A web-based appointment system to reduce waiting for outpatients: A retrospective study

<p>Abstract</p> <p>Background</p> <p>Long waiting times for registration to see a doctor is problematic in China, especially in tertiary hospitals. To address this issue, a web-based appointment system was developed for the Xijing hospital. The aim of this study was to investigate the efficacy of the web-based appointment system in the registration service for outpatients.</p> <p>Methods</p> <p>Data from the web-based appointment system in Xijing hospital from January to December 2010 were collected using a stratified random sampling method, from which participants were randomly selected for a telephone interview asking for detailed information on using the system. Patients who registered through registration windows were randomly selected as a comparison group, and completed a questionnaire on-site.</p> <p>Results</p> <p>A total of 5641 patients using the online booking service were available for data analysis. Of them, 500 were randomly selected, and 369 (73.8%) completed a telephone interview. Of the 500 patients using the usual queuing method who were randomly selected for inclusion in the study, responses were obtained from 463, a response rate of 92.6%. Between the two registration methods, there were significant differences in age, degree of satisfaction, and total waiting time (<it>P </it>< 0.001). However, gender, urban residence, and valid waiting time showed no significant differences (<it>P </it>> 0.05). Being ignorant of online registration, not trusting the internet, and a lack of ability to use a computer were three main reasons given for not using the web-based appointment system. The overall proportion of non-attendance was 14.4% for those using the web-based appointment system, and the non-attendance rate was significantly different among different hospital departments, day of the week, and time of the day (<it>P </it>< 0.001).</p> <p>Conclusion</p> <p>Compared to the usual queuing method, the web-based appointment system could significantly increase patient's satisfaction with registration and reduce total waiting time effectively. However, further improvements are needed for broad use of the system.</p

In situ Biological Dose Mapping Estimates the Radiation Burden Delivered to ‘Spared’ Tissue between Synchrotron X-Ray Microbeam Radiotherapy Tracks

Microbeam radiation therapy (MRT) using high doses of synchrotron X-rays can destroy tumours in animal models whilst causing little damage to normal tissues. Determining the spatial distribution of radiation doses delivered during MRT at a microscopic scale is a major challenge. Film and semiconductor dosimetry as well as Monte Carlo methods struggle to provide accurate estimates of dose profiles and peak-to-valley dose ratios at the position of the targeted and traversed tissues whose biological responses determine treatment outcome. The purpose of this study was to utilise γ-H2AX immunostaining as a biodosimetric tool that enables in situ biological dose mapping within an irradiated tissue to provide direct biological evidence for the scale of the radiation burden to ‘spared’ tissue regions between MRT tracks. Γ-H2AX analysis allowed microbeams to be traced and DNA damage foci to be quantified in valleys between beams following MRT treatment of fibroblast cultures and murine skin where foci yields per unit dose were approximately five-fold lower than in fibroblast cultures. Foci levels in cells located in valleys were compared with calibration curves using known broadbeam synchrotron X-ray doses to generate spatial dose profiles and calculate peak-to-valley dose ratios of 30–40 for cell cultures and approximately 60 for murine skin, consistent with the range obtained with conventional dosimetry methods. This biological dose mapping approach could find several applications both in optimising MRT or other radiotherapeutic treatments and in estimating localised doses following accidental radiation exposure using skin punch biopsies

Risky use of alcohol, drugs and cigarettes in a psychosis unit: a 1 1/2 year follow-up of stability and changes after initial screening

<p>Abstract</p> <p>Background</p> <p>Co-morbidity with substance use disorders negatively influences overall functioning in patients with psychosis. However, frequencies and courses of risky use of alcohol, drugs and cigarettes are rarely investigated in patients at psychosis units.</p> <p>The purpose of this study is to describe the use of alcohol, drugs and cigarettes in patients at a psychosis unit over a 1 1/2 year period after them having taken part in a screening investigation including a feed-back of the results to personnel. Relationships with sex and age are also described.</p> <p>Methods</p> <p>The patients' use of the substances was examined at baseline and at follow-up using three self-reporting instruments: Alcohol Use Disorders Identification Test (AUDIT), Drug Use Disorders Identification Test (DUDIT) and Fagerstrom Test for Nicotine Dependence (FTND).</p> <p>Results</p> <p>One hundred and eighty-six patients out of 238 at baseline (78 percent) took part in the follow-up. Total AUDIT score decreased in women. Older men more often developed a risky alcohol use. Older women tended to reduce their risky drug habits. On a group level the habits mostly were stable, but 11 percent changed their alcohol habits and 15 percent changed their smoking habits from risky to no/low risky use, or vice versa. Nine percent changed their drug habits, predominantly from risky to no/low risky use.</p> <p>Conclusion</p> <p>A more active approach towards alcohol, drug and smoking habits in psychosis units would probably be beneficial.</p

Augmented Lung Inflammation Protects against Influenza A Pneumonia

Influenza pneumonia causes high mortality every year, and pandemic episodes kill millions of people. Influenza-related mortality has been variously ascribed to an ineffective host response that fails to limit viral replication, an excessive host inflammatory response that results in lung injury and impairment of gas exchange, or to bacterial superinfection. We sought to determine whether lung inflammation promoted or impaired host survival in influenza pneumonia.To distinguish among these possible causes of influenza-related death, we induced robust lung inflammation by exposing mice to an aerosolized bacterial lysate prior to challenge with live virus. The treatment induced expression of the inflammatory cytokines IL-6 and TNF in bronchoalveolar lavage fluid 8- and 40-fold greater, respectively, than that caused by lethal influenza infection. Yet, this augmented inflammation was associated with striking resistance to host mortality (0% vs 90% survival, p = 0.0001) and reduced viral titers (p = 0.004). Bacterial superinfection of virus infected lungs was not observed. When mice were repeatedly exposed to the bacterial lysate, as would be clinically desirable during an influenza epidemic, there was no tachyphylaxis of the induced viral resistance. When the bacterial lysate was administered after the viral challenge, there was still some mortality benefit, and when ribavirin was added to the aerosolized bacterial lysate, host survival was synergistically improved (0% vs 93.3% survival, p<0.0001).Together, these data indicate that innate immune resistance to influenza can be effectively stimulated, and suggest that ineffective rather than excessive inflammation is the major cause of mortality in influenza pneumonia

The Impact of the Human DNA Topoisomerase II C-Terminal Domain on Activity

Type II DNA topoisomerases (topos) are essential enzymes needed for the resolution of topological problems that occur during DNA metabolic processes. Topos carry out an ATP-dependent strand passage reaction whereby one double helix is passed through a transient break in another. Humans have two topoII isoforms, alpha and beta, which while enzymatically similar are differentially expressed and regulated, and are thought to have different cellular roles. The C-terminal domain (CTD) of the enzyme has the most diversity, and has been implicated in regulation. We sought to investigate the impact of the CTD domain on activity.We have investigated the role of the human topoII C-terminal domain by creating constructs encoding C-terminally truncated recombinant topoIIalpha and beta and topoIIalpha+beta-tail and topoIIbeta+alpha-tail chimeric proteins. We then investigated function in vivo in a yeast system, and in vitro in activity assays. We find that the C-terminal domain of human topoII isoforms is needed for in vivo function of the enzyme, but not needed for cleavage activity. C-terminally truncated enzymes had similar strand passage activity to full length enzymes, but the presence of the opposite C-terminal domain had a large effect, with the topoIIalpha-CTD increasing activity, and the topoIIbeta-CTD decreasing activity.In vivo complementation data show that the topoIIalpha C-terminal domain is needed for growth, but the topoIIbeta isoform is able to support low levels of growth without a C-terminal domain. This may indicate that topoIIbeta has an additional localisation signal. In vitro data suggest that, while the lack of any C-terminal domain has little effect on activity, the presence of either the topoIIalpha or beta C-terminal domain can affect strand passage activity. Data indicates that the topoIIbeta-CTD may be a negative regulator. This is the first report of in vitro data with chimeric human topoIIs

Agents increasing cyclic GMP amplify 5-HT4-elicited positive inotropic response in failing rat cardiac ventricle

Activation of 5-HT4 receptors in failing ventricles elicits a cAMP-dependent positive inotropic response which is mainly limited by the cGMP-inhibitable phosphodiesterase (PDE) 3. However, PDE4 plays an additional role which is demasked by PDE3 inhibition. The objective of this study was to evaluate the effect of cGMP generated by particulate and soluble guanylyl cyclase (GC) on the 5-HT4-mediated inotropic response. Extensive myocardial infarctions were induced by coronary artery ligation in Wistar rats, exhibiting heart failure 6 weeks after surgery. Contractility was measured in left ventricular preparations. Cyclic GMP was measured by EIA. In ventricular preparations, ANP or BNP displayed no impact on 5-HT4-mediated inotropic response. However, CNP increased the 5-HT4-mediated inotropic response as well as the β1-adrenoceptor (β1-AR)-mediated response to a similar extent as PDE3 inhibition by cilostamide. Pretreatment with cilostamide eliminated the effect of CNP. Inhibition of nitric oxide (NO) synthase and soluble GC by l-NAME and ODQ, respectively, attenuated the 5-HT4-mediated inotropic response, whereas the NO donor Sin-1 increased this response. The effects were absent during PDE3 inhibition, suggesting cGMP-dependent inhibition of PDE3. However, in contrast to the effects on the 5-HT4 response, Sin-1 inhibited whereas l-NAME and ODQ enhanced the β1-AR-mediated inotropic response. cGMP generated both by particulate (NPR-B) and soluble GC increases the 5-HT4-mediated inotropic response in failing hearts, probably through inhibition of PDE3. β1-AR and 5-HT4 receptor signalling are subject to opposite regulatory control by cGMP generated by soluble GC in failing hearts. Thus, cGMP from different sources is functionally compartmented, giving differential regulation of different Gs-coupled receptors

Synergistic TLR2/6 and TLR9 Activation Protects Mice against Lethal Influenza Pneumonia

Lower respiratory tract infections caused by influenza A continue to exact unacceptable worldwide mortality, and recent epidemics have emphasized the importance of preventative and containment strategies. We have previously reported that induction of the lungs' intrinsic defenses by aerosolized treatments can protect mice against otherwise lethal challenges with influenza A virus. More recently, we identified a combination of Toll like receptor (TLR) agonists that can be aerosolized to protect mice against bacterial pneumonia. Here, we tested whether this combination of synthetic TLR agonists could enhance the survival of mice infected with influenza A/HK/8/68 (H3N2) or A/California/04/2009 (H1N1) influenza A viruses. We report that the TLR treatment enhanced survival whether given before or after the infectious challenge, and that protection tended to correlate with reductions in viral titer 4 d after infection. Surprisingly, protection was not associated with induction of interferon gene expression. Together, these studies suggest that synergistic TLR interactions can protect against influenza virus infections by mechanisms that may provide the basis for novel therapeutics