Steroids are used in management of coronavirus disease 2019 (COVID-19) patients with severe illness and their use has been demonstrated to decrease mortality. Although life-saving, steroids are well documented as risk factors for osteonecrosis.Osteonecrosis of the hip can be debilitating and surgery may be required to improve the quality of life. With the increasing number of COVID-19 cases, osteonecrosis of the hip and other joints resulting from steroid use is expected to show a sharp rise in the coming years. In this review we discuss the association between steroids and osteonecrosis, indications for steroid therapy in COVID-19 patients, and incidence, diagnosis, and treatment of osteonecrosis secondary to steroids in COVID-19.

Background and Objectives: The widespread use of mobile phones and personal listening devices (PLDs) poses potential health risks, particularly noise-induced hearing loss. Among younger generations, high-volume PLD use is associated with auditory and vestibular system changes. Clinical vestibular testing, including vestibular-evoked myogenic potentials (VEMP) and the video head impulse test (vHIT), may reveal peripheral vestibular impacts from prolonged PLD exposure at volumes over 60%. This study examines VEMP and vHIT results in individuals with normal hearing who have had extended high-volume PLD exposure. Subjects and Methods: A cross-sectional comparative study was conducted on individuals aged 15-24 years. All the participants had normal pure tone thresholds with “A” type tympanogram, present acoustic reflexes, and history of PLD usage. Participants were divided into groups according to PLD exposure of <1 year (group A), 1.1-2 years (group B), 2.1-3 years (group C), and 3.1-4 years (group D). The output sound pressure level (dB SPL) near the tympanic membrane was measured. Furthermore, cervical VEMP, ocular VEMP, and vHIT were assessed. Results: The VEMP and vHIT findings were statistically analyzed and compared across groups. The peak-to-peak amplitudes of VEMP showed a statistically significant difference between groups A and D. Conclusions Potential subclinical damage to the otolith organs can be associated with increased PLD exposure. No damage to the semi-circular canals was observed as the participants used lower dBA values by the PLDs.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Background: Pectus excavatum (PE), the most common congenital chest wall deformity, is increasingly treated with minimally invasive repair (MIRPE). However, postoperative complications such as bar displacement remain a significant challenge, occurring in approximately 9.5% of cases. While surgical modifications and stabilization techniques aim to reduce risks, bar displacement persists as a critical concern. Methods: This PROSPERO-registered systematic review followed PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A search of PubMed, Scopus, and CINAHL through October 2024 identified studies evaluating bar displacement in PE patients undergoing MIRPE or alternative surgical approaches. The inclusion criteria focused on risk factors, stabilization techniques, and reoperation strategies. Data extraction and risk-of-bias assessments were independently conducted by multiple reviewers to ensure accuracy and quality. Results: Thirteen studies spanning 23 years were included. Bar displacement rates varied widely (0.9%–33.3%), with key risk factors including patient age, chest wall rigidity, bar length, and placement technique. Advanced stabilization methods—such as bridge fixation, shorter bars, multipoint fixation, and adjunct stabilizers—significantly reduced displacement rates. Common postoperative complications included wound infections, seromas, pleural effusions, and bar re-dislocation. Imaging modalities like chest X-rays and 3-dimensional computed tomography scans proved critical for early detection. Heterogeneity in stabilization approaches underscores a shift toward patient-specific strategies to optimize outcomes. Conclusion Tailored stabilization techniques are essential for successful PE correction.Although advancements in fixation methods have reduced displacement risks, standardized postoperative protocols and multicenter studies are needed to validate these innovations and improve long-term outcomes (PROSPERO: CRD42024595337).

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.

Steroids are used in management of coronavirus disease 2019 (COVID-19) patients with severe illness and their use has been demonstrated to decrease mortality. Although life-saving, steroids are well documented as risk factors for osteonecrosis.Osteonecrosis of the hip can be debilitating and surgery may be required to improve the quality of life. With the increasing number of COVID-19 cases, osteonecrosis of the hip and other joints resulting from steroid use is expected to show a sharp rise in the coming years. In this review we discuss the association between steroids and osteonecrosis, indications for steroid therapy in COVID-19 patients, and incidence, diagnosis, and treatment of osteonecrosis secondary to steroids in COVID-19.

Background and Objectives: The widespread use of mobile phones and personal listening devices (PLDs) poses potential health risks, particularly noise-induced hearing loss. Among younger generations, high-volume PLD use is associated with auditory and vestibular system changes. Clinical vestibular testing, including vestibular-evoked myogenic potentials (VEMP) and the video head impulse test (vHIT), may reveal peripheral vestibular impacts from prolonged PLD exposure at volumes over 60%. This study examines VEMP and vHIT results in individuals with normal hearing who have had extended high-volume PLD exposure. Subjects and Methods: A cross-sectional comparative study was conducted on individuals aged 15-24 years. All the participants had normal pure tone thresholds with “A” type tympanogram, present acoustic reflexes, and history of PLD usage. Participants were divided into groups according to PLD exposure of <1 year (group A), 1.1-2 years (group B), 2.1-3 years (group C), and 3.1-4 years (group D). The output sound pressure level (dB SPL) near the tympanic membrane was measured. Furthermore, cervical VEMP, ocular VEMP, and vHIT were assessed. Results: The VEMP and vHIT findings were statistically analyzed and compared across groups. The peak-to-peak amplitudes of VEMP showed a statistically significant difference between groups A and D. Conclusions Potential subclinical damage to the otolith organs can be associated with increased PLD exposure. No damage to the semi-circular canals was observed as the participants used lower dBA values by the PLDs.

Background: Pectus excavatum (PE), the most common congenital chest wall deformity, is increasingly treated with minimally invasive repair (MIRPE). However, postoperative complications such as bar displacement remain a significant challenge, occurring in approximately 9.5% of cases. While surgical modifications and stabilization techniques aim to reduce risks, bar displacement persists as a critical concern. Methods: This PROSPERO-registered systematic review followed PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. A search of PubMed, Scopus, and CINAHL through October 2024 identified studies evaluating bar displacement in PE patients undergoing MIRPE or alternative surgical approaches. The inclusion criteria focused on risk factors, stabilization techniques, and reoperation strategies. Data extraction and risk-of-bias assessments were independently conducted by multiple reviewers to ensure accuracy and quality. Results: Thirteen studies spanning 23 years were included. Bar displacement rates varied widely (0.9%–33.3%), with key risk factors including patient age, chest wall rigidity, bar length, and placement technique. Advanced stabilization methods—such as bridge fixation, shorter bars, multipoint fixation, and adjunct stabilizers—significantly reduced displacement rates. Common postoperative complications included wound infections, seromas, pleural effusions, and bar re-dislocation. Imaging modalities like chest X-rays and 3-dimensional computed tomography scans proved critical for early detection. Heterogeneity in stabilization approaches underscores a shift toward patient-specific strategies to optimize outcomes. Conclusion Tailored stabilization techniques are essential for successful PE correction.Although advancements in fixation methods have reduced displacement risks, standardized postoperative protocols and multicenter studies are needed to validate these innovations and improve long-term outcomes (PROSPERO: CRD42024595337).

Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis.Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.