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Biomedical subjects

Armond S Goldman

Publications and source records attributed to Armond S Goldman.

6 recordsLinked to original sources
PubMed2005

What caused the epidemic of Pneumocystis pneumonia in European premature infants in the mid-20th century?

An epidemic of interstitial pneumonia principally involving premature infants occurred in Germany and nearby European countries between the 1920s and 1960s. Fatalities were due to Pneumocystis. Because the principal defenses against Pneumocystis are T cells, an acquired T-cell deficiency was postulated. A number of potential causes including malnutrition were considered. All were implausible except for a retrovirus that was benign in adults but virulent in premature infants. Furthermore, we suspect that the virus was imported into Germany from former German African colonies. Premature infants were vulnerable because of the developmental status of their T cells. Given the practices in that part of Europe at that time, the virus was most likely transmitted by contaminated blood transfusions and subsequent contamination of reusable needles and syringes used in injections. Although the epidemic ended 4 decades ago, a search for the postulated retrovirus can be conducted if tissues from affected infants are available.

Blood Transfusion↗
PubMed2003

What was the cause of Franklin Delano Roosevelt's paralytic illness?

In 1921, when he was 39 years of age, Franklin Delano Roosevelt contracted an illness characterized by: fever; protracted symmetric, ascending paralysis; facial paralysis; bladder and bowel dysfunction; numbness; and dysaesthesia. The symptoms gradually resolved except for paralysis of the lower extremities. The diagnosis at the onset of the illness and thereafter was paralytic poliomyelitis. Yet his age and many features of the illness are more consistent with a diagnosis of Guillain-Barré syndrome, an autoimmune polyneuritis. The likelihoods (posterior probabilities) of poliomyelitis and Guillain-Barré syndrome were investigated by Bayesian analysis. Posterior probabilities were calculated by multiplying the prior probability (disease incidence in Roosevelt's age group) by the symptom probability (likelihood of a symptom occurring in a disease). Six of eight posterior probabilities strongly favoured Guillain-Barré syndrome.

Diagnosis, Differential↗
PubMed2002

Immune consequences of mutations in the human common gamma-chain gene.

A mutation (c.878T>A) in the common gamma chain (gamma(c)) causes an X-linked combined immunodeficiency (XCID) in a large kindred of British origin. In the disease, gamma(c) is expressed, but its binding to Jak3 is reduced. The immune deficiencies and clinical course were less marked in toddlers and school age children with XCID(L293Q) than in severe combined immunodeficiency (SCID). However, affected newborns were profoundly deficient in thymic size and T cells. In some affected infants, thymic size and numbers of T cells gradually increased during the first year. Their clinical course was relatively benign. In affected infants of one lineage, the number of blood T cells failed to increase substantially. They succumbed to opportunistic infections. T cell deficiencies in XCID(L293Q) progressively worsened during adolescence. Decreased thymic function, failure to rescue T cells from apoptosis, and replication senescence were possible causes. Blood T cells with the phenotype CD45RA(+)CD62L(+) (unstimulated T cells) were most depressed. CD4(+) T cells were also deficient in a specific marker of recent thymic emigrants, episomal DNA deletion circles created during TcR gene rearrangements. Apoptosis of T cells was increased, but neither apoptosis nor cell death was age-related. In contrast, telomere shortening in T cells increased with age. Unlike murine gamma(c) gene deletions, gamma delta T cells were prominent in affected adolescents and young adults. Furthermore, T cells with a V delta 2/V gamma 9 specificity declined with age and were replaced in the oldest male with a V delta 1 specificity. Thus, the mutation provides many insights concerning the role of gamma(c) in the biology of T cells.

Chromosomes, Human, X↗
PubMed2002

Evolution of the mammary gland defense system and the ontogeny of the immune system.

A decisive event in the evolution of mammals from synapsid reptiles was the modification of ventral thoracic-abdominal epidermal glands to form the mammary gland. The natural selection events that drove the process may have been the provision of certain immunological agents in dermal secretions of those nascent mammals. This is mirrored by similar innate immune factors in mammalian sebum and in protherian and eutherian milks. On the basis of studies of existing mammalian orders, it is evident that immune agents in milk such as immunoglobulins, iron-binding proteins, lysozyme, oligosaccharides, and leukocytes compensate for developmental delays in early postnatal production of antimicrobial factors. At least in human milk, anti-inflammatory and immunomodulating agents also evolved to provide different types of protection for the offspring. In addition, investigations reveal that the types or concentrations of immunological agents in milk vary depending upon the type of placenta, lactation pattern, and environment of the species.

Animals↗