Inoculation of baboons and macaques with simian immunodeficiency virus/Mne, a primate lentivirus closely related to human immunodeficiency virus type 2

A primate lymphotropic lentivirus was isolated on the human T-cell line HuT 78 after cocultivation of a lymph node from a pig-tailed macaque (Macaca nemestrina) that had died with malignant lymphoma. This isolate, originally designated M. nemestrina immunodeficiency virus (MnIV) and now classified as simian immunodeficiency virus (SIV/Mne), was inoculated intravenously into three juvenile rhesus monkeys (Macaca mulatta), three juvenile pig-tailed macaques (M. nemestrina), and two juvenile baboons (Papio cynocephalus). All six macaques became viremic by 3 weeks after inoculation, whereas neither of the baboons developed viremia. One pig-tailed macaque died at 15 weeks with suppurative peritonitis secondary to ulcerative, necrotizing colitis. Immunologic abnormalities included a marked decrease in CD4+ peripheral blood lymphocytes. Although five macaques mounted an antibody response to SIV/Mne, the animal that died at 15 weeks remained antibody negative. Three other macaques (two rhesus and one pig-tailed) died 66 to 87 weeks after inoculation after exhibiting progressive weight loss, anemia, and diarrhea. Histopathologic findings at necropsy included various manifestations of immune deficiency, nephropathy, subacute encephalitis, pancreatitis, adenocarcinoma, and lymphoid atrophy. SIV/Mne could be readily isolated from the spleens and lymph nodes of all necropsied macaques, and from the cerebrospinal fluid, brains, bone marrow, livers, and pancreas of some of the animals. SIV antigens were localized by avidin-biotin immunohistochemistry to pancreatic islet cells and to bone marrow endothelial cells. The data suggest that African baboons may be resistant to infection by SIV/Mne, whereas Asian macaques are susceptible to infection with this pathogenic primate lentivirus.     

Regional chromosomal localisation of APOA2 to 1q21–1q23

Summary Using in situ hybridisation, we have mapped APOA2 to the 1q21–1q23 region of chromosome 1. DNA hybridisation to somatic cell hybrids made from cells carrying a balanced translocation between X and 1 confirms the localisation as proximal to 1q23. This was further confirmed by the presence of two polymorphic alleles in a cell line carrying a deletion of 1q25–1q32.     

L-dihydroxyphenylalanine-induced asymmetric changes in striatal uric acid peak: determination by in vivo electrochemical detection in rats with unilateral nigrostriatal lesions

Rats were unilaterally lesioned with 6-hydroxydopamine to destroy the nigrostriatal pathway. Following injection with 25 mg/kg L-dopa, circling behavior away from the lesioned side was monitored. Concurrently, in vivo electrochemical detection was used to compare changes in striatal extracellular levels of ascorbic acid (Peak 1) and uric acid (Peak 2) on the lesioned and unlesioned sides. Peak 1 changes did not differ, but Peak 2 changed asymmetrically on the two sides. The difference in the changes in Peak 2 was highly correlated with the circling behavior, with the greater increase on the lesioned side.     

Connective tissue reinforcing structures of the digital tendon sheaths of the human hand

At a greater number of humid preparated human hands, all the ligamentous supports of the digital tendon sheath were exposed and their dimensions were determined. The osteofibrous channels, which contain the long flexor tendons of the digits, were bounded on the one hand by transversely concave shaft areas of the phalanges and the palmar ligaments and on the other side by the fibrous parts of the tendon sheath. From the second to the 5th finger, it has a regular extension of length, which begins proximal at the heads of the metacarpal bones and runs distal to the base of the nail phalanx. In some cases, there is a continuous communication between the digital tendon sheath of the little finger and the carpal synovial sheath. The tendon sheath of the flexor pollicis longus muscle in comparison with it is always in an open communication with the radial synovial sac of the wrist. At the fibrous supports of the digital tendon sheath, one can find constant and inconstant ligamentous structures. Regular shaped ligaments consist of annular fibers (A1 to A5). The proximal complex of fiber supports is a formation of the A1 and A2 ligaments. The band A1 can be divided into 2 ligaments both of roughly equal length, which lay between the head of the metacarpal bone and the base of the proximal phalanx. The strongest fibrous support of the whole digital tendon sheath represents the band A2. It is attached to the midth of the proximal phalanx and increases in strength from proximal to distal. The middle length varies between 6.7 mm at the thumb and 18.7 mm at the middle finger. The distal margin is strengthened by fibrocartilage tissue to be in accordance with the important function as a pulley. The annular band A4 forms the distal supporting complex height above the shaft of the middle phalanx. At the 2nd to the 5th finger it is, with a middle length of 6 to 7 mm, very much shorter than A2 and restrains first of all the tendon of the flexor digitorum profundus muscle. In the area of the interphalangeal joints, we can find the annular bands A3 and A5, which fiber texture is formed variable. Both ligaments are attached on either both sides with the joint capsule and the palmar plate. The other inconstant supports of the digital sheaths are systematically recorded indeed (C1 to C3), but only in exceptional cases they exist of cruciform fibers (Lig. cruciatum).(ABSTRACT TRUNCATED AT 400 WORDS)     

Rapid, Sensitive Assay for Staphylococcal Enterotoxin and a Comparison of Serological Methods

Reversed passive hemagglutination was used to assay enterotoxin in culture filtrates and in food samples. With cells tanned and then sensitized with antitoxin globulin and preserved with either formaldehyde or pyruvic aldehyde, as little as 0.0007 mug of enterotoxin was detectable. The results of hemagglutination tests compared well with those obtained by quantitative precipitin tests or by immunodiffusion, but hemagglutination was 50 to 100 times more sensitive than the immunodiffusion technique. In addition, results of the hemagglutination test were available within a few hours, and neither elimination of interfering proteins from food extracts nor concentration of the sample, both of which are necessary for immunodiffusion, was required for this procedure.     

Coronal breadth of human primary anterior teeth

Original data for mesiodistal diameter of deciduous anterior teeth on 180 White children show: (1) mean size is smallest for the lower central incisor and largest for the upper canine, (2) means from combining widths on the left anterior teeth of each arch are larger in the maxilla than the mandible by 4.0 mm, (3) individual differences for widths of the upper central and lateral incisors extend from one child with these teeth of similar size to another child with the central incisor larger than the lateral by 2.3 mm, and (4) anterior tooth correlations are positive, varying from r = 0.4 for upper canine width with width of lower central incisor, to r = 0.8 for combined widths of left anterior teeth in the maxilla with combined widths of their antagonists. Comparative findings are drawn from investigations on Australian aborigines, South African Bushmen, Liberian Negroes, Tristan da Cunha islanders, Japanese, Japanese-Negro admixtures, Japanese-White admixtures, White groups living in several parts of Europe, and North American Whites. Among these ethnic groups, Australian aborigines have the largest deciduous anterior teeth. Composite means on each sex for North American Whites show boys to have slightly larger anterior deciduous teeth than girls.     

Kinetics of gonadotropin binding by receptors of the rat testis. Analysis by a nonlinear curve-fitting method.

The kinetics of the reaction between human chorionic gonadotropin (hCG) and specific gonadotropin receptors in the rat testis were determined at 24 and 37 degrees, over a wide range of hormone concentrations. Hormone concentrations were corrected for the binding activity of the (-125I)hCG tracer preparations. Analysis of the experimental data was performed with an interactive nonlinear curve fitting program, based upon the second-order chemical kinetic differential equation. The mean values for the association rate constant (k1) were 4.7 x 10-7 M-1 min-1 at 24 degrees, and 11.0 x 10-7 M-1 min-1 at 37 degrees. At both temperatures, the values of kl were independent of hormone concentration. Initial dissociation rates were consistent with first order kinetics, with dissociation rate constant (k2) of 1.7 x 10 minus -3 and 4.6 x 10 minus -3 min minus -1 at 24 and 37 degrees, respectively. When studied over longer periods at 24 degrees, the dissociation process appeared to be multiexponential. The kinetics of degradation of (-125I)hCG and receptors were determined at both temperatures, and a mathematical model was developed by modification of the second-order chemical kinetic differential equation to take these factors into account. The application of such a model to hCG kinetic binding data demonstrated that reactant degradation had little significant effect on the derivation of the association rate constant (k1), but caused significant overestimation of the dissociation rate constant (k2) values derived from association experiments. The model was also applied by computer simulation to a theoretical analysis of the effects of degradation of free hormone and receptor sites upon kinetic and steadystate binding data. By this method, the initial velocities of hormone binding were shown to be less affected by degradation than the steady-state levels of hormone-receptor complex. Also, reactant degradation in simulated steady-state experiments caused an underestimate of the apparent equilibrium association constant, but had relatively less effect on the determination of binding site concentration.     

Enhanced mutagenesis parallels enhanced reactivation of herpes virus in a human cell line.

U.v. irradiation of human NB-E cells results in enhanced mutagenesis and enhanced reactivation of u.v.-irradiated H-1 virus grown in those cells ( Cornelis et al., 1982). This paper reports a similar study using herpes simplex virus (HSV) in NB-E cells. The mutation frequency of HSV (resistance of virus plaque formation to 40 micrograms/ml iododeoxycytidine ) increased approximately linearly with exposure of the virus to u.v. radiation. HSV grown in unirradiated cells gave a slope of 1.8 X 10(-5)m2/J, with 3.2 X 10(-5)m2/J for HSV grown in cells irradiated (3 J/m2) 24 h before infection. There was no evidence for mutagenesis of unirradiated virus by irradiated cells, as seen with H-1 virus. Enhanced reactivation of irradiated HSV in parallel cultures increased virus survival, manifested as a change in slope of the final component of the two-component survival curve from a D0 of 27 J/m2 in unirradiated cells to 45 J/m2 in irradiated cells. Thus, enhanced mutagenesis and enhanced reactivation occurred for irradiated HSV in NB-E cells. The difference in the enhanced mutagenesis of HSV (dependent on damaged DNA sites) and of H-1 virus (primarily independent of damaged DNA sites) is discussed in terms of differences in DNA polymerases.