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31.
Comparison of isolation of Haemophilus vaginalis (Corynebacterium vaginale) from peptone-starch-dextrose agar and Columbia colistin-nalidoxic acid agar.
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A total of 447 cervical or vaginal specimens were inoculated in parallel onto peptone-starch-dextrose (PSD) and Columbia colistin (10 mg/ml)-nalidixic acid (15 mug/ml) (CNA) agar and were incubated for 48 h at 35 degrees C in an atmosphere with 2 to 10% CO2. One hundred (22.4%) of the cultures were positive for Haemophilus vaginalis. Forty-eight of the isolates were recovered from both PSD and Columbia CNA agar, five from PSD only, and 47 from Columbia CNA agar only (P less than 0.001). On Columbia CNA agar, 76 of the isolates were detected after 24 h of incubation, and the remainder were detected within 4 days of incubation. 相似文献
32.
Transforming potential of deletion mutants of the SV40 T antigen coding gene in Syrian hamster cells 总被引:2,自引:0,他引:2
Thymidine kinase-deficient syrian hamster cells were cotransfected with recombinant plasmids containing the thymidine kinase (TK) gene of Herpes Simplex Virus Type 1, and either intact or partially deleted SV40 T antigen-coding genes. The transformants were selected by their ability to grow in gHAT medium. After selection and cloning, the TK-positive transformants that also expressed T antigen were tested for the extent of their transformation with respect to a number of characteristics, which included saturation density, ability to grow in soft agar, resistance to butyrate and to dibutyryl-cAMP, and plating efficiency. The combined results of these various tests indicate that cells containing partially deleted SV40 T antigen-coding genes are less transformed than cells containing an intact SV40 T antigen-coding gene. However, the amounts of T antigen are lower in cells transformed by deletion mutants than in cells transformed by wild-type T antigen-coding gene. Our data indicate that both the quantity and the quality of T antigen may be important in determining the degree of transformation in Syrian hamster cells. 相似文献
33.
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35.
The purpose of the study was to investigate the characteristics of shock attenuation during high-speed running. Maximal running
speed was identified for each subject [n=8 males, 25 (SD 4.6) years; 80 (8.9) kg; 1.79 (0.06) m] as the highest speed that could be sustained for about 20 s on a
treadmill. During testing, light-weight accelerometers were securely mounted to the surface of the distal antero-medial aspect
of the leg and frontal aspect of the forehead. Subjects completed running conditions of 50, 60, 70, 80, 90, and 100% of their
maximal speeds with each condition lasting about 20 s. Stride length, stride frequency, leg and head peak impact acceleration
were recorded from the acceleration profiles. Shock attenuation was analyzed by extracting specific sections of the acceleration
profiles and calculating the ratio of head to leg power spectral densities across the 10–20 Hz frequency range. Both stride
length and stride frequency increased across speeds (P<0.05) and were correlated with running speed (stride length r=0.92, stride frequency r=0.89). Shock attenuation increased about 20% per m·s–1 across speeds (P<0.05), which was similar to the 17% increase in stride length per m·s–1. Additionally, shock attenuation was correlated with stride length (r=0.71) but only moderately correlated with stride frequency (r=0.40) across speeds. It was concluded that shock attenuation increased linearly with running speed and running kinematic
changes were characterized primarily by stride length changes. Furthermore, the change in shock attenuation was due to increased
leg not head peak impact acceleration across running speeds.
Electronic Publication 相似文献
36.
C1-esterase inhibitor blocks T lymphocyte proliferation and cytotoxic T lymphocyte generation in vitro 总被引:1,自引:0,他引:1
We have previously shown that activated C1s complement and activated T
cells cleave beta2-microglobulin (beta2m) in vitro leading to the formation
of desLys58 beta2m. This process can specifically be inhibited by
C1-esterase inhibitor (C1-inh). Furthermore we showed that exogenously
added desLys58 beta2m in nanomolar amounts to a one-way allogenic mixed
lymphocyte culture (MLC) increased the endogenous production of IL-2 and
the generation of allo-specific cytotoxic T lymphocytes. C1-inh was
purified from fresh human plasma and added to human or murine MLC and
mitogen-stimulated lymphocyte cultures grown in the presence of
complement-inactivated serum. Read-outs were cell proliferation, lymphokine
production and development of T cell-mediated cytotoxicity. We found that
addition of C1-inh to MLC and mitogen- exposed murine and human lymphocyte
cultures inhibited proliferation, the development of allospecific cytotoxic
activity, and changed the endogenous production of IL-2, IL-4, IL-10, IL-12
and IFN-gamma. These data clearly demonstrate a regulatory function of
C1-inh on T cell- mediated immune functions.
相似文献
37.
The CTLA-4 gene region of chromosome 2q33 is linked to, and associated with, type 1 diabetes. Belgian Diabetes Registry 总被引:8,自引:1,他引:8
Nistico L; Buzzetti R; Pritchard LE; Van der Auwera B; Giovannini C; Bosi E; Larrad MT; Rios MS; Chow CC; Cockram CS; Jacobs K; Mijovic C; Bain SC; Barnett AH; Vandewalle CL; Schuit F; Gorus FK; Tosi R; Pozzilli P; Todd JA 《Human molecular genetics》1996,5(7):1075-1080
Susceptibility to autoimmune insulin-dependent (type 1) diabetes mellitus
is determined by a combination of environmental and genetic factors, which
include variation in MHC genes on chromosome 6p21 (IDDM1) and the insulin
gene on chromosome 11p15 (IDDM2). However, linkage to IDDM1 and IDDM2
cannot explain the clustering of type 1 diabetes in families, and a role
for other genes is inferred. In the present report we describe linkage and
association of type 1 diabetes to the CTLA-4 gene (cytotoxic T lymphocyte
associated-4) on chromosome 2q33 (designated IDDM12). CTLA-4 is a strong
candidate gene for T cell- mediated autoimmune disease because it encodes a
T cell receptor that mediates T cell apoptosis and is a vital negative
regulator of T cell activation. In addition, we provide supporting evidence
that CTLA-4 is associated with susceptibility to Graves' disease, another
organ- specific autoimmune disease.
相似文献
38.
Burwinkel B; Maichele AJ; Aagenaes O; Bakker HD; Lerner A; Shin YS; Strachan JA; Kilimann MW 《Human molecular genetics》1997,6(7):1109-1115
Glycogen storage disease due to phosphorylase kinase deficiency occurs in
several variants that differ in mode of inheritance and tissue-
specificity. This heterogeneity is suspected to be largely due to mutations
affecting different subunits and isoforms of phosphorylase kinase. The gene
of the ubiquitously expressed beta subunit, PHKB, was a candidate for
involvement in autosomally transmitted phosphorylase kinase deficiency of
liver and muscle. To identify such mutations, the complete PHKB coding
sequence was amplified by RT-PCR of RNA isolated from blood samples of
patients and analyzed by direct sequencing of PCR products. The
characterization of mutations was complemented by PCR of genomic DNA. In
one female and four male patients, we identified five independent nonsense
mutations (Y418ter; R428ter; Y974H+E975ter; Q656ter in two cases), one
single-base insertion in codon N421, one splice-site mutation affecting
exon 31, and a large deletion involving the loss of exon 8. Although these
severe translation-disrupting mutations occur in constitutively expressed
sequences of the only known beta subunit gene of phosphorylase kinase,
PHKB, they are associated with a surprisingly mild clinical phenotype,
affecting virtually only the liver, and relatively high residual enzyme
activity of approximately 10%.
相似文献
39.
Is fecundability associated with month of birth? An analysis of 19th and early 20th century family reconstitution data from The Netherlands 总被引:1,自引:4,他引:1
Smits LJ; Van Poppel FW; Verduin JA; Jongbloet PH; Straatman H; Zielhuis GA 《Human reproduction (Oxford, England)》1997,12(11):2572-2578
The relationship between fecundability and month of birth was investigated
in a cohort of 1526 women who married between 1802 and 1929, using only
women whose first marriage occurred before the age of 35 years. On the
basis of their time to pregnancy (TTP, calculated as time between wedding
and first birth minus gestational length), women were categorized into two
groups: fecunds (TTP up to 12 months or prenuptial conceptions, n = 1348)
and subfecunds (TTP >18 months, n = 118). By use of logistic regression,
cosinor functions with a period of 1 year or 6 months and variable shift
and amplitude were fitted through the monthly odds of subfecunds versus
fecunds. The best fitting curve was unimodal, with a zenith in September (P
= 0.13 for H0: no differences). Exclusion of childless women (n = 36,
minimum follow-up 5 years) from the subfecunds led to a similar curve (P
< 0.01), while childless women, as compared with fecunds, showed a birth
distribution that was best represented with a bimodal curve with zeniths in
January and July (P = 0.06). This study provides evidence for the existence
of differences in fecundability by month of birth. The cause of this
relationship is unclear, but may lie in a melatonin-dependent circannual
variability of the quality of the oocyte.
相似文献
40.
Mutations in the Ca(2+)-sensing receptor gene cause autosomal dominant and sporadic hypoparathyroidism 总被引:3,自引:0,他引:3
Baron J; Winer KK; Yanovski JA; Cunningham AW; Laue L; Zimmerman D; Cutler GB Jr 《Human molecular genetics》1996,5(5):601-606
Parathyroid hormone secretion is negatively regulated by a 7- transmembrane
domain, G-protein coupled Ca(2+)-sensing receptor. We hypothesized that
activating mutations in this receptor might cause autosomal dominant
hypoparathyroidism (ADHP). Consistent with this hypothesis, we identified,
in two families with ADHP, heterozygous missense mutations in the
Ca(2+)-sensing receptor gene that cosegregated with the disorder. None of
50 normal controls had either mutation. We also identified a de novo,
missense Ca(2+)-sensing receptor mutation in a child with severe sporadic
hypoparathyroidism. The amino acid substitution in one ADHP family affected
the N-terminal, extracellular domain of the receptor. The other mutations
involved the transmembrane region. Unlike patients with acquired
hypoparathyroidism, patients with these mutations had hypercalciuria even
at low serum calcium concentrations. Their greater hypercalciuria
presumably reflected activation of Ca(2+)-sensing receptors in kidney
cells, where the receptor negatively regulates calcium reabsorption. This
augmented hypercalciuria increases the risk of renal complications and thus
has implications for the choice of therapy.
相似文献