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Research seeking to explain intraspecific variations in plant phenolics has focused on two general paradigms, the resource availability (carbon/nutrient balance) and induced-defense models. We experimentally tested both hypotheses to explain changes in phlorotannin concentrations in the brown alga Fucus vesiculosus. Fucus was collected monthly from two estuarine sites (Cape Cod, Massachusetts, USA) differing in nitrogen availability, and analyzed for polyphenolic levels and tissue-nitrogen concentrations. In situ nutrient enrichment experiments were conducted to measure changes in polyphenolic levels related to N availability. Simulated grazing experiments examined the possibility of induced increases in polyphenolic concentrations in Fucus vesiculosus. Paired choice ex- periments conducted in the laboratory examined feeding selectivity by the snail Littorina littorea for either Fucus population. Field measurements and experiments revealed temporal and site-related changes in tissue constituents. Polyphenolic concentrations were consistently, sometimes two times, higher in Fucus vesiculosus from the low-N site compared with algae from the high-N site; tissue-N content was higher in the population from the high-N site. For both populations, tissue N was inversely correlated with polyphenolic concentrations. Only Fucus from the low-N site showed a significant reduction in polyphenolic concentrations under experi- mental enrichment. Regression analysis revealed a significant inverse relationship (R2 = 0.71) between phenolic concentrations and growth rates for Fucus at the high-N, but not the low-N site. This suggests a growth cost associated with phlorotannin production for this phenolic-poor population due, perhaps, to C-limited growth. Phlorotannin concentra- tions increased significantly in clipped Fucus at the low-N site in two of three simulated grazing experiments, indicating an inducible response. We did not find a significant in- ducible response for the high-N, phenolic-poor population, and our choice experiments revealed a clear preference for this population by Littorina littorea. Our results offer support for both the induced-defense and carbon/nutrient balance hypotheses as explanation for variations in phlorotannin concentrations in Fucus vesiculosus. We suggest that within- species variation in polyphenolics is due to a complex interaction of environmental (nutrient availability, irradiance levels) and defense-related (grazing activity) factors.

Lung dendritic cells (DCs) from mice were enriched to 92-99% purity using a multistep enrichment protocol which included fluorescence-activated cell sorting. DCs were analyzed for expression of cell surface molecules, function in a mixed leukocyte reaction (MLR), and dependence on accessory molecules in stimulating an MLR. DCs possessed potent accessory properties in vitro, while interstitial macrophages (IM), which are Ia-negative, displayed little MLR-stimulating function of their own. However, IM were capable of enhancing DC-initiated T cell proliferation via a cell contact mechanism. These results indicated that murine lung DCs functioned as stimulators of primary T cell responses, and that cells in the local environment influenced their function. Lung DCs expressed surface molecules typical of DCs from other sites including CD11a, CD54, CD80, and CD86. As is true for DCs in other sites, costimulatory molecules including CD80, CD86, CD40L, CD2, CD54, and CD11a played important roles in lung DC-initiated T cell proliferation. Interestingly, anti-CD86 monoclonal antibody (mAb) had little inhibitory effect on the MLR unless it was added in combination with anti-CD80 mAb. These studies suggest that CD80 on lung DCs can provide a costimulatory signal to allogeneic T cells in the absence of CD86 signaling, but that CD86 functions poorly except when CD80 is also engaged.

Understanding how lung immunity develops against pulmonary pathogens should lead to more rational approaches in vaccine design and to the use of recombinant cytokines in lung disease. T lymphocytes are central to the development of effective immune responses; therefore, understanding how lung immunity develops will require a study of how and where T cells respond to respiratory antigens. Our laboratory has helped define the phenotype and function of lung dendritic cells, which likely play an essential role in stimulating naive T cells to respond to antigens. We found that both interstitial and alveolar macrophages can regulate the function of these cells, the former to enhance activity, the latter to suppress. In addition, we developed a murine pulmonary infection model using the fungus, Cryptococcus neoformans, in which T-cell-mediated immunity is essential for effective host clearance of the organism. The role of T cells in this model is to recruit and activate effector cells to resolve the lung infection; both CD4 and CD8 T-cell subsets are required for optimal effector cell recruitment. These studies are summarized as examples of current approaches to understanding pulmonary immunity.

Effective pulmonary immune responses likely require both local antigen presenting cells (APC) and regulatory suppressor cells. Bronchoalveolar cells (BAC), which consist primarily of alveolar macrophages (AM), are poor APC in most species and are often suppressive. However, dendritic cell (DC)-enriched populations from both lung interstitium and BAC have potent APC activity as measured by their capacity to stimulate both alloantigen and antigen-induced lymphoproliferative T cell responses. To determine if BAC could down-regulate pulmonary immune responses, BAC were mixed with DC-enriched loosely adherent lung interstitial cells (LAd) in a mixed leukocyte reaction (MLR). With high numbers of BAC, MLRs were consistently suppressed and suppression was partially reversed by the addition of indomethacin and catalase. Supernatants from BAC cultured with either syngeneic or allogeneic T lymphocytes in the presence of indomethacin and catalase markedly suppressed an MLR, while supernatants from BAC cultured alone were inconsistently suppressive. Antibodies to TGF-beta completely reversed the BAC-T cell supernatant-induced suppression of the MLR. However, TGF-beta antibody only partially reversed BAC-induced suppression when BAC were added directly to MLR cultures that contained indomethacin and catalase, suggesting that, in addition to TGF-beta, prostaglandins, and H2O2, BAC in culture with LAd and allogeneic T cells also produced short-lived suppressive factors and/or mediated suppression by direct cell contact. Thus, resident BAC likely utilize multiple mechanisms including TGF-beta secretion to suppress intra-alveolar immune responses initiated by lung DC.

A recent study by the National Athletic Trainers Association indicated that injuries occur more often during practice than during games in high school athletics. Results of the 3-year study indicated that 60% of basketball injuries occurred in boys and young men during practice and 59% occurred in women. About 2/3 of the estimated 120,000 injuries suffered by prep wrestlers each year happen during practice. The study found that an average of 331,865 high school football players (1/3 of the million who play football each year) were sidelined by an injury at least once. With these statistics in mind, our study looks at the approach to the management of injury in the public schools that make up the Oahu Inter-scholastic Association (OIA) in the state of Hawaii. The estimated number of student athletes that participate in organized athletics in the OIA is 7,960 and the number of coaches is 1,189.

The nuclei Se 76 and Se 78 have been Coulomb excited with 37 MeV oxygen ions. In both isotopes 2′ + and 4 + levels have been observed at approximately twice the energy of the first-excited state. The spins of these levels were determined in O 16 -γ angular correlation measurements, and the transition strengths were interpreted from the γ-ray yields. There is evidence that both nuclei may have collective 0 + levels in this energy region. Effects arising from the static quadrupole moments of excited states are discussed.

A search was made for gamma rays following the positron decay of Ne/ sup 18/ in order to locate the 0/sup +/, T = 1 level in F/sup 18/. Ne/sup 18/ was produced in the reaction O/sup 16/(He/sup 3/,N)Ne/sup 18/. Th e He/sup 3/ beam could be interrupted by a tantalum shutter. Pulseheight spectra obtained during "beam-off" periods showed a gamma ray with an energy of about 1 Mev. The possibility of the peak arising from random coincidences between 0.511Mev annihilation quanta was ruled out. The observed gamma ray was identified with a transition from the 1.04-Mev level in F/sup 18/. It is probable that the level excited is the analog of the ground state of Ne/sup 18/ and has the assignmert 0/ sup +/, T = 1. (M.C.G.)

Decay studies on three energy levels of F/sup 18/ were performed; 0.930 Mev (prompt alpha rays), 1.08 Mev (prompt alpha rays), and 1.12 Mev (delayed alpha rays). The decay- of the 1.12-Mev level of F/sup 18/ was of particular interest. The lifetime of the three levels was found to be less than 10/sup -8/ second for the 0.93- and 1.08-Mev levels and 0.1x 10/sup 6/ second for the 1.12- Mev level. (B.O.G.)

PART I Vital capacity, the largest expiration following the deepest inspiration, varies with age and sex, height and weight, health and disease, and after periods of rest and exertion. It is a fair criterion of life, reaching its peak when physiologic competence is highest, diminishing as incompetence increases and becoming zero when respiration ceases. A just evaluation of the therapeutic significance of vital capacity depends primarily on recognition of the anatomic and physiologic factors that establish it and secondarily on knowledge of their interrelationships, which control it. These are the means to understand the causes and effects of the numerous, considerable and at times abrupt fluctuations in vital capacity known to occur in health and in disease spontaneously and to be provoked by operations. They are also the means to better therapy. Answers to the questions implied are to be found in studies of the processes that control oxygen metabolism

Histoplasmosis was considered a rare and always fatal disease for many years after it was first described by Darling in 1906. However, recent epidemiological studies in the United States have revealed that in some states in the endemic area 60% to 70% of males aged 17 through 21 years have been infected with Histoplasma capsulatum . 1 The respiratory tract is the usual portal of entry of the fungus with the primary lesion occurring in the lungs. 2 Cases of histoplasmosis having skin lesions have been reported, but the skin lesions were usually the result of dissemination of the infection. 3,4 The purpose of this paper is to report a case of primary cutaneous histoplasmosis which resulted from direct inoculation of the fungus through the skin. Report of Case On Jan 12, 1959, a 32-year-old white male who had recently moved into the endemic area for histoplasmosis assisted with an autopsy

All who escape untimely death from other causes are infected with tubercle bacilli. The majority are insusceptible and develop no recognized evidence of infection. The minority are of three grades of susceptibility. Those of least susceptibility recover spontaneously, often despite maltreatment. The moderately susceptible may recover if aided promptly and properly, or may arrest the progress of the disease spontaneously. The disease in the most susceptible may be arrested if treatment is favorable, or its progress may be only retarded. The strength or weakness of resistance, defense and repair determines insusceptibility and the grades of susceptibility. Because they are the products of activities of cells, they are not static but dynamic, and are constantly fluctuating. Fluctuations are irregularly periodic and tend to take two courses. The more common course is downward. Through fatigue and exhaustion caused by unhygienic living, by intercurrent diseases and by age, people tend to forfeit more

The publication at this time of the result of our endeavors to cultivate an organism from the tissues of patients with Hodgkin's disease is occasioned by the publication by Negri and Mieremet 1 of the successful cultivation from two cases of Hodgkin's disease of a diphtheroid organism which they designate as the Corynebacterium granulomatis maligni . While Hodgkin's disease, or malignant granuloma of the lymphatic apparatus, has of late years come to be generally regarded as of infectious nature, the etiological agent has remained undetermined. The work in this country of Reed 2 and of Longcope 3 showed definitely that the condition was independent of tuberculosis, and that the theory supported by Sternberg 4 that it was a manifestation of the activity of the tubercle bacillus could not be maintained. In 1900 Fraenkel and Much 5 reported that by treating Hodgkin's nodes with a strong alkalin solution of sodium hypochlorid

Pure cultures of diphtheroid organisms apparently identical with or closely related to the Bacillus hodgkini have recently been obtained by us from two spleens removed surgically in the treatment of splenic anemia. Case 1 was under the care of Dr. J. J. Bellin of Green Bay, Wis., who kindly submitted blood-smears for examination before operation and sent the spleen immediately after its removal. The spleen was carefully sterilized externally by boiling before cultures were made from its interior. Case 2 was a patient in the Milwaukee County Hospital, where the blood was studied before and after splenectomy and where part of the bacteriologic and experimental observations were made. Histologic studies of the two spleens confirmed the clinical diagnosis of splenic anemia or the early stage of Banti's disease. Inoculation of dogs and rabbits was made with cultures of the organism obtained from Case 2 and with a culture obtained from

In this summary of our clinical experience in treating sixty-three cases of Hodgkin's disease of certain diagnosis over a period of eight years, we shall exclude, so far as practicable, hypotheses and technical details. We offer an interpretation of the effects of our therapy that is to some extent both incomplete and unsatisfactory. Many of our patients began treatment comparatively recently, and approximate accuracy in the estimation of results depends on a series of well controlled observations extending over a period of at least five years. On the other hand, this is the largest series of cases reported from one group of observers, the only one that has been followed at frequent intervals by coordinated workers, consecutive records thus being obtained of variation in the blood picture, general physical condition and roentgenographic evidence. These observations, so far as possible, have been made independently in an effort to eliminate bias. Pending

In a recent publication 1 we have described a diphtheroid organism obtained in pure culture in four cases of Hodgkin's disease, and observed in three others. In order to determine the possibility of an etiologic relationship between this organism and the disease, the Macacus rhesus monkey has been used for inoculation experiments. While the experiments have been under way but a comparatively short time, histologic examination of a portion of a group of enlarged lymph-nodes, removed for transplantation to another animal, is of so encouraging a nature that a report seems justified. While we cannot yet claim that by the inoculation of the organism in question we have produced Hodgkin's disease (meaning the firm establishment of the organism in the animal and a continued and progressive enlargement of the general lymphadenoid tissue), we can say, that by repeated injections we have produced progressive enlargement of a single group of lymph-nodes which

In a preliminary note recently published,1we reported that by repeated injection of the diphtheroid organism cultivated by us from cases of Hodgkin's disease, there had been produced in monkeys lesions of the lymphnodes showing all the essential features of early Hodgkin's disease in man. Up to that time we had been unable to demonstrate that the organism could survive in the monkey for any great length of time, and therefore we felt that we could not assert that we had produced Hodgkin's disease in the monkey, or that we had even demonstrated any great pathogenicity of the diphtheroid organism for that species. Since making that report, however, the course of our experimental work has demonstrated fully the pathogenicity of the culture we were using, and has further shown that the virulence of the organism to the monkey may easily be increased even to the point of producing death