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1.
The most common cause of illness in infancy and childhood is acute infection of the respiratory tract. Several recent studies have reported that life-threatening respiratory disease in infancy, such as pneumonia and bronchiolitis, is directly related to the smoking habits of parents. The effects of smoking are more hazardous to youngsters because babies and young children breathe more rapidly than adults. Because of this higher breathing rate, they inhale more air—and more pollution—in comparison to their total body weight. The harmful effects of cigarette smoking on infants and children and recommendations for specific interventions to minimize or eliminate this health hazard are discussed. 相似文献
2.
Resection of the adrenal glands precludes participation in many immunotherapy protocols for metastatic renal cell carcinoma. We performed radical nephrectomy with adrenalectomy and contralateral partial adrenalectomy, including adrenal vein ligation for a 4 cm. hilar metastasis without perioperative complications or local recurrence after 30 months. Adrenal function, measured by cosyntropin stimulation tests 6 weeks and 10 months postoperatively, was normal. Partial adrenalectomy with preservation of adrenal function is possible. 相似文献
3.
Previous reports in the literature have described correlation of increasing repeat length with severity of the phenotype, in Kennedy syndrome. We describe male siblings with different repeat lengths, with lack of expression of the phenotype in the sibling with the longer repeat length. The phenotype was identical to motor neurone disease. There is variability of expression in Kennedy syndrome and repeat length even in siblings cannot be taken as a conclusive indicator of severity. CAG repeat length cannot be used to predict the natural history of Kennedy disease. The diagnosis of Kennedy syndrome should be considered in male patients presenting with atypical motor neurone disease. 相似文献
4.
5.
Uroscopy in the 21st century: high-field NMR spectroscopy 总被引:1,自引:1,他引:0
Neild GH; Foxall PJ; Lindon JC; Holmes EC; Nicholson JK 《Nephrology, dialysis, transplantation》1997,12(3):404-417
From the experiments described, it can be seen that there are different
research approaches that can be taken and these are summarized in Table 1.
Whereas much scientific research is principally hypothesis led, there
remains, nevertheless, an important place for exploratory research. High
resolution NMR can measure, directly and simultaneously, a wide range of
endogenous metabolites in biological fluids and has the unique capability
of providing structural information on the metabolites detected. It has
proved to be a powerful research tool with which to study inherited
metabolic diseases, renal disease, drug metabolism, and toxicity, and can
be used to monitor the effects of drug therapy. For instance, by using a
library of experimental toxins one can map the metabolic profile of
site-specific nephron injury. With this approach in man one could
eventually take an unknown disease such as Balkan nephropathy and predict
the initial site of tubular injury, the mode of injury and therefore the
kind of toxin capable of producing that injury. NMR spectroscopic
techniques are still advancing rapidly, with ever increasing sensitivity
and sophistication of NMR pulse sequences to enhance structural elucidation
in complex mixtures. Given the advances in directly coupled HPLC-NMR and
even HPLC-NMR-mass spectroscopy it is likely that these technologies in
conjunction with pattern recognition will make major contribution to our
understanding of renal processes and provide new diagnostic insights in the
21st century.
相似文献
6.
Leukotriene B4 (LTB4) and the protein kinase C activator, 4-beta-phorbol dibutyrate (PDBu), both induced a pronounced and concentration-dependent stimulation of hydrogen peroxide (H2O2) generation by purified guinea pig peritoneal eosinophils in the concentration range 1 nM-1 microM. The LTB4 response was inhibited competitively by the specific LTB4 receptor antagonist, U-75302, with a KB of 25 nM, while the concentration-response curves for both stimuli were shifted rightwards (3.8-fold and 2.8-fold for LTB4 and PDBu, respectively) by the competitive protein kinase C inhibitor, 1-O-hexadecyl-2-O-methylglycerol at a concentration of 300 microM. LTB4 appears, therefore, to induce respiratory burst in eosinophils via a receptor-mediated mechanism involving protein kinase C. 相似文献
7.
A large proportion of mice rendered neonatally tolerant of class II MHC antigens respond to the tolerogen in vitro in an MLR, while simultaneously maintaining tolerance in vivo as evidenced by acceptance of a skin graft bearing the tolerated antigens. To determine whether this discrepancy between in vivo and in vitro tolerance is reflective of differences in the amount and/or type of lymphokines produced by tolerant lymphocytes, we have examined the ability of tolerogen-reactive lymphocytes to produce IL-2, IL-4/5, and IFN in vitro in an MLR. Our results demonstrate that when stimulated with the tolerogen, lymphocytes from both normal and tolerant responders produce IL-2 and interferon. However, in comparison to normal cells, 2 alterations in the tolerogen-specific responses of lymphocytes obtained from tolerant mice were identified. (1) The amount of IL-2 in the supernatants derived from tolerant cultures declines prematurely compared to normal cultures. This premature decline in IL-2 production was due neither to a lower frequency of Th cells as judged by limit dilution analysis nor to an increase in IL-2R expression on tolerant lymphocytes as measured by FACS analysis. (2) IL-4 and presumably IL-5 can be demonstrated in supernatants of tolerant, but not normal, lymphocytes stimulated by the tolerogen. Thus although lymphocytes from MLR-positive tolerant mice generate substantial quantities of lymphokines in response to the tolerogen, the pattern of lymphokine production is unusual when compared to that of normal lymphocytes. These results are inconsistent with the notion that a global lack of helper activity, per se, is responsible for the maintenance of tolerance in these mice and furthermore suggest that tolerance could be the result of "inappropriate" lymphokine production. 相似文献
8.
Localization of a gene for otosclerosis to chromosome 15q25-q26 总被引:5,自引:0,他引:5
Tomek MS; Brown MR; Mani SR; Ramesh A; Srisailapathy CR; Coucke P; Zbar RI; Bell AM; McGuirt WT; Fukushima K; Willems PJ; Van Camp G; Smith RJ 《Human molecular genetics》1998,7(2):285-290
Among white adults otosclerosis is the single most common cause of hearing
impairment. Although the genetics of this disease are controversial, the
majority of studies indicate autosomal dominant inheritance with reduced
penetrance. We studied a large multi- generational family in which
otosclerosis has been inherited in an autosomal dominant pattern. Five of16
affected persons have surgically confirmed otosclerosis; the remaining nine
have a conductive hearing loss but have not undergone corrective surgery.
To locate the disease- causing gene we completed genetic linkage analysis
using short tandem repeat polymorphisms (STRPs) distributed over the entire
genome. Multipoint linkage analysis showed that only one genomic region, on
chromosome 15q, generated a lod score >2.0. Additional STRPs were typed
in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and
D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis
gene.
相似文献
9.
Hendrickx J; Dams E; Coucke P; Lee P; Fernandes J; Willems PJ 《Human molecular genetics》1996,5(5):649-652
X-linked liver glycogenosis type II (XLG II) is a recently described X-
linked liver glycogen storage disease, mainly characterized by enlarged
liver and growth retardation. These clinical symptoms are very similar to
those of XLG I. In contrast to XLG I patients, however, XLG II patients do
not show an in vitro enzymatic deficiency of phosphorylase kinase (PHK).
Recently, mutations were identified in the gene encoding the liver alpha
subunit of PHK (PHKA2) in XLG I patients. We have now studied the PHKA2
gene of four unrelated XLG II patients and identified four different
mutations in the open reading frame, including a deletion of three
nucleotides, an insertion of six nucleotides and two missense mutations.
These results indicate that XLG II is due to mutations in PHKA2. In
contrast to XLG I, XLG II is caused by mutations that lead to minor
structural abnormalities in the primary structure of the liver alpha
subunit of PHK. These mutations are found in a conserved RXX(X)T motif,
resembling known phosphorylation sites that might be involved in the
regulation of PHK. These findings might explain why the in vitro PHK
enzymatic activity is not deficient in XLG II, whereas it is in XLG I.
相似文献
10.