Homozygous osteogenesis imperfecta unlinked to collagen I genes

Summary In a consanguineous pedigree in which a severe type of osteogenesis imperfecta was segregating as an autosomal recessive trait, analysis of genetic markers for both collagen I structural loci COL1A1 and COL1A2 showed that the phenotype was unlinked to either locus.     

Seasonal variation in cell volume of epilimnetic bacteria

The relationship between bacterial cell volume and temperature was examined for field data collected over a 4-year period and through controlled chemostat incubations of aPseudomonas sp. Volumes of planktonic bacteria were found to decrease as water temperature increased. Changes in temperature accounted for 38% of the variation in average cell volume (P<0.001). Average planktobacterial cell volume fell 42% from 0.217m³ in mid-winter to 0.127m³ in mid-summer. Similar results were found for the size distribution of epibacterial cells. Controlled chemostat incubations of aPseudomonas sp. indicated that cell volume was significantly affected by temperature, growth rate, and the interaction of temperature and growth rate. The data suggest that a change in cell volume as a result of a change in temperature is an intrinsic property of planktonic bacteria.     

Structural Features of Human Monoamine Oxidase A Elucidated from cDNA and Peptide Sequences

Monoamine oxidase (MAO), an important enzyme for the degradation of amine neurotransmitters, has been implicated in neuropsychiatric illness. The amino acid sequence for one form of the enzyme, MAO-A, has been deduced from human cDNA clones and verified against proteolytic peptides. The covalent binding site for the flavin adenine dinucleotide (FAD) cofactor is near the C-terminal region. The presence of features characteristic of the ADP-binding fold suggests that the N-terminal region is also involved in the binding of FAD. These cDNAs should facilitate the study of the structure, function, and intracellular targeting of MAO, as well as the analysis of its expression in normal and pathological states.     

A molecularly cloned hepatitis B virus produced in vitro is infectious in a chimpanzee.

The infectivity of hepatitis B virus (HBV) produced in vitro by HepG2 cells transfected with HBV DNA (HepG2T14) has been assayed in a chimpanzee. Following inoculation, the chimpanzee underwent a typical course of type B hepatitis infection, characterized by elevation of serum aminotransferases and by histological identification of hepatic damage. Hepatitis B surface antigen and core-related antigen appeared in the serum at weeks 5 and 7, respectively, after infection. HBV DNA was detected in serum samples, and replicative forms of the HBV genome were identified in liver biopsies. Subtype identification of hepatitis B surface antigen and restriction enzyme analysis of HBV DNA in both the inoculum and the serum of the infected chimpanzee confirmed that the hepatitis B infection observed in this animal was caused by viral particles produced by HepG2T14 cells. These findings indicate that, although HepG2 cells do not seem to be susceptible to infection by HBV in vitro, they can produce biologically active infectious virions after transfection with cloned HBV DNA.     

Expression of the Opc protein correlates with invasion of epithelial and endothelial cells by Neisseria meningitidis

Whereas capsulate strains of Neisseria meningitidis are dependent on pili for adhesion to human endothelial and epithelial cells, strains which lacked assembled pili and were partially capsule-deficient adhered to and invaded human endothelial and epithelial cells if they expressed the Opc protein. Bacteria expressing low or undetectable levels of Opc protein failed to adhere to or invade eukaryotic cells. In addition, the presence of OpaAC751 protein on the surface of bacteria did not increase bacterial interactions with host cells. Association of Opc-expressing bacteria was inhibited by antibodies against Opc. Invasion was dependent on the host-cell cytoskeletal activity and was inhibited by cytochalasin D. In some cells, infected at the apical surface, bacteria emerging from basal surface were detected by electron microscopy. Opc is found in diverse meningococci and may represent a common virulence factor which facilitates adherence and invasion by these bacteria.     

Luteinizing hormone-independent luteinization and ovulation in the hypophysectomized rat: a possible role for the oocyte?

Immature hypophysectomized, estrogen-treated rats were used to study the regulation of luteinization. Particular attention was focused on the potential role of the oocyte in this process. Rats were injected for 2 days with follicle-stimulating hormone (FSH) to stimulate follicular development. Within 48 h following FSH treatment, many follicles became luteinized, as determined by morphometric analysis. This luteinization occurred in the absence of detectable levels of luteinizing hormone (LH). The number of follicles undergoing luteinization was dependent on the FSH dose. In addition, ovulation occurred in some of the animals receiving the highest doses of FSH (3-micrograms or 5-micrograms injections). The majority of follicles undergoing luteinization or ovulation were greater than 400 microns in diameter. Luteinized follicles exhibited positive reactivity for cholesterol side-chain cleavage enzyme, 3 beta-hydroxysteroid dehydrogenase, lipid, and alkaline phosphatase, which was similar to that found in corpora lutea of the cycle. Serum progesterone (P0) and 20 alpha-hydroxypregn-4-en-one levels were elevated in animals with luteinized follicles, especially in those animals that also underwent ovulation. Morphological evaluation of oocytes showed that the majority of luteinized follicles contained a degenerating oocyte. Oocyte degeneration was highly correlated (r = 0.94) to luteinization. These results demonstrate that luteinization and ovulation can occur in the FSH/estrogen-primed hypophysectomized rats in the absence of detectable serum LH. Furthermore, LH-independent luteinization was strongly correlated to degenerative changes in the oocyte. These results provide new evidence to support the concept that the oocyte may be an intraovarian regulator of luteinization.