Benjamin H. Landing

Bio: Benjamin H. Landing is an academic researcher from University of Southern California. The author has contributed to research in topics: Myenteric plexus & Cystic fibrosis. The author has an hindex of 29, co-authored 105 publications receiving 2955 citations. Previous affiliations of Benjamin H. Landing include University of California, Los Angeles & Boston Children's Hospital.

Cultivation in vitro of cells derived from a human osteosarcoma

Abstract: A cell line was derived from an osteosarcoma. Cells grew to high population density in liquid medium and formed colonies in agar medium. The cell line consisted of polygonal or fusiform cells resembling the cells of the original tumor. No collagen fibers or calcium apatite microcrystals could be demonstrated in the cultured cells by electron microscopy nor were virus particles detected. Isoenzyme studies of the cell line revealed the “B” band of glucose-6-phosphate dehydrogenase. Chromosome studies of the cell line revealed a range of stem line number from 58 to 65; chromosome counts ranged from 47 to 183. Some cells had marker chromosome of varied morphology and some had minute chromosomes. Chromosome breaks were found in 30.5% of the cells.

Generalized gangliosidosis: another inborn error of ganglioside metabolism?

Abstract: Introduction IN 1959 Norman et al1described a patient with a specific form of amaurotic idiocy which they called "Tay-Sachs Disease With Visceral Involvement." In this patient the clinical and pathological picture resembled Tay-Sachs disease, plus accumulation of lipid-laden histiocytes in liver, spleen, thymus, and other organs. Their patient's case differed chemically from Niemann-Pick disease, in which there is also combined neural and visceral involvement, in that the stored material in the brain was a ganglioside. In Niemann-Pick disease the characteristic lipid, which accumulates to a moderate degree in the brain and to a marked degree in the viscera, is sphingomyelin. Their patient's case also differed from classical Tay-Sachs disease since visceral involvement is absent in this disease. Also in 1959, Craig et al2described an infant with "foam-cell" histiocytosis of the viscera, involvement of renal glomerular epithelium, and clinical and radiological features suggestive of Hurler's disease. Since

Thirteen boys with progressive septic granulomatosis

Abstract: 1. Thirteen boys are described who present a syndrome of chronic suppurative lymphadenitis, chronic dermatitis, chronic pulmonary disease, and hepatosplenomegaly, with an eventually fatal outcome. 2. The cases described appear to have the same basic disorder as those previously reported by Landing and Shirkey and by Bridges, Berendes, and Good. 3. Despite the frequent finding of hypergammaglobulinemia, no defect of antibody synthesis has been demonstrated. 4. The existence of an as yet unidentified physiological defect common to these patients is suggested.

Xeroderma Pigmentosum: Clinical and Laboratory Investigation of Its Basic Defect

Abstract: Xeroderma pigmentosum is characterized by sunlight sensitivity, multiple cutaneous malignancies, and autosomal recessive inheritance. Some patients also demonstrate neurological manifestations, ie, mental deficiency, microcephaly, ataxia, choreoathetosis, and deafness. Five patients were studied, four with neurological disease, one of whom also had lymphatic leukemia. Autopsy of one patient disclosed cerebral and olivopontocerebellar atrophy. There was nuclear atypia of pancreatic islet cells and liver cells similar to that seen in ataxia-telangiectasia. Normal skin fibroblasts can repair ultraviolet radiation damage to deoxyribonucleic acid by inserting new bases into DNA in the form of small patches. However, cells from patients with xeroderma pigmentosum carry a mutation such that repair replication of DNA is either absent or greatly reduced in comparison to normal fibroblasts. The failure of DNA repair in the skin may be related to carcinogenesis which occurs in sun-exposed areas of the skin.

Infantile systemic hyalinosis: report of four cases of a disease, fatal in infancy, apparently different from juvenile systemic hyalinosis.

Abstract: Four female Mexican-American infants, two siblings, had widespread deposit of hyaline material in skin, gastrointestinal tract, adrenals, urinary bladder, ovaries, skeletal muscles, thymus, parathyroids, and other loci. Clinical features included thickness and focal nodularity of skin, relatively short limbs and neck, gum hypertrophy, hypotonia and reduced movement, joint contractures, osteoporosis, growth failure, diarrhea, and recurrent infections. Clinical onset was in the first week, and all 4 patients died by age 20 months. Infantile systemic hyalinosis appears to be a specific, presumably autosomal recessive, genetic disease, differing from the disorder called systemic hyalinosis, juvenile hyaline fibromatosis, or Puretic syndrome. The biochemical defect and the pathogenetic mechanisms responsible for the pathologic and clinical features of this condition remain to be established.

Antimicrobial reactive oxygen and nitrogen species: concepts and controversies

Abstract: Phagocyte-derived reactive oxygen and nitrogen species are of crucial importance for host resistance to microbial pathogens. Decades of research have provided a detailed understanding of the regulation, generation and actions of these molecular mediators, as well as their roles in resisting infection. However, differences of opinion remain with regard to their host specificity, cell biology, sources and interactions with one another or with myeloperoxidase and granule proteases. More than a century after Metchnikoff first described phagocytosis, and more than four decades after the discovery of the burst of oxygen consumption that is associated with microbial killing, the seemingly elementary question of how phagocytes inhibit, kill and degrade microorganisms remains controversial. This review updates the reader on these concepts and the topical questions in the field.

Bone morphogenetic protein-2 converts the differentiation pathway of C2C12 myoblasts into the osteoblast lineage.

Abstract: The implantation of bone morphogenetic protein (BMP) into muscular tissues induces ectopic bone formation at the site of implantation. To investigate the mechanism underlying this process, we examined whether recombinant bone morphogenetic protein-2 (BMP-2) converts the differentiation pathway of the clonal myoblastic cell line, C2C12, into that of osteoblast lineage. Incubating the cells with 300 ng/ml of BMP-2 for 6 d almost completely inhibited the formation of the multinucleated myotubes expressing troponin T and myosin heavy chain, and induced the appearance of numerous alkaline phosphatase (ALP)-positive cells. BMP-2 dose dependently induced ALP activity, parathyroid hormone (PTH)-dependent 3',5'-cAMP production, and osteocalcin production at concentrations above 100 ng/ml. The concentration of BMP-2 required to induce these osteoblastic phenotypes was the same as that required to almost completely inhibit myotube formation. Incubating primary muscle cells with 300 ng/ml of BMP-2 for 6 d also inhibited myotube formation, whereas induced ALP activity and osteocalcin production. Incubation with 300 ng/ml of BMP-2 suppressed the expression of mRNA for muscle creatine kinase within 6 h, whereas it induced mRNA expression for ALP, PTH/PTH-related protein (PTHrP) receptors, and osteocalcin within 24-48 h. BMP-2 completely inhibited the expression of myogenin mRNA by day 3. By day 3, BMP-2 also inhibited the expression of MyoD mRNA, but it was transiently stimulated 12 h after exposure to BMP-2. Expression of Id-1 mRNA was greatly stimulated by BMP-2. When C2C12 cells pretreated with BMP-2 for 6 d were transferred to a colony assay system in the absence of BMP-2, more than 84% of the colonies generated became troponin T-positive and ALP activity disappeared. TGF-beta 1 also inhibited myotube formation in C2C12 cells, and suppressed the expression of myogenin and MyoD mRNAs without inducing that of Id-1 mRNA. However, no osteoblastic phenotype was induced by TGF-beta 1 in C2C12 cells. TGF-beta 1 potentiated the inhibitory effect of BMP-2 on myotube formation, whereas TGF-beta 1 reduced ALP activity and osteocalcin production induced by BMP-2 in C2C12 cells. These results indicate that BMP-2 specifically converts the differentiation pathway of C2C12 myoblasts into that of osteoblast lineage cells, but that the conversion is not heritable.

Neurogenesis in the Neocortex of Adult Primates

Abstract: In primates, prefrontal, inferior temporal, and posterior parietal cortex are important for cognitive function. It is shown that in adult macaques, new neurons are added to these three neocortical association areas, but not to a primary sensory area (striate cortex). The new neurons appeared to originate in the subventricular zone and to migrate through the white matter to the neocortex, where they extended axons. These new neurons, which are continually added in adulthood, may play a role in the functions of association neocortex.

The adaptations to strength training : morphological and neurological contributions to increased strength.

Abstract: High-resistance strength training (HRST) is one of the most widely practiced forms of physical activity, which is used to enhance athletic performance, augment musculo-skeletal health and alter body aesthetics. Chronic exposure to this type of activity produces marked increases in muscular strength, which are attributed to a range of neurological and morphological adaptations. This review assesses the evidence for these adaptations, their interplay and contribution to enhanced strength and the methodologies employed. The primary morphological adaptations involve an increase in the cross-sectional area of the whole muscle and individual muscle fibres, which is due to an increase in myofibrillar size and number. Satellite cells are activated in the very early stages of training; their proliferation and later fusion with existing fibres appears to be intimately involved in the hypertrophy response. Other possible morphological adaptations include hyperplasia, changes in fibre type, muscle architecture, myofilament density and the structure of connective tissue and tendons. Indirect evidence for neurological adaptations, which encompasses learning and coordination, comes from the specificity of the training adaptation, transfer of unilateral training to the contralateral limb and imagined contractions. The apparent rise in whole-muscle specific tension has been primarily used as evidence for neurological adaptations; however, morphological factors (e.g. preferential hypertrophy of type 2 fibres, increased angle of fibre pennation, increase in radiological density) are also likely to contribute to this phenomenon. Changes in inter-muscular coordination appear critical. Adaptations in agonist muscle activation, as assessed by electromyography, tetanic stimulation and the twitch interpolation technique, suggest small, but significant increases. Enhanced firing frequency and spinal reflexes most likely explain this improvement, although there is contrary evidence suggesting no change in cortical or corticospinal excitability. The gains in strength with HRST are undoubtedly due to a wide combination of neurological and morphological factors. Whilst the neurological factors may make their greatest contribution during the early stages of a training programme, hypertrophic processes also commence at the onset of training.