Iris Reconstruction: A Surgeon's Guide.

Objectives: The aim of this review paper is to summarise surgical options available for repairing iris defects at the iris-lens plane, focusing on suturing techniques, iridodialysis repair, and prosthetic iris devices. Methods: A thorough literature search was conducted using multiple databases, including Medline, PubMed, Web of Science Core Collection, and the Cochrane Library, from inception to February 2024. Relevant studies were screened based on predefined criteria, and primary references cited in selected articles were also reviewed. Results: Various surgical techniques were identified for iris defect repair. Suturing methods such as interrupted full-thickness sutures and the McCannel technique offer solutions for smaller defects, while iridodialysis repair techniques address detachment of the iris from the ciliary body. Prosthetic iris devices, including iris-lens diaphragm devices, endocapsular capsular tension ring-based devices, and customizable artificial iris implants, provide options for larger defects, each with its own advantages and limitations. Conclusions: Successful iris reconstruction requires a personalised approach considering factors like defect size, ocular comorbidities, and patient preference. Surgeons must possess a thorough understanding of available techniques and prosthetic devices to achieve optimal outcomes in terms of both visual function and, nonetheless, cosmetic appearance.

Excess pancreatic elastase alters acinar-ß cell communication by impairing the mechano-signaling and the PAR2 pathways.

Type 1 (T1D) or type 2 diabetes (T2D) are caused by a deficit of functional insulin-producing ß cells. Thus, the identification of ß cell trophic agents could allow the development of therapeutic strategies to counteract diabetes. The discovery of SerpinB1, an elastase inhibitor that promotes human ß cell growth, prompted us to hypothesize that pancreatic elastase (PE) regulates ß cell viability. Here, we report that PE is up-regulated in acinar cells and in islets from T2D patients, and negatively impacts ß cell viability. Using high-throughput screening assays, we identified telaprevir as a potent PE inhibitor that can increase human and rodent ß cell viability in vitro and in vivo and improve glucose tolerance in insulin-resistant mice. Phospho-antibody microarrays and single-cell RNA sequencing analysis identified PAR2 and mechano-signaling pathways as potential mediators of PE. Taken together, our work highlights PE as a potential regulator of acinar-ß cell crosstalk that acts to limit ß cell viability, leading to T2D.

Analysing the Society for Vascular Surgery and American Association for Vascular Surgery scoring systems for outcomes post-endovascular aortic repair.

BACKGROUND AND AIMS: Assess the association between the Society for Vascular Surgery/American Association for Vascular Surgery (SVS/AVSS) (Rutherford et al., J Vasc Surg 26: 517-38, 1997; Chaikof et al., J Vasc Surg 35:1061-6, 2002) medical comorbidity scoring scheme (MCS), and the global scoring system (GS) and major morbidity and mortality after elective endovascular aneurysm repair. Primary end points were peri-operative morbidity and mortality. Secondary end points were intensive care unit admission, high dependency unit admission, total stay > 5 days and 2-year mortality. METHODS: The project was approved by the Galway Clinical Research Ethics Committee. This project followed the Declaration of Helsinki. Binary logistic regression was performed to assess the association of the scores and their individual components with the primary and secondary outcomes. Results were reported as odds ratio (OR) per point increase in score with 95% confidence intervals (CI) and the Hosmer-Lemeshow (HL). RESULTS: Between 2002 and 2015, 401 patients underwent elective EVARs. MCS was calculated for 396 patients while GS was calculated for 183 patients. The MCS (OR 1.906, CI 1.017-3.574, p = 0.044) was associated with perioperative morbidity. The MCS was associated with perioperative mortality (OR 8.875, CI 1.918-41.070, p = 0.005). The GS was associated with perioperative morbidity (OR 11.929, CI 1.151-123.584, p = .038) but not associated with perioperative mortality (OR 3.62, CI 0.006-2118.148, p = .692). CONCLUSIONS: The MCS shows association with perioperative morbidity and mortality. GS shows association with perioperative morbidity but not perioperative mortality; however, this may be due to our study being underpowered. We believe that the analysis of higher numbers of patients could unmask trends in both of these scores and individual components of both scores changed.

The rise and fall of pneumococcal serotypes carried in the PCV era.

Streptococcus pneumoniae is a major cause of meningitis, sepsis and pneumonia worldwide. Vaccination using pneumococcal conjugate vaccines (PCV) has therefore been part of the UK's childhood immunisation programme since 2006. Here we describe pneumococcal carriage rates in children under five years of age attending the paediatric department of a large UK hospital in response to vaccine implementation over seven winter seasons from 2006 to 2013. S. pneumoniae (n=696) were isolated from nasopharyngeal swabs (n=2267) collected during seven consecutive winters, October to March, 2006/7 to 2012/13. This includes the period immediately following the introduction of the seven-valent pneumococcal conjugate vaccine (PCV7) in 2006 in addition to pre- and post-PCV13 introduction in 2010. We show a decrease in PCV13 vaccine serotypes (VT) in the three years following PCV13 vaccine implementation (2010/11 to 2012/13). Serotype 6A represented the only observed VT following PCV13 implementation with all others (including PCV7 serotypes) absent from carriage. Overall pneumococcal carriage, attributable to non-VT (NVT), was consistent across all sampling years with a mean of 31·1%. The ten most frequently isolated NVTs were 6C, 11A, 15B, 23B, 15A, 21, 22F, 35F, 23A and 15C. Fluctuations in the prevalence of each were however noted. Comparing prevalence at 2006/07 with 2012/13 only 15A was shown to have increased significantly (p value of 0·003) during the course of PCV implementation. These data support the increasing evidence that the primary effect of PCVs is due to population immunity by reducing or eliminating the carriage of invasive VT serotypes. With IPD being increasingly attributed to non-vaccine serotypes, surveillance of carriage data continues to act as an early warning system for vaccine design and public health policy that require continual data of both carried pneumococcal serotypes and IPD attributed serotype data.