Carrying on with life as a lung cancer survivor: a qualitative study of Australian survivors' employment, finances, relationships, and healthcare experiences.

Background: With novel therapies, more individuals are living longer with lung cancer (LC). This study aimed to understand the impacts of LC on life domains such as employment, finances, relationships, and healthcare needs.

Methods: Individuals 18+, diagnosed with LC, 6-24 months post-treatment were recruited through an Australian LC cohort study (Embedding Research and Evidence in Cancer Healthcare-EnRICH).

Application of a revised model for coping with advanced cancer to qualitatively explore lung cancer survivors' experiences of ongoing physical effects, novel treatments, uncertainty, and coping.

Purpose: Lung cancer remains underrepresented in cancer survivorship research. This study aimed to understand survivors' physical/psychological challenges, experiences of immunotherapy (IO) and targeted therapy (TT), and psychological adjustment through application of the Roberts et al. (2017) advanced cancer adaptation of Folkman and Greer's appraisal and coping model.

type D epsilon toxin produces a rapid and dose-dependent cytotoxic effect on cerebral microvascular endothelial cells in vitro.

type D epsilon toxin (ETX) is responsible for a severe and frequently fatal neurologic disorder in ruminant livestock. Light microscopic, immunohistochemical, and ultrastructural studies have suggested that ETX injury to the cerebral microvasculature, with subsequent severe, generalized vasogenic edema and increased intracranial pressure, is critically important in producing neurologic dysfunction. However, the effect of ETX on brain capillary endothelial cells in vitro has not been examined previously, to our knowledge.

Tumour angiogenesis, anti-angiogenic therapy and chemotherapeutic resistance.

In order for a tumour to continue to grow and disseminate, it must acquire a new blood supply. Neovascularisation can be enacted by a number of different mechanisms. This dependence of tumour progression on an augmented vascular supply has been exploited by the development of anti-angiogenic drugs, which are designed to inhibit new blood vessel formation or disrupt existing tumour-associated vasculature, both leading to ischaemic-hypoxic tumour cell death.

Loss of Endothelial Barrier Antigen Immunoreactivity in Rat Retinal Microvessels is Correlated with Clostridium perfringens Type D Epsilon Toxin-induced Damage to the Blood-Retinal Barrier.

Clostridium perfringens type D epsilon toxin (ETX) is a potent neurotoxin producing a severe, and often fatal, neurological disorder in ruminant livestock. Microvascular damage appears to be the fundamental action of ETX in the brain and, recently, similar vascular injury, with subsequent severe vasogenic oedema, has been reported in the retina of rats given ETX. Endothelial barrier antigen (EBA) is a useful marker of an intact blood-brain barrier in rats and it has been shown that loss of EBA immunoreactivity is correlated with ETX-induced cerebral microvascular damage in this species.

Characterization of an 'Amyloid Only' Transgenic (B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax) Mouse Model of Alzheimer's Disease.

The spatiotemporal pattern of cerebral amyloid deposition, detectable as light microscopically recognizable aggregates in an 'amyloid only' transgenic mouse model of Alzheimer's disease, B6C3-Tg(APPswe,PSEN1dE9)85Dbo/Mmjax, is reported for the first time in this strain. Monoclonal and polyclonal antibodies were used to detect amyloid deposition immunohistochemically in brains collected from these mice at 3-12 months of age. Amyloid aggregates (20-200 μm) were first found in serial, whole coronal sections of brain at 4 months of age and these increased progressively, plateauing at 11-12 months.

Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation.

Background: The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary injury factor that can drive ongoing neuronal injury. Despite this, treatments that have targeted aspects of the inflammatory pathway have not shown significant efficacy in clinical trials.

Main Body: We suggest that this may be because classical inflammation only represents part of the story, with activation of neurogenic inflammation potentially one of the key initiating inflammatory events following TBI.

Cytokine-mediated blood brain barrier disruption as a conduit for cancer/chemotherapy-associated neurotoxicity and cognitive dysfunction.

Neurotoxicity is a common side effect of chemotherapy treatment, with unclear molecular mechanisms. Clinical studies suggest that the most frequent neurotoxic adverse events affect memory and learning, attention, concentration, processing speeds and executive function. Emerging preclinical research points toward direct cellular toxicity and induction of neuroinflammation as key drivers of neurotoxicity and subsequent cognitive impairment.

Toll-like receptor 4 signaling: a common biological mechanism of regimen-related toxicities: an emerging hypothesis for neuropathy and gastrointestinal toxicity.

Regimen-related toxicities remain a priority concern within the field of supportive care in cancer. Despite this, many forms of toxicity are under reported and consequently poorly characterised. Although there have been significant improvements in our understanding of regimen-related toxicities, symptom management continues to occur independently raising concerns such as drug interactions and the tendency to emphasise management of a single symptom at the expense of others.

Advancing drug therapy for brain tumours: a current review of the pro-inflammatory peptide Substance P and its antagonists as anti-cancer agents.

Evidence for the involvement of the Substance P (SP)/NK1 receptor system in the development and progression of cancer strongly supports its potential as a therapeutic target in malignancies. Novel strategies for approaching cancer treatment are urgently required particularly with regard to tumours of the central nervous system (CNS), which are notoriously difficult to effectively treat and associated with extremely poor prognosis for many patients. This is due, in part, to the presence of the highly specialised blood-brain barrier, which is known to restrict common treatments such as chemotherapy and hinder early tumour diagnosis.

Multiple fractures following camel bite of the face (a case report).

A rare case of multiple fractures following camel bite of the face in a young male, producing facial deformity and open bite is described. Fractures were confirmed by X-rays and CT scan. Treatment consisted of an open reduction and interosseous wiring of fractures to attain normal occlusion which was maintained by intermaxillary and suspension wire fixation followed by soft tissue repair.

Goldenhar's syndrome--a case report.

A case of Goldenhar's syndrome in a three months old male child with epibulbar dermoid (Fig. 1), accessory auricular appendages (Fig. 2), transverse facial cleft (Figs.

Syringe suction drain.

A mini suction drain made up of a 20 cc glass syringe, a stainless steel spring and a scalp vein cannula (whose needle end has been cut off and multiple holes made in the distal 2.5-5 cm) is described. It is very useful in preventing postoperative haematoma formation, in nasogastric tube suction, in easy drawing up of fluids from vials, and in exploration of deep seated abscesses and collections.