Energy expenditure during physiotherapist-assisted and self-treatment in cystic fibrosis

Cystic fibrosis (CF) results in increased energy requirements at rest. However, the energy expended during physiotherapy management is unknown. The aim of this study, therefore, is to examine the energy expended during two commonly used forms of chest physiotherapy in CF subjects. Twenty-six CF subjects completed a randomised crossover trial with 48 hours between treatments. Two regimens of treatment were conducted: therapist-assisted treatment (active cycle of breathing, ACBT, with percussion, vibration), and independent treatment (ACBT alone, under the supervision of a physiotherapist). Subjects completed pulmonary function tests before and after either treatment. Indirect calorimetry and oximetry parameters were recorded at rest, during, and following treatment. Treatment groups were compared using ANOVA and two-sample crossover t-tests. When compared to resting values, physiotherapy treatment resulted in significant increases in VO₂, VCO₂ and respiratory exchange ratio. No difference was evident between treatment regimens for the change in VO₂ between baseline and treatment. The increase in ventilation (baseline to treatment) was significantly greater for the therapist-assisted treatment. The therapist-assisted ACBT was associated with a significant carryover effect for forced expiratory flow at 50% of vital capacity (FEF₅₀). Oxygen requirements for the two treatments were similar. However, the assisted regimen resulted in greater changes in minute ventilation during treatment and improved 48-hour post-treatment pulmonary function after only one treatment session. These findings suggest that the inclusion of percussion and vibration within the ACBT may influence respiratory muscle activity during treatment and result in improved pulmonary function.     

Heterogeneity of B cell involvement in acute nonlymphocytic leukemia

In order to study the pattern of B cell involvement in acute nonlymphocytic leukemia (ANLL), multiple B lymphoid cell lines were established by Epstein-Barr virus transformation of peripheral blood mononuclear cells from two patients with the disease who were heterozygous for the X chromosome-linked glucose-6-phosphate dehydrogenase (G6PD). In one patient, the progenitor cells involved by the leukemia exhibited multipotent differentiative expression, whereas in the other patient the cells showed differentiative expression restricted to the granulocytic pathway. In the patient whose abnormal clone showed multipotent expression, the ratio of B-A G6PD in B lymphoid cell lines was skewed in the direction of type B (the enzyme characteristic of the leukemia clone) and significantly different from the 1:1 ratio expected. It is, therefore, likely that the neoplastic event occurred in a stem cell common to the lymphoid series as well as to the myeloid series. In contrast, evidence for B cell involvement was not detected in the patient whose ANLL progenitor cells exhibited restricted differentiative expression. These findings underscore the heterogeneity of ANLL. Clinically and morphologically similar malignancies in these two patients originated in progenitors with different patterns of stem cell differentiative expression. This difference may reflect differences in cause and pathogenesis.     

CGA-7 and HHF, two monoclonal antibodies that recognize muscle actin and react with adherent cells in human long-term bone marrow cultures

The CGA-7, a monoclonal antibody that reacts with smooth muscle cell actin but not with endothelial cell or fibroblast actin, and HHF, a monoclonal antibody that reacts with smooth muscle, skeletal muscle, and cardiac muscle actin, both recognize microfilaments present within adherent cells from actively hematopoietic human long-term marrow cultures. Macrophages, monocytes, and cultured marrow fibroblasts do not react with either antibody. These data suggest that the anti-actin antibodies may serve as useful markers for in vitro microenvironmental cells and lend support to the hypothesis that stromal cells from long- term marrow cultures are different from marrow fibroblasts and may constitute a unique cell lineage.     

Injury to a patent left internal thoracic artery graft at coronary reoperation

BACKGROUND: The purpose of this study was to determine the prevalence, outcome, and operative strategies for patients having injury to a patent left internal thoracic artery (LITA) graft to the left anterior descending coronary artery (LAD) at coronary reoperation. METHODS: Of 655 patients with a patent LITA graft to the LAD undergoing coronary reoperation from 1986 to 1997, 35 (5.3%) sustained intraoperative injury to the LITA graft. RESULTS: Strategies to restore flow to the LAD included new saphenous vein graft to the LAD in 15 patients, saphenous vein graft to the LITA stump in 7, saphenous vein graft to the LAD and repair of the LITA graft in 6, and other strategies in 7. All or part of the LITA graft to the LAD was salvaged in 20 patients (57%). Fourteen patients (40%) sustained perioperative myocardial infarction, and 3 patients died (8.6%). The 3 patients who died all had stenosis or thrombosis of the graft to the LAD documented at autopsy. CONCLUSIONS: We conclude that (1) the prevalence of injury to a patent LITA graft is 5.3%; (2) a variety of techniques can be used to restore blood flow to the LAD; and (3) ineffective revascularization of the LAD in this situation is associated with operative mortality. At primary coronary artery bypass grafting, the LITA pedicle should be positioned in the left chest away from the posterior sternal table; this strategy may minimize the risk of LITA graft injury at coronary reoperation.     

Lymphography--current role in oncology

A review of the use of lymphography at this hospital, a major oncology centre, is presented. The advent of computed tomography has brought a dramatic reduction in the number of lymphograms currently performed for diseases such as lymphoma, testicular tumours and gynaecological malignancies. This study analyses the reasons for this decline, and concludes that valuable information can still be obtained from lymphography in certain selected groups of patients.     

Obesity Is Associated with Increased Prostate Growth and Attenuated Prostate Volume Reduction by Dutasteride

Background

Although obesity has been associated with larger prostate volumes (PV), few studies have actually investigated whether obesity enhances PV growth, especially among men using 5α-reductase inhibitors.

Objective

To examine whether obesity is associated with enhanced PV growth measured by serial transrectal ultrasound (TRUS) measurements.

Design, setting, and participants

We conducted a secondary analysis of the REduction by DUtasteride of prostate Cancer Events (REDUCE) trial, which was originally aimed at cancer risk reduction among high-risk men with a single negative prestudy biopsy.

Intervention

Per-protocol randomization to placebo or dutasteride and mandatory TRUS-guided biopsies at 2 yr and 4 yr.

Outcome measurements and statistical analysis

Percentage change in PV at 2 yr and 4 yr from baseline. We tested its association with baseline body mass index (BMI) groups of <25, 25–29.9, and ≥30 kg/m² using multivariable linear regression. Secondarily, we tested whether BMI was associated with the likelihood of having no PV reduction among men randomized to dutasteride using multivariable logistic regression.

Results and limitations

Of 8122 participants, we analyzed 71.8% and 54.5% with complete 2-yr and 4-yr PV data, respectively. In multivariable analysis, men on placebo with BMI ≥30 versus <25 kg/m² had enhanced PV growth from baseline (at 2 yr: 17.0% vs 10.7%, p < 0.001; at 4 yr: 29.4% vs 20.1%; p = 0.001). Men on dutasteride with BMI ≥30 versus <25 kg/m² had attenuated PV reduction from baseline (at 2 yr: −14.3% vs −18.5%; p = 0.002; at 4 yr: −13.2% vs −19.3%; p = 0.001) and higher likelihood of having no PV reduction (at 2 yr: odds ratio [OR]: 1.44; 95% confidence interval [CI], 1.08–1.93; p = 0.014; at 4 yr: OR: 1.62; 95% CI, 1.18–2.22; p = 0.003). We found no significant interactions between BMI and dutasteride on PV change at 2 yr and 4 yr (p interaction ≥0.36). No clinical outcomes or effects of weight change were assessed.

Conclusions

Obesity enhanced PV growth and attenuated PV reduction by dutasteride. The null interaction between obesity and dutasteride for PV change implies that the effect of obesity on dutasteride-treated men is likely a combination of dutasteride-driven PV reduction with obesity-driven PV growth rather than decreased dutasteride efficacy.

ClinicalTrials.gov identifier

NCT00056407.