The Queen Elizabeth Hospital (Q.E.H.) is located in Barbados' capital city Bridgetown, which is located in the parish of Saint Michael. The hospital is the main General Hospital for the southern part of the island.The hospital can perform most surgeries, and specialized care includes the areas of: gynaecology, paediatrics, obstetrics, cardiac surgery, plastic surgery, psychotherapy, radiology, radiography and ophthalmology. The Q.E.H. boasts also having a series of operating theaters.The Q.E.H. is a 600-bed complex lying in the Eastern section of Bridgetown, located on the southeast bank of the Constitution River. The current hospital building was constructed in 1963–1964, and officially opened on 14 November 1964.In December 2004, the Barbados Ministry of Health disclosed that based on foreign-investment into the country, there is a future possibility that genetic re-constructive surgery may be performed at the Q.E.H.The Accident and Emergency Department, formerly known as QEH Casualty, was transformed in 1990 into the new A&E Department. The department was pioneered by Dr Irvine Brancker and Dr Van Tyne. It opened with a team of initially 12 junior doctors and 2 consultants. Presently, there are 20 doctors in the department. As the busiest department in the hospital, they attend to approximately 45,000 patients each year. Offering patient care on par with some first world countries, Dr Chaynie Williams, the first female head of the department, applauds the skill set of her staff and also notes that the A&E improvement programme has put measures in place to make the visit to A&E a more comfortable one, including the addition of patient advocates, a redesign of the physical space, improvements to staffing complements, improved outreach and efficiencies plus a concerted, ongoing effort to reduce waiting times.In 2006 it was stated that the Government of Barbados was spending $112 million (US$56 million) annually running the hospital.In 2008 the former Minister of Health Dr. Jerome Walcott said that the current hospital which is over 40 years old should be replaced by a new state of the art hospital complex. He classified it as nonsensical to spend over $400 million (US$200 million) on an extension of the current facility saying that it may cost upwards of $600 million (US$300 million) in the end. He went on to suggest the current QEH might be better off turned into a nursing home. Later in 2011 the government's Donville Inniss gave the figure of around $800 million to build a new Hospital for Barbados. It was stated the government will need to review several factors including cost(s) and possible locations.PAHO has rated the current facility as a Category B hospital facility..
Microbial biofilms are increasingly recognized as critical modulators of chronic airway inflammation and immune dysregulation in pulmonary diseases. This review summarizes current evidence on how biofilm formation and persistence alter host immune responses, contributing to the pathogenesis of chronic lung disorders. We first outline the characteristics of respiratory biofilms and the major pathogens involved. We then discuss how biofilms reshape innate and adaptive immunity—impairing pattern recognition receptor signaling, promoting neutrophil extracellular trap (NET) formation, altering macrophage polarization, and skewing T-cell differentiation. These immune alterations sustain low-grade inflammation, tissue remodeling, and immune tolerance, driving disease progression in chronic obstructive pulmonary disease, bronchiectasis, severe asthma, and even lung cancer. We further highlight emerging diagnostic biomarkers and therapeutic approaches targeting biofilm-associated immune pathways, including combined antibiofilm and immunomodulatory strategies. Finally, we identify key knowledge gaps and propose future research directions, emphasizing multi-omics approaches and personalized interventions to better define and target biofilm-driven immune dysregulation in chronic respiratory diseases.
Multiple myeloma (MM) is a complex hematologic malignancy characterized by the abnormal proliferation of plasma cells in the bone marrow. Despite advances in therapy, resistance remains a significant obstacle to curing the disease. Long non-coding RNAs (lncRNAs), a broad family of regulatory RNA molecules, have recently been recognized as important players in MM biology, influencing disease progression and treatment response. This review explores current insights into the diverse roles of lncRNAs in MM, focusing on their involvement in key molecular processes, including miRNA sponging, epigenetic regulation, apoptosis, and interactions with signaling pathways such as PI3K/Akt and STAT3. Additionally, the review evaluates emerging treatment strategies targeting lncRNAs, including RNA-based therapeutics, CRISPR/Cas9 technology, and exosome-mediated delivery systems, assessing their potential to overcome drug resistance and improve clinical outcomes. By integrating molecular research with clinical implications, this review emphasizes the promise of lncRNAs as biomarkers and therapeutic targets in MM and offers a framework for future research and development.
Dysregulation of the nuclear factor kappa B (NF-κB) signaling pathway is closely associated with inflammation-driven carcinogenesis, tumor progression and resistance to conventional therapies. Sustained NF-κB activation enhances malignant cell survival, proliferation and immune evasion by promoting proinflammatory and antiapoptotic gene expression. This review aims to critically evaluate natural dietary compounds that modulate NF-κB signaling and explore their translational relevance in cancer prevention and therapy. We analyzed key classes of phytochemicals such as polyphenols (curcumin, resveratrol), flavonoids (EGCG, quercetin), alkaloids (berberine), and terpenoids (celastrol), focusing on their molecular mechanisms of NF-κB inhibition, preclinical anticancer efficacy, and emerging strategies to overcome pharmacokinetic limitations. Preclinical evidence consistently demonstrates that these compounds inhibit NF-κB activity by targeting upstream kinases, preventing nuclear translocation, and suppressing downstream protumorigenic gene expression. Notably, advances in nanotechnology-based delivery systems, including liposomes and polymeric nanoparticles, have markedly enhanced the stability, bioavailability, and tumor-specific delivery of these agents in vivo. In conclusion, natural NF-κB-targeting compounds offer a promising multitargeted strategy for integrative cancer therapy. Continued development of optimized formulations and well-designed clinical trials will be essential to translate their potential into effective nutraceutical or adjuvant interventions in oncology.
Uraemic cardiomyopathy is a term widely used to describe the severe myocardial disease characterized by left ventricular hypertrophy and diffuse interstitial fibrosis that occurs in kidney failure. The causative factors are multiple and include many of the haemodynamic and metabolic abnormalities that are present in patients with chronic kidney disease (CKD). These abnormalities start to cause left ventricular damage and dysfunction in the early stages of CKD, probably from an estimated glomerular filtration rate of approximately 60 ml/min/1.73 m2. The term ‘uraemic cardiomyopathy’ is therefore misleading and inaccurate, and we suggest instead using the term ‘CKD-associated cardiomyopathy’. In this Review, we describe the clinical manifestations and myocardial abnormalities seen on imaging in both CKD and kidney failure, discuss the multiple and interacting causative factors, and consider both established and prospective treatment options. A better understanding of the pathogenesis of CKD-associated cardiomyopathy is likely to lead to the introduction of effective preventive therapies, with success measured as a reduction in the proportion of patients reaching kidney failure with severe cardiomyopathy and ultimately in a reduction in the mortality from this condition. Chronic kidney disease (CKD)-associated cardiomyopathy, also known as uraemic cardiomyopathy, describes the myocardial abnormalities that occur in patients with CKD or kidney failure. In this Review, Edwards and colleagues discuss the pathophysiological mechanisms of this condition, as well as the imaging, prevention and treatment options.
To evaluate the long-term efficacy and safety of gilteritinib compared with salvage chemotherapy (SC) in patients with relapsed/refractory FMS-like tyrosine kinase 3 (FLT3)-mutated acute myeloid leukemia (AML). In the phase 3 COMMODORE (NCT03182244) trial, patients with relapsed/refractory FLT3-mutated AML from China, Russia, Singapore, Thailand, and Malaysia were randomized to gilteritinib (120 mg/day) or SC. The long-term follow-up included assessments every 3 months for a maximum of 3 years from the end-of-treatment visit. The primary endpoint was overall survival (OS). Secondary endpoints included event-free survival (EFS), complete remission (CR) rate, hematopoietic stem cell transplantation (HSCT) rate, and transfusion maintenance and conversion rates. Overall, 276 patients (gilteritinib, n = 137; SC, n = 139) completed the long-term follow-up. Most (88.0%) patients were Asian. The median (95% confidence interval [CI]) OS was longer with gilteritinib versus SC (10.3 [8.8, 12.7] vs 5.4 [4.1, 8.1] months, respectively; hazard ratio [HR; 95% CI], 0.612 [0.451, 0.832]), with a median follow-up of 34.6 months. The median (95% CI) EFS was longer with gilteritinib versus SC (2.1 [< 0.1, 3.2] vs 0.6 [0.2, 1.2] months, respectively; HR [95% CI], 0.589 [0.438, 0.792]). The CR rate was 20.4% and 11.5% in the gilteritinib and SC arms, respectively. During the entire study period, 22.6% and 7.9% of patients in the gilteritinib and SC arms underwent HSCT, respectively; 18.2% of patients in the gilteritinib arm received on-study HSCT. No new safety concerns were identified. Long-term gilteritinib treatment improved clinical outcomes compared with SC and was well-tolerated in a predominantly Asian population with relapsed/refractory FLT3-mutated AML.
