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41.
A case of infantile digital fibromatosis was studied by light and electron microscopic histochemistry. Using two different acidic solutions of phosphotungstic acid at varying pHs, the round inclusions characteristic of this tumor were shown to have a high protein content with little or no carbohydrate. The histochemical reactivity of the inclusions was similar to that of the cytoplasmic microfibrils in the tumors cells and consistent with the idea that both the inclusions and the microfibrils represent actin. There is, however, no definite proof that the tumor cells are myofibroblasts. At the present time, this tumor should be viewed as a peculiar expression of deranged assembly or metabolism of filamentous proteins or both. 相似文献
42.
This study analyses the influence of female and male patient age and human
menopausal gonadotrophin (HMG) requirements on clinical pregnancy rates and
live birth rates with ovulation stimulation using HMG in combination with
intrauterine insemination (IUI). In this study, 363 consecutive HMG/IUI
treatment cycles in 184 patients carried out at a university fertility
centre were analysed in a retrospective fashion. The main outcomes measured
were clinical pregnancy rates and live birth rates. Increased female
partner age (> or = 35) and male partner age (> or = 40) were found
to negatively influence pregnancy rates with HMG/ IUI therapy. In addition,
this study demonstrated a critical threshold of HMG requirements beyond
which pregnancy did not occur. No pregnancies occurred in treatment cycles
requiring > 25 ampoules (1875 IU) of menotrophins to achieve follicular
maturity, irrespective of patient age. In conclusion, female partner age,
male partner age, and HMG requirements all significantly influence
pregnancy rates with HMG/IUI therapy.
相似文献
43.
Background
Ischemic stroke is the most common cause of disability in North America and in addition to the generally accepted risk factors, there is increasing evidence for the potential pathophysiological role of genes. One of these genes, the endothelial nitric oxide synthase gene (NOS3) has been reported as a genetic risk factor for ischemic stroke. To independently confirm and extend the results of these previous reports, we investigated this gene as a risk factor for stroke in an ethnically diverse study population. 相似文献44.
Ferrand PE Fujimoto T Chennathukuzhi V Parry S Macones GA Sammel M Kuivaniemi H Romero R Strauss JF 《Molecular human reproduction》2002,8(11):1031-1034
Infection is believed to be a leading cause of preterm premature rupture of membranes (PPROM). The bacterial cell wall component, lipopolysaccharide (LPS), is thought to initiate tissue responses leading to PPROM in the setting of Gram negative infection. LPS is recognized by the innate immune system, including the proteins encoded by the CARD15 and TLR4 genes. A recently described mutation (2936insC) in CARD15 and a polymorphism in TLR4 896 A>G impair responses to LPS. The objective of this study was to determine if African Americans, who have a higher incidence of PPROM than Caucasians, have different frequencies of the mutant CARD15 allele and the TLR4 hyporesponsive variant, and if risk of PPROM is influenced by fetal carriage of these alleles. The allele frequencies for the CARD15 mutation and the TLR4 896G variant in African Americans were similar to those reported for Caucasians. There was no association between the TLR4 alleles examined and PPROM. However, the CARD15 mutation was only detected in controls and not in PPROM cases. We conclude that the CARD15 mutation and hyporesponsive TLR4 allele do not contribute to ethnic variation in the incidence of PPROM. 相似文献
45.
Effects of estradiol with and without testosterone on body composition and relationships with lipids in postmenopausal women 总被引:1,自引:0,他引:1
OBJECTIVE: The cardioprotective effects of postmenopausal estrogen replacement therapy are mediated by several mechanisms, including favorable effects on lipids and lipoproteins. The extent to which the latter reflects modification of body fat distribution by sex steroids is not known. Hence, we investigated the relationships between changes in lipids and measures of body composition in postmenopausal women who were administered estrogen therapy with and without testosterone. DESIGN: We randomized 33 postmenopausal women to treatment with either estradiol 50 mg (E) alone or estradiol 50 mg plus testosterone 50 mg implants (E&T) administered every 3 months for 2 years in conjunction with cyclic oral progestins for women with an intact uterus. RESULTS: Both therapies were associated with sustained reductions in total cholesterol and low-density lipoprotein (LDL) cholesterol. In women who received E but not E&T, hip (p < 0.001) and abdominal circumferences (p < 0.05) and fat mass:fat-free mass (FM:FFM) ratio over the abdomen (p < 0.05) declined. E&T but not E resulted in increased FFM (p < 0.001) and a reduced FM:FFM ratio (p < 0.05). For E but not E&T, the decrease in LDL cholesterol was significantly related to changes in total and compartmental body fat and to change in the FM:FFM ratio (p < 0.05). CONCLUSION: Estrogen replacement has effects on body fat distribution in postmenopausal women that are associated with improved lipid parameters. Addition ofparenteral testosterone does not negate the favorable effects of estrogen on LDL cholesterol levels but may attenuate the reduction in centralized body fat achieved with E implants. 相似文献
46.
S McGregor J Strauss N Bulgin V De Luca C J George M Kovacs J L Kennedy 《American journal of medical genetics. Part B, Neuropsychiatric genetics》2007,(5):696-700
Recently, evidence has accumulated for the role of neurotrophic processes in mood disorders. Neurotrophins operate on receptors, one of which is the p75 neurotrophin receptor (p75(NTR)). We examined three p75(NTR) markers at the p75(NTR) gene, including a missense polymorphism that changes serine to leucine (S205L), for association with suicide attempt (SA) in 203 childhood-onset mood disorder (COMD) cases. There was no difference between COMD suicide attempters and COMD non-attempters with logistic regression models for any of the three markers. We also compared the three polymorphisms between 192 COMD cases and 192 matched healthy controls and found no significant differences between COMD and healthy controls. Our results do not support an association of the p75(NTR) S205L polymorphism with risk for COMD or SA in COMD. 相似文献
47.
Recombinant troponin I substitution and calcium responsiveness in skinned cardiac muscle 总被引:1,自引:0,他引:1
John D. Strauss Jennifer E. Van Eyk Zacharias Barth Lan Kluwe Rudolf J. Wiesner K. Maéda J. Caspar Rüegg 《Pflügers Archiv : European journal of physiology》1996,431(6):853-862
Using treatment with vanadate solutions, we extracted native cardiac troponin I and troponin C (cTnI and cTnC) from skinned
fibers of porcine right ventricles. These proteins were replaced by exogenously supplied TnI and TnC isoforms, thereby restoring
Ca2+-dependent regulation. Force then depended on the negative logarithm of Ca2+ concentration (pCa) in a sigmoidal manner, the pCa for 50% force development, pCa50, being about 5.5. For reconstitution we used fast-twitch rabbit skeletal muscle TnI and TnC (sTnI and sTnC), bovine cTnI
and cTnC or recombinant sTnIs that were altered by site-directed mutagenesis. Incubation with TnI inhibited isometric tension
in TnI-extracted fibers in the absence of Ca2+, but restoration of Ca2+ dependence required incubation with both TnI and TnC. Relaxation at low Ca2+ levels and the steepness of the force/pCa relation depended on the concentration of exogenously supplied TnI in the reconstitution
solution (range 20–150 μM), while Ca2+ sensitivity, i.e. the pCa50, was dependent on the isoform, and also on the concentration of TnC in the reconstitution solution. At pH 6.7, skinned fibers
reconstituted with optimal concentrations of sTnC and sTnI (120 μM and 150 μM, respectively) were more sensitive to Ca2+ than those reconstituted with cTnC and cTnI (difference in pCa50 approx. 0.2 units). Rabbit sTnI was cloned and expressed in Escherichia coli using a high yield expression plasmid. We introduced point mutations into the TnI inhibitory region comprising the sequence
of the minimal common TnC/actin binding site (-G104-K-F-K-R-P-P-L-R-R-V-R115-). The four mutants produced by substitution of T for P110, G for P110, G for L111, and G for K105 were chosen, based on previous work with synthetic peptides showing that single amino acid substitution in this region diminished
the capacity of these peptides to inhibit acto-S1 ATPase or contraction of skinned fibers. Therefore, all amino acid residues of the inhibitory region are thought to contribute
to biological activity of TnI. However, each of the recombinant TnIs could substitute for endogenous TnI. In combination with
exogenous TnC, Ca2+ dependence could be restored when gly110sTnI, thr110sTnI or gly111sTnI was used for reconstitution. The mutant gly105sTnI, on the other hand, reduced the ability of skinned fibers to relax at low Ca2+ concentrations and it caused an increase in Ca2+ sensitivity.
Received: 5 October 1995/Received after revision and accepted: 1 December 1995 相似文献
48.
Zeidán Q Strauss M Porras N Anselmi G 《Journal of submicroscopic cytology and pathology》2002,34(3):315-321
In order to evaluate the heart and liver responses after adriamycin (ADR) toxic aggression, with and without exogenous L-carnitine (CAR) protection, female Sprague-Dawley rats, body weight 40-60 g, were randomized into four groups: CON, ADR, CAR and CAR-ADR. ADR was injected i.v. at a dose of 15-18 mg/kg body wt (0.1 ml). CAR was administered i.v. at a dose of 20 mg (0.1 ml) before each subdose of ADR, and then orally at 180 mg/kg body wt daily for 12 weeks. Long-term cardiac and hepatic subcellular damage were determined by transmission electron microscopic analysis of ultrathin sections. The ADR-induced long-term cardiac subcellular pathology included loss, disruption and disassembly of myofibrils, and mitochondrial swelling and condensation. On the other hand, the ADR-induced subcellular hepatic alterations consisted of polymorphic mitochondria, cytoplasmic vacuolization and accumulation of lipid droplets. Apparently, cardiac tissue was more affected by ADR toxic aggression than hepatic tissue. However, these alterations were of less severity in protected groups, in both heart and liver, suggesting CAR as a possible hepatoprotector agent against ADR toxicity. Because of the liver-L-carnitine-heart relationship, studying ADR-hepatotoxicity could be helpful in the further understanding of severe ADR-cardiotoxicity. 相似文献
49.
50.
Analysis of the steroidogenic acute regulatory protein (StAR) gene in Japanese patients with congenital lipoid adrenal hyperplasia 总被引:1,自引:0,他引:1
Nakae J; Tajima T; Sugawara T; Arakane F; Hanaki K; Hotsubo T; Igarashi N; Igarashi Y; Ishii T; Koda N; Kondo T; Kohno H; Nakagawa Y; Tachibana K; Takeshima Y; Tsubouchi K; Strauss JF rd; Fujieda K 《Human molecular genetics》1997,6(4):571-576
Genomic DNA from 19 Japanese patients with congenital lipoid adrenal
hyperplasia (lipoid CAH) representing 16 different families was examined to
identify the genetic alterations of steroidogenic acute regulatory protein
(StAR). Ten of 19 patients had a 46,XX karyotype and nine had a 46,XY
karyotype. Six of the 46,XX patients have experienced spontaneous pubertal
changes including breast development and irregular menstruation whereas
none of the 46,XY subjects displayed pubertal changes. Eight different
mutations were identified. Sixteen patients were either homozygotes or
compound heterozygotes for the Q258X mutation. The seven other mutations
identified were 189delG, 246insG, 564del13bp, 838delA, Q212X, A218V and
M225T. The 189delG, 246insG, 546del13bp and Q212X mutants encode truncated
proteins. COS-1 cells transfected with expression vectors encoding cDNAs
for the mutant StAR proteins which affect the C-terminus, 838delA, A218V
and Q258X, exhibited no steroidogenesis enhancing activity. However, the
M225T mutant retained some steroidogenic activity. The patient with the
M225T mutation had late onset of this disorder and some capacity to secrete
testosterone in response to hCG. These findings suggest: (i) that the Q258X
mutation can be used as a genetic marker for the screening of Japanese for
lipoid CAH, (ii) that the C-terminus of StAR plays an important role in the
protein's activity and (iii) that there are differences in the extent of
functional impairment of the testis and ovaries in lipoid CAH.
相似文献