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111.
Jasna Dietz Thomas Kaercher Anne-Theres Schneider Theodor Zimmermann Kenneth Huttner Ramsey Johnson Holm Schneider 《European journal of pediatrics》2013,172(8):1023-1031
X-linked hypohidrotic ectodermal dysplasia (XLHED; ectodysplasin deficiency) has been classically described as affecting hair, sweat glands, and dentition. What may be underappreciated is the effect ectodysplasin deficiency has on glands surrounding the airways and eyes and the resulting chronic health issues. In this study, 12 male children (age range 6–13 years) and 14 male adults with XLHED (18–58 years of age) were investigated by pulmonary function tests, measurement of fractional exhaled nitric oxide, and by ophthalmologic assessments. Twelve healthy individuals (six children, six adults) served as controls. Signs of airway constriction and inflammation were detected in eight children with XLHED, including the youngest subject, and in ten adult XLHED patients. Increased tear osmolarity, reduced tear film break-up time, and other ocular abnormalities were also present at an early age. Five of 12 XLHED subjects not reporting a history of asthma and 7 of the 12 patients not reporting a history of dry eye issues showed at least two abnormal test results in the respective organ system. The presence of residual sweat ducts, suggestive of partial ectodysplasin gene expression, correlated with milder disease in two XLHED subjects with mutations affecting the collagen-like domain of ectodysplasin. Conclusion: The high prevalence of asthma-like symptoms in XLHED patients as young as 6 years and a similar prevalence of dry eye problems indicate that screening evaluation, regular monitoring, and consideration of therapeutic intervention should begin in early childhood. 相似文献
112.
Zidar P Kaschl UI Drobne D Bozic J Strus J 《Arhiv za higijenu rada i toksikologiju》2003,54(3):177-181
This paper describes a study of behavioural response in terrestrial isopod Oniscus asellus when offered two food pellets of different quality. One group had a choice of sterilised food and food pellets covered with mould. The other group had a choice of uncontaminated and cadmium-dosed food. During the behavioural test, the animals were monitored by a video camera and each visit to food pellets and time spent around it was counted. The results show that animals spent significantly less time near sterilised and cadmium-dosed food than with uncontaminated or mould-covered food. Discrimination between offered food pellets showed that avoidance behaviour can be used as an indicator of different food quality. 相似文献
113.
114.
Oligonephronia, not exuberant apoptosis, accounts for the development of glomerulosclerosis in the bcl-2 knockout mouse 总被引:2,自引:1,他引:1
Gassler N; Elger M; Inoue D; Kriz W; Amling M 《Nephrology, dialysis, transplantation》1998,13(10):2509-2518
Background. A main function attributed to B cell
leukaemia/lymphoma 2 gene (bcl-2) is its ability to confer resistance
against apoptosis. In bcl-2 deficient mice, extensive apoptosis occurs
during abnormal nephrogenesis, and renal failure is found very quickly
after birth. However, the underlying mechanisms remain poorly understood.
The aim of the present study was to clarify whether the degenerative
process in the kidneys seen after birth is based either on increased
apoptosis of glomerular cells or on mechanisms independent from the genetic
defect. Materials and methods. Kidneys from
7-56-day-old bcl-2 knockout mice and wild-type litter mates were studied.
Glomerula number, glomerular tuft volume, cell counts in 'non-sclerotic'
glomeruli as well as the glomerular damage score were determined by
histomorphometrical studies. Apoptosis was evaluated by morphological
criteria and the terminal deoxynucleotidyl transferase-mediated dUTP nick
end-labelling (TUNEL)-technique. Results.
The number of nephrons at birth was severely decreased in bcl-2
knockout mice compared to controls (<20%;
P<0.001). These nephrons undergo dramatic
hypertrophy with an approximately 4-fold increase in volume
(P<0.001). In hypertrophic, but 'non-sclerotic'
glomeruli, the number density of glomerular cells progressively declined
with time (P<0.001). Starting with day 20,
enlarged glomeruli developed sclerosis beginning with a segmental
distribution, but quickly progressing to global sclerosis. Apoptosis was
neither detected in non-sclerotic glomeruli nor in stages prior to fully
established sclerosis. As shown by the glomerular damage score, post-natal
degeneration of kidneys from bcl-2 knockout animals proceeded rapidly.
Conclusions. Bcl-2 knockout mice exhibit deficient
nephrogenesis resulting in severe oligonephronia at birth. Post-partum
development of glomerulosclerosis does not seem to be due to augmented
apoptosis. The degenerative process appears to be based on a glomerular
overload with increased mechanical stress to the filtration barrier,
leading via glomerula hypertrophy, podocyte damage and formation of tuft
adhesions to glomerulosclerosis. 相似文献
115.
David A Ishola Dionne M van der Giezen Brunhilde Hahnel Roel Goldschmeding Wilhelm Kriz Hein A Koomans Jaap A Joles 《Nephrology, dialysis, transplantation》2006,21(3):591-597
BACKGROUND: The availability of genetically modified mice has increased the need for relevant mouse models of renal disease, but widely used C57BL/6 mice often show resistance to proteinuria. 129/Sv mice are considered more sensitive to certain renal models. Albumin overload, an important model of proteinuric disease, induces marked proteinuria in rats but barely in C57BL/6 mice. We hypothesized that albumin overload would induce more proteinuria in 129S2/Sv than C57BL/6J mice. METHODS: Male and female C57BL/6J and 129S2/Sv mice received bovine serum albumin (BSA) for 11 days. Control groups received saline injections. Injected BSA was immunohistochemically localized to study intrarenal handling of overloaded protein. Renal macrophage infiltration (F4/80 immuno-staining) and glomerular ultrastructure (electron microscopy) were assessed. RESULTS: The BSA-treated groups were similarly hyperproteinemic at Day 11 (D11). Proteinuria differed widely. In C57BL/6J mice, it remained unchanged in females but significantly, though mildly, increased in males (from 3+/-1 to 8+/-2 mg/day, P < 0.05). In 129S2/Sv, proteinuria was marked in both males and females (4+/-1 to 59+/-14, and 0.6+/-0.2 to 29+/-9 mg/day, respectively, both P < 0.01). Proteinuria was accompanied by tubulo-interstitial macrophage infiltration in 129S2/Sv mice. Injected BSA was visualized within glomeruli in both strains and in the urinary space and tubules of 129S2/Sv but not C57BL/6J mice, indicating much greater glomerular leakage in the former. No glomerular macrophages or ultra-structural differences were detected. CONCLUSION: There are major strain differences in the proteinuria and renal inflammatory response of mice to albumin overload, which are not due to structural variation in the filtration barrier but possibly to functional differences in glomerular protein permeability. 相似文献
116.
117.
Some N,N′-diacyl-p-phenylenediamines substituted with halogens ( 2a - c ) were prepared. Their polarographic reduction in N,N-dimethylformamide with Et4NClO4 was performed and discussed. The mechanism of the electrochemical reduction is stated. Large-scale electrolytic reductions of 2a - b to 3a - b were performed. 相似文献
118.
We studied conduction velocity in peripheral nerves and the block of synaptic transmission produced by lack of glucose in hippocampal slices from 4- and 12-month-old streptozotocin-induced diabetic rats and their age-matched controls. In sural nerves of young and old diabetic rats, the conduction velocity was reduced by 30–35%. In slices from young diabetics, CA1 synaptic transmission was more sensitive to aglycemia than in control slices. However, all slices from older rats showed comparable increases in CA1 synaptic sensitivity to aglycemia. We conclude that the cerebral adaptation to diabetic hyperglycemia apparent in the hippocampus of young rats is masked in older rats by an age-dependent increase in sensitivity to lack of glucose. 相似文献
119.
120.
Spot-like or smudge-like film artifacts produced by static electric discharges may mimic lesions when superimposed on filmed CT images. These artifacts are typically round with a dark center that fades peripherally. Automatic film loading, low atmospheric humidity, and dirty film cassettes increase production of these artifactual pseudolesions. Misdiagnosis is prevented by familiarity with the artifacts' appearance and review of images on the viewing console. 相似文献