Our findings suggest that these molecules may be involved in the pathogenetic mechanisms acting as potential markers of Th17 cells activation in ALS.

Background-Dyspnea and fatigue are the main causes of exercise limitation in chronic heart failure (CHF) patients, whose peak inspiratory (Pi max ) and expiratory pressures (Pe max ) are often reduced. The aim of this study was to examine the relationship between respiratory muscle performance and oxygen kinetics. Methods and Results-A total of 55 patients (NYHA class I to III) and 11 healthy subjects underwent cardiopulmonary exercise tests (CPET) on a treadmill. In 45 of the 55 patients (group I) and in healthy subjects (group II), pulmonary function tests, Pi max , and Pe max were measured before and 10 minutes after exercise, and oxygen kinetics were monitored throughout and during early recovery from CPET. The first degree slope of oxygen consumption (V O 2 ) decline during early recovery (V O 2 /t-slope) and V O 2 half-time (T 1/2 ) were calculated. In 10 of the 55 CHF patients (group III), the measurements of Pi max were repeated 2, 5, and 10 minutes after CPET. A Ͼ10% reduction in Pi max after CPET (subgroup IA) was measured in 11 of 45 patients. In contrast, 34 of 45 CHF patients (subgroup IB) and all control subjects (group II) had Pi max Ͼ90% of baseline value after CPET. Subgroup IA patients had significantly lower peak V O 2 (13.5Ϯ2.1 versus 17.8Ϯ5.6 mL ⅐ kg Ϫ1 ⅐ min Ϫ1 ; PϽ0.001), lower anaerobic thresholds (10.1Ϯ2.4 versus 13.6Ϯ4.6 mL ⅐ kg Ϫ1 ⅐ min

BACKGROUNDAdverse effects of paclitaxel and carboplatin have been well described; however, pulmonary toxicity after patients receive this regimen has not been investigated extensively.METHODSTo clarify this issue, 33 consecutive patients who were treated with paclitaxel and carboplatin underwent prospective evaluation of respiratory function, which included pulmonary symptoms, pulmonary function tests (PFTs), arterial blood gas levels, and radiographic studies. Assessment was performed before and after completion of chemotherapy in all patients. Patients with substantial declines in PFTs, defined as a decline ≥ 20 percent in forced expiratory volume in 1 second (FEV1), total lung capacity (TLC), or diffusion capacity for carbon monoxide (DLCO), were reassessed 5 months later.RESULTSAfter chemotherapy, there were no significant changes in forced vital capacity (FVC; 111% ± 21% of the predicted value before chemotherapy vs. 111 ± 20% of the predicted value after chemotherapy), FEV1 (108% ± 24% of the predicted value before chemotherapy vs. 107% ± 22% of the predicted value after chemotherapy), FEV1/FVC ratio (79% ± 8% before chemotherapy vs. 78% ± 6% after chemotherapy), alveolar volume (VA; 95% ± 14% of the predicted value before chemotherapy vs. 96% ± 14% of the predicted value after chemotherapy), or TLC (96% ± 14% of the predicted value before chemotherapy vs. 97% ± 13% of the predicted value after chemotherapy). In contrast, there was a significant decline in DLCO (101% ± 20% of the predicted value before chemotherapy vs. 96 ± 21% of the predicted value after chemotherapy; P < 0.05). Arterial blood gas levels did not change after treatment. No patient had decreased FEV1 or TLC levels by ≥ 20%, whereas 4 of 33 patients (12%) exhibited a substantial decline (≥ 20%) in DLCO that persisted 5 months after treatment (DLCO at baseline, immediately after chemotherapy, and 5 months after the completion of chemotherapy, respectively: 99% ± 36% of the predicted value vs. 75% ± 28% of the predicted value vs. 74% ± 31% of the predicted value; P < 0.05). None of the 33 patients developed respiratory symptoms or had radiologic signs suggestive of lung toxicity. Among the various risk factors examined, baseline DLCO and FEV1 levels were associated with changes in DLCO post‐treatment.CONCLUSIONSThis prospective analysis showed that the combination of paclitaxel with carboplatin induced an isolated decrease in DLCO level in the absence of clinical or radiologic evidence of toxicity. Further studies are needed to clarify whether this reduction in DLCO is predictive of subsequent pulmonary impairment. Cancer 2002;94:452–8. © 2002 American Cancer Society.

A fatal case is reported of Balantidium coli pneumonia in a 71-y-old woman suffering from anal cancer. The diagnosis was made by the discovery of motile trophozoites in a wet mount from bronchial secretions. The usual habitat of the parasite is the colon; lung balantidiasis is very rare.

Background: There is evidence that immunological factors may be involved in pathogenic mechanisms of amyotrophic lateral sclerosis (ALS). Interleukin (IL)-15 and IL-12 are proinflammatory cytokines produced by activated blood and glial cells. They promote T cell differentiation and proliferation. Patients and Methods: We measured by ELISA serum and cerebrospinal fluid (CSF) levels of IL-15 and IL-12 in 21 patients with ALS and 19 patients with other noninflammatory neurological disorders (NIND) studied as a control group. IL-15 and IL-12 serum and CSF levels were also correlated with duration of the disease, the disability level determined using the revised ALS Functional Rating Scale and the clinical subtype of the disease onset in patients with ALS. Results: IL-15 and IL-12 serum levels were higher in patients with ALS as compared with patients with NIND (p = 0.014 and p = 0.011, respectively). IL-15 and IL-12 CSF levels were also increased in patients with ALS (p = 0.011 and p = 0.005, respectively). IL-15 and IL-12 levels were not correlated with disease duration, disability scale or clinical subtype of the disease onset in ALS patients. Conclusions: Our findings suggest that these molecules may be involved in the pathogenic mechanisms acting as potential markers of immune activation in ALS.