Variations of the flexor digitorum superficialis tendon of the little finger.

Seventy cadaveric hands were dissected to study variations of the flexor digitorum superficialis tendon (FDS) to the little finger. Anatomical variations were present in 13% of hands and 10% of the hands showed an anatomical variation that would preclude independent FDS function in the little finger. The distance of the decussation from the metacarpophalangeal joint was measured. A ratio of this distance to proximal phalangeal length was calculated. The ratio indicated that decussation position was independent of phalangeal size.

Developmental abnormalities of terminal deoxynucleotidyl transferase positive bone marrow cells and thymocytes in New Zealand mice: effects of prostaglandin E1.

The enzyme TdT was used as a marker with which to study the ontogeny of primitive lymphopoietic cells in NZ strain mice. A marked accumulation of abnormally large, rapidly proliferating TdT+ cells was seen in the subcapsular region of the thymus cortex in the NZB and NZB/W mice. This abnormal accumulation of TdT+ thymocytes was most pronounced in the NZB/W hybrid and persisted for at least the first 16 wk of life. In addition, significantly elevated percentages of TdT+ bone marrow cells (presumptive prothymocytes) were present in NZB, NZW, and NZB/W mice between 1 and 4 wk of age, with the highest mean peak levels occurring in the NZB strain. Treatment of both normal and adrenalectomized BALB/c and NZB/W mice with pharmacologic doses (7 to 10 mg/kg) of PGE1 caused a marked, dose-dependent decrease in thymus weight and thymus cell number within 12 to 18 hr. Histologic and cell separation studies showed that this was due to the selective depletion of PNA+ TdT+ cortical thymocytes. Similarly, PGE1 caused a reversible, dose-dependent decrease in the percentage of TdT+ bone marrow cells. In contrast, PGF2 alpha, which is not therapeutically active against autoimmunity in NZB/W mice, had no detectable effect on TdT+ bone marrow cells or thymocytes in BALB/c or NZB/W mice. These results directly document the existence of abnormalities in the development of lymphopoietic precursor cells in the bone marrow and thymus cortex of NZ strain mice prior to the onset of autoimmune phenomena. The results also raise the possibility that the therapeutic efficacy of exogenous PGE1 in autoimmune NZ strain mice may be related, at least in part, to its ability to rectify the abnormal development of these early lymphoid cells.

Ocular disease induced in mice by anterior chamber inoculation of herpes simplex virus.

Herpes simplex virus type 1 (HSV-1) inoculated directly into the anterior chamber of the mouse eye induced an acute inflammatory process in both the injected eye and its uninjected (contralateral) counterpart. In the former, a rapid intense inflammatory reaction developed in the anterior segment (cornea, anterior chamber) and anterior portion of the uveal tract (iris and ciliary body). The retina of the injected eye was spared. In contrast, in the uninjected eyes, a delayed massive destructive reaction also developed, but was limited almost exclusively to the posterior segment ( vitreous, retina and choroid); retinas of the uninjected eyes were destroyed completely. When HSV-1 was inoculated bilaterally into both anterior chambers, destructive inflammatory responses developed in both corneas and anterior segments, but the retinas were spared bilaterally. These results indicate that (1) a unique and interesting pattern of bilateral ocular disease occurs after uniocular anterior chamber injection of HSV-1 in mice; (2) the distribution of the destructive lesions differs between the injected eye and its uninjected counterpart; and (3) local factors, perhaps produced within the eye itself, modify the progression of the virus-induced reaction within the globe.

Role of suppressor T cells in herpes simplex virus-induced immune deviation.

Herpes simplex virus type 1 inoculated into the anterior chamber of the mouse eye induces suppression of anti-herpes simplex virus T-cell-mediated delayed hypersensitivity. This suppression is virus-specific, and mediated by splenic T lymphocytes, and it can be adoptively transferred to naive recipients.

Alloantigen presentation to the anterior chamber of the eye subverts specific in vitro cell-mediated immune responses.

Aberrant cell-mediated immune responses are produced when minor histocompatibility antigens expressed on tumor cells are placed in the anterior chamber of the mouse eye. Mice bearing intraocular histoincompatible tumors fail to develop alloimmunity as expressed by their failure to reject orthotopic skin grafts syngeneic with the tumor cells. The cellular basis of anterior chamber-associated immune deviation (ACAID) was examined in vitro by studying lymphoid cells from BALB/c mice that had received intracameral inoculations of P815 tumor cells. It was found that both proliferative and cytotoxic T cell responses to DBA/2 alloantigens were either low or absent. Splenectomy prior to intracameral inoculation of P815 cells produced the opposite effect, i.e., lymphoid cells from these animals performed in in vitro assays as though they were specifically primed to the DBA/2 alloantigens. In an effort to identify an active process of suppression as the possible basis for ACAID, mixing experiments were conducted in which the alloreactivities of normal lymphoid cells were subjected to putative regulator cells from animals with ACAID. No evidence of suppression of the response of animal cells to DBA/2 alloantigens was discerned. Thus, the aberrant cell-mediated responses of lymphoid cells from BALB/c mice bearing intraocular P815 tumors appear to be consistent with the hypothesis that clonal deletion among mature immunocompetent cells is responsible for the ACAID phenomenon.

Intracameral inoculation of herpes simplex virus type I induces anterior chamber associated immune deviation.

Herpes simplex virus Type 1 (HSV-1) inoculated intracamerally (IC) into the anterior chamber of BALB/c eyes induces anterior chamber associated immune deviation (ACAID) in which T cell-mediated delayed type hypersensitivity (DTH) responses to HSV-1 are impaired while B cell-mediated anti-HSV neutralizing antibody responses are intact or enhanced.

Trachoma in a rural Haitian community.

We selected 43 patients, aged 15 days to 57 yesrs, for intensive study after screening 975 people for clinical evidence of trachoma in rural Haiti. Trachoma was present in Haiti with low endemicity and was followed by relatively mild sequelae. Laboratory studies confirmed the disease through demonstration of conjunctival inclusion bodies by immunofluoresence and serotyping of antibody in sera or eye secretions, or both. Of 23 patients (age 1 to 36 years) with active trachoma, all had serum antibody to chlamydia (range 1:10 to 1:640), nine had eye secretion antibody (range 1:10 to 1:1280), and one was inclusion positive. The remaining 20 patients (age 15 days to 57 years) had the following diagnosis: atypical follicles (eight), conjunctivitis with or without mucopurulent discharge (ten) innactive pannus only (one), and severe anemia (one). Only 16 of the 20 were tested for serum antibody and all were positive (1:10 to 1:5,120), 11 of 20 had eye secretion antibody (1:10 to less than or equal to 1:640), and one was inclusion positive. Serotyping attempted on 22 patients yielded 16 patients with antibodies specific for type A, one patient with type B, and five who were not typed.