A nurse-led approach to urgent results management at Sydney Sexual Health Centre demonstrates benefits to client outcomes and cost savings: a time efficiency and health system cost analysis.

BACKGROUND: The timely provision of test results to facilitate early access to treatment is an essential component of sexually transmissible infection (STI) control and contributes to a significant proportion of the workload at sexual health services. We aimed to estimate the time to deliver client results and treatment as well as the health system costs of the nurse-led urgent results management model at the Sydney Sexual Health Centre (SSHC) compared to an alternative 'ordering clinician' model. METHODS: We conducted a retrospective analysis of urgent results managed by the results nurse over 2weeks in 2019 and an observational study over 2weeks in 2021, where 10 clinicians managed five of their own urgent results. Additional activity data were gathered to determine the annual health system costs for both models. RESULTS: In the nurse-led model 211 of 280 clients required notification; 156 (73.9%) were notified on the day their results became available, and the median time to treatment (n =137) was 1day. The annual health system cost for the nurse-led model was A$3922143. In the ordering clinician model, 17 (42.5%) clients were notified on the same day, and of the 27 clients treated at SSHC, the median time to treatment increased to 4days. The annual health system cost for the ordering clinician model was A$4043667.28 compared with the nurse-led model, and an additional 33.3h per week of clinician time was required for the same level of service provision. CONCLUSIONS: This study highlights the strengths of the nurse-led results model at SSHC, demonstrating improved client outcomes for STI notification and treatment times and health systems savings.

Early initiation of antiretroviral therapy (ART): from point-of-care test to ART at a peer-led community-based testing site in Sydney.

The effect of performing baseline HIV investigations (BLHIVI) at the time of a reactive HIV point-of-care test in the pathway to antiretroviral therapy (ART) in a community setting has not been described. In this study, 67 men newly diagnosed with HIV across three service models were analysed. The median time to ART was 30, 29.5 and 38 days (P=0.29) at a peer-led community testing site intervention group, in a historical control group and in an urban publicly funded sexual health service respectively. In a community setting, the inclusion of BLHIVI has the potential to reduce the time to early ART initiation.

Current literature and imaging techniques of aseptic lymphocyte-dominated vasculitis-associated lesions (ALVAL).

Aseptic lymphocyte-dominated vasculitis-associated lesions (ALVAL) are a recognized complication of metal-on-metal bearing hip prostheses. There is an impending concern regarding the future investigation and management of patients who have received such implants. The current literature is discussed, and the current guidelines for management of these patients in the UK are reviewed. The various imaging techniques available, such as computed tomography, metal artefact reduction magnetic resonance imaging, and ultrasound are discussed and evaluated with respect to the assessment of patients with suspected ALVAL. The histopathological findings are discussed with images of the tissue changes provided. Images of the radiological findings are also provided for all general radiological methods. ALVAL and its radiological presentation is an important issue that unfortunately may become a significant clinical problem.

Using social network analysis and agent-based modelling to explore information flow using common operational pictures for maritime search and rescue operations.

The concept of common operational pictures (COPs) is explored through the application of social network analysis (SNA) and agent-based modelling to a generic search and rescue (SAR) scenario. Comparing the command structure that might arise from standard operating procedures with the sort of structure that might arise from examining information-in-common, using SNA, shows how one structure could be more amenable to 'command' with the other being more amenable to 'control' - which is potentially more suited to complex multi-agency operations. An agent-based model is developed to examine the impact of information sharing with different forms of COPs. It is shown that networks using common relevant operational pictures (which provide subsets of relevant information to groups of agents based on shared function) could result in better sharing of information and a more resilient structure than networks that use a COP. PRACTITIONER SUMMARY: SNA and agent-based modelling are used to compare different forms of COPs for maritime SAR operations. Different forms of COP change the communications structures in the socio-technical systems in which they operate, which has implications for future design and development of a COP.

Multimodal control of sensors on multiple simulated unmanned vehicles.

The use of multimodal (speech plus manual) control of the sensors on combinations of one, two, three or five simulated unmanned vehicles (UVs) is explored. Novice controllers of simulated UVs complete a series of target checking tasks. Two experiments compare speech and gamepad control for one, two, three or five UVs in a simulated environment. Increasing the number of UVs has an impact on subjective rating of workload (measured by NASA-Task Load Index), particularly when moving from one to three UVs. Objective measures of performance showed that the participants tended to issue fewer commands as the number of vehicles increased (when using the gamepad control), but, while performance with a single UV was superior to that of multiple UVs, there was little difference across two, three or five UVs. Participants with low spatial ability (measured by the Object Perspectives Test) showed an increase in time to respond to warnings when controlling five UVs. Combining speech with gamepad control of sensors on UVs leads to superior performance on a secondary (respond-to-warnings) task (implying a reduction in demand) and use of fewer commands on primary (move-sensors and classify-target) tasks (implying more efficient operation). STATEMENT OF RELEVANCE: Benefits of multimodal control for unmanned vehicles are demonstrated. When controlling sensors on multiple UVs, participants with low spatial orientation scores have problems. It is proposed that the findings of these studies have implications for selection of UV operators and suggests that future UV workstations could benefit from multimodal control.

Contributions to accelerating atmospheric CO2 growth from economic activity, carbon intensity, and efficiency of natural sinks.

The growth rate of atmospheric carbon dioxide (CO(2)), the largest human contributor to human-induced climate change, is increasing rapidly. Three processes contribute to this rapid increase. Two of these processes concern emissions. Recent growth of the world economy combined with an increase in its carbon intensity have led to rapid growth in fossil fuel CO(2) emissions since 2000: comparing the 1990s with 2000-2006, the emissions growth rate increased from 1.3% to 3.3% y(-1). The third process is indicated by increasing evidence (P = 0.89) for a long-term (50-year) increase in the airborne fraction (AF) of CO(2) emissions, implying a decline in the efficiency of CO(2) sinks on land and oceans in absorbing anthropogenic emissions. Since 2000, the contributions of these three factors to the increase in the atmospheric CO(2) growth rate have been approximately 65 +/- 16% from increasing global economic activity, 17 +/- 6% from the increasing carbon intensity of the global economy, and 18 +/- 15% from the increase in AF. An increasing AF is consistent with results of climate-carbon cycle models, but the magnitude of the observed signal appears larger than that estimated by models. All of these changes characterize a carbon cycle that is generating stronger-than-expected and sooner-than-expected climate forcing.

Carbon pools and flux of global forest ecosystems.

Forest systems cover more than 4.1 x 10(9) hectares of the Earth's land area. Globally, forest vegetation and soils contain about 1146 petagrams of carbon, with approximately 37 percent of this carbon in low-latitude forests, 14 percent in mid-latitudes, and 49 percent at high latitudes. Over two-thirds of the carbon in forest ecosystems is contained in soils and associated peat deposits. In 1990, deforestation in the low latitudes emitted 1.6 +/- 0.4 petagrams of carbon per year, whereas forest area expansion and growth in mid- and high-latitude forest sequestered 0.7 +/- 0.2 petagrams of carbon per year, for a net flux to the atmosphere of 0.9 +/- 0.4 petagrams of carbon per year. Slowing deforestation, combined with an increase in forestation and other management measures to improve forest ecosystem productivity, could conserve or sequester significant quantities of carbon. Future forest carbon cycling trends attributable to losses and regrowth associated with global climate and land-use change are uncertain. Model projections and some results suggest that forests could be carbon sinks or sources in the future.

Global deforestation: contribution to atmospheric carbon dioxide.

A study of effects of terrestrial biota on the amount of carbon dioxide in the atmosphere suggests that the global net release of carbon due to forest clearing between 1860 and 1980 was between 135 x 10(15) and 228 x 10(15) grams. Between 1.8 x 10(15) and 4.7 x 10(15) grams of carbon were released in 1980, of which nearly 80 percent was due to deforestation, principally in the tropics. The annual release of carbon from the biota and soils exceeded the release from fossil fuels until about 1960. Because the biotic release has been and remains much larger than is commonly assumed, the airborne fraction, usually considered to be about 50 percent of the release from fossil fuels, was probably between 22 and 43 percent of the total carbon released in 1980. The increase in carbon dioxide in the atmosphere is thought by some to be increasing the storage of carbon in the earth's remaining forests sufficiently to offset the release from deforestation. The interpretation of the evidence presented here suggests no such effect; deforestation appears to be the dominant biotic effect on atmospheric carbon dioxide. If deforestation increases in proportion to population, the biotic release of carbon will reach 9 x 10(15) grams per year before forests are exhausted early in the next century. The possibilities for limiting the accumulation of carbon dioxide in the atmosphere through reduction in use of fossil fuels and through management of forests may be greater than is commonly assumed.

Consistent land- and atmosphere-based U.S. carbon sink estimates.

For the period 1980-89, we estimate a carbon sink in the coterminous United States between 0.30 and 0.58 petagrams of carbon per year (petagrams of carbon = 10(15) grams of carbon). The net carbon flux from the atmosphere to the land was higher, 0.37 to 0.71 petagrams of carbon per year, because a net flux of 0.07 to 0.13 petagrams of carbon per year was exported by rivers and commerce and returned to the atmosphere elsewhere. These land-based estimates are larger than those from previous studies (0.08 to 0.35 petagrams of carbon per year) because of the inclusion of additional processes and revised estimates of some component fluxes. Although component estimates are uncertain, about one-half of the total is outside the forest sector. We also estimated the sink using atmospheric models and the atmospheric concentration of carbon dioxide (the tracer-transport inversion method). The range of results from the atmosphere-based inversions contains the land-based estimates. Atmosphere- and land-based estimates are thus consistent, within the large ranges of uncertainty for both methods. Atmosphere-based results for 1980-89 are similar to those for 1985-89 and 1990-94, indicating a relatively stable U.S. sink throughout the period.

Response to Comment on "Tropical forests are a net carbon source based on aboveground measurements of gain and loss".

The Hansen et al critique centers on the lack of spatial agreement between two very different datasets. Nonetheless, properly constructed comparisons designed to reconcile the two datasets yield up to 90% agreement (e.g., in South America).

Tropical forests are a net carbon source based on aboveground measurements of gain and loss.

The carbon balance of tropical ecosystems remains uncertain, with top-down atmospheric studies suggesting an overall sink and bottom-up ecological approaches indicating a modest net source. Here we use 12 years (2003 to 2014) of MODIS pantropical satellite data to quantify net annual changes in the aboveground carbon density of tropical woody live vegetation, providing direct, measurement-based evidence that the world's tropical forests are a net carbon source of 425.2 ± 92.0 teragrams of carbon per year (Tg C year-1). This net release of carbon consists of losses of 861.7 ± 80.2 Tg C year-1 and gains of 436.5 ± 31.0 Tg C year-1 Gains result from forest growth; losses result from deforestation and from reductions in carbon density within standing forests (degradation or disturbance), with the latter accounting for 68.9% of overall losses.

Identification and characterization of prostein, a novel prostate-specific protein.

In this report, we describe the application of a systematic, genome-based approach to identify prostein, a novel prostate-specific protein expressed in normal and malignant prostate tissues. Characterization of the prostein gene shows that prostein cDNA encodes a 553-amino acid protein. The protein is predicted to be a type IIIa plasma membrane protein with a cleavable signal peptide and 11 transmembrane-spanning regions. The prostein gene is located on chromosome 1 at the WI-9641 locus between q32 and q42. Prostein mRNA is shown to be uniquely expressed in normal and cancerous prostate tissues using Northern blot, eDNA microarray, and real-time PCR analyses. Furthermore, prostein mRNA expression does not appear to be prostate tumor grade related and is restricted exclusively to prostate cell lines. Immunohistochemical staining using a mouse monoclonal antibody generated against prostein demonstrates that this protein is specifically detected in prostate tissues both at the plasma membrane and in the cytoplasm. Prostein expression is androgen responsive because treatment of LNCaP cells with androgen up-regulates prostein message and protein expression levels. These results validate prostein as a prostate-specific marker with potential utility in the diagnosis and treatment of prostate cancer.

Identification of differentially expressed genes in human prostate cancer using subtraction and microarray.

We have identified human prostate cancer- and tissue-specific genes using cDNA library subtraction in conjunction with high throughput microarray screening. Subtracted cDNA libraries of prostate tumors and normal prostate tissue were generated. Characterization of subtracted libraries showed enrichment of both cancer- and tissue-specific genes. Highly redundant clones were eliminated by colony hybridization. The remaining clones were selected for microarray to determine gene expression levels in a variety of tumor and normal tissues. Clones showing overexpression in prostate tumors and/or normal prostate tissues were selected and sequenced. Here we report the identification of two genes, P503S and P504S, from subtracted libraries and a third gene, P510S, by subtraction followed by microarray screening. Their expression profiles were further confirmed by Northern blot, real-time PCR (TaqMan), and immunohistochemistry to be overexpressed in prostate tissues and/or prostate tumors. Full-length cDNA sequences were cloned, and their subcellular locations were predicted by a bioinformatic algorithm, PSORT, to be plasma membrane proteins. The genes identified through these approaches are potential candidates for cancer diagnosis and therapy.

Identification of genes differentially over-expressed in lung squamous cell carcinoma using combination of cDNA subtraction and microarray analysis.

In order to develop effective vaccine products against human cancer, we are interested in identifying genes over-expressed in tumor cells. Through a combination of cDNA library subtraction and microarray technology, we identified seventeen genes preferentially expressed in lung squamous cell carcinoma, including four novel genes. To date, expression profiles of these genes were confirmed by Northern and/or real-time analysis, and several genes were also found to be expressed in head and neck squamous tumors. Thus, these combined methods represent a high throughput approach for identifying tumor specific genes. Furthermore, the report of characterization on these genes will allow them to be exploited for their diagnostic, prognostic, and therapeutic potentials including immunotherapy and antibody based anticancer therapy.

Energy-linked and energy-independent transhydrogenase activities in Escherichia coli vesicles.

Active transport vesicles of Escherichia coli were shown to possess low levels of energy-independent and energy-dependent nicotinamide nucleotide transhydrogenase activities. Breakage of such vesicles in a French pressure cell resulted in a fraction which had an 8-10-fold increased respiration- and ATP-driven transhydrogenase activities. Stimulation of the ATPase activity in vesicles with Triton X-100 was also paralledled by a 2-fold increase in the energy-independent transhydrogenase. Disruption of the vesicles similarly resulted in increases in the energy-independent transhydrogenase, NADH and succinate oxidase activities but a decrease in succinate supported proline uptake. In the light of these findings, the "sidedness' of the vesicle membranes is discussed.

Occurrence of proteins immunoreactive with anti-coupling factor B in phosphorylating membrane preparations.

Coupling factor B has been isolated from beef heart mitochondria, apparently in multiple forms which differ in molecular weight and specific activity. Since it has no known intrinsic catalytic activity, detection and quantitation have been based upon the factor B-dependent stimulation of ATP-linked activities in factor B-deficient sub-mitochondrial particles. This communication reports the development of a reliable and more universally applicable enzyme-linked immunosorbent assay (ELISA) for detection and quantitation of factor B in soluble or membranous preparations. The assay requires nanoliter volumes of rabbit antiserum raised against purified factor B and will detect nanogram amounts of the coupling factor. Analysis of beef heart submitochondrial particles using a competitive binding ELISA indicated a factor B content of 0.27 nmol/mg protein, making factor B stoichiometric with F1 (0.3--0.6 nmol/mg). Furthermore, application of the factor B ELISA has indicated the presence of material cross-reacting with the beef heart factor B-antiserum in phosphorylating membranes from chloroplasts, Escherichia coli, Paracoccus denitrificans and the thermophilic bacterium, PS3. Negative results were obtained with mitochondria and microsomes from rat liver, purple membranes from Halobium halobacterium and sarcoplasmic reticulum from rabbit skeletal muscle.

WT1-specific serum antibodies in patients with leukemia.

WT1 is an oncogenic protein expressed by the Wilms' tumor gene and overexpressed in the majority of acute myelogenous leukemias (AMLs) and chronic myelogenous leukemias (CMLs). The current study analyzed the sera of patients with AML and CML for the presence of antibodies to full-length and truncated WT1 proteins. Sixteen of 63 patients (25%) with AML had serum antibodies reactive with WT1/full-length protein. Serum antibodies from all 16 were also reactive with WT1/NH2-terminal protein. By marked contrast, only 2 had reactivity to WT1/COOH-terminal protein. Thus, the level of immunological tolerance to the COOH terminus may be higher than to the NH2 terminus. The WT1/COOH-terminal protein contains four zinc finger domains with homology to other self-proteins. By implication, these homologies may be related to the increased immunological tolerance. Results in patients with CML were similar with antibodies reactive to WT1/full-length protein detectable in serum of 15 of 81 patients (19%). Antibodies reactive with WT1/NH2-terminal protein were present in the serum of all 15, whereas antibodies reactive with WT1/COOH-terminal protein were present in only 3. By contrast to results in leukemia patients, antibodies reactive with WT1/full-length protein were detected in only 2 of 96 normal individuals. The greater incidence of antibody in leukemia patients provides strong evidence that immunization to the WT1 protein occurred as a result of patients bearing malignancy that expresses WT1. These data provide further stimulus to test therapeutic vaccines directed against WT1 with increased expectation that the vaccines will be able to elicit and/or boost an immune response to WT1.

Heparin inhibition of antibody-dependent complement-mediated lysis.

The effect of heparin on the monoclonal antibody-dependent complement-mediated lysis of human lymphoid cell lines and peripheral blood T-lymphocytes was studied. T-lymphoid cell lines (CEM and MOLT-3) were lysed by optimal concentrations of monoclonal antibodies and rabbit complement. Heparin at concentrations as low as 0.5 U/ml partially inhibited the complement-mediated lysis of all antibody-cell combinations while a heparin concentration of 25 U/ml produced complete inhibition. Lysis mediated by an IgG monoclonal antibody (J5) to the common acute lymphoblastic leukemia antigen (CALLA) was more sensitive to heparin inhibition than that due to an IgM antibody (VIL A1). Bovine and porcine heparin were equally inhibitory. Peripheral blood T-lymphocytes collected in heparin (100 U/ml) were resistant to complete lysis when treated with 17F12 and complement immediately after isolation; complete lysis was achieved only when they were incubated for 2 h prior to treatment. The role of monoclonal antibody and complement in the in vitro lysis of normal and leukemic lymphocytes is discussed.

A p53 homologue and a novel serine proteinase inhibitor are over-expressed in lung squamous cell carcinoma.

LSCC is a common type of lung cancer and accounts for approximately 30% of all lung cancers. We have used a combination of subtraction and cDNA microarray technology to identify genes preferentially over-expressed in LSCC. Here we report extensive molecular characterization of two novel full-length cDNA sequences, L530S and L531S. Although L530S and L531S were found to be differentially over-expressed in LSCC, the expression profiles for these two genes were not identical. L530S expression was specifically elevated in LSCC whereas L531S transcript was up regulated in both LSCC and head and neck squamous cell carcinoma samples. L530S is a homologue of p53, and L531S belongs to a new member of serine proteinase inhibitors with significant homology to SCCA1 and SCCA2. Furthermore, L531S protein was found to be expressed in lung cancers by IHC analysis. The distinct as well as similar expression profiles exhibited by L530S and L531S suggest that each gene may play a unique role for tumorgenesis of LSCC. Identification of these genes not only allows us to further explore their diagnostic and therapeutic potentials for LSCC, but also provides us with additional tools and reagents for understanding the biology behind LSCC, and differentiating LSCC from other types of lung cancer at the molecular level.