Investigating the expression profiles of cysteine string proteins (CSPs) in cochlear tissue.

Objective: This study aims to explore the expression patterns of cysteine string protein alpha (CSPα) and cysteine string protein beta (CSPβ) in the mammalian inner ear, with an emphasis on their temporal dynamics during the developmental stages of C57BL/6 mice.

Methods: We utilized immunofluorescence staining to assess the localization and distribution of CSPα and CSPβ within the inner ears of C57BL/6 mice and miniature pigs. Additionally, this method facilitated the investigation of their temporal expression profiles.

Effects of trypsin and pepsin detection on chronic otitis media with effusion.

Chronic otitis media with effusion (COME) is a common cause of hearing loss in children and adults. Laryngopharyngeal reflux (LPR) is often overlooked in the clinical management of COME complicated by LPR. This study aimed to investigate the presence and concentration of trypsin and pepsin in the middle ear effusion (MEE), as well as the recurrence rate of otitis media with effusion (OME) in COME patients with trypsin-/pepsin-positive MEE after acid-suppressive treatment (AST).

The expression and significance of Epac1 and Epac2 in the inner ear of guinea pigs.

Objective: To detect the expression of Epac1 and Epac2 in the inner ear of guinea pigs and its association with microcirculation in the inner ear.

Methods: The temporal bones of 30 healthy red-eye guinea pigs (60 ears) weighing 200-350 g were collected, then the surrounding bone wall of the cochlea was removed under a dissection microscope. Real-time quantitative PCR (RT-qPCR) and Western blot were used to detect mRNA and protein expression, respectively, of Epac1 and Epac2 in the inner ear and to compare their expression in heart, liver, kidney, intestine, and lung tissues.

Oridonin ameliorates noise-induced hearing loss by blocking NLRP3 - NEK7 mediated inflammasome activation.

Inflammation is involved in noise-induced hearing loss (NIHL), but the mechanism is still unknown. The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which triggers the inflammatory cascade, has been implicated in several inflammatory diseases in response to oxidative stress. However, whether the NLRP3 inflammasome is a key factor for permanent NIHL is still unknown.

Specific deletion of CDC42 in pancreatic β cells attenuates glucose-induced insulin expression and secretion in mice.

Insulin is a key hormone for maintaining glucose homeostasis in organisms. In general, deficiency of insulin synthesis and secretion results in type I diabetes, whereas insulin resistance leads to type 2 diabetes. Cell division cycle 42 (CDC42), a member of Rho GTPases family, has been shown as an essential regulator in the second phase of glucose-induced insulin secretion in pancreatic islets β cells in vitro.

Follicle-stimulating hormone inhibits cervical cancer via NF-κB pathway.

Background: Follicle-stimulating hormone (FSH) has multiple biological functions. It is currently considered that FSH can inhibit cervical cancer, and our aim was to explore the underlying molecular mechanisms.

Materials And Methods: An in vivo experiment using nude mice injected with HeLa cells was performed.

Berberine exerts antioxidant effects via protection of spiral ganglion cells against cytomegalovirus-induced apoptosis.

Cytomegalovirus (CMV) is the leading cause of sensorineural hearing loss (SNHL) in children because of its damage to the cochlea and spiral ganglion cells. Therefore, it has become a top priority to devise new methods to effectively protect spiral ganglion cells from damage. Berberine (BBR) has gained attention for its vast beneficial biological effects through immunomodulation, and its anti-inflammatory and anti-apoptosis properties.

MCMV triggers ROS/NLRP3-associated inflammasome activation in the inner ear of mice and cultured spiral ganglion neurons, contributing to sensorineural hearing loss.

Congenital cytomegalovirus (CMV) infection is the most common infectious cause of sensorineural hearing loss in children. While the importance of CMV‑induced SNHL has been described, the mechanisms underlying its pathogenesis and the role of inflammatory responses remain elusive. The present study established an experimental model of hearing loss after systemic infection with murine CMV (MCMV) in newborn mice.

Cochlear Spiral Ganglion Neuron Apoptosis in Neonatal Mice with Murine Cytomegalovirus-Induced Sensorineural Hearing Loss.

Background: Sensorineural hearing loss (SNHL) is the most common consequence of congenital cytomegalovirus (CMV) infection, and could result in neurological abnormalities and intellectual and developmental disabilities.

Purpose: To explore the mechanism of murine CMV (MCMV)-induced SNHL in neonatal mice model.

Research Design: A repeated measures design was used.

Pathological changes of the inner ear cochlea in different time windows of murine cytomegalovirus-induced hearing loss in a mouse model.

Conclusions: Murine congenital cytomegalovirus (CMV) (MCMV) infection of the inner ear cochlea, which caused continuous pathological change, occurred on the third day after intracerebral injection and persisted for a very long time.

Objective: Our study used the MCMV-induced hearing loss neonatal mouse model to investigate the pathological changes of the cochlea in different time windows.

Methods: Sixty newborn BALB/c mice were randomly and equally divided into the experimental group (MCMV intracerebral injection) and control group (normal saline intracerebral injection).

Changes in calcium/calmodulin level and mitochondrial membrane potential in cochlear neurons of newborn mice infected with murine cytomegalovirus.

We sought to elucidate the pathogenesis of hearing loss in newborns due to congenital cytomegalovirus. We used the model of murine cytomegalovirus (MCMV) infection and evaluated concentrations of free calcium, calmodulin levels, and mitochondrial membrane potential in cochlear neurons of infected newborn mice. MCMV infection was established by intracranial inoculation of newborn mice with viral suspension (20 μl of MCMV TCID(50)--10(4) IU/0.

[Changes of hearing threshold and calcium/calmodulin in the cochlear nucleus cells of mice with cytomegalovirus intracranial infection].

Objective: To explore the changes in the threshold of auditory brainstem response (ABR) and [Ca(2+)]I and calmodulin (CaM) in cochlear nucleus of newborn mice infected by murine cytomegalovirus (MCMV) in the brain.

Methods: Sixty-nine newborn mice were randomized into model group and control group. The model group (54 mice) was established by intracranial injection with MCMV viral suspension 20 l and the same volume of 0.