the preovulatory LH surge and ovulation in farmed fallow deer, Dama dama

A study was conducted to determine the timing of ovulation relative to the onset of oestrus and the preovulatory LH surge in fallow deer. Mature fallow does were randomly allocated to two treatments (N = 10 per treatment) designed to synchronize oestrus on or about 17 May. Does assigned to Group 1 (prostaglandin-induced oestrus) each initially received single intravaginal CIDR [Controlled Internal Drug Release] devices for 13 days followed by an i.m. injection of 750 mg cloprostenol on Day 12 (15 May) of the subsequent luteal cycle. Does assigned to Group 2 (progesterone-induced oestrus) each received CIDR devices for 13 days, with withdrawal occurring on 15 May. All does were run with crayon-harnessed bucks (10:1 ratio) from the start of synchronization (18:00 h 15 May). Ten does (5 per group) were blood sampled via indwelling jugular cannulae every 2 h for 72 h from cloprostenol injection or CIDR device withdrawal and the plasma was analysed for concentrations of progesterone and LH by radioimmunoassay. Does within each treatment were randomly allocated to an ovarian examination time of 12, 16, 20 or 24 h after the onset of oestrus. Laparoscopy was repeated at 12-h intervals until ovulation was recorded. The ovaries of does failing to exhibit oestrus were examined 72 and 86 h after cloprostenol injection or CIDR device withdrawal. A total of 17 does were observed to exhibit oestrus at a mean (+/- s.e.m.) interval from treatment of 44.6 +/- 3.6 h for Group 1 (N = 9) and 34.1 +/- 2.5 h for Group 2 (N = 8).(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship between the onset of oestrus, the preovulatory surge in luteinizing hormone and ovulation following oestrous synchronization and superovulation of farmed red deer (Cervus elaphus).

The timing of ovulation relative to the onset of oestrus and the preovulatory surge in luteinizing hormone (LH) was studied in red deer following treatments to synchronize oestrus and induce either a monovulatory or superovulatory response. Mature hinds (n = 36) were allocated randomly to two mating groups (n = 16 + 20), with respective treatments staggered by 4 weeks during the 1990 rut (March-April). Each hind was treated with an intravaginal controlled internal drug releasing (CIDR)-type S device for 14 days. Treatments to induce a monovulatory response included CIDR device alone (treatment A; n = 4 + 8) and additional injection of 200 iu pregnant mares' serum gonadotrophin (PMSG) at device removal (treatment B; n = 4 + 4). Treatments to induce a superovulatory response included injections of 200 iu PMSG and 0.5 units ovine follicle-stimulating hormone (FSH) at about time of removal of CIDR devices (treatment C; n = 4 + 4) and further treatment with gonadotrophin-releasing hormone (GnRH) analogue 18 h after removal of CIDR devices (treatment D; n = 4 + 4). The hinds were run with crayon-harnessed stags from insertion of CIDR devices (12 March or 9 April) and blood samples were taken every second day to determine plasma progesterone. Further blood samples were collected for determination of plasma LH and progesterone via indwelling jugular cannulae every 2 h for 72 h from removal of CIDR devices. Hinds were allocated randomly to an initial ovarian examination by laparoscopy at either 16 or 20 h (A and B), or 12 or 16 h (C and D) after the onset of oestrus, with laparoscopy repeated at intervals of 8 h until either ovulation was recorded (A and B), or for four successive occasions (C and D). All hinds received cloprostenol injections 15 days after device removal. A total of 28 hinds (78%) exhibited oestrus and a preovulatory LH surge, with mean (+/- SEM) times to onset of oestrus of 44.6 +/- 1.0 h (A; n = 7), 37.4 +/- 2.0 h (B; n = 7), 16.3 +/- 1.7 h (C; n = 6) or 14.0 +/- 1.7 h (D; n = 8). Failure to exhibit oestrus or LH surge was most prevalent among hinds in treatment A early in the rut.(ABSTRACT TRUNCATED AT 400 WORDS)     

Association of the lipoprotein receptor-related protein 2 gene with gout and non-additive interaction with alcohol consumption

Introduction

The T allele of a single nucleotide polymorphism (SNP: rs2544390) in lipoprotein receptor-related protein 2 (LRP2) is associated with higher serum urate and risk of gout in Japanese individuals. SNP rs2544390 also interacts with alcohol consumption in determining hyperuricemia in this population. We investigated the association of rs2544390 with gout, and interaction with all types of alcohol consumption in European and New Zealand (NZ) Māori and Pacific subjects, and a Māori study cohort from the East Coast region of NZ’s North Island.

Methods

Rs2544390 was genotyped by Taqman®. From NZ a total of 1205 controls and 1431 gout cases clinically ascertained were used. Publicly available genotype and serum urate data were utilized from the Atherosclerosis Risk in Communities (ARIC) study and the Framingham Heart Study (FHS). Alcohol consumption data were obtained by consumption frequency questions in all study cohorts. Multivariate adjusted logistic regression was done using STATA.

Results

The T allele of rs2544390 was associated with increased risk of gout in the combined Māori and Pacific Island cohort (OR = 1.20, P = 0.009), and associated with gout in the European subjects, but with a protective effect (OR = 0.79, P_Unadjusted = 0.02). Alcohol consumption was positively associated with risk of gout in Māori and Pacific subjects (0.2% increased risk/g/week, P = 0.004). There was a non-additive interaction between any alcohol intake and the risk of gout in the combined Māori and Pacific cohorts (P_Interaction = 0.001), where any alcohol intake was associated with a 4.18-fold increased risk in the CC genotype group (P = 6.6x10^-5), compared with a 1.14-fold increased risk in the CT/TT genotype group (P = 0.40). These effects were not observed in European subjects.

Conclusions

Association of the T-allele with gout risk in the Māori and Pacific subjects was consistent with this allele increasing serum urate in Japanese individuals. The non-additive interaction in the Māori and Pacific subjects showed that alcohol consumption over-rides any protective effect conferred by the CC genotype. Further exploration of the mechanism underlying this interaction should generate new understanding of the biological role of alcohol in gout, in addition to strengthening the evidence base for reduction of alcohol consumption in the management of gout.     

Neanderthal hand and foot remains from Moula‐Guercy,Ardèche,France

The hand and foot remains from Moula‐Guercy cave (Ardèche, France) comprise 24 specimens of Eemian age (ca. 120 ka). The specimens include primarily complete elements, which are rare among the Moula‐Guercy postcrania. The hand remains have several characteristic Neanderthal traits including a laterally facing (parasagittally oriented) second metacarpal‐capitate articulation, a short styloid process, a wide proximal articular surface on the third metacarpal, and absolutely expanded apical tuberosities on the distal hand phalanges relative to modern humans. The foot remains include several incomplete elements along with an antimeric pair of naviculars, a medial cuneiform and cuboid, and a single complete element from each of the distal segments (one each: metatarsal, proximal foot phalanx, intermediate foot phalanx, distal foot phalanx). Consistent among the specimens are relatively wide diaphyses for length in the metatarsals and phalanges and large and prominent muscle attachments, both consistent with previously published Neanderthal morphology. The hand and foot collection from Moula‐Guercy is an important dataset for future studies of Neanderthal functional morphology, dexterity, and behavior as it represents a previously undersampled time period for European Neanderthals. Am J Phys Anthropol 152:516–529, 2013. © 2013 Wiley Periodicals, Inc.     

The Caenorhabditis elegans CED-9 protein does not directly inhibit the caspase CED-3, in vitro nor in yeast

A genetically defined pathway orchestrates the removal of 131 of the 1090 somatic cells generated during the development of the hermaphrodite nematode Caenorhabditis elegans. Regulation of apoptosis is highly evolutionarily conserved and the nematode cell death pathway is a valuable model for studying mammalian apoptotic pathways, the dysregulation of which can contribute to numerous diseases. The nematode caspase CED-3 is ultimately responsible for the destruction of worm cells in response to apoptotic signals, but it must first be activated by CED-4. CED-9 inhibits programmed cell death and considerable data have demonstrated that CED-9 can directly bind and inhibit CED-4. However, it has been suggested that CED-9 may also directly inhibit CED-3. In this study, we used a yeast-based system and biochemical approaches to explore this second potential mechanism of action. While we confirmed the ability of CED-9 to inhibit CED-4, our data argue that CED-9 can not directly inhibit CED-3.     

Unanswered ethical and scientific questions for trials of invasive interventions for coronary disease: The case of single vessel disease

Trials in the 1990s demonstrated that medical therapy is as effective as invasive therapies for treating single-vessel coronary disease. Yet more recent studies enrolling patients with this condition have focused on evaluating only invasive approaches, namely, stenting versus coronary artery bypass surgery. Several ethical and scientific questions remain unanswered regarding the conduct of these later trials. Were they justified? Why wasn't a medical therapy arm included? Were subjects informed about the availability of medical therapy as an equivalent option? Was optimized medical therapy given prior to randomization? The absence of clear answers to these questions raises the possibility of serious bias in favor of invasive interventions. Considering that medical therapy is underutilized in patients with coronary disease, efforts should focus more on increasing utilization of medical therapy and proper selection of noninvasive interventions.     

Biological effects of power frequency magnetic fields: Neurochemical and toxicological changes in developing chick embryos

BACKGROUND: There are several reports that indicate a linkage between exposure to power frequency (50 - 60 Hz) magnetic fields with abnormalities in the early embryonic development of the chicken. The present study was designed to understand whether power frequency electromagnetic fields could act as an environmental insult and invoke any neurochemical or toxicological changes in developing chick embryo model. METHODS: Fertilized chicken eggs were subjected to continuous exposure to magnetic fields (50 Hz) of varying intensities (5, 50 or 100 microT) for a period of up to 15 days. The embryos were taken out of the eggs on day 5, day 10 and day 15. Neurochemical (norepinephrine and 5-hydroxytryptamine) and amino acid (tyrosine, glutamine and tryptophan) contents were measured, along with an assay of the enzyme glutamine synthetase in the brain. Preliminary toxicological investigations were carried out based on aminotransferases (AST and ALT) and lactate dehydrogenase activities in the whole embryo as well as in the liver. RESULTS: The study revealed that there was a significant increase (p < 0.01 and p < 0.001) in the level of norepinephrine accompanied by a significant decrease (p < 0.01 and p < 0.001) in the tyrosine content in the brain on day 15 following exposure to 5, 50 and 100 microT magnetic fields. There was a significant increase (p < 0.001) in glutamine synthetase activity resulting in the significantly enhanced (p < 0.001) level of glutamine in the brain on day 15 (for 100 microT only). The possible mechanisms for these alterations are discussed. Further, magnetic fields had no effect on the levels of tryptophan and 5-hydroxytryptamine in the brain. Similarly, there was no effect on the activity of either aminotransferases or lactate dehydrogenase in the whole embryo or liver due to magnetic field exposure. CONCLUSIONS: Based on these studies we conclude that magnetic field-induced changes in norepinephrine levels might help explain alterations in the circadian rhythm, observed during magnetic field stress. Also, the enhanced level of glutamine can act as a contributing factor for developmental abnormalities.