Ways of Reasoning Used by Nurses in Postoperative Pain Assessment.

BACKGROUND: Postoperative pain is a major concern of patients undergoing surgery. Pain assessment for patients undergoing surgery is a common requirement for surgical nurses and is the most important nursing approach to ensuring patient comfort. AIMS: The purpose of this study was to identify the reasoning used by nurses when assessing postoperative pain in patients. METHODS: Phenomenography was the research approach chosen to analyze the nurses' experiences. This approach is used to acquire qualitative knowledge about the ways individuals experience the world. RESULTS: The reasoning used by nurses in postoperative pain assessment was identified from two perspectives: the frames of reference used to interpret a patient's perception of pain and the strategic efforts used to assess the pain. An outcome space for the various categories of reasoning employed by the nurses with regard to postoperative pain assessment was constructed to determine how these categories were logically related. CONCLUSIONS: These findings have the potential to lead to a diverse range of nursing education modalities related to the adoption of different focuses and actions in postoperative pain assessment.

Clinical and Molecular Delineation of a Novel Cys1050Phe Missense Mutation in the ABCC9 Gene in a Korean Patient with Cantú Syndrome.

Cantú syndrome is characterized by congenital hypertrichosis, cardiomegaly, and osteochondrodysplasia and is recognized as a rare syndrome. Although it has previously been reported that the majority of affected individuals have a relatively good prognosis, there are no reports on long-term follow up. Here we report the first case of Cantú syndrome in Korea and the associated changes in overall development with rehabilitation over several months.

Rac1 promotes chondrogenesis by regulating STAT3 signaling pathway.

The small GTPase protein Rac1 is involved in a wide range of biological processes including cell differentiation. Previously, Rac1 was shown to promote chondrogenesis in micromass cultures of limb mesenchyme. However, the pathways mediating Rac1's role in chondrogenesis are not fully understood. This study aimed to explore the molecular mechanisms by which Rac1 regulates chondrogenic differentiation. Phosphorylation of signal transducer and activator of transcription 3 (STAT3) was increased as chondrogenesis proceeded in micromass cultures of chick wing bud mesenchyme. Inhibition of Rac1 with NSC23766, janus kinase 2 (JAK2) with AG490, or STAT3 with stattic inhibited chondrogenesis and reduced phosphorylation of STAT3. Conversely, overexpression of constitutively active Rac1 (Rac L61) increased phosphorylation of STAT3. Rac L61 expression resulted in increased expression of interleukin 6 (IL-6), and treatment with IL-6 increased phosphorylation of STAT3. NSC23766, AG490, and stattic prohibited cell aggregation, whereas expression of Rac L61 increased cell aggregation, which was reduced by stattic treatment. Our studies indicate that Rac1 induces STAT3 activation through expression and action of IL-6. Overexpression of Rac L61 increased expression of bone morphogenic protein 4 (BMP4). BMP4 promoted chondrogenesis, which was inhibited by K02288, an activin receptor-like kinase-2 inhibitor, and increased phosphorylation of p38 MAP kinase. Overexpression of Rac L61 also increased phosphorylation of p38 MAPK, which was reduced by K02288. These results suggest that Rac1 activates STAT3 by expression of IL-6, which in turn increases expression and activity of BMP4, leading to the promotion of chondrogenesis.

Operando spectroscopic characterization of formamidinium lead iodide perovskite quantum dots for tracking electrochemical reactions.

Multidimensional ABX3 hybrid perovskites three-dimensionally confined dot-shaped structure demonstrate versatile potential to photoelectrochemical cells for water splitting, hydrogen generation, solar cells, and light-emitting diodes. To apply perovskite quantum dots (PQDs) to solar-driven chemistry and optoelectronic devices, understanding the photoinduced charge carrier dynamics of PQDs under electrochemical conditions or applied bias are important. In this study, the detailed transformation mechanism of formamidinium lead iodide perovskite quantum dots under electrochemical conditions was studied by tracking the products of the reaction through cyclic voltammetry, X-ray photoemission spectroscopy, in-situ UV-visible spectroelectrochemistry, etc. Through comprehensive characterizations, the mechanism of irreversible oxidative transformation of perovskite quantum dots was presented. This study provides deeper insight into the electrochemical behavior of PQDs for successful solar-driven chemistry and optoelectronic device applications.

P- and N-type InAs nanocrystals with innately controlled semiconductor polarity.

InAs semiconductor nanocrystals (NCs) exhibit intriguing electrical/optoelectronic properties suitable for next-generation electronic devices. Although there is a need for both n- and p-type semiconductors in such devices, InAs NCs typically exhibit only n-type characteristics. Here, we report InAs NCs with controlled semiconductor polarity. Both p- and n-type InAs NCs can be achieved from the same indium chloride and aminoarsine precursors but by using two different reducing agents, diethylzinc for p-type and diisobutylaluminum hydride for n-type NCs, respectively. This is the first instance of semiconductor polarity control achieved at the synthesis level for InAs NCs and the entire semiconductor nanocrystal systems. Comparable field-effective mobilities for holes (3.3 × 10-3 cm2/V·s) and electrons (3.9 × 10-3 cm2/V·s) are achieved from the respective NC films. The mobility values allow the successful fabrication of complementary logic circuits, including NOT, NOR, and NAND comprising photopatterned p- and n-channels based on InAs NCs.

Giant maxillary mucocele occurring after reduction malarplasty.

Reduction malarplasty for patients with a prominent malar complex is a popular procedure in Asia. However, a range of complications have been reported after reduction malarplasty, such as hematoma, orbital complications, asymmetric face, and nonunion. A medially displaced fracture or bony fragment can induce sinusitis and subsequent trauma to bones in combination with chronic inflammatory processes, which can lead to chronic obstruction of mucus-secreting glands. In our case, 46-year-old man presented with a large mucocele in the maxillary sinus after malar reduction approximately 20 years ago.

Exploring nurses' end-of-life care for dying patients in the ICU using focus group interviews.

PURPOSE: The aim of this study is to illuminate how nurses working in an intensive care unit perceive their professional duties regarding end-of-life care based on their end-of-life care experience. DESIGN AND METHODS: A qualitative research design utilising focus-group interviews was employed. Two focus groups with twelve nurses were recruited, one consisting of nurses with less than five years of clinical experience in intensive care units and the other with more than five years of experience. FINDINGS: An analysis of the nurses' explorations of end-of-life care in an intensive care unit for patients facing impending death revealed three main themes: (1) facing an extreme change in human existence, (2) being in the presence of the patient's transition and (3) being prepared as an intensive care unit nurse. These three themes covered a total of 16 subthemes. CONCLUSION: The findings of this study outline how intensive care unit nurses perceive dying patients and how they manage end-of-life care. It also illustrates how patients and their families can be included in the process, and this should be a component of nurses' education regarding end-of-life care.

Staurosporine induces chondrogenesis of chick embryo wing bud mesenchyme in monolayer cultures through canonical and non-canonical TGF-ß pathways.

Staurosporine has been known to induce chondrogenesis in monolayer cultures of mesenchymal cells by dissolving actin stress fibers. The aim of this study was to further elucidate how the alteration of actin filaments by staurosporine induces chondrogenesis. Specifically, we examined whether the transforming growth factor (TGF)-ß pathway is implicated. SB505124 strongly suppressed staurosporine-induced chondrogenesis without affecting the drug's action on the actin cytoskeleton. Staurosporine increased the phosphorylation of TGF-ß receptor I (TßRI) but had no significant effect on the expression levels of TGF-ß1, TGF-ß2, TGF-ß3, TßRI, TßRII, and TßRIII. Phosphorylation of Smad2 and Smad3 was not increased by staurosporine. However, SB505124 almost completely suppressed the phosphorylation of Smad2 and Smad3. In addition, inhibition of Smad3 blocked staurosporine-induced chondrogenesis. Inhibition of Akt, p38 mitogen-activated protein kinase (MAPK), and c-jun N-terminal kinase (JNK) suppressed chondrogenesis induced by staurosporine. Phosphorylation of Akt, p38 MAPK, and JNK was increased by staurosporine. SB505124 reduced the phosphorylation of Akt and p38 MAPK, while it had no effect on the phosphorylation of JNK. The phosphorylation level of extracellular signal-regulated kinase (ERK) was not significantly affected by staurosporine. In addition, inhibition of ERK with PD98059 alone did not induce chondrogenesis. Taken together, these results suggest that staurosporine induces chondrogenesis through TGF-ß pathways including canonical Smads and non-canonical Akt and p38 MAPK signaling.

Hypoxia-inducible factor-1α upregulates tyrosine hydroxylase and dopamine transporter by nuclear receptor ERRγ in SH-SY5Y cells.

Hypoxia-inducible factor-1α (HIF-1α) is a transcription factor relevant to the development of many mammalian organs including the brain. However, the molecular mechanisms by which signaling events mediate neuronal differentiation have not been fully elucidated. In the present study, we show for the first time that the orphan nuclear receptor estrogen-related receptor γ (ERRγ) is upregulated by HIF-1α and plays essential roles in HIF-1α-induced upregulation of dopaminergic marker molecules such as tyrosine hydroxylase and dopamine transporter. We found that deferoxamine upregulated HIF-1α and enhanced the dopaminergic phenotype and neurite outgrowth of SH-SY5Y cells. Deferoxamine activated transcription and protein expression of ERRγ, and deferoxamine-induced upregulation of tyrosine hydroxylase and dopamine transporter was attenuated by using the ERRγ inverse agonist or silencing ERRγ. Altogether, these results suggest that HIF-1α can positively regulate the dopaminergic phenotype through ERRγ. This study could provide new perspectives for understanding the mechanisms underlying the promotion of dopaminergic neuronal differentiation by hypoxia.