Pioneering the 12-hour shift in Australia – implementation and limitations

Twelve-hour shift rostering offers an alternative to the traditional 8- and 10-hour shifts usually worked in Australian nursing practice. This paper outlines the implementation process involved in introducing 12-hour shifts in a Melbourne hospital intensive care unit. The process was instigated by the nursing staff. After extensive consultation with the union and hospital management, a roster pattern of two 12-hour days, followed by 12-hour night shifts then days off, was introduced. Independent researchers were engaged to evaluate the impact of the 12-hour shifts on staff well-being and work performance. Effects on staff retention, sick leave and inservice education were examined. The researchers found that well-being and work performance were minimally affected by the 12-hour shift roster, while staff retention and sick leave were unaffected. Further, the pattern of 12-hour shifts, which was democratically implemented, was preferred by the nursing staff and did not diminish their well-being and work performance.     

Clinical and cytogenomic findings in OAV spectrum

The oculoauriculovertebral spectrum (OAVS) is characterized by anomalies involving the development of the first and second pharyngeal arches during the embryonic period. The phenotype is highly heterogeneous, involving ears, eyes, face, neck, and other systems and organs. There is no agreement in the literature for the minimum phenotypic inclusion criteria, but the primary phenotype involves hemifacial microsomia with facial asymmetry and microtia. Most cases are sporadic and the etiology of this syndrome is not well known. Environmental factors, family cases that demonstrate Mendelian inheritance, such as preauricular appendages, microtia, mandibular hypoplasia, and facial asymmetry; chromosomal abnormalities and some candidate genes suggest a multifactorial inheritance model. We evaluated clinical, cytogenomic and molecularly 72 patients with OAVS, and compared our findings with patients from the literature. We found 15 CNVs (copy number variations) considered pathogenic or possibly pathogenic in 13 out of 72 patients. Our results did not indicated a single candidate genomic region, but recurrent chromosomal imbalances were observed in chromosome 4 and 22, in regions containing genes relevant to the OAVS phenotype or related to known OMIM diseases suggesting different pathogenic mechanisms involved in this genetically and phenotypic heterogeneous spectrum.

     

Evolutionary development of three gonadotropin-releasing hormone (GnRH) systems in vertebrates

Gonadotropin-releasing hormone (GnRH) is the neuropeptide that links the brain to the reproductive system. Most vertebrate species express two forms of GnRH, which differ in amino acid sequence, localization, distribution, and embryological origin. The GnRH system in the ventral forebrain produces a species-specific GnRH form and projects toward the gonadotropic cell in the pituitary. The GnRH neurons of this system originate from the olfactory placode and migrate into the brain during early development. The other GnRH system is localized in a nucleus in the midbrain, where large cells express chicken-GnRH-II, of which the function is still unclear. In modern teleosts, a third GnRH system is present in the terminal nerve, which contains salmon GnRH. The three GnRH systems appear at different times during fish evolution. Besides the two accepted lineages in GnRH evolution (of conserved chicken GnRH-II in the midbrain and of mammalian GnRH or species-specific GnRH in the hypophysiotropic system), we propose a third lineage: of salmon GnRH in the terminal nerve.     

Irritable bowel syndrome among patients attending General Outpatients' clinics in Jos, Nigeria

Irritable bowel syndrome (IBS) is a common disorder in the Western world. Its prevalence is yet to be fully determined in the African setting. This was a cross-sectional study of patients attending three General Outpatient clinics in Jos, Nigeria. Four hundred and eighteen randomly selected patients were interviewed using a structured questionnaire based on the Rome II diagnostic criteria for IBS. Excluded from the study were patients with established organic disease, memory problems, and pregnant women. Eighteen patients were excluded based on these criteria and 400 were analysed using Epi Info 2000 (Atlanta, Georgia, USA) statistical computer software. One hundred and thirty-two (33%) out of the 400 patients fulfilled the criteria for the diagnosis of IBS, the female to male ratio being 1.13 : 1. IBS was significantly associated with increasing age (P=0.03) and depression (P<0.001). The prevalence of IBS is high among patients attending primary care in the African setting with depression being the likely reason for seeking care.     

Neutrophil granulocytes as host cells and transport vehicles for intracellular pathogens: apoptosis as infection-promoting factor

Polymorphonuclear neutrophil granulocytes (PMN) are primary antimicrobial effector cells of the innate immune system and serve to destroy invading pathogens. Although most ingested microorganisms are killed readily inside PMN, several obligate or facultative intracellular pathogens survive even in this hostile environment. Extension of the life span of neutrophils is a general escape mechanism of pathogens residing in PMN. However, after 2-4 days, even infected neutrophils become apoptotic and are phagocytosed by macrophages. Since microbes entering macrophages via the uptake of infected apoptotic PMN may survive and multiply in macrophages, apoptotic neutrophils can serve as "Trojan horses" for certain pathogens. Interfering with activating signaling pathways appears to be another potent mechanism by which intracellular microorganisms suppress cellular activation in neutrophils. In addition to provide a short overview of the topic, the present review aims to summarize our own findings regarding the interaction between human neutrophils and intracellular pathogens as well as regarding the disease promoting role of apoptotic cells after infection with Leishmania major.     

RNF11 modulates microglia activation through NF-κB signalling cascade

Microglia are resident macrophages in the central nervous system (CNS) that play a major role in neuroinflammation and pathogenesis of several neurodegenerative diseases. Upon activation, microglia releases a multitude of pro-inflammatory factors that initiate and sustain an inflammatory response by activating various signalling pathways, including the NF-κB pathway in a feed forward cycle. In microglial cells, activation of NF-κB signalling is normally transient, while sustained NF-κB activation is associated with persistent neuroinflammation. RING finger protein 11 (RNF11), in association with A20 ubiquitin-editing complex, is one of the key negative regulators of NF-κB signalling pathway in neurons. In this study, we have demonstrated and confirmed this role of RNF11 in microglia, the immune cells of the CNS. Coimmunoprecipitation experiments showed that RNF11 and A20 interact in a microglial cell line, suggesting the presence of A20 ubiquitin-editing protein complex in microglial cells. Next, using targeted short hairpin RNA (shRNA) knockdown and over-expression of RNF11, we established that RNF11 expression levels are inversely related to NF-κB activation, as evident from altered expression of NF-κB transcribed genes. Moreover our studies, illustrated that RNF11 confers protection against LPS-induced cell cytotoxicity. Thus our investigations clearly demonstrated that microglial RNF11 is a negative regulator of NF-κB signalling pathway and could be a strong potential target for modulating inflammatory responses in neurodegenerative diseases.