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Strangulated right Richter's inguinal hernia of the cecum is relatively rare. A case of this unusual hernia was successfully managed with a wedge resection and closure of the infarcted bowel wall in conjunction with complementary tube cecostomy. The procedure is easy to perform and relatively safe and is therefore recommended for use in selected cases of Richter's hernia of the cecum.

In this study, cellular requirements for rejection are examined by the use of adoptive transfer assays in the ACI to Lewis cardiac allograft model. The findings show that adoptive transfer of 1 x 10(8) spleen cells (SpL), 5 x 10(7) T-cells, and 2 x 10(7) helper T-cells (W3/25+) obtained from normal, nonsensitized donors restores acute ACI graft rejection in sublethally irradiated (750 rad) Lewis recipients. In contrast, reconstitution with 2 x 10(7) cytotoxic T-cells (0X8+) does not restore first-set graft rejection. Reconstitution of the irradiated recipients with either W3/25+ or 0X8+ T-cells obtained from specifically sensitized syngeneic donors resulted in acute rejection. The W3/25+ T-cell subset was significantly more potent (P less than 0.01) in effecting rejection on a per-cell basis. Adoptive transfer of SpL, T-cells, and 0X8+ T-cells obtained from sensitized rats led to accelerated cardiac allograft rejection in the naive secondary recipients while W3/25+ T-cells did not. This study suggests that although the W3/25+ T-cells alone have the capacity to initiate first-set graft rejection, both W3/25+ and 0X8+ subsets appear to be critical to the completion of rejection of heart allografts. We also examined the capacity of adoptively transferred B-cells from sensitized donors to influence graft rejection. Our findings suggest that while B-cells fail to restore the capacity for graft rejection in irradiated recipients, they can, however, present MHC antigens to the secondary naive host thus causing allosensitization which results in accelerated rejection of a subsequent graft.

Lewis rats pretreated with UV-B-irradiated donor leukocytes (UV-DL) and peritransplant cyclosporine (CsA...CsA, 20 mg/kg on days 0, +1, and +2) accepted W/F heart allografts permanently. This study of donor-specific immunologic unresponsiveness and its cellular mechanisms shows that the induction phase of unresponsiveness is partially mediated by W3/25+ T cells, while its maintenance is dependent on the presence of 0 x 8+ T cells. In vivo adoptive transfer of either splenocytes, T lymphocytes (T cells), or W3/25+ T cells from ungrafted, UV-DL-transfused rats into unmodified syngeneic Lewis rats that received test grafts 24 hr later led to significant prolongation of donor-specific graft survival. Adoptive transfer of 0 x 8+ cells did not influence donor-type (W/F) test graft rejection. Adoptive transfer of SpL, T cells and 0 x 8+ cells from UV-DL and CsA-treated recipients of W/F heart allografts at 20 or 180 days after transplantation led to significant donor-specific graft prolongation in naive syngeneic hosts, while adoptive transfer of W3/25+ cells, in this group, did not affect test graft survival. However, the adoptive transfer of SpL or of T cell subsets did not influence third-party (ACI) graft survival. In-vitro mixed lymphocyte reaction between thoracic duct lymphocytes obtained at various intervals following grafting from UV-DL and CsA treated Lewis recipients of W/F heart allografts and donor-type SpL resulted in significantly reduced reactivity by 78%, 75%, 69% (P less than 0.001) and 43% (P less than 0.02) compared with controls when responder TDL were obtained at 20, 50, 100, and 180 days after transplantation, respectively. In coculture studies, the MLR response to donor SpL was specifically suppressed by 60%, 57%, 46%, and 50% (P less than 0.01) at 20, 50, 100, and 180 days after transplantation, respectively, compared with controls. These data indicate that the induction of specific unresponsiveness to heart allografts in this model is mediated, in part, initially by the appearance in the host of specific W3/25+ cells either induced or recalled by UV-DL transfusion, and that a stable state of immunologic unresponsiveness is subsequently dependent on the presence of 0 x 8+ suppressor cells.

Effects of thymosin fraction 5 on T-lymphocyte rosette formation in vitro were assessed in fourteen patients with hepatocellular carcinoma, twenty-one with Burkitt's lymphoma, thirteen with Hodgkin's disease and fifteen with breast cancer. Thymosin was found to cause a significant increase in T-lymphocyte rosette formation in patients with Burkitt's lymphoma and Hodgkin's disease but not in those with hepatocellular carcinoma and cancer of the breast. The significance of these results is discussed.

Chronic leg ulcers in sickle cell anemia occur mainly around the ankles. The prevalence is up to 75% in adults. These ulcers are painful and debilitating, yet medical treatment is unsuccessful. Surgical treatment consists of repeated skin grafting procedures, which eventually deplete the patient's available donor sites. Thus, in vitro generation of human epidermal autograft for potential treatment of leg ulcers in sickle cell anemia was initiated. However, because epidermal cells need a supporting matrix in order to be applied to the ulcer, the authors decided to assess the independent effect of a collagen matrix alone in promoting healing of sickle cell leg ulcers. Collistat (Hellistex, Inc) dressing was applied directly to the ulcers. The ulcers were reviewed every 2 weeks, and the dressing reapplied every 4 weeks. Collagen matrix caused the chronic ulcers to heal completely in fewer than 3 months. This encouraging performance of collagen alone should be greatly enhanced by the in vitro epidermal autograft.

In continuation of our studies using UV-B-irradiated DST and donor leukocyte (DL) recipient pretreatment to induce specific unresponsiveness to organ allografts, we have examined the relative contributions of splenic lymphocyte populations and T lymphocyte subsets in the induction of immunologic unresponsiveness. Our data show that enriched populations of MHC class II-positive B lymphocytes and the W3/25+ T cell subset obtained from splenic leukocytes using immunoadsorbent columns in conjunction with mAbs led to indefinite graft survival (greater than 100 days) in the Lewis-to-ACI rat cardiac allograft model. In contrast, pretreatment with T lymphocytes or the Ox8+ T subset was relatively ineffective in prolonging cardiac allograft survival. In addition, third-party (W/F) W3/25+ T cell recipient pretreatment did not influence the survival of Lewis cardiac allografts in ACI recipients, thus confirming the specificity of pretreatment with the T cell subset in graft prolongation. Furthermore, we have examined the underlying mechanisms of donor-specific unresponsiveness induced by donor spleen cells, B lymphocytes, and W3/25+ T cells using adoptive transfer assays. Serial adoptive transfer studies demonstrated the presence of 0x8+ suppressor T cells in the spleens of unresponsive recipients bearing well-functioning cardiac allografts and of serum "suppressor factors" that have the capacity for specifically prolonging donor-type test graft survival in naive syngeneic rats. Our findings suggest that the induction of specific unresponsiveness in this model is dependent on a sequential collaboration between the appearance of donor-specific serum factor(s) (humoral phase) and donor-specific suppressor T cells (cellular phase). These results may be potentially useful in planning future strategies for the induction of unresponsiveness to clinical organ allografts by immunologic manipulation of the host with MHC class II-positive B cell and CD4+ T cell clones.

Rectal duplication is a rare congenital anomaly. The authors describe the case of a 52-year-old man with this condition, which caused chronic constipation. An unusual sequence of events led to the diagnosis of this anomaly at a repeat laparotomy and its eventual successful management. Awareness of the anomaly would greatly influence its early diagnosis and treatment.

We have previously demonstrated that pretreatment of ACI recipients with ultraviolet-irradiated donor-specific blood transfusion (UV-DST) leads to permanent cardiac allograft survival without further host immunosuppression (ACI rats are weak responders to Lewis lymphocytes in mixed-lymphocyte reaction). This study examines the effect of UV-DST and the timing of transfusions on ACI cardiac allograft survival in Lewis recipients with and without the addition of peritransplant cyclosporine (CsA) (20 mg/kg i.m.) given on days 0, +1, and +2 in relation to the time of transplantation. The mean survival time (MST) of ACI cardiac allografts in Lewis recipients was significantly increased to 33.6 +/- 5.7 days (P less than 0.001) by CsA treatment alone as compared to 6.5 +/- 0.5 days survival in control. When DST was given on day -3 combined with CsA, graft survival was increased to 42.0 +/- 9.3 days (P less than 0.01), as compared to 5.8 +/- 1.3 days when DST alone was used. When DST was irradiated with ultraviolet B (UV-DST) and administered on day -3 combined with peritransplant CsA, the MST was increased to 68.83 +/- 16.1 days as compared to an MST of 10.0 +/- 1.0 days in controls treated with UV-DST alone. When UV-DST was given on day -7 and combined with peritransplant CsA immunosuppression, the results were similar. However, when UV-DST was peritransplant CsA course, 4 of 6 recipients maintained their ACI heart allografts indefinitely (greater than 300 days) in contrast to the effect of UV-DST alone (MST of 13.5 days). Third-party (W/F) UV-irradiated blood transfusions were ineffective in prolonging ACI cardiac allografts in Lewis rats, regardless of whether the transfusions were given alone or in combination with peritransplant immunosuppression with CsA. In conclusion, these results demonstrate that UV-DST combined with a brief peritransplant immunosuppression with CsA induces prolonged heart allograft survival in a histoincompatible, strong responder host, and that such effect is donor specific. The use of UV-DST combined with peritransplant CsA immunosuppression offers a promising approach to achieving organ transplant unresponsiveness, and decreased sensitization to the donor blood elements, which eventually may have important clinical implications.

An analysis of 294 enlarged peripheral lymph node biopsies in Ife, Nigeria, revealed that the underlying disease in 51.7% was chronic inflammation while malignant diseases accounted for 48.3%. The order of frequency of the lesions was reactive hyperplasia (29.3%), metastatic cancer (24.5%), malignant lymphoma (23.8%), tuberculosis (15.6%) and toxoplasmosis (3.7%). One-third of the metastases were of undetermined origin. The neck which accounted for 53% of the biopsies, was the most frequent site for tuberculous adenitis, toxoplasmic lymphadenitis, and malignancies. The axilla was involved in 15% of the cases and was the most common site for metastatic breast carcinoma. The inguinal lymph nodes were also involved in 24% of the cases and had the highest occurrence of melanoma, reactive hyperplasia and parasitic granuloma. The habit of bare-foot walking leading to repeated trauma and infection is implicated in the high incidence of inguinal node reactive hyperplasia. This study demonstrates that lymph node malignancies and chronic granulomatous infections present a problem of increasing diagnostic and therapeutic importance and furthermore, it emphasizes that physicians in Nigeria should consider toxoplasmosis in the differential diagnosis of peripheral lymphadenopathy.

A clinicopathologic analysis of 202 benign breast lesions in black women is presented. The study shows that the peak incidence of fibroadenoma occurs at an earlier age in black than in white patients. Fibrocystic disease is most frequent in both black and white patients between 25 and 45 years of age. It is noteworthy that nulliparous adolescent blacks have a higher risk of fibroadenoma developing and our findings confirm the observation made by Funderburk et al [5] and Nigro and Organ [6] that the incidence of fibroadenoma in blacks is high. The low incidence of fibrocystic disease in our patients does not reflect the clinical incidence of the disease because most patients with fibrocystic disease do not undergo biopsy. We are unable to draw any conclusions about the relation between the use of oral contraceptives and the incidence of benign breast disease. In conclusion, a review of the literature and an analysis of our data suggest a relatively higher incidence of fibroadenoma among black patients. In contrast to the finding in the white population, it appears that in blacks fibroadenoma is more common than carcinoma of the breast.

Perforated bowel or diseases of the retroperitoneal organs may be complicated by retroperitoneal abscess formation. Six cases of retroperitoneal abscess treated at Ife University Teaching Hospital, Ile-Ife, Nigeria, over a two-year period are reported. Delayed presentation was responsible for the only death in the series and was also associated with prolonged morbidity in the remaining five cases. Early presentation and diagnosis, use of appropriate antibiotics, and prompt surgical intervention are factors that appear to influence the morbidity of the disease.

The role of humoral immunity in graft rejection in the rat model remains controversial. Passive transfer of cytotoxic alloantibody (CAA) has resulted either in hyperacute rejection or in graft enhancement. This study examines the effect of transfer of CAA on cardiac allograft survival in three rat strain combinations that are fully mismatched at the major histocompatibility (MHC) loci. Strain-specific immune responsiveness in donor-recipient pairs varied from low (Lewis-to-ACI) to high (ACI-to-Lewis) as measured by mixed lymphocyte reactions. CAA was obtained from rats sensitized by three successive skin grafts at weekly intervals. Group 1 (high responder recipients), which consisted of Lewis rats presensitized to ACI and had a lymphocytotoxicity titer of 1:512 to 1:2048, rejected ACI cardiac allografts in 10.8 +/- 7.2 hr compared with 6.5 +/- 0.5 days in naive controls (p less than 0.001). Injection of 1 ml of high-titer CAA into naive Lewis rats immediately after ACI cardiac grafting led to hyperacute rejection of ACI hears in 2.1 +/- 0.8 hr while 1 ml of CAA followed by 2 ml of guinea pig complement (GPC) resulted in even faster rejection (mean survival time (MST) of 23.8 +/- 4.7 min). Injection of 2 ml GPC alone or in combination with 1 ml naive Lewis serum had no effect on graft survival. Multiple pretransplant injections of 1 ml of CAA on days -3, -2,-1, and 0 relative to transplantation resulted in significant prolongation of allograft survival (MST of 10.3 +/- 0.3 days; P less than 0.01). In group 2 (intermediate responder recipients), where Lewis rats were presensitized to WF strain and where cytotoxicity titer was 1:16 to 1:256, the recipients rejected WF hearts in 23.8 +/- 5.8 hr compared with 6.8 +/- 0.8 days in unsensitized control recipients (P less than 0.001). Injection of 1 ml of Lewis anti-WF CAA resulted in prolonged graft survival of 9.7 +/- 3.5 days, while injection of 1 ml of CAA followed by 2 ml of GPC caused hyperacute rejection in 104 +/- 61.7 min. Pretransplant injections of CAA on days -3, -2, -1, and 0 resulted in enhancement, with an MST of 16.3 +/- 1.3 days (P less than 0.001). In group 3 (low responder recipients), ACI presensitized to Lewis developed a cytotoxicity titer of 1:2 to 1:32 and rejected Lewis hearts in 5.3 +/- 0.4 days compared with 10.6 +/- 1.0 days in naive recipients.(ABSTRACT TRUNCATED AT 400 WORDS)

This study examines the effect of pretreatment with 10(8) ultraviolet B-irradiated donor leukocytes (UV-DL) with or without peritransplant cyclosporine (CyA) treatment (20 mg/kg on days 0, +1, and +2 relative to transplantation) on rat cardiac allograft survival across major histocompatibility loci. A single UV-DL pretreatment on day -3 or -7 (before transplantation) significantly prolonged survival of heart allografts from Wistar-Furth rats (W/F) in Lewis recipients from 6.8 +/- 0.8 days to 18.4 +/- 2.1 and 17.6 +/- 1.5 days (p less than 0.001), respectively. Multiple UV-DL infusions on days -14 and -7 increased the mean survival time to 20.0 +/- 0.9 days (p less than 0.001). Similarly, UV-DL infusion on day -3 or -7 significantly prolonged the mean survival time of heart allografts from ACI rats in Lewis rats. A single or multiple UV-DL infusions combined with peritransplant CyA led specifically to permanent W/F cardiac allograft survival (more than 200 days) in all recipients. Similarly, UV-DL infusion combined with peritransplant CyA led to indefinite survival of ACI cardiac allografts in two thirds of Lewis recipients. Adoptive transfer of splenocytes from long-term recipients of cardiac allografts, which specifically prolonged donor test grafts in syngeneic hosts, suggests that unresponsiveness to cardiac allografts is, in part, dependent on suppressor cells. This study emphasizes the importance of UV irradiation of DLs in the modulation of alloreactivity and the induction of donor-specific unresponsiveness in adult animals.

The effect of donor-specific blood transfusion was compared to that of UVB-irradiated donor-specific blood transfusion on heart allograft survival in inbred rats with major histocompatibility differences. In one series ACI rats received heterotopic heart grafts from Lewis rats and 1 mL transfusion of donor-type blood at 1, 2, and 3 weeks prior to the transplantation. Fifty percent of the grafts were permanently accepted (survival greater than 200 days). Following UVB-irradiated donor-specific blood transfusion, 55% of the grafts survived indefinitely. In a mixed lymphocyte reaction ACI lymphocytes are weak responders to Lewis lymphocytes. In another series, Lewis rats received ACI hearts. Donor-specific transfusions at 1, 2, and 3 weeks prior to transplantation did not significantly alter the survival of heart allografts. Lewis lymphocytes react strongly to ACI stimulator cells in a mixed lymphocyte reaction. However, when the donor blood was UVB-irradiated prior to transfusion, the ACI allograft survival was significantly prolonged in this ACI-to-Lewis strain combination. When Lewis rats received W/F hearts following either donor-specific or UVB-irradiated donor-specific transfusions, the hearts' survival was similarly and significantly prolonged, but did not become permanent. Mixed lymphocyte reaction reveals that the stimulation index of Lewis lymphocytes against W/F lymphocytes is greater than that of ACI versus Lewis, but is less than that between Lewis responder cells against ACI stimulators.(ABSTRACT TRUNCATED AT 250 WORDS)

For the purpose of defining the distribution of breast diseases in Nigeria, a review of 671 cases seen in Ife over a 10 year period was undertaken. Twenty-six (3.9 per cent) of the patients were males. The frequency of breast diseases in this population was fibro-adenoma, 48 per cent; carcinoma, 21 per cent; breast abscess, 8.6 per cent; fibrocystic disease, 5.5 per cent; sclerosing adenosis, 5.4 per cent and gynaecomastia, 2.7 per cent. The other breast lesions were the same type of disease as documented in white patients. The most striking difference was the relatively high incidence of fibro-adenoma, especially in nulliparous adolescent females, while carcinoma and fibrocystic disease were fewer than expected. Breast carcinoma presented a decade earlier in Nigerian women and was usually advanced at presentation and of aggressive histological type. Of the breast carcinomas, 4.3 per cent were associated with pregnancy.

Two unusual presentations of carcinoma of the right colon are described. One of the two patients presented with a right gluteal abscess and the other presented with a colocutaneous fistula to the anterior abdominal wall at the site of a previous appendectomy scar. Despite extensive local tumor invasion of adjacent structures in both cases, all the regional lymph nodes were free of cancer and the tumors were of low-grade malignancy. A review of the literature indicates that bulky colonic tumors with extensive local invasion and negative mesenteric lymph nodes have a relatively good prognosis if adequate resection is performed.

Recipient pretreatment with UV-B irradiated donor-specific blood transfusions (UV-DST) combined with peritransplant cyclosporine on days 0, +1, and +2 leads to permanent cardiac allograft survival in the ACI-to-Lewis rat strain combination. This study investigates the mechanisms of immunologic unresponsiveness induced by UV-DST and CsA by examining several in vitro and in vivo parameters in long-term cardiac allograft recipients. The results of the in vitro studies demonstrate that thoracic duct lymphocytes (TDL) of treated and allografted Lewis rats respond less in a mixed lymphocyte reaction to donor splenic lymphocytes (SpL) by 69%, 75%, and 73% (P less than 0.001) at 30, 50, and 100 days after transplantation, respectively, compared with controls, while the response to a third-party (W/F) SpL is unimpaired. In coculture experiments, the TDL from treated recipients specifically suppressed the response of unmodified Lewis TDL to ACI SpL by 59% and 40% (P less than 0.01) at 30 and 50 days after transplantation, respectively, while responses to W/F SpL were suppressed by only 3-6%. The sera obtained from ungrafted rats transfused with UV-DST suppressed the MLR between unmodified Lewis TDL and ACI SpL by 31% (P less than 0.05) while the sera from UV-DST and CsA-treated and allografted rats specifically suppressed the MLR by 75%, 80% (P less than 0.001) and 37% (P less than 0.01) at 10, 30, and 50 days after transplantation, respectively. In vivo adoptive transfer of 10(4) donor-type dendritic cells (DC) into recipients of beating cardiac allografts at 40 or 60 days after transplantation led to rapid and acute allograft rejection, while the adoptive transfer of 10(8) unseparated SpL obtained at 50 days after transplantation from treated Lewis recipients to syngeneic naive hosts led to a modest but significant prolongation of ACI test cardiac allografts. The transfer of serum from treated and allografted recipients at 10, 30, and 50 days after transplantation led to specific and significant prolongation of test grafts in syngeneic naive hosts. These findings suggest that the mechanisms underlying the in vivo immunologic unresponsiveness induced by pretreatment with UV-DST and peritransplant CsA include inactivation without elimination of class II-antigen presenting cells (APC), generation of specific serum suppressor factor(s) and/or antiidiotypic antibody, and induction of donor-specific suppressor cells.