A narrative review of nursing in Saudi Arabia: prospects for improving social determinants of health for the female workforce.

Introduction: Nurses represent the backbone of global healthcare systems where women typically deliver care and men lead. The Kingdom of Saudi Arabia (KSA) highly relies on foreign female nurses despite Saudisation policies designed to localize its workforce. Yet, in the context of an ambitious 2016-30 national health transformation program to modernize public health in a high-income and rapidly developing country, intersectional inequalities persist for migrant and local nurses in KSA.

Blood Transfusions in Patients with Advanced Cancer at the End-of-Life: Are They Really Beneficial?

Objectives: Anaemia is prevalent in individuals with advanced cancer and may contribute to adversely affecting their quality of life. In palliative care (PC), red blood cell (RBC) transfusions are regularly administered to address bothersome symptoms such as fatigue and dyspnoea. However, they are not without risks and adverse effects in individuals who are often frail at the end of life.

Intensity of Care at the End-of-Life in Pediatrics: A Single Center Analysis With Implications for Advanced Care Planning in Saudi Arabia.

Advances in medicine have altered the progression of several pediatric disorders. However, this progress also comes with medical, economic, and ethical challenges, which can negatively affect children's quality of life. This study examines the quality of care of children with malignant and non-malignant conditions at the end of life.

Prevalence of Anxiety, Depression, and Distress and Their Association With Problems Encountered by Advanced Cancer Patients in a Tertiary Hospital in Saudi Arabia.

Background: Patients with advanced cancer often suffer from significant psychological distress, anxiety, and depression, which can profoundly influence their quality of life. This study aimed to evaluate the prevalence and severity of these psychological factors in advanced cancer patients. Additionally, it sought to identify related psychosocial, practical, emotional, and physical problems and their association with the psychological factors.

Coping with change.

Although the NHS is continually changing, the qualifications and skills I have acquired will always be valuable. I have also learned that change provides an opportunity to develop new skills.

Neuronal apoptosis induced by endoplasmic reticulum stress is regulated by ATF4-CHOP-mediated induction of the Bcl-2 homology 3-only member PUMA.

An increasing body of evidence points to a key role of endoplasmic reticulum (ER) stress in acute and chronic neurodegenerative conditions. Extensive ER stress can trigger neuronal apoptosis, but the signaling pathways that regulate this cell death remain unclear. In the present study, we demonstrate that PUMA, a Bcl-2 homology 3 (BH3)-only member of the Bcl-2 family, is transcriptionally activated in cortical neurons by ER stress and is essential for ER-stress-induced cell death.

The Chk1/Cdc25A pathway as activators of the cell cycle in neuronal death induced by camptothecin.

Cell cycle regulators appear to play a paradoxical role in neuronal death. We have shown previously that cyclin-dependent kinases (CDKs), along with their downstream effectors, Rb (retinoblastoma) and E2F/DP1 (E2 promoter binding factor/deleted in polyposis 1), regulate neuronal death evoked by the DNA damaging agent camptothecin. However, the mechanism by which CDKs are activated in this model is unclear.

Regulation of axotomy-induced dopaminergic neuron death and c-Jun phosphorylation by targeted inhibition of cdc42 or mixed lineage kinase.

Mechanical transection of the nigrostriatal dopamine pathway at the medial forebrain bundle (MFB) results in the delayed degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). We have previously demonstrated that c-Jun activation is an obligate component of neuronal death in this model. Here we identified the small GTPase, cdc42, and mixed lineage kinases (MLKs) as upstream factors regulating neuronal loss and activation of c-Jun following MFB axotomy.

Apical role for BRG1 in cytokine-induced promoter assembly.

IFN-gamma induction of the CIITA (class II transactivator) promoter (pIV) requires Brahma-related gene 1 (BRG1), a chromatin-remodeling enzyme. However, the events that lead to pIV activation are only partially understood, and the point at which BRG1 acts is unknown. The first IFN-gamma-induced event triggers nuclear translocation of STAT1 (signal transducer and activator of transcription 1), which binds IFN-gamma-responsive promoters.

Differential roles of nuclear and cytoplasmic cyclin-dependent kinase 5 in apoptotic and excitotoxic neuronal death.

Cyclin-dependent kinase 5 (cdk5) is a member of the cyclin-dependent kinase family whose activity is localized mainly to postmitotic neurons attributable to the selective expression of its activating partners p35 and p39. Deregulation of cdk5, as a result of calpain cleavage of p35 to a smaller p25 form, has been suggested to be a central component of neuronal death underlying numerous neurodegenerative diseases. However, the relevance of cdk5 in apoptotic death that relies on the mitochondrial pathway is unknown.

Multiple cyclin-dependent kinases signals are critical mediators of ischemia/hypoxic neuronal death in vitro and in vivo.

The mechanisms involving neuronal death after ischemic/hypoxic insult are complex, involving both rapid (excitotoxic) and delayed (apoptotic-like) processes. Recent evidence suggests that cell cycle regulators such as cyclin-dependent kinases are abnormally activated in neuropathological conditions, including stroke. However, the function of this activation is unclear.

p53 activation domain 1 is essential for PUMA upregulation and p53-mediated neuronal cell death.

The p53 tumor suppressor gene has been implicated in the regulation of apoptosis in a number of different neuronal death paradigms. Because of the importance of p53 in neuronal injury, we questioned the mechanism underlying p53-mediated apoptosis in neurons. Using adenoviral-mediated gene delivery, reconstitution experiments, and mice carrying a knock-in mutation in the endogenous p53 gene, we show that the transactivation function of p53 is essential to induce neuronal cell death.

The proapoptotic gene SIVA is a direct transcriptional target for the tumor suppressors p53 and E2F1.

The p53 tumor suppressor gene is believed to play an important role in neuronal cell death in acute neurological disease and in neurodegeneration. The p53 signaling cascade is complex, and the mechanism by which p53 induces apoptosis is cell type-dependent. Using DNA microarray analysis, we have found a striking induction of the proapoptotic gene, SIVA.

Cyclin-dependent kinase 5 is a mediator of dopaminergic neuron loss in a mouse model of Parkinson's disease.

Recent evidence indicates that cyclin-dependent kinases (CDKs, cdks) may be inappropriately activated in several neurodegenerative conditions. Here, we report that cdk5 expression and activity are elevated after administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a toxin that damages the nigrostriatal dopaminergic pathway. Supporting the pathogenic significance of the cdk5 alterations are the findings that the general cdk inhibitor, flavopiridol, or expression of dominant-negative cdk5, and to a lesser extent dominant-negative cdk2, attenuates the loss of dopaminergic neurons caused by MPTP.

Apoptosis-inducing factor is involved in the regulation of caspase-independent neuronal cell death.

Caspase-independent death mechanisms have been shown to execute apoptosis in many types of neuronal injury. P53 has been identified as a key regulator of neuronal cell death after acute injury such as DNA damage, ischemia, and excitotoxicity. Here, we demonstrate that p53 can induce neuronal cell death via a caspase-mediated process activated by apoptotic activating factor-1 (Apaf1) and via a delayed onset caspase-independent mechanism.