APP gene promoter constructs are preferentially expressed in the CNS and testis of transgenic mice.

Transgenic animals were used to examine the spatial and temporal regulation of the human beta amyloid precursor protein (APP) gene promoter region in vivo. A 2.9 kb DNA fragment encompassing the APP gene promoter was fused to the chloramphenical acetyltransferase (CAT) reporter gene (pAMY-CAT) or a partial cDNA encoding the potentially amyloidogenic C-terminal 100 amino acid region of APP (pAMY-C100). Expression of these transgenes occurred primarily, but not exclusively, in the central nervous system (CNS) and testis in multiple independent lineages of transgenic mice. Temporal expression of the CAT reporter gene during development paralleled that reported for the endogenous APP gene. These studies suggest that a CNS-responsive cis-acting element(s) may exist in the promoter/5'-flanking region of the APP gene.

Acquired immunodeficiency syndrome--a review and update. History, characteristics of human immunodeficiency virus infection, its replication, biologic factors, and pathogenicity.

The search to find a cure for acquired immunodeficiency syndrome has led to an unprecedented explosion of knowledge about viruses in general, especially retroviruses, of which the human immunodeficiency viruses (HIV) types 1 and 2 are members. We attempt to describe how retroviruses work, particularly HIV-1, and what regulates their expression in the host-cell system. Viral stability and its implications for health care workers is also discussed. One of the many mysteries of HIV is the ability it has to elude normal immune responses. Even though B- and T-cell responses are mounted by people infected with HIV, such responses are restricted and increasingly ineffective as the disease progresses. Host susceptibility plays a major role in the virus' ability to infect individuals. Finally, some current treatment options and the key role of the family physician in the battle against acquired immunodeficiency syndrome are discussed.

Monoclonal antibody detection of laminin in minor salivary glands of patients with Sjögren's syndrome.

The potential roles of the basement membrane proteins, laminin and fibronectin, and the cytoskeletal protein, tubulin, were assessed in the pathogenesis of Sjögren's Syndrome (SS) by comparing their expressions in SS with normal labial salivary gland (LSG) tissue. Laminin, fibronectin and tubulin expression were determined using well characterized monoclonal antibodies in the peroxidase anti-peroxidase technique on formalin-fixed LSG's from patients with SS and normal controls. Characteristic periductal staining for laminin occurred in the LSG's of 14/18 SS patients scored by one observer and 16/18 scored by the second observer. Staining of LSG's for laminin occurred in 2/35 control specimens consisting of 15 normal LSG's and 20 inflammatory lesions with attached normal LSG. The staining which occurred in the two controls was diffuse and 'non-specific' in one case, and indistinguishable from the characteristic periductal staining found in SS in the other case. Among the 20 controls containing inflammatory lesions, four showed diffuse staining for laminin within the actual lesion, but the adjacent LSG's did not stain. No statistically significant difference between SS and normal tissues stained by anti-fibronectin and anti-tubulin was observed. The study concluded that there was an increase in laminin or a laminin-like substance on salivary ductal epithelia of SS patients. This suggests a potential role for laminin in the pathologic mechanism and may indicate that increased laminin expression is a marker for SS.

Stage-specific embryonic antigen 3 as a marker of visceral extraembryonic endoderm.

The distribution of the stage-specific embryonic antigen SSEA-3 was studied immunohistochemically on postimplantation mouse embryos. This carbohydrate antigen, identified as an epitope of a globo-series ganglioside isolated from human teratocarcinoma cells (Kannagi et al., 1983, J. Biol. Chem. 258, 8934-8942) was originally detected on the zygote and mouse early cleavage-stage embryos. It disappears on the early blastocyst and reappears on the primitive endoderm of the implanting blastocyst (Shevinsky et al., 1982, Cell 30, 697-705). We now show in the early egg cylinder (on the sixth day of pregnancy) SSEA-3 is present in the entire visceral endoderm but not in any other part of the conceptus. From Day 7 of pregnancy onward, SSEA-3 is restricted to the extraembryonic visceral endoderm and the visceral yolk sac cells. Therefore, SSEA-3 is a useful marker for this endodermal cell lineage in midgestational mouse embryos.