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The purpose of the study was to determine the effect of alpha-ketoglutarate sodium salt (AKG) treatment on the mineralization of the tibia in female rats during the development of osteopenia (Experiment-1) and in the condition of established osteopenia (Experiment-2). Thirty-two female rats were ovariectomized (OVX) to induce osteopenia and osteoporosis and another 32 female rats were sham-operated (SHO) and then randomly divided between the two experiments. In Experiment-1, the treatment with AKG started after a 7-day period of convalescence, whereas in Experiment-2 the rats were subjected to a 60-day period of osteopenia fixation, after which the actual experimental protocol commenced. AKG was administered in the experimental solution for drinking at a concentration of 1.0?mol/l and a placebo (PLC) was used as a control solution. After 60?days of experimental treatment the rats in both experiements were sacrificed, the body weight recorded, and blood serum and isolated tibia were stored for further analysis. The bones were analyzed using tomography and densitometry, and for estimation of mechanical properties the 3-point bending test was used. Serum concentrations of osteocalcin and collagen type I crosslinked C-telopeptide were measured. The anabolic effects of AKG on bone during osteopenia development in Experiment-1 not only stopped the degradation of bone tissue, but also stimulated its mineralization. The usage of AKG in animals with established osteopenia (Experiment-2) was not able to prevent bone atrophy, but markedly reduced its intensity. The stimulation of tibia mineralization after AKG treatment has been also argued in healthy SHO animals. The results obtained prove the effectiveness of AKG usage in the prophylaxis and therapy of osteopenia and osteoporosis, induced by bilateral gonadectomy. Additionally, the results clearly prove that treatment with AKG improves the mineralization of bone tissue in healthy animals.  相似文献   
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The fibroblast growth factor 1 (FGF1) gene is expressed primarily in the kidney and may contribute to hypertension. However, the biologic mechanisms underlying the association between FGF1 and BP regulation remain unknown. We report that the major allele of FGF1 single nucleotide polymorphism rs152524 was associated in a dose-dependent manner with systolic BP (P=9.65×10−5) and diastolic BP (P=7.61×10−3) in a meta-analysis of 14,364 individuals and with renal expression of FGF1 mRNA in 126 human kidneys (P=9.0×10−3). Next-generation RNA sequencing revealed that upregulated renal expression of FGF1 or of each of the three FGF1 mRNA isoforms individually was associated with higher BP. FGF1-stratified coexpression analysis in two separate collections of human kidneys identified 126 FGF1 partner mRNAs, of which 71 and 63 showed at least nominal association with systolic and diastolic BP, respectively. Of those mRNAs, seven mRNAs in five genes (MME, PTPRO, REN, SLC12A3, and WNK1) had strong prior annotation to BP or hypertension. MME, which encodes an enzyme that degrades circulating natriuretic peptides, showed the strongest differential coexpression with FGF1 between hypertensive and normotensive kidneys. Furthermore, higher level of renal FGF1 expression was associated with lower circulating levels of atrial and brain natriuretic peptides. These findings indicate that FGF1 expression in the kidney is at least under partial genetic control and that renal expression of several FGF1 partner genes involved in the natriuretic peptide catabolism pathway, renin-angiotensin cascade, and sodium handling network may explain the association between FGF1 and BP.  相似文献   
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In the present work, for the first time, the possibility of formation of CrAl2O4 was shown from the equimolar mixture of co-precipitated Al2O3 and Cr2O3 oxides under a reductive environment. The crystallographic properties of the formed compound were calculated using the DICVOL procedure. It was determined that it has a cubic crystal structure with space group Fd-3m and a unit cell parameter equal to 8.22(3) Å. The formed CrAl2O4 is not stable under ambient conditions and easily undergoes oxidation to α-Al2O3 and α-Cr2O3. The overall sequence of the phase transformations of co-precipitated oxides leading to the formation of spinel structure is proposed.  相似文献   
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Introduction

Traumatic brain injury (TBI) affects cardiac electrical function, and several extra-cerebral factors, including intra-abdominal pressure (IAP), might further modulate this brain-heart interaction. The purpose of this study was to investigate the impact of TBI, and of increased IAP during TBI, on cardiac electrical function as measured by vectorcardiographic (VCG) variables.

Methods

Survival, IAP and changes in VCG variables including spatial QRS-T angle and QTc interval were measured in consecutive adult patients with either isolated TBI (iTBI), or with TBI accompanied by polytrauma to the abdomen and/or limbs (pTBI). For all patients, observations were performed just after the admission to the ICU (baseline) and at 24, 48, 72 and 96 h after admission.

Results

74 patients aged 45 ± 18 were studied. 44 were treated for iTBI and 30 for pTBI. In all patients, spatial QRS-T angle and QTc interval increased after TBI (p < 0.001), relatively more so in patients with pTBI. Compared to survivors, non-survivors also ultimately had greater widening of the spatial QRS-T angle (p < 0.001), most notably just before foraminal herniation. Wider spatial QRS-T angle and longer QTc interval were also noted in patients with IAP > 12 mmHg (p < 0.001), and with right compared to left hemispheric injury (p < 0.001). ST segment level at the J point decreased 24 and 48 h after TBI in leads I, II, III, aVR, aVF, V1, V2, V3 and V6, and increased in lead V1, especially in non-survivors.

Conclusions

Spatial QRS-T angle and QTc interval increase after TBI. If foraminal herniation complicates TBI, further widening of the spatial QRS-T angle typically precedes it, followed by notable narrowing thereafter. Increased IAP also intensifies TBI-associated increases in spatial QRS-T angle and QTc interval.  相似文献   
8.

Objective

Amongst middle-aged men, haplogroup I is associated with ≈50% higher risk of coronary artery disease than other paternal lineages of Y chromosome. We hypothesised that carriers of haplogroup I had higher levels of aggression and estrogens and/or lower levels of androgens early in life and thus might be more prone to cardiovascular disease than men with other lineages of Y chromosome.

Methods

We reconstructed phylogenetic tree of the Y chromosome in >1000 young apparently healthy white men from the general population. Each Y chromosome was classified into one of 13 most common European lineages. Androgens (DHEA-S, androstenedione, total testosterone) and their metabolites (total estradiol, estrone) were measured by radioimmunoassays. Information on five dimensions of aggression (total, physical, verbal, anger and hostility) was collected using Buss and Perry questionnaire.

Results

Approximately 17% men inherited haplogroup I from their fathers. Carriers of haplogroup I showed lower scores of verbal aggression than men with other haplogroups (β = −0.72, SE = 0.29, P = 0.012) and when further compared to carriers of most common R1a lineage and other haplogroups (β = −1.03, SE = 0.34, P = 0.003). However, these associations did not survive a correction for multiple testing. Sex steroids did not show even nominal level of association with haplogroup I.

Conclusion

Our data show no overall association between haplogroup I and sex-related phenotypes in young white men. These results also suggest that the previously identified association between haplogroup I and coronary artery disease is not likely mediated by unfavourable profile of sex steroids or heightened aggression early in life.  相似文献   
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Common Carotid Artery Remodeling Studied by Sonomorphological Criteria   总被引:1,自引:0,他引:1  
BACKGROUND AND PURPOSE: Only a few attempts have been made to establish the impact of critical intima-media thickness (IMT) on narrowing of the lumen of the common carotid artery (CCA). In the present study, sonomorphological criteria have been used to assess how intima-media thickening in the CCA may influence the artery geometry. METHODS: High-resolution ultrasonography was employed in 233 patients (466 arteries) to quantify the selected parameters of CCA biometry: IMT, arterial lumen diameter (LD), interadventitial diameter (IAD), and outer artery diameter (OAD). RESULTS: With an increase of CCA IMT up to the critical point of 1.2 mm, the LD showed parallel compensatory increases. Above the inflection point of 1.3 mm, the lumen became progressively narrower proportionally to the increasing IMT. CONCLUSION: There are limits to the compensatory enlargement of the CCA lumen. Above the inflection point of CCA IMT of 1.3 mm, the artery lumen becomes progressively narrower with increasing IMT.  相似文献   
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