Cairns Hospital, known as the Cairns Base Hospital between 1932 and 2013, is the largest major hospital in Far North Queensland, Australia. It is located at 165 The Esplanade, Cairns North, Cairns. The hospital offers general service to Cairns' population of about 155,000 and other nearby communities. The building complex has a 667 space multi-storey car park with a pedestrian overpass linking it to the rest of the hospital.In 2011, a shortage of beds for mental health patients meant some were staying for more than 100 hours in the emergency department.
Melioidosis is caused by Burkholderia pseudomallei, a Gram-negative environmental saprophyte found in tropical and subtropical regions globally. The aims of treatment for melioidosis are to prevent death and other complications of septic shock, and to eradicate B. pseudomallei and prevent relapse. To achieve these aims, treatment comprises an intensive phase involving minimum 10-14 days of intravenous ceftazidime, meropenem, or imipenem, and a prolonged eradication phase of at least 3 months of oral trimethoprim-sulfamethoxazole. Here, we review the clinical trial and other evidence that supports melioidosis treatment guidelines, and the approach to complications including treatment side effects, relapse, and antimicrobial resistance.
Endometrial cancer (EC) is a hormonally driven malignancy with a strikingly uneven global distribution, interestingly occurring far more frequently in developed countries. Central to its pathogenesis is endocrine imbalance, which is most notably due to prolonged exposure to unopposed oestrogen, which fuels tumour initiation and progression. The dynamic interplay between oestrogen and progesterone signalling shapes disease biology and underpins the widespread use of hormonal therapies, particularly in early-stage disease and in patients who are not surgical candidates. Current EC management relies on a multimodal approach, integrating surgery, radiotherapy, hormonal therapy, and chemotherapy. However, the therapeutic landscape is rapidly evolving. Ongoing clinical trials are investigating innovative immunotherapeutic strategies, including biomarker-driven treatments, rational combination regimens, and adoptive cellular therapies. Immune checkpoint inhibitors have already demonstrated clinical benefit in mismatch repair-deficient EC. In parallel, cancer vaccines targeting tumour-associated antigens such as folate-binding protein (FBP), along with emerging modalities like CAR T-cell therapy, are being explored for their potential to reduce recurrence and improve long-term outcomes. Recent advances have highlighted the PI3K/AKT/mTOR signalling cascade as a key therapeutic target, offering opportunities to enhance the effectiveness of endocrine treatments. At the same time, growing evidence underscores the importance of crosstalk between hormonal dysregulation and immune mechanisms within the tumour microenvironment, a relationship that profoundly influences tumour behaviour and therapeutic response. In this review, we present a comprehensive overview of the current state of EC management and emerging therapeutic directions, with particular emphasis on treatment options available in Poland, the authors' country of origin.
Background/Objectives: Traumatic brain injury (TBI) is a leading cause of morbidity and mortality worldwide. Electrolyte disturbances are common in this patient cohort, with serum chloride frequently elevated. Chloride dysregulation may be associated with poor neurological outcomes through mechanisms including paradoxical gamma amino butyric acid receptor excitation, cytotoxic edema, and ferroptosis. The aim of this review was to evaluate the relationship between serum chloride levels and outcomes in patients with TBI. Methods: A literature review was performed to identify all potential studies that reported on serum chloride levels and TBI. All study types and patient groups were included. Studies were included if they reported on serum chloride measurements as well as outcomes such as mortality, surgical intervention, intracranial pressure, and neurological/functional outcome scores in patients with TBI. References and citations were also reviewed. Results: A small number of mostly retrospective studies with modest patient numbers demonstrate an association between high chloride levels and increased mortality in patients with TBI, with this relationship persisting independent of hypernatremia. Recent large, randomized trials showed that balanced crystalloid solutions, despite lower chloride content, may be associated with worse outcomes in TBI patients compared to saline. No studies directly correlated chloride levels with intracranial pressure measurements. Chloride level rather than total chloride load appears more strongly associated with adverse outcomes, with non-hypertonic saline sources contributing substantially to chloride burden. Mechanistic evidence links chloride channel dysregulation to ferroptosis and cytotoxic edema, with sex-specific patterns of transporter expression. Conclusions: Limited available evidence suggests that hyperchloremia is independently associated with increased mortality in TBI though causality remains unestablished. The findings regarding balanced solutions challenge conventional fluid management assumptions and highlight the complexity of chloride's role in TBI pathophysiology. The absence of studies directly correlating chloride with intracranial pressure represents a critical evidence gap. Future studies with larger patient numbers, prospective designs, and multimodal neuromonitoring should further define these relationships to inform evidence-based chloride management strategies.
