The immunomodulator AS I0 I has been demonstrated to exhibit radioprotective and chemoprotective effects in mice. Following phase-I studies, preliminary resulk from phase-ll clinical trials on non-small-cell-lung-cancer patients showed a reduction in the severity of alopecia in patients treated with A S l O l in combination with chemotherapy. To further substantiate these findings, the present study was extended to include 58 patienk treated either with the optimal dose of 3 mg/rn2 AS I0 I combined with carboplatin and VP-16, or with chemotherapy alone. As compared with patienk treated with chemotherapy alone, there was a significant decrease in the level of alopecia in patients receiving the combined therapy. The newly developed rat model was used to elucidate the protective mechanism involved in this effect. We show that significant prevention of chemotherapy-induced alopecia is obtained in rats treated with Ara-C combined with AS 10 I, administered i.p. or S. C. or applied topically to the dorsal skin. We show that this protection by AS I0 I is mediated by macrophage-derived factors induced by AS I0 I. Protection by AS I0 I can be ascribed, at least in part, to IL-I, since treatment of rats with IL-IRA largely abrogated the protective effect of AS I0 I. Moreover, we demonstrate that in humans there is an inverse correlation between the grade of alopecia and the increase in IL-la. In addition, protection by A S l O l could be related to PGE2 secretion, since injection of indomethacin before treatment with AS I0 I and Ara-C partly abrogated the protective effect of AS 10 I. To assess the ability of AS 10 I to protect against chemotherapy-induced alopecia, phase-ll clinical trials have been initiated with cancer patienk suffering from various malignancies.o 1996 Wiley-Liss, Inc.The psychological impact of chemotherapy-induced alopecia represents one of the more devastating side effects of cancer chemotherapy and, in some instances, leads patients to refuse potentially curative chemotherapy (Hood, 1986). Although this complication has been known for many decades, little progress has been made in its prevention or treatment (Wood, 1985), in part because of lack of a suitable, reproducible experimental model. A new model has now been developed in which chemotherapy induces total alopecia in 8-dayold rats (Hussein et al., 1990). This model enables the investigation of agents that might protect against chemotherapyinduced alopecia, and the elucidation of their mechanism of action.The immunomodulator ASlOl [ammonium trichloro (dioxyethylene-0,O') tellurate] has been shown by us to exhibit radioprotective properties when injected into mice prior to sub-lethal and lethal doses of irradiation (Kalechman et al., 1990). In addition, AS101 was found to protect mice from hemopoietic damage caused by sub-lethal doses of various chemotherapeutic drugs, and to increase the rate of survival of mice treated with lethal doses of these agents. These include cyclophosphamide (Kalechman et al., 1991a), 5-FU (Kalechman et al., 1991b)...

AS101 has significant bone marrow (BM)-sparing effects and prevents hair loss in chemotherapy-treated patients, with minimal overall toxicity. These effects are probably due to increased production of IL-1 alpha, IL-6, and granulocyte-macrophage (GM)-CSF.

Of 162 patients with chronic interstitial lung disease, eight (seven of them male) had active tuberculosis. This was 4-5 times higher than the incidence in the general population. The frequency of tuberculosis was similar in patients treated with and without corticosteroids.

Home monitoring of asthmatic patients with the telespirometry system may improve the management of the disease and the quality of life and reduce costly hospitalizations.

The hypothesis that the surface tension of the fluid film which lines the lung alveoli reduces the pericapillary pressure in air-filled lungs was tested by perfusing the excised lungs of dogs with saline, 6% dextran in saline, and blood. After almost maximal inflation with air from low volumes or the degassed state (inflation state) the pulmonary arterial pressure, relative to the base of the lungs, was lower than the alveolar pressure with flows up to 50 ml/min. It was higher than the alveolar pressure at any flow when the air-liquid interface had been abolished by filling the lungs to the same volume with fluid. The pulmonary arterial pressure at the same flow and alveolar pressure was lower in the inflation state than after deflation from higher volumes (the deflation state). However, lung volume was larger in the deflation state. The possibility of some low resistance channels in the inflation state could not be excluded. However, histological examinations showed that the alveolar capillaries were patent and failed to show any airless lung. pulmonary circulation; pericapillary pressure in lungs; surface tension and pulmonary vascular resistance Submitted on July 29, 1963