Placental development is highly sensitive to maternal nutrition and influences fetal growth and reproductive success. Moderate maternal feed restriction (FR) during gestation can reduce feeding costs on farms, but its impact on the placenta and productive performance in females and offspring remains unclear. This study characterised compartment-specific placental adaptations and their productive consequences in multiparous rabbit does subjected to a 40% nutritional restriction during the first two-thirds of gestation (Day 0 to 21), followed by ad libitum refeeding. On day 28 of gestation, seven days after refeeding began, placental morphometry, histology, efficiency, and gene expression was characterized alongside fetal growth and viability. Maternal body weight and feed intake during gestation, fertility, prolificacy, and postnatal outcomes during lactation were also assessed. Placental efficiency was reduced (P < 0.05), and was accompanied by proportional decreases in fetal head and body weight (P < 0.05), consistent with a generalized restriction of fetal growth. The labyrinth exhibited hemorrhage and fibrosis with subsequent reduced cellularity. Furthermore, the main glucose transporter (SLC2A1) was donwregulated in both placental compartments, whereas genes related to anaerobic glycolysis (LDHA, GAPDH), NO-related signalling (eNOS), and fetal growth regulation (IGF2R) were upregulated in the fetal placenta compartment of FR does (P < 0.05). VEGF expression and localization were not affected by the restriction-refeeding protocol. Late-gestation refeeding restored maternal body weight, and did not compromise fertility or offspring survival, althought lower stillbirths in FR does were found (P < 0.05). Overall, the restriction-refeeding regime induces compartment-specific placental adaptations associated with reduced placental efficiency and fetal growth, while fetal survival and postnatal viability areunaffected. These findings highlight placental plasticity in response to maternal nutrition and support the rabbit as a valuable model for placental adaptation to maternal undernutrition.

BackgroundA petrous apex mucocele is a rare benign cystic lesion that can present with symptoms due to pressure on surrounding structures, including the internal carotid artery, Meckel's cave and the fifth and sixth cranial nerves, as well as the cavernous sinus region and inner ear.MethodsA 36-year-old male presented with 8 months of diplopia when looking to the right, a right-sided temporoparietal headache, and paresthesia in the right half of his face. An MRI revealed a 26 × 32 × 37 mm lesion in the right petrous apex. The lesion's signal characteristics were most consistent with a mucocele. We performed an endoscopic endonasal transclival marsupialization and created a wide drainage opening, which we supported by inserting a stent containing mometasone furoate.ResultsThe postoperative course was marked by transient arterial hypertension, which required antihypertensive treatment. Postoperative imaging studies revealed no intracranial complications and confirmed that the drainage pathway remained patent.ConclusionIn the differential diagnosis of lesions in the medial portion of the petrous apex, a mucocele should be considered. In appropriately selected cases, endoscopic endonasal marsupialization can be an effective option. To maintain postoperative patency of the drainage pathway, an implant containing mometasone furoate may also be used.

Autoimmune inner ear disease (AIED) is a spectrum of diseases that may present solely as fluctuating sensorineural hearing loss triggered by unknown stimuli, or it may occur in association with other systemic rheumatic diseases. This article will review primary AIED as well as the etiologies of secondary AIED. It will also describe the epidemiology, pathophysiology, diagnosis, and management, including corticosteroids and steroid-sparing treatments.

Congenital nasal encephaloceles are rare anterior skull base defects that may predispose patients to cerebrospinal fluid (CSF) leakage and subsequent meningitis. While sensorineural hearing loss (SNHL) is a known complication of pediatric meningitis, progression from an unrecognized nasal encephalocele to meningitis and bilateral profound hearing loss is infrequently reported. We describe a seven-month-old male who presented with pneumococcal meningitis and status epilepticus requiring intensive care management. Following recovery, he developed severe-to-profound bilateral SNHL. Further evaluation revealed labyrinthitis ossificans and a previously unrecognized nasal encephalocele. The patient underwent bilateral cochlear implantation followed by successful endoscopic repair of the skull base defect. Postoperatively, he demonstrated hearing thresholds within normal ranges and no evidence of recurrence. This case highlights the importance of early recognition of congenital skull base defects in infants presenting with meningitis. It underscores the role of timely imaging and multidisciplinary management in preventing irreversible complications.

Sensorineural hearing loss in mammals is essentially irreversible. Mature cochlear hair cells, once lost, do not regenerate. Non-mammalian vertebrates retain this ability, but in the mammalian organ of Corti, supporting cells lose their proliferative and transdifferentiation competence after birth. Reactivation of classical developmental pathways has also shown limited success in the adult cochlea. In this review, we first synthesize published evidence on Hippo-Yes-associated protein(YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling in the inner ear, including studies of inner-ear progenitors, organ of Corti growth, vestibular sensory epithelia, cochlear hair-cell injury, neonatal cochlear regeneration models, and emerging adult cochlear data. On this basis, we then evaluate the biomechanical brake hypothesis, which proposes that injury-associated mechanical remodeling may interact with Hippo-YAP/TAZ signaling to restrict supporting-cell plasticity in the mature mammalian cochlea. Rather than presenting this hypothesis as an established mechanism, we treat it as an evidence-graded framework that must be tested against alternative explanations, including protective epithelial repair, cell-cycle inhibition, epigenetic restriction, and loss of developmental competence. The available literature suggests that Hippo-YAP/TAZ signaling participates in several inner-ear processes, including progenitor expansion, sensory epithelial growth, species-dependent vestibular repair, otoprotective responses, and supporting-cell proliferation under defined experimental conditions. However, direct evidence that injury-induced mechanical remodeling causally suppresses YAP/TAZ-dependent regeneration in the adult cochlea remains limited. We therefore distinguish among developmental, neonatal, vestibular, ex vivo, and adult in vivo evidence, and identify where current findings support, weaken, or remain insufficient to establish the biomechanical brake model. Finally, we outline specific gaps that should guide future work: comprehensive tabulation of Hippo-related inner-ear studies, adult supporting-cell lineage tracing, spatial mapping of cochlear mechanical properties and Hippo activity, cell-subtype-specific perturbation of YAP/TAZ signaling, functional assessment by auditory brainstem response and distortion product otoacoustic emission, and long-term evaluation of epithelial stability. This organization is intended to clarify what Hippo-YAP/TAZ signaling has already been shown to do in the inner ear, what remains speculative, and which experiments are required before mechanobiological modulation can be considered a plausible regenerative strategy.

Fetal Alcohol Spectrum Disorder, caused by prenatal alcohol exposure, remains a major public health concern, affecting up to 1 in 20 U.S. schoolchildren. Pregnancy is typically not recognized until six weeks of gestation, alcohol exposure often occurs unknowingly during the peri-conceptional period, a highly vulnerable developmental window of oocyte maturation. The placenta is increasingly recognized as a mediator of alcohol-induced neurodevelopmental risk through the placenta-brain axis. We characterize peri-conceptional alcohol exposure on placental development in a mouse PCA model mimicking human drinking patterns. Single-cell transcriptomic analyses on late gestation placentas revealed disruption of extracellular matrix and collagen-remodeling pathways within the labyrinth; processes essential for placental vascular development. Mitochondria isolated from E17.5 placentas showed compromised respiration. We assess placental vascular functions with non-invasive dynamic contrast-enhanced MRI, enabling analysis across placental compartments for longitudinal evaluation of perfusion, substrate delivery, and contractile function. We demonstrate that PCA exposure arrests placental vascularization, perfusion, and morphological maturation. PCA exposure before implantation altered long-term placental programming, resulting in impaired placental perfusion and mitochondrial functions across gestation. These findings implicate placental dysfunction as a critical mechanism in Fetal Alcohol Spectrum Disorder pathogenesis and identify extracellular matrix remodeling and mitochondria as potential therapeutic targets following PCA exposure.

Oral endotracheal intubation in rats is useful for cranial, thoracic, and survival experiments but remains technically demanding. We evaluated a simple method using a modified 5-Fr vascular sheath and a smartphone-connected ear-pick endoscope in 30 male Sprague-Dawley rats (8-12 weeks, 300-400 g). Under 3% isoflurane anesthesia and vecuronium bromide-induced neuromuscular blockade, the sheath was shortened to approximately 8 cm, and its modified inner dilator was advanced into the trachea under endoscopic visualization; the sheath was then advanced over the dilator and connected to mechanical ventilation. Intubation was successful in all rats, with first-attempt success in 28/30 (93.3%). No major complications occurred, although minor oral bleeding was observed in several rats. This method may provide a practical option for rat airway management.