[Gender-inclusive care of victims of violence : The model project "Gender Gewaltkonzept" at the University Hospital Aachen]. / Gendergerechte Versorgung von Gewaltopfern : Das Modellprojekt "Gender Gewaltkonzept" an der Uniklinik Aachen.

Violence is a topic of great social relevance, frequently causing tremendous health consequences for those affected and high consequential costs for health care and the national economy. The established consulting and assistance services are usually restricted to offers for ambulant supply, mainly from private agencies or societies. As a result, there is no identification and care for patients who have experienced violence and who are treated in hospital. Another deficiency is the identification and care of male victims of violence. Despite wide-ranging offers of assistance, only very few gender-specific consulting and support services have been available to date.Therefore, the model project "Gender Gewaltkonzept" was initiated at Aachen University Hospital to assess the prevalence of violence and the potential consequences of the violence experienced on the patients' health. In addition, we investigated whether males and females are in need of different supply requirements.Based on the results of the project "Gender Gewaltkonzept" so far, and on prevalence estimates proving that there is a high rate of violent experiences in both males and females, this overview is aimed at presenting the aid and protection concepts available for victims of violence, in addition to the existing deficiencies of the care system. We present approaches to resolving these deficiencies to be able to establish all-encompassing gender-appropriate support for victims of violence.

Neural network of cognitive emotion regulation--an ALE meta-analysis and MACM analysis.

Cognitive regulation of emotions is a fundamental prerequisite for intact social functioning which impacts on both well being and psychopathology. The neural underpinnings of this process have been studied intensively in recent years, without, however, a general consensus. We here quantitatively summarize the published literature on cognitive emotion regulation using activation likelihood estimation in fMRI and PET (23 studies/479 subjects). In addition, we assessed the particular functional contribution of identified regions and their interactions using quantitative functional inference and meta-analytic connectivity modeling, respectively. In doing so, we developed a model for the core brain network involved in emotion regulation of emotional reactivity. According to this, the superior temporal gyrus, angular gyrus and (pre) supplementary motor area should be involved in execution of regulation initiated by frontal areas. The dorsolateral prefrontal cortex may be related to regulation of cognitive processes such as attention, while the ventrolateral prefrontal cortex may not necessarily reflect the regulatory process per se, but signals salience and therefore the need to regulate. We also identified a cluster in the anterior middle cingulate cortex as a region, which is anatomically and functionally in an ideal position to influence behavior and subcortical structures related to affect generation. Hence this area may play a central, integrative role in emotion regulation. By focusing on regions commonly active across multiple studies, this proposed model should provide important a priori information for the assessment of dysregulated emotion regulation in psychiatric disorders.

Nonequilibrium and thermal effects in mode-locked VECSELs.

Ultrafast femtosecond timescale dynamics in Vertical External Cavity Surface Emitting Lasers (VECSELs) have recently been employed to achieve record average power and duration mode-locked pulses by employing different types of saturable absorbers and Kerr Lens elements. Microscopic many-body dynamics are expected to dominate when attempting to push pulse durations below 100 fs. We present a preliminary microscopic simulation of ultrafast mode-locking in order to expose the role of hot carrier distributions in establishing ultrafast mode-locking.

Cost-efficient delay generator for fast terahertz imaging.

We present a fast and low-cost delay generator for terahertz (THz) waves that transfers a rotational motion of a transparent dielectric cube into an effective THz delay. The device is easily implemented in the THz beam path and allows for coherent sampling over 40 ps with a scan rate of hundreds of hertz. Furthermore, we show that our approach is particularly suitable for fast THz imaging.

Inflammatory signals from fatty bone marrow support DNMT3A driven clonal hematopoiesis.

Both fatty bone marrow (FBM) and somatic mutations in hematopoietic stem cells (HSCs), also termed clonal hematopoiesis (CH) accumulate with human aging. However it remains unclear whether FBM can modify the evolution of CH. To address this question, we herein present the interaction between CH and FBM in two preclinical male mouse models: after sub-lethal irradiation or after castration. An adipogenesis inhibitor (PPARγ inhibitor) is used in both models as a control. A significant increase in self-renewal can be detected in both human and rodent DNMT3AMut-HSCs when exposed to FBM. DNMT3AMut-HSCs derived from older mice interacting with FBM have even higher self-renewal in comparison to DNMT3AMut-HSCs derived from younger mice. Single cell RNA-sequencing on rodent HSCs after exposing them to FBM reveal a 6-10 fold increase in DNMT3AMut-HSCs and an activated inflammatory signaling. Cytokine analysis of BM fluid and BM derived adipocytes grown in vitro demonstrates an increased IL-6 levels under FBM conditions. Anti-IL-6 neutralizing antibodies significantly reduce the selective advantage of DNMT3AMut-HSCs exposed to FBM. Overall, paracrine FBM inflammatory signals promote DNMT3A-driven clonal hematopoiesis, which can be inhibited by blocking the IL-6 pathway.

Comparative analysis of an intestinal strain of Bifidobacterium longum and a strain of Bifidobacterium animalis subspecies lactis in Cheddar cheese.

Bifidobacteria cultures were incorporated into Cheddar cheeses to conduct a comparative analysis between the commercially available strain Bifidobacterium animalis ssp. lactis Bb-12 and the wild-type intestinal isolate, Bifidobacterium longum DJO10A. They were incorporated as starter adjuncts in separate vats and as a mixed culture, and survival through manufacturing and cheese ripening was assessed. For cheese using only Bb-12, the cells may have grown during cheese manufacture as 133% of the inoculum was incorporated into the cheese, resulting in 8.00 log cfu/g. Counts remained high during ripening showing less than 1 log decrease over a 12-mo period. For cheese using a mixed culture of Bb-12 and DJO10A, both strains were incorporated at much lower levels: 3.02 and 1.11%, respectively. This resulted in cheese with 6.00 and 5.04 log cfu/g for Bb-12 and DJO10A, respectively. Bifidobacteria survival rates were low, most likely due to the moisture of the cheese being below 38%. The Bb-12 demonstrated almost 100% viability during ripening. Numbers of DJO10A started to decline after 2 mo of ripening and dropped below the level of detection (2 log cfu/g) after 4.5 mo of ripening. Neither DJO10A nor Bb-12 fortified cheeses produced detectable amounts of organic acids during ripening other than lactic acid, indicating the lack of detectable metabolic contribution from bifidobacteria during cheese production and ripening such as production of acetic acid. To determine if sublethal stresses could improve the viability of DJO10A, 2 more vats were made, 1 with DJO10A exposed to sublethal acid, cold, and centrifugation stresses, and 1 exposed to none of these stresses. Although stress-primed DJO10A survived cheese manufacture better, as 72.8% were incorporated into the cheese compared with 41.1% of the unprimed, the statistical significance of this difference is unknown. In addition, the difference in moisture levels in the cheese cannot be excluded as influencing this difference. However, the rate of decline during ripening was similar for both. After 6 mo of ripening, cell counts in cheese were 4.68 and 4.24 log cfu/g for primed and unprimed cultures, respectively. These results suggest that whereas priming bifidobacteria with sublethal stresses before incorporation in a cheese fermentation may improve the number of viable cells that get incorporated into the cheese, it does not affect viability during cheese ripening.

Impact of the contact metallization on the performance of photoconductive THz antennas.

Both AuGe based alloys and Ti/Au metal layer stacks are widely used as ohmic metal contacts for photoconductive THz antennas made of low temperature grown GaAs. Here, we present the first systematic comparison between these two metallization types. A series of antennas of both kinds is excited by femtosecond laser pulses and by the emission from two diode lasers, i.e. we test the structures as pulsed THz emitters and as photomixers. In both cases, coherent and incoherent detection schemes are employed. We find that the power emitted from the antennas with AuGe metallization is 50% higher than that of antennas with a Ti/Au metal layer. From a comparison with a photomixer model we conclude that the higher output power results from a lower contact resistance of the AuGe contacts leading to an increased current flow. However, Ti/Au contacts have a higher thermal stability which might be advantageous if high system stability is called for.

MK-801, an excitatory amino acid antagonist, does not improve neurologic outcome following cardiac arrest in cats.

The excitatory amino antagonist MK-801 was administered to cats following resuscitation from cardiac arrest to evaluate its effect on neurologic and neuropathologic outcome in a clinically relevant model of complete cerebral ischemia. In 29 cats studied, cardiac arrest (ventricular fibrillation) was maintained for 18 min and resuscitation was successfully performed in 21 cats. Four animals underwent a sham arrest. MK-801 or placebo was administered in a blinded, randomized manner. Beginning at 5 min post resuscitation (PR), MK-801 330 micrograms/kg over 2 min followed by 73 micrograms/kg/h for 10 h or the same volume of placebo was administered. Resuscitated animals remained paralyzed and sedated in an intensive care setting for 24-30 h PR. Neurologic examinations were performed at 2, 4, and 7 days PR by observers blinded to the treatment groups. Seventeen cats were entered into data analysis (nine MK-801-treated and eight placebo-treated). MK-801-treated animals had a significantly greater neurologic deficit score (NDS) rank (0 = normal, 100 = brain death) 2 days PR (mean rank 12.1 vs. 5.6; p = 0.008). This difference is most likely due to ongoing sedative actions of MK-801. There were no significant differences in NDS rank at 4 (10.3, MK-801 vs. 7.5, placebo) and 7 (9.6, MK-801 vs. 8.3, placebo) days PR. There were no significant differences in frontal cortex, hippocampus, occipital cortex, or cerebellar neuropathology between groups. Sham-arrested cats had normal neurologic and neuropathologic evaluations. In the circumstance of complete cerebral ischemia as employed in the current study, MK-801 had no beneficial effect upon neurologic or neuropathologic outcome.

The noncompetitive N-methyl-D-aspartate receptor antagonist, MK-801 profoundly reduces volatile anesthetic requirements in rabbits.

Rabbits anesthetized with volatile anesthetics were given bolus doses of the n-methyl-D-aspartate (NMDA) receptor antagonist MK-801. Following observation and recording of the hemodynamic and electroencephalographic effects of MK-801, the animals were tested for requirements of volatile anesthetic to prevent movement to a noxious stimulus. It was demonstrated that MK-801 significantly reduced anesthetic requirements in a dose-dependent manner, while also affecting hemodynamics and the electroencephalogram in a manner consistent with the production of a deeper plane of anesthesia.

A comparison of the effects on neuronal Golgi morphology, assessed with electron microscopy, of cardiopulmonary bypass, low-flow bypass, and circulatory arrest during profound hypothermia.

Adult swine (n = 18) were studied to compare the effects on neuronal morphology of hypothermic circulatory arrest with hypothermic very-low-flow cardiopulmonary bypass. Animals were anesthetized with halothane and prepared in a standard manner for nonpulsatile cardiopulmonary bypass. Monitored variables included mean arterial pressure, arterial blood gases, the processed electroencephalogram, and subdural brain temperature. Bypass was initiated with pump flows of 100 ml.kg-1.min-1, and mean arterial pressure was kept above 50 mm Hg at all times. Animals were cooled to 18 degrees C, using a heat exchanger, and were randomly assigned to one of three groups. Group 1 animals were control animals who underwent 1 hour of hypothermic cardiopulmonary bypass. Group 2 animals underwent 1 hour of circulatory arrest. Group 3 animals underwent 1 hour of very-low-flow cardiopulmonary bypass (10% of normal). At the end of the 1 hour of hypothermic bypass, very-low-flow bypass, or arrest period, animals were rewarmed to 37 degrees C with normal bypass flows, and normothermic perfusion continued for 1 additional hour. Animals were then perfusion fixed with formalin and the brains were removed for electron microscopic analysis. Electron microscopic analysis was used to determine the effects of treatment and was limited to 20 neurons of the CA1 sector of the hippocampus in each animal. Golgi bodies were identified and classified as normal, mildly affected, or severely affected. Animals subjected to either very-low-flow bypass or circulatory arrest had significantly more severely affected and significantly fewer normal Golgi bodies than control animals (p < 0.001). Animals maintained with very-low-flow bypass, however, had significantly more severely affected and fewer normal Golgi bodies than animals subjected to circulatory arrest (p < 0.001). We conclude that under the conditions of this experiment very-low-flow hypothermic cardiopulmonary bypass is associated with significantly greater neuronal Golgi abnormalities than total circulatory arrest.

Effect of hyperglycemia on peri-ischemic neurotransmitter levels in the rabbit hippocampus.

This study examined the effect of preexisting hyperglycemia on the extracellular concentrations of glutamate and glycine in the rabbit hippocampus using in vivo microdialysis during brief episodes of transient global ischemia. Hyperglycemia has repeatedly been shown to exacerbate the neurologic injury produced by episodes of global cerebral ischemia. Under hypoxic conditions, glucose may be metabolized to glutamate, a known neurotoxin which has been implicated as a mediator of ischemic neuronal cell death. In this study, microdialysis probes were stereotactically inserted into the dorsal hippocampus of anesthetized rabbits. Animals were randomized to receive an i.v. infusion of either saline or dextrose. Global cerebral ischemia was then produced by the combination of neck tourniquet inflation and the induction of systemic hypotension. Administration of dextrose had no effect on these basal levels of glutamate or glycine. During ischemia, glutamate and glycine concentrations increased several-fold when compared with baseline. However, hippocampal glutamate concentrations were lower in the dextrose-treated groups during the peri-ischemic period (P = 0.02). Glycine concentrations were higher during the reperfusion period in the dextrose-treated animals when compared with saline controls (P = 0.03). The increased concentration of extracellular glycine which was observed in the dextrose-treated animals may contribute to the neurologic injury which occurs during episodes of global ischemia. The results of this study suggest that hyperglycemia does not exert its detrimental effects by increasing the extracellular concentration of glutamate.

Butanol effects on gamma-amino butyric acid concentration-responses in human alpha1beta2gamma2L gamma-amino butyric acid type A receptors with a mutation at alpha1S270.

Alcohol enhancement of gamma-amino butyric acid type A receptor (GABA(A)R) gating at low GABA is reduced by a serine-to-isoleucine mutation at residue alphaS270, suggesting that alphaS270 forms an enhancement site. However, whether the alphaS270I mutation strengthens alcohol inhibition of GABA(A)Rs remains unexplored. Furthermore, alphaS270 mutations have not been studied in the most prevalent form of mammalian GABA(A)Rs consisting of alpha1, beta2, and gamma2 subunits. In voltage-clamped Xenopus oocytes expressing recombinant alpha1beta2gamma2L GABA(A)Rs, electrophysiological analysis of GABA concentration-responses demonstrates that the alpha1(S270I) mutation increases apparent GABA affinity and significantly reduces the Hill coefficient of GABA(A)R activation. Butanol-induced leftward-shifts in GABA concentration-responses for both wild-type alpha1beta2gamma2L and alpha1(S270I)beta2gamma2L GABA(A)Rs are equal. At high GABA, butanol neither enhances nor inhibits alpha1(S270I)beta2gamma2L responses. Thus, in the dominant mammalian GABA(A)R isoform, the alphaS270I mutation affects neither enhancement nor inhibition by butanol, but alters the gating mechanism by reducing cooperativity, producing an apparent reduction in alcohol enhancement at low GABA.

Failure of nimodipine to improve neurologic outcome after eighteen minutes of cardiac arrest in the cat.

The calcium entry blocker nimodipine was administered to cats following resuscitation from 18 min of cardiac arrest to evaluate its effect on neurologic and neuropathologic outcome in a clinically relevant model of complete cerebral ischemia. Cardiac arrest (ventricular fibrillation) was maintained for 18 min and resuscitation was performed by a standardized protocol in 40 cats. Beginning at 5 min post-resuscitation, nimodipine, 10 micrograms/kg over 2 min followed by 1 microgram/kg per min for 10 h, or the same volume of placebo was administered in a randomized, blinded fashion. Neurologic deficits were scored at 2, 4, and 7 days post-resuscitation by observers blinded to the treatment group. Thirty cats were evaluated neurologically at 7 days post-resuscitation and were entered into data analysis (n = 15 per group). Neither neurologic deficit scores nor neuropathologic scores were significantly different between groups. The authors conclude that nimodipine administration in the manner and doses stated does not improve neurologic outcome in cats following resuscitation from cardiac arrest.

The NO synthase inhibitors L-Name and L-NMMA, but not L-arginine, block the mammalian nicotinic acetylcholine receptor channel.

(1) Nitric oxide (NO) synthase inhibitors (NOS-I) such as L-Name (N(G)-nitro L-arginine methyl ester) and L-NMMA (N(G)-monomethyl L-arginine) may enhance anesthesia indirectly by inhibiting the NO pathway. Moreover, NOS-I interact directly with receptor proteins. In an animal study, L-NMMA potentiated muscle relaxants. (2) The present experiments investigate the effects of L-NMMA, L-Name, and L-arginine on the nicotinic acetylcholine receptor channel (nAChR) using patch clamp techniques and a piezo-driven application system. Both NOS-I appear to directly interact with the nAChR in the open as well as in the closed conformation. L-Arginine has no effect.

Hospital admissions for malaria in Basel, Switzerland: an epidemiological review of 150 cases.

The increase in international travel and immigration from tropical countries has led to a growing number of imported malaria cases in industrialized countries. We analyzed the charts of every patient hospitalized for malaria from 1970-1992 in Basel, Switzerland. A period lasting from 1970-1986 was compared to 1987-1992. There were 150 malaria-episodes recorded. Over time, the number of immigrants increased from 12 to 27% (p <.05). More patients were admitted with Plasmodium falciparum-infection (49 vs. 75%, p <.005). The number of untypable malaria decreased from 30 to 9% (p <.005). In the more recent period, more diagnosis were done within a week (66 vs. 50%, p <.05). Twenty-three (15%) patients were admitted to the ICU, four (2. 6%) patients died of cerebral malaria. Twenty-seven (18%) patients developed malaria while taking correct prophylaxis. Despite some progress, malaria is still causing considerable morbidity and mortality. Non adherence to chemoprophylaxis was a major risk factor for acquiring malaria in hospitalized patients.

A comparison of the cerebral and hemodynamic effects of mannitol and hypertonic saline in a rabbit model of acute cryogenic brain injury.

There has recently been an increased interest in the use of hypertonic saline solutions in the fluid resuscitation of trauma victims and patients with uncontrollable intracranial hypertension. In this study, the cerebral and hemodynamic effects of 3.2% hypertonic saline solution were compared with those of an equiosmolar (20%) mannitol solution or 0.9% saline in a rabbit model of acute cryogenic brain injury. Forty-five minutes following the creation of a left hemispheric cryogenic brain lesion, equal volumes (10 ml/kg) of hypertonic saline, 0.9% saline, or mannitol were infused over a 5-min period. Monitored variables over the ensuing 120 min included mean arterial pressure, central venous pressure, intracranial pressure (ICP), hematocrit, and serum osmolality. At the conclusion of the 2-h study period, hemispheric water contents were determined by gravimetric analysis and the wet/dry weight method. There were no significant differences in mean arterial pressure between the three groups at any time during the experiment. Plasma osmolality was significantly increased by +/- 10 mOsm/kg following infusions in both the mannitol and hypertonic groups compared to the saline group. The infusion of either mannitol or hypertonic saline produced a transient and significant decrease in ICP during the first 60-90 min but not at 120 min after cryogenic brain lesion, whereas animals in the saline group demonstrated a continual increase in ICP. However, there appeared to be no significant differences in ICP between animals receiving mannitol or hypertonic saline at any time point following infusion of solutions. We conclude that following acute cryogenic brain injury, infusions of equal volumes of equiosmolar solutions of hypertonic saline or mannitol will transiently reduce ICP as compared to equal volumes of normal saline. However, hypertonic saline is not superior to mannitol in its ability to reduce ICP in this model of intracranial hypertension.

Sevoflurane versus halothane anesthesia after acute cryogenic brain injury in rabbits: relationship between arterial and intracranial pressure.

The relationship between intracranial pressure and arterial blood pressure during sevoflurane or halothane anesthesia was evaluated in New Zealand white rabbits after cryogenic brain injury. Fourteen rabbits were randomized to be anesthetized with 1.5 MAC of sevoflurane or halothane in oxygen. All animals were paralyzed with pancuronium, and mechanically ventilated. A cryogenic lesion was created over the left hemisphere. Thirty minutes later, the intracranial pressure had risen to a mean value of 15 mm Hg. The inhaled concentration of anesthetic drugs was then increased to achieve a blood pressure of 35 mm Hg. Baseline measurements were made of monitored variables including mean arterial pressure, intracranial pressure, esophageal temperature, end-tidal CO2, and arterial blood gases. Neosynephrine was then infused to raise the blood pressure from 35 to 100 mm Hg during 20 min. The PaCO2 was maintained between 38 and 42 mm Hg. At baseline, there were no significant differences in mean arterial pressure, intracranial pressure, and blood gas values between the two groups. The intracranial pressure in the sevoflurane anesthesia group increased from 11 +/- 1 to 44 +/- 4 mm Hg as mean arterial pressure increased from 35 to 100 mm Hg. Intracranial pressure in the halothane anesthesia group increased from 9 +/- 1 to 32 +/- 3 mm Hg during the same range of blood pressure. Linear regressions of intracranial pressure on mean arterial pressure were performed for each of the two anesthetic groups. The slope of the regression line for the sevoflurane animals (0.491) was significantly greater than that for the halothane animals (0.323, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of THAM and sodium bicarbonate on intracranial pressure and mean arterial pressure in an animal model of focal cerebral injury.

Episodes of arterial hypotension are associated with an increased mortality in head injury patients. Rapid infusion of sodium bicarbonate in such patients may cause hypotension and elevate intracranial pressure. Therefore, we examined the effects of tromethamine (THAM) versus bicarbonate on intracranial pressure and blood pressure in a model of focal cerebral injury. THAM is a buffer that in previous studies has been shown to lower intracranial pressure. After creation of a cryogenic lesion in 13 New Zealand white rabbits, equivalent infusions (15 s duration) of sodium bicarbonate and THAM (2 mEq/kg) were administered sequentially to each animal in random order. Rapid infusion was chosen to simulate the administration of these drugs during a resuscitation. THAM infusion was associated with a significantly lower intracranial pressure and blood pressure than bicarbonate. The fall in blood pressure was great enough that cerebral perfusion pressure after THAM infusion was significantly lower than after bicarbonate infusion. In this model of cerebral injury, rapid infusion of THAM offered no therapeutic advantage over bicarbonate.

The effects of fentanyl and sufentanil on intracranial pressure and cerebral blood flow in rabbits with an acute cryogenic brain injury.

The cerebrovascular response to the administration of equipotent doses of fentanyl and sufentanil was evaluated in New Zealand white rabbits following cryogenic brain injury. In a preliminary study consisting of 10 animals, it was documented that the cerebral blood flow response to alterations in the PaCO2 remained intact in this model of brain injury. Subsequently, 28 rabbits were anesthetized with 1.5% halothane in oxygen, paralyzed with pancuronium, and mechanically ventilated. A cryogenic lesion was created over the left hemisphere. One hour later, the intracranial pressure had risen to a mean value of 15 mm Hg. Baseline measurements were then made of monitored variables, which included heart rate, mean arterial pressure, central venous pressure, intracranial pressure, temperature, and arterial blood gases. Global cerebral blood flow was measured utilizing a hydrogen clearance technique. The animals were then randomized to receive an infusion of fentanyl (N = 9, 200 microg/kg), sufentanil (N = 10, 20 microg/kg), or an equal volume of normal saline (N = 9) by i.v. infusion over 5 min. At the conclusion of the opioid infusions, repeated measurements of hemodynamic variables and intracranial pressure were recorded for 15 min and a second cerebral blood flow measurement was made. There were no significant differences in mean arterial pressure, heart rate, central venous pressure, intracranial pressure, cerebral blood flow, or blood gas values between the three groups prior to the administration of fentanyl, sufentanil, or normal saline. At the conclusion of the 5 min infusion, the intracranial pressure had increased by approximately 5 mm Hg in all three groups. The mean arterial pressure decreased to a similar degree in the fentanyl and sufentanil groups and was significantly lower than the mean arterial pressure in the saline group. Although the cerebral perfusion pressure decreased in all three groups, cerebral blood flow was not significantly affected. These results suggest that there is no significant difference in the effects of fentanyl vs. sufentanil on mean arterial pressure, intracranial pressure, or cerebral blood flow in this model of acute brain injury and elevated intracranial pressure.

Sex ratios in mule duck embryos at various stages of incubation.

Mule duck hatcheries have long reported varying degrees of unbalance in the sex ratio, with a preponderance of male mules at hatching. The aim of the present study was to assess the distributions of sex ratios at various stages of development in embryos originating from intra- and intergeneric crosses between parental lineages (Muscovy male x Muscovy female, Pekin male x Pekin female, Muscovy male x Pekin female or Mule, and Pekin male x Muscovy female or Hinny). In Experiment I, embryo sexing was performed on Days 1 and 5 of incubation (by multiplex PCR) and at hatching (by vent observation). The sex ratio was not significantly modified during the early stages of embryo development whatever the genetic origin (P>0.05, Days 1 and Day 5) but our results in mule and hinny ducklings confirmed the preponderance of males among normally hatched ducklings originating from the intergeneric lineage (58.9 and 55.4% males in mules and hinnies, respectively; P<0.05 in both cases). Sex ratio (vent sexing) in second grade (cull) ducklings revealed that 68% of these ducklings were females (P<0.05). In Experiment II, the distribution of sex ratio was also performed in mule duck eggs from 6 batches (400,000 eggs/batch) first examined for fertility (candling) on Day 18 of incubation. These results indicate that the percentage of males present in the population of normally hatched ducklings increases when fertility decreases. In addition, this experiment also revealed that 83.7-90.5% of viable male mule embryos develop up to hatching, compared to only 43.0-51.0% of female mule embryos. Given that a deviation in sex ratio during the first stages of incubation is unlikely (Experiment I), it is concluded that the skewed sex ratio of mule ducks at hatching is primarily due to increased late mortality in female mule embryos occurring between egg transfer and hatching. This mortality originated, at least in part, from the intergeneric origin of female mules, and was marked to a greater or lesser extent depending on the initial success of fertilization in a given batch, a possible indication that the initial quality of gametes may selectively exert its influence at the later stages of embryo development.