No abstract

The self-management of asthma can improve clinical outcomes. Recently, mobile telephones have been widely used as an efficient, instant personal communication tool. This study investigated whether a self-care system will achieve better asthma control through a mobile telephone-based interactive programme.This was a prospective, controlled study in outpatient clinics. From 120 consecutive patients with moderate-to-severe persistent asthma, 89 were eventually recruited for the study, with 43 in the mobile telephone group (with a mobile telephone-based interactive asthma self-care system).In the mobile telephone group, mean¡SEM peak expiratory flow rate significantly increased at 4 (378.2¡9.3 L?min ; n543; p50.001) compared to the control group. Mean¡SEM forced expiratory volume in 1 s significantly increased at 6 months (65.2¡3.2% predicted; n543; p,0.05). Patients in the mobile telephone group had better quality of life after 3 months, as determined using the Short Form-121 physical component score, and fewer episodes of exacerbation and unscheduled visits than the control group. Patients in the mobile telephone group significantly increased their mean daily dose of either systemic or inhaled corticosteroids compared with the control group.The mobile telephone-based interactive self-care system provides a convenient and practical self-monitoring and -management of asthma, and improves asthma control.

Our study provided evidence of an increased pool of CD11b+/CD14⁻/CD15+/CD33+ MDSCs in the peripheral blood of NSCLC patients. For the suppressive effect of the cells on CD8+ T lymphocytes, these findings suggest the important role of the CD11b+/CD14⁻/CD15+/CD33+ MDSCs in mediating immunosuppression in NSCLC.

Circulating fibrocytes are increased in patients with asthma with CAO and can be transformed by TGF-beta(1) to myofibroblasts. Fibrocytes may contribute to airway obstruction in asthma.

The application of a supervised endurance exercise training programme in a home setting offering convenience and prolonged effects is a challenge.In total, 48 patients were initially assessed by the incremental shuttle walk test (ISWT), spirometry and the Short Form-12 (SF-12) quality-of-life questionnaire, and then every 4 weeks for 3 months thereafter and again after 1 yr. During the first 3 months, 24 patients in the cell phone group were asked to perform daily endurance walking at 80% of their maximal capacity by following the tempo of music from a program installed on a cell phone. The level of endurance walking at home was readjusted monthly according to the result of ISWT. In the control group, 24 patients received the same protocol and were verbally asked to take daily walking exercise at home.Patients in the cell phone group significantly improved their ISWT distance and duration of endurance walking after 8 weeks. The improvements in ISWT distance, inspiratory capacity and SF-12 scoring at 12 weeks persisted until the end of the study, with less acute exacerbations and hospitalisations.In the present pilot study, the cell phone-based system provides an efficient, home endurance exercise training programme with good compliance and clinical outcomes in patients with moderate-to-severe chronic obstructive pulmonary disease.

Nitric oxide (NO) plays a major role in the pulmonary host-defence mechanism in response to infections and is implicated in bacteriostatic as well as bactericidal processes [1,2]. NO is generated through the L-arginine pathway and is converted to the related reactive nitrogen intermediates (RNI) . In inflammatory responses, NO is produced by the inducible form of NO synthase (iNOS), which is mostly from inflammatory cells, such as macrophages [3][4][5]. NO production and iNOS expression by alveolar macrophages (AM) is upregulated in response to heat-killed Mycobacterium tuberculosis instilled into the lungs of rats [6] and plays a role in limiting the growth of Mycobacterium avium complex [7,8]. Murine macrophages activated by interferon (IFN)-γ and tumour necrosis factor (TNF)-α are capable of killing M. tuberculosis in vitro via the generation of RNI by iNOS [9]. In addition, pretreatment with NO synthase (NOS) inhibitors profoundly increases bacterial burden, pathological tissue damage and mortality in mice infected with M. tuberculosis [10], thus indicating that NO plays an important role in resistance to M. tuberculosis infection in the mouse. A recent report has shown that iNOS messenger ribonucleic acid (mRNA) is upregulated on AM in patients with active pulmonary tuberculosis (TB) [11], however, it is not known whether the iNOS enzyme activity is also enhanced and leads to increased generation of RNI by AM against M. tuberculosis.NO can be detected in the expired air of animals and humans [12]. Recent reports have shown that the level of exhaled NO is elevated in patients with bronchial asthma and bronchiectasis [13,14], and have suggested that this is due to iNOS upregulation induced by cytokines such as IFN-γ, TNF-α and interleukin (IL)-1β [15] released in chronic airway inflammation. Thus, the measure of exhaled NO concentration may gauge the extent of NOmediated inflammatory responses in the airways. In this study, we measured exhaled NO levels in patients with active pulmonary TB and determined the cellular source of NO by examining the expression of iNOS and the release of RNI from AM. Material and methods Study populationNineteen patients with active pulmonary TB (13 males and 6 females, aged 59.1±4.5 yrs) were studied prior to anti-TB treatment. None of these patients were current smokers. For all patients, at least one recent sputum specimen We conclude that the increase in exhaled nitric oxide observed in patients with active pulmonary tuberculosis is due to an upregulation of inhaled NO synthase expression in alveolar macrophages which have an enhanced capacity for nitric oxide production. Eur Respir J 1998; 11: 809-815.

In patients with severe H1N1 pneumonia, early adjuvant treatment with corticosteroids and an mTOR inhibitor was associated with improvement in outcomes, such as hypoxia, multiple organ dysfunction, virus clearance, and shortened liberation of ventilator and ventilator days.

We evaluated whether a goal-directed protocol, without measurement of central venous oxygen saturation, would improve survival in medical intensive care unit (ICU) patients with septic shock. This is a prospective, controlled study in a 24-bed medical ICU at a tertiary care hospital. From a total of 241 consecutive patients with septic shock, 224 were randomly assigned to receive therapy with or without a written protocol using central venous pressure, mean arterial pressure, and urine output as therapeutic goals. Baseline characteristics were similar between groups. Implementation of goal-directed therapy caused a more rapid reversal of persistent shock (47 +/- 22.8 vs. 65.4 +/- 32.1 h, P = 0.006) and decreases of ICU (50% vs. 67.2%, P = 0.009) and in-hospital (53.7% vs. 71.6%, P = 0.006) mortality rates compared with non-goal-directed therapy. Patients receiving goal-directed therapy also had less risk for developing central nervous system or renal failure than patients without. Patients with goal-directed therapy received more fluid during the period of persistent shock (136.2 +/- 119 vs. 88.6 +/- 57.7 mL h, P = 0.034) and less delay in vasopressor administration (78 +/- 22.2 vs. 104.4 +/- 29 min, P = 0.001) than patients with non-goal therapy. Implementation of a goal-directed protocol improves survival and clinical outcomes in ICU patients with septic shock. These benefits may arise from adequate fluid resuscitation, earlier vasopressor administration, rapid shock reversal, and protection of major organ function. With central venous oxygen saturation measurement to detect tissue perfusion, the clinical outcomes may be further improved.