An ultrastructural study on anterior cruciate ligament reconstruction using autogenous patellar tendon grafts in dogs

An ultrastructural study was undertaken concerning morphological changes within the autografted patellar tendon (PT) after being transplanted to the anterior cruciate ligament (ACL) in mongrel dogs. After 4 weeks, the arrangements of both large and small collagen fibrils in the PT graft became disordered, and the number of inflammatory cells increased. However, the same PT grafts revealed postsurgical signs of newly-produced collagen fibrils around activated fibroblasts at 12 to 24 weeks. At 52 weeks after the transplantation, small collagen fibrils increased in both number and density, showing a remarkable morphological similarity to the collagen fibrils of normal ACL. These data indicate that the characteristics of the PT graft eventually resemble those of a normal ACL. This paper was presented in part at the Combined Meeting of the Orthopedic Research Societies of the USA, Japan and Canada in Banff, Alberta, Canada, October, 1991.     

Benastatins A and B, new inhibitors of glutathione S-transferase, produced by Streptomyces sp. MI384-DF12. I. Taxonomy, production, isolation, physico-chemical properties and biological activities.

Benastatins have been isolated as part of a program designed to find microorganism-produced inhibitors of glutathione S-transferase from Streptomyces sp. MI384-DF12. They were purified by chromatography of reversed-phase silica gel, silica gel and Capcell Pak C18 (HPLC) followed by solvent extraction and then isolated as yellow powders. Benastatins A and B have the molecular formulae, C30H28O7 and C30H30O7, respectively. They were competitive with 3,4-dichloronitrobenzene as the substrate, and the inhibition constants (Ki) of benastatins A and B were 5.0 x 10(-6) and 3.7 x 10(-6), respectively.     

A case of multiple leiomyomatous lesions of the lung: An analysis of flowcytometry and hormone receptors

A 36 year old woman was admitted to our department because of a chest X-ray which showed multiple developing shadows. She underwent bilateral exploratory thoracotomies and a total 5 tumors were resected and pathologically diagnosed as benign metastasizing leiomyoma, the largest of which was positive for the progesterone receptor and negative for the estrogen receptor. A histogram of this tumor using a flow cytometer showed a diploid pattern and 4.6 percent of the S phase which was not more than that of a leiomyoma of the uterus from another patient. Two months later, she underwent a hysterectomy and bilateral salpingo-oophorectomy for treatment of the positive progesterone receptor in the pulmonary lesions. The resected uterine myoma and normal myometrium showed positive estrogen and progesterone receptors. For the subsequent 28 months she has been free of any further symptoms. Benign metastasizing leiomyoma of the uterus is a rare disease and very interesting because of its histological benignity and hormonal dependency. However, according to the literature, it is often confused in entity due to the fact that normal lung tissue also possesses hormone receptors. Considering our data on hormone receptors, it is rational to think that multiple leiomyomatous lesions in the lung should only be diagnosed as benign metastasizing leiomyomas when they possess positive estrogen and progesterone receptors.     

A case of a probable "cancer family syndrome" presenting four synchronous malignancies of the colon

A 72-year-old male was admitted because of right lower quadrant pain, Barium enema and total colonoscopy disclosed multiple colon cancers and sequentially, a subtotal colectomy was performed. The resected specimen demonstrated 3 advanced carcinomas and an adenomatous cancer with additional multiple polyps. Investigation of his family history revealed that his mother and his elder sister had died of uterine cancer, and that his elder brother, his nephew, and his niece had been operated on for colorectal cancer. We thus supposed a case of "Cancer Family Syndrome" presenting multiple neoplasms of the colon.     

GAMMA HEAVY CHAIN DISEASE

Electron microscopic and immunohistochemical studies were carried out on materials obtained from three patients of gamma heavy chain disease ( λ -HCD). Electron microscopically, proliferating cells showed various stages of maturation from immunoblast to plasma cell, and the majority of proliferating cells were proplasmacytes and plasma cells. From the intracytoplasmic immunoglobulin studies by immunoperoxidase method (PAP method) and electron microscopical enzyme-labeled antibody technique, proliferating cells, such as the immunoblast, plasmablast, proplasmacyte, and plasma cell, showed positive reaction to anti- λ -heavy chain serum and anti-Fc fragment (IgG) serum, and also in a third case with Bence Jones protein, proliferating cells showed positive reaction to anti_-K light chain serum. We would conclude that proliferating cells in λ -HCD might be a single clone proliferation of B-cell synthesizing λ -HCD protein, and the predominant proliferation cells are proplasmacytes and plasma cells situated near mature plasma cells in the B-cell line.     

Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia

We report here that loss of the Sprouty2 gene (also known as Spry2) in mice resulted in enteric nerve hyperplasia, which led to esophageal achalasia and intestinal pseudo-obstruction. Glial cell line-derived neurotrophic factor (GDNF) induced hyperactivation of ERK and Akt in enteric nerve cells. Anti-GDNF antibody administration corrected nerve hyperplasia in Sprouty2-deficient mice. We show Sprouty2 to be a negative regulator of GDNF for the neonatal development or survival of enteric nerve cells.     

T-cell acute lymphoblastic leukemia with add(1)(p36) and del(12)(p11) following acute myelocytic leukemia with partial deletion of 9p

We describe the case of a 40-year-old man whose disease was initially diagnosed as acute myelocytic leukemia. The patient achieved remission with chemotherapy, but relapsed shortly afterwards with an acute T-cell lymphoblastic leukemia. He died of intracranial bleeding. Karyotyping analysis showed a del(9p?) as a common abnormality in the leukemic cells at onset and relapse. Fluorescence in situ hybridization analysis demonstrated allelic loss of the CDKN2A gene in cells from both stages of the disease. At relapse the leukemia cells had additional abnormalities such as add(1)(p36) and del(12)(p11). We postulate that the loss of CDKN2A is involved in leukemogenesis but does not determine the lineage of the leukemic cells. Instead, abnormalities of genes at 1p36, 12p11, or both may be involved in driving a lymphoid phenotype.