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Background: Compared to other types of abdominal protrusions, Spigelian hernias are not very common. In prosthetic repair of abdominal protrusions, mesh fixation and defect overlap are an open issue, as they are a source of complications. A newly developed tentacle-shaped mesh has been used to ensure a fixation-free repair with a broader defect overlap in the repair of abdominal hernias. This study describes the long-term results of a fixation-free repair of Spigelian hernias carried out with a tentacle mesh.
Methods: A proprietary mesh composed of a central body with integrated radiating arms was used for repairing Spigelian hernias in 54 patients. The implant was positioned in preperitoneal sublay, and the straps were delivered across the abdominal musculature with a needle passer, and then, after fascia closure, cut short in the subcutaneous layer.
Results: The friction of the straps passing through the abdominal wall served to hold the mesh in place, guaranteeing a wide overlap over the defect without fixation. In a long-term follow-up of 6 to 84 months (mean 64 months), a very low rate of complications occurred, but no recurrence was reported.
Conclusions: The tentacle strap system of the prosthesis allowed for an easy, fast and safe fixation-free placement granting a wide overlap, avoiding intraoperative complications. Greatly reduced pain and a negligible amount of postoperative complications characterized the postoperative outcome.
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http://dx.doi.org/10.3390/jcm12123866 | DOI Listing |
JACC Case Rep
September 2025
Department of Cardiovascular Medicine, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
Background: Cardiac sarcoidosis (CS) usually affects the left ventricle and presents with nonspecific features like conduction abnormalities and ventricular arrhythmias. However, right ventricle (RV)-dominant involvement has been increasingly reported, making diagnosis difficult.
Case Summary: A 55-year-old man presented with palpitations.
Invest Ophthalmol Vis Sci
September 2025
The University of Leicester Ulverscroft Eye Unit, School of Psychology and Vision Sciences, University of Leicester, Leicester, United Kingdom.
Purpose: To define the genetic architecture of foveal morphology and explore its relevance to foveal hypoplasia (FH), a hallmark of developmental macular disorders.
Methods: We applied deep-learning algorithms to quantify foveal pit depth from central optical coherence tomography (OCT) B-scans in 61,269 UK Biobank participants. A genome-wide association study (GWAS) was conducted using REGENIE, adjusting for age, sex, height, and ancestry.
Medicine (Baltimore)
September 2025
Department of Pediatrics, Affiliated Hospital of Jining Medical University, Jining, Shandong Province, China.
Rationale: Weaver syndrome is a rare congenital overgrowth disorder characterized by a wide spectrum of clinical manifestations that often overlap with other overgrowth syndromes. It is primarily caused by pathogenic variants in the Enhancer of Zeste Homolog 2 (EZH2) gene on chromosome 7q36.1.
View Article and Find Full Text PDFGene
September 2025
Department of Cardiac Surgery, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital(Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China; Department of Neck and Thoracic Surgery, Yingde People's Hospital, Yingde, Guangdong, China. Electronic add
Background: Recurrent 10p15.3 microdeletion syndrome is a rare multisystem disorder characterized by abnormal facial features, global developmental delay (DD)/intellectual disability (ID), short stature, hand/foot malformation, and congenital heart defects (CHDs). However, the specific genetic defects that contribute to the cardiac phenotype remain unclear.
View Article and Find Full Text PDFLancet Rheumatol
September 2025
Leeds Institute for Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, UK; NIHR Leeds Biomedical Research Centre, Leeds, UK.
Vacuoles, E1 enzyme, X-linked, autoinflammatory, and somatic (VEXAS) syndrome is a newly identified disorder caused by an acquired monogenic somatic UBA1 gene mutation, affecting nuclear and cytoplasmic ubiquitination. This mutation triggers immune dysregulation, leading to diverse clinical and pathological features resembling inflammatory rheumatic diseases. Blood abnormalities stem from myeloid precursor dysfunction, presenting as elevated concentrations of inflammatory markers and cytokines, leukopenia, and macrocytosis.
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