Agricultural intensification and loss of matrix habitat over 23 years in the West Wimmera, south-eastern Australia

The global trend toward more intensive forms of agriculture is changing the nature of matrix habitat in agricultural areas. Removal of components of matrix habitat can affect native biota at the paddock and the landscape scale, particularly where intensification occurs over large areas. We identify the loss of paddock trees due to the proliferation of centre pivot irrigation in dryland farming areas as a potentially serious threat to the remnant biota of these areas. We used a region of south-eastern Australia as a case study to quantify land use change from grazing and dryland cropping to centre pivot irrigation over a 23-year period. We also estimated rates of paddock tree loss in 5 representative landscapes within the region over the same period. The total area affected by centre pivots increased from 0 ha in 1980 to nearly 9000 ha by 2005. Pivots were more likely to be established in areas which had originally been plains savannah and woodlands containing buloke (Allocasuarina luehmannii), a food source for an endangered bird. On average, 42% of paddock buloke trees present in 1982 were lost by 2005. In the two landscapes containing several centre pivots, the loss was 54% and 70%. This accelerated loss of important components of matrix habitat is likely to result in species declines and local extinctions. We recommend that measures to alleviate the likely negative impacts of matrix habitat loss on native biota be considered as part of regional planning strategies.

Recovery following laparoscopic cholecystectomy in either a 23 hour or an 8 hour facility

Research confirms that laparoscopic cholecystectomy (LC) results in shorter lengths of hospital stay and earlier return to usual activity than the traditional cholecystectomy procedure. Research in this area, however, focuses more on the medical aspects of patient recovery, but very few studies have evaluated how these patients manage their recovery at home or what types of problems they encounter. A total of 28 LC patients were randomly assigned to two groups: (1) 23 h stay (overnight) in a general surgical ward or (2) day procedure unit (DPU) stay. Data was collected by a self-administered Postoperative Symptoms Diary and telephone interview. Results showed no significant difference between the two groups of patients recovery symptoms scores. Problems with mobility, pain and elimination recorded the highest mean scores for both groups of patients. Overnight patients also experienced problems with tiredness and eating. All DPU patients were able to manage their postoperative symptoms, compared to only 44% of patients who had stayed in overnight. Carer assistance was needed with regard to activities of daily living, child care and reassurance. Results showed that with careful selection of patients, LC cases performed as day procedures did not impact at all on the patients' recovery trajectory.

Skew arcs and Wagner's [23, 14, 5] code

In 1966, Wagner used computational search methods to construct a  [23,14,5] code. This code has been examined with much interest since that time, in hopes of finding a geometric construction and possible code extensions. In this article, we give a simple geometric construction for Wagner's code and consider extensions of this construction.

Somatostatin modulates G-CSF-induced but not interleukin-3-induced proliferative responses in myeloid 32D cells via activation of somatostatin receptor subtype 2

Somatostatin, originally identified as a peptide involved in neurotransmission, functions as an inhibitor of multiple cellular responses, including hormonal secretion and proliferation. Somatostatin acts through activation of G-protein-coupled receptors of which five subtypes have been identified. We have recently established that human CD34/c-kit expressing hematopoietic progenitors and acute myeloid leukemia (AML) cells exclusively express SSTR2. A major mechanism implicated in the antiproliferative action of somatostatin involves activation of the SH2 domain-containing protein tyrosine phosphatase SHP-1. While 0.1-1 x 10(-9) M of somatostatin, or its synthetic stable analog octreotide, can inhibit G-CSF-induced proliferation of AML cells, little or no effects are seen on GM-CSF- or IL-3-induced responses.
MATERIALS AND METHODS: To study the mechanisms underlying the antiproliferative responses of myeloblasts to somatostatin, clones of the IL-3-dependent murine cell line 32D that stably express SSTR2 and G-CSF receptors were generated. RESULTS: Similar to AML cells, octreotide inhibited G-CSF-induced but not IL-3-induced proliferative responses of 32D[G-CSF-R/SSTR2] cells. Somatostatin induced SHP-1 activity and inhibited G-CSF-induced, but not IL-3-induced, activation of the signal transducer and activator of transcription proteins STAT3 and STAT5.
CONCLUSION: Based on these data and previous results, we propose a model in which recruitment and activation of the tyrosine phosphatase SHP-1 by SSTR2 is involved in the selective negative action of somatostatin on G-CSF-R signaling.

Exercise-induced activation of STAT3 signaling is increased with age

Activation of the transcription factor signal transducers and activators of transcription (STAT) 3 is common to many inflammatory cytokines and growth factors, with recent evidence of involvement in skeletal muscle regeneration. The purpose of this study was to determine whether STAT3 signaling activation is regulated differentially, at rest and following intense resistance exercise, in aged human skeletal muscle. Skeletal muscle biopsies were harvested from healthy younger (n = 11, 20.4 ± 0.8 years) and older men (n = 10, 67.4 ± 1.3 years) under resting conditions and 2 h after the completion of resistance exercise. No differences were evident at rest, whereas the phosphorylation of STAT3 was significantly increased in old (23-fold) compared to young (5-fold) subjects after exercise. This correlated with significantly higher induction of the STAT3 target genes including; interleukin-6 (IL-6), JUNB, c-MYC, and suppressor of cytokine signaling (SOCS) 3 mRNA in older subjects following exercise. Despite increased SOCS3 mRNA, cellular protein abundance was suppressed. SOCS3 protein is an important negative regulator of STAT3 activation and cytokine signaling. Thus, in aged human muscle, elevated responsiveness of the STAT3 signaling pathway and suppressed SOCS3 protein are evident following resistance exercise. These data suggest that enhanced STAT3 signaling responsiveness to proinflammatory factors may impact on mechanisms of muscle repair and regeneration.

Dorsal and ventral medullary catecholamine cell groups contribute differentially to systemic interleukin-1beta-induced hypothalamic pituitary adrenal axis responses

Medial parvocellular paraventricular corticotropin-releasing hormone (mPVN CRH) cells are critical in generating hypothalamic-pituitary-adrenal (HPA) axis responses to systemic interleukin-1beta (IL-1beta). However, although it is understood that catecholamine inputs are important in initiating mPVN CRH cell responses to IL-1beta, the contributions of distinct brainstem catecholamine cell groups are not known. We examined the role of nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM) catecholamine cells in the activation of mPVN CRH, hypothalamic oxytocin (OT) and central amygdala cells in response to IL-1beta (1 microg/kg, i.a.). Immunolabelling for the expression of c-fos was used as a marker of neuronal activation in combination with appropriate cytoplasmic phenotypic markers. First we confirmed that PVN 6-hydroxydopamine lesions, which selectively depleted catecholaminergic terminals, significantly reduced IL-1beta-induced mPVN CRH cell activation. The contribution of VLM (A1/C1 cells) versus NTS (A2 cells) catecholamine cells to mPVN CRH cell responses was then examined by placing ibotenic acid lesions in either the VLM or NTS. The precise positioning of these lesions was guided by prior retrograde tracing studies in which we mapped the location of IL-1beta-activated VLM and NTS cells that project to the mPVN. Both VLM and NTS lesions reduced the mPVN CRH and OT cell responses to IL-1beta. Unlike VLM lesions, NTS lesions also suppressed the recruitment of central amygdala neurons. These studies provide novel evidence that both the NTS and VLM catecholamine cells have important, but differential, contributions to the generation of IL-1beta-induced HPA axis responses.