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In this catalogue, 54 Annelida OTUs collected by the IN2021_V04 and IN2022_V08 expeditions to the Australian Christmas Island and Cocos (Keeling) Islands Territories are diagnosed and illustrated. [ABSTRACT FROM AUTHOR]

More public institutions are now required to assess student learning outcomes. A look at Virginia and New Jersey shows these requirements vary, but mandated assessment may not produce needed improvements. Inadequate assessment methodologies, faculty resistance, and a lack of clarity about the use of results make this movement uncertain. (Author/MLW)

Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease, in which the body's immune system targets its own cells for destruction. The cells that are destroyed in IDDM are the beta-cells, the insulin-producing cells located in the pancreatic islets of Langerhans. However, the way this destruction is brought about remains unknown. To learn more concerning this, the role of macrophages (a type of immune cell) was investigated in a series of experiments using the non-obese diabetic mouse, an animal model used in diabetes research. Mice were treated with a protein (monoclonal antibody 5C6) known to block the migration of macrophages to sites of inflammation, and were then subjected to conditions that promote the onset of diabetes. Results showed that 5C6-treated mice had a greatly reduced tendency (from 93 to 8 percent) to become diabetic compared with controls (untreated mice). Moreover, animals that received 5C6 throughout the experiment preserved their insulin-containing islet cells, while untreated animals had very few intact cells left. Since the entry of T cells (another type of immune cell) seems to occur only after initial migration of macrophages into tissue, the hypothesis was advanced that the protective effect of 5C6 may result from its ability to suppress macrophage migration. If macrophages do not enter the tissue, then T cells and other components of the immune system do not exert their destructive effects. Ideas regarding the physiological mechanisms that could be active in such processes are presented. (Consumer Summary produced by Reliance Medical Information, Inc.)

THE ORGANISMS LIVING ON THE OCEAN FLOOR ARE LINKED TO THOSE LIVING IN THE OCEAN ABOVE, BUT WHETHER OR HOW THE BIODIVERSITY IN THESE TWO REALMS IS LINKED REMAINS LARGELY [...]

The spontaneous development of insulin dependent diabetes mellitus in non-obese diabetic (NOD) mice has been shown to be mediated by a Th1 response against beta cell antigens. It is known that in murine models of Schistosoma mansoni infection, egg production is associated with a switch from a Th1 to Th2 response. This subsequent dominance of a Th2 response in S.mansoni infected mice has been shown to influence the response to other infectious agents or antigens. We therefore determined whether infection with S.mansoni could influence the spontaneous incidence of insulin dependent diabetes mellitus (IDDM) in NOD mice. Infection with this helminth significantly reduced the spontaneous incidence of IDDM. IDDM was also prevented by injecting parasite eggs alone. Because until relatively recently humans might expect to succumb to a variety of infectious agents, the current freedom from infection might permit the expression of a genetic predisposition to autoimmune pathology and be responsible for the increased incidence of IDDM. [ABSTRACT FROM AUTHOR]

When normal mice are immunized with rat RBC, autoantibodies to mouse red cells and antigen-specific suppressor cells are generated. Suppressor cell activity is found in T-enriched populations and suppresses only the induction of autoantibody, not ongoing or secondary autoantibody responses. Using anti- bodies lytic for either B cells or distinct T-cell subpopulations, we are able to show that suppression is dependent on the presence of Lyt 1 + T cells. [ABSTRACT FROM AUTHOR]

This paper describes some of the characteristics of a suppressor cell which is capable of regulating a rat RBC-induced autoantibody response against mouse RBCs. This cell, which appears to function as an inducer of suppression on transfer to naive recipients, is sensitive to Iow doses of cyclophosphamide, and its generation is affected by iow doses of irradiation. However, the recipients of these cells arc insensitive to cyclophosphamide treatment, suppression still being induced in such animals. [ABSTRACT FROM AUTHOR]

When SJL mice are hyperimmunized with rat red blood cells (RBC), tolerance to self is readily broken and these animals develop a high autoantibody response to their own RBC. However, these mice also fail to generate those antigen-specific suppressor cells which normally regulate this induced autoantibody response. [ABSTRACT FROM AUTHOR]

Passive administration of monoclonal IgM anti-sheep red blood cell antibody 2 hr prior to a low dose of sheep red blood cells (SR BC) markedly enhances the specific antibody response. This IgM enhancement of the response to SRBC is highly reproducible and can furthermore be demonstrated in vitro. The time course and dose dependency of the response indicate that a critical antibody: antigen ratio is necessary for enhancement to occur. The IgM enhancement phenomenon has been demonstrated in several strains of mice, providing strong evidence against an idiotype-related mechanism. [ABSTRACT FROM AUTHOR]