scholarly journals Relative growth of the skull and postcranium in giant transgenic mice

1990 ◽  
Vol 56 (1) ◽  
pp. 21-34 ◽  
Author(s):  
Brian T. Shea ◽  
Robert E. Hammer ◽  
Ralph L. Brinster ◽  
Matthew R. Ravosa
Keyword(s):  
Transgenic Mice ◽  
Growth Patterns ◽  
Cross Sectional ◽  
Relative Growth ◽  
Normal Littermate ◽  
Skeletal Size ◽  
Body Weights ◽  
Igf I ◽  
Growth Controls ◽  
Normal Controls

SummaryCross-sectional allometric growth patterns of the cranial and postcranial skeleton were compared between giant transgenic (MT-rGH) mice and their normal littermate controls. Body weights, external body dimensions, and a series of cranial and postcranial linear dimensions of the skeleton were determined for samples of known age. Comparative bivariate and multivariate allometric analyses were completed in order to determine whether (1) the larger transgenic mice differed significantly from the normal controls in aspects of body and skeletal proportions, and (2) any such proportion differences resulted from general allometric effects of overall weight or skeletal size increase. Results demonstrate that the transgenic mice do exhibit significantly different body and skeletal proportions than normal control adults. Allometric comparisons of the skeletal dimensions relative to body weight reveal similar coefficients of growth allometry but several differences in y-intercept values in the transgenic vs. control groups. The comparisons among the skeletal dimensions of the skull and postcranium generally reveal the sharing and differential extension of common growth allometries in the two groups. Thus, the elevated levels of growth hormone (GH) and insulin-like growth factor I (IGF-I) in the transgenic mice appear to result in increased overall growth for the various skeletal elements, but in the relative proportions determined by intrinsic growth controls within that system.

Androgen regulation of circulating insulin-like growth factor-I during puberty in male hypogonadal mice

1993 ◽  
Vol 139 (1) ◽  
pp. 57-65 ◽  
Author(s):  
B. A. Crawford ◽  
J. Singh ◽  
J. M. Simpson ◽  
D. J. Handelsman
Keyword(s):  
Growth Factor ◽  
Seminal Vesicles ◽  
Insulin Like Growth Factor ◽  
Male Mice ◽  
Cross Sectional ◽  
Factor I ◽  
Body Weights ◽  
Igf I ◽  
Kidney Liver ◽  
Normal Controls

ABSTRACT This study aimed at determining the relationship of sex steroids, particularly in the perinatal period, to the pubertal insulin-like growth factor-I (IGF-I) surge in male mice. We used hypogonadal (hpg) mice, which have a major deletion in the gonadotrophin-releasing hormone (GnRH) gene, in order to have a model lacking all GnRH-induced gonadotrophin and sex steroid secretion throughout pre- and postnatal life. Cross-sectional data on body weights and weights of testes, seminal vesicles, kidneys, liver and spleen from 9 to 77 days of age were obtained in male hpg, heterozygous (Hz) and homozygous normal (N/N) littermates (n = 75–78/group). These data did not reveal any difference between Hz and N/N mice. Hpg mice had decreased body weights which by 70–77 days of age were approximately 18% less than normal controls. Testes and seminal vesicles of hpg mice did not demonstrate any significant postnatal growth. Relative to body weight, kidney weights were also markedly reduced in hpg mice (P<0·0001), deviating significantly from normal by 28–35 days of age, reflecting the impact of androgen deficiency on a non-reproductive organ. From the cross-sectional data it was concluded that puberty commenced soon after weaning (21 days) in the male and that maturity was achieved within 4–5 weeks. Longitudinal study showed that, compared with normal controls, untreated hpg mice had an exaggerated pubertal IGF-I surge (P<0·005) which peaked in mid-puberty. This, together with their reduced body weights (P<0·05), were normalized by treatment from 21 to 70 days of age with two 1 cm s.c. implants of testosterone (n=6) or dihydrotestosterone (n=7). There was no difference in IGF-I levels or in weights of testes, seminal vesicles, kidney, liver or spleen between testosterone and dihydrotestosterone treatments (P>0·05). Prolonged high levels of androgen also restored testicular and seminal vesicle weights to 40% of phenotypically normal controls, while kidney, liver and spleen weights were also significantly increased. The pubertal IGF-I surge in mice does not, therefore, require androgens in either the pre- or postnatal periods, and it is exaggerated in androgen-deficient male mice and dampened to normal regardless of aromatization. Journal of Endocrinology (1993) 139, 57–65

scholarly journals Transgenic Mice Overexpressing Des-Acyl Ghrelin Show Small Phenotype

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 355-364 ◽  
Author(s):  
Hiroyuki Ariyasu ◽  
Kazuhiko Takaya ◽  
Hiroshi Iwakura ◽  
Hiroshi Hosoda ◽  
Takashi Akamizu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Biological Effects ◽  
Lower Body ◽  
Acid Modification ◽  
Male And Female ◽  
Body Weights ◽  
Igf I ◽  
Actin Promoter ◽  
Acyl Ghrelin ◽  
Serum Gh

Ghrelin, a 28-amino acid acylated peptide, displays strong GH-releasing activity in concert with GHRH. The fatty acid modification of ghrelin is essential for the actions, and des-acyl ghrelin, which lacks the modification, has been assumed to be devoid of biological effects. Some recent reports, however, indicate that des-acyl ghrelin has effects on cell proliferation and survival. In the present study, we generated two lines of transgenic mice bearing the preproghrelin gene under the control of chicken β-actin promoter. Transgenic mice overexpressed des-acyl ghrelin in a wide variety of tissues, and plasma des-acyl ghrelin levels reached 10- and 44-fold of those in control mice. They exhibited lower body weights and shorter nose-to-anus lengths, compared with control mice. The serum GH levels tended to be lower, and the serum IGF-I levels were significantly lower in both male and female transgenic mice than control mice. The responses of GH to administered GHRH were normal, whereas those to administered ghrelin were reduced, especially in female transgenic mice, compared with control mice. These data suggest that overexpressed des-acyl ghrelin may modulate the GH-IGF-I axis and result in small phenotype in transgenic mice.

Increased neural activity in transgenic mice with brain IGF-I overexpression

Neuroreport ◽  
1997 ◽  
Vol 8 (13) ◽  
pp. 2907-2911 ◽  
Author(s):  
Gabriel Gutiérrez-Ospina ◽  
Leilani Saum ◽  
Ali Suha Calikoglu ◽  
Sofía Díaz-Cintra ◽  
Fernando A. Barrios ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Neural Activity ◽  
Igf I

Interactions of insulin-like growth factor (IGF)-II and growth hormone in vivo: circulating levels of IGF-I and IGF-binding proteins in transgenic mice

1997 ◽  
pp. 701-708 ◽  
Author(s):  
A Blackburn ◽  
RA Dressendorfer ◽  
WF Blum ◽  
M Erhard ◽  
G Brem ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Transgene Expression ◽  
High Protein Diet ◽  
High Protein ◽  
Protein Diet ◽  
Standard Diet ◽  
Igf I ◽  
Igf Binding ◽  
B Mice

To study interactions between insulin-like growth factor-II (IGF-II) and growth hormone (GH) in vivo, we crossed hemizygous transgenic mice carrying phosphoenolpyruvate carboxykinase (PEPCK)-IGF-II fusion genes with hemizygous PEPCK-bovine GH (bGH) transgenic mice. Offspring harbouring both transgenes (IB), the IGF-II transgene (I) or the bGH transgene (B), and non-transgenic littermates (C) were obtained. Blood samples were taken before (end of week 12) and after (end of week 14) the mice had received a diet high in protein and low in carbohydrates to stimulate PEPCK promoter-controlled transgene expression. Mean serum GH concentrations of both B and IB mice corresponded to 900 ng/ml and increased more than twofold (P < 0.001) after 1 week of the high-protein diet. GH concentrations in controls and I mice were less than 20 ng/ml. Serum IGF-II concentrations in I and IB mice were three-to fourfold higher than those in C and B mice. Whereas IGF-II concentrations were not changed by the high-protein diet in the last two groups, serum IGF-II increased significantly in I (P < 0.001) and IB mice (P < 0.05). This increase was significantly (P < 0.05) less pronounced in IB than in C and I mice. Circulating IGF-I concentrations were about twofold (P < 0.001) higher in B and IB than in C and I mice, and showed a tendency to be lower in I than in C and in IB than in B mice when animals were maintained on the standard diet. The high-protein diet did not change circulating IGF-I concentrations in controls and B mice, but resulted in a significant reduction of serum IGF-I concentrations in I (P < 0.05) and IB mice (P < 0.001). Consequently, after PEPCK-IGF-II transgene expression was stimulated, serum IGF-I concentrations were significantly (P < 0.05) lower in I than in C and in IB than in B mice. Serum IGF-binding protein (IGFBP)-2 concentrations were significantly (P < 0.05) higher in I mice than in all other groups when mice were maintained on the standard diet, with a tendency to reduced IGFBP-2 concentrations in B mice. After the high-protein diet, serum IGFBP-2 concentrations did not change in C and I mice, but increased by two- to threefold in B and IB mice (P < 0.001). Serum IGFBP-3 concentrations tended to be greater in B and IB than in C and I mice, but these differences were mostly not significant. IGFBP-4 concentrations were significantly (P < 0.001) increased by GH overproduction in B and IB mice. Our data suggest that the reduction in circulating IGF-I concentrations by increased IGF-II is most probably due to the limited serum IGF binding capacity and the short half-life of free IGFs, rather than to a reduction in GH-dependent IGF-I production. Effects of GH overproduction on serum IGFBP-2 concentrations depend on dietary factors and may be both inhibitory and stimulatory.

A cross-sectional study of IGF-I determinants in women

2001 ◽  
Vol 10 (5) ◽  
pp. 443-452 ◽  
Author(s):  
A Lukanova ◽  
P Toniolo ◽  
A Akhmedkhanov ◽  
K Hunt ◽  
S Rinaldi ◽  
...  
Keyword(s):  
Cross Sectional Study ◽  
Sectional Study ◽  
Cross Sectional ◽  
Igf I

Abstract 12008: Nos1 Adapter Protein Nos1ap Overexpression Alters Qtc Intervals in Transgenic Mice

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tatjana Williams ◽  
Anahi P Arias-Loza ◽  
Marco Abeßer ◽  
Joachim Schmitt ◽  
Kai Schuh ◽  
...  
Keyword(s):  
Ion Channels ◽  
Sudden Cardiac Death ◽  
Transgenic Mice ◽  
Cardiac Death ◽  
Genetic Alterations ◽  
Luciferase Assay ◽  
Qtc Interval ◽  
Cross Sectional ◽  
Programmed Stimulation ◽  
Increased Susceptibility

Background: Congenital long- or short-QT syndrome may lead to life-threatening ventricular tachycardia and sudden cardiac death. Apart from rare disease-causing mutations in ion channels, common genetic variations in the neuronal nitric oxide synthase (NOS1) regulator NOS1AP, have recently been associated with QT interval variations in a human whole-genome association study. In fact, NOS1AP SNPs have been linked to increases in QTc intervals and sudden cardiac death. We therefore speculate that myocardial NOS1AP overexpression may lead to a decrease of the QTc interval and an increased susceptibility to rhythm disorders. Methods and Results: We generated transgenic mice (TG) with a conditional myocardial NOS1AP overexpression and focused on electrical alterations. Conditional overexpression of NOS1AP resulted in a 147% ventricular increase in TG mice compared to WT littermates. NOS1AP was mainly located at the sarcolemma where it interacted with NOS1 and the L-type Ca2+- channel. HW/BW ratio, ventricular ANP expression, ventricular cross-sectional area and collagen deposition were not altered in NOS1AP mice under baseline conditions. However, NOS1AP overexpressing mice showed a clear decrease of QTc intervals (33 vs. 48 ms). They were more prone to bradycardia (resting heart rate 467 bpm vs. 666 bpm). Atrial programmed stimulation repeatedly caused atrial tachycardia. Ventricular programmed stimulation caused VT in some mice with NOS1AP overexpression. We also investigated the functional effect of the human rs16847548 (T/C). We found that this SNP decreased NOS1AP promoter activity in a viral NOS1AP luciferase assay, suggesting that this SNP downregulates NOS1AP expression in humans. Conclusion: Myocardial overexpression of NOS1AP leads to a significant shortening of the QTc interval with an increased susceptibility to atrial and ventricular rhythm disorders. SNP rs16847548 in NOS1AP resulted in downregulation of NOS1AP expression which provides an explanation for elongation of QTc intervals. In summary, not only a mutation in ion channels itself but also genetic alterations in expression of ion channel modifiers, such as NOS1AP, have an impact on QTc intervals.

scholarly journals The Relationship between Dioxin-Like Polychlorobiphenyls and IGF-I Serum Levels in Healthy Adults: Evidence from a Cross-Sectional Study

PLoS ONE ◽  
2012 ◽  
Vol 7 (5) ◽  
pp. e38213 ◽  
Author(s):  
Octavio P. Luzardo ◽  
Luis Alberto Henríquez-Hernández ◽  
Pilar F. Valerón ◽  
Pedro C. Lara ◽  
Maira Almeida-González ◽  
...  
Keyword(s):  
Serum Levels ◽  
Cross Sectional Study ◽  
Healthy Adults ◽  
Sectional Study ◽  
Cross Sectional ◽  
Igf I ◽  
The Relationship

scholarly journals Obesity, The Single Most Important Risk Factor for OSA: A Case Report

Pulse ◽  
2018 ◽  
Vol 10 (1) ◽  
pp. 38-41
Author(s):  
SMAA Mamun
Keyword(s):  
Magnetic Resonance Imaging ◽  
Magnetic Resonance ◽  
Clinical Symptoms ◽  
Upper Airway ◽  
Resonance Imaging ◽  
Cross Sectional ◽  
Airway Narrowing ◽  
Fat Deposits ◽  
Obstructive Sleep ◽  
Normal Controls

Obstructive sleep apnea (OSA) is characterized by repetitive airflow reduction caused by collapse of the upper airway during sleep in addition to daytime sleepiness, clinical symptoms include fatigue, insomnia, and snoring. The condition is associated with adverse clinical outcomes, including cardiovascular disease, hypertension, cognitive impairment, and metabolic abnormalities.1 Among the risk factors for OSA, obesity is probably the most important. Several studies have consistently found an association between increased body weight and risk of OSA. Tomographic scanned images have shown that obesity causes increased fatty deposits in the pharyngeal area.2 The deposits encroach on the airway and contribute to airway narrowing. Also, among obese patients as compared to normal controls, fat deposits appear to alter the shape of the upper airway without necessarily reducing the cross-sectional area. M. A. Ciscar et al used magnetic resonance imaging to investigate differences between obese and normal controls.2 Ultrafast magnetic resonance imaging was used to study the upper airway and surrounding soft tissue in 17 patients with OSA during wakefulness and sleep, and in eight healthy subjects whilst awake. Coronal sections of awake OSA patients showed elliptical-shaped airways with long axes that were oriented anteroposterior; normal controls had airways that were oriented transversely. Studies using computed tomography have produced similar results.14Pulse Vol.10 January-December 2017 p.38-41

scholarly journals Growth and body weight of free-range reindeer in western Alaska

Rangifer ◽  
2000 ◽  
Vol 20 (2-3) ◽  
pp. 221 ◽  
Author(s):  
Greg L. Finstad ◽  
Alexander K. Prichard
Keyword(s):  
Body Weight ◽  
Growth Rates ◽  
Total Body Weight ◽  
Growth Patterns ◽  
Spatial And Temporal Variation ◽  
Adult Males ◽  
Body Weights ◽  
Total Body ◽  
Reproductive Females ◽  
Average Body

Total body weight of 9749 reindeer calves and 4798 adult reindeer were measured from 1984 to 1999 on the Seward Peninsula, western Alaska, USA. Growth rates of male and female calves, and annual growth patterns of adults were determined. Male calves grew faster than female calves. Reproductive females were lighter than non-reproductive females during summer but there was no effect of reproduction on average body weights the following winter. Adult males age 3-5 were heavier during summer than winter. Castrated males weighed the same as uncastrated males in summer, but were significantly heavier in winter, and did not display the large annual fluctuations in weight typical of reproductive males and females. Growth rates were higher and body weights greater in this herd than many other cir-cumpolar reindeer populations. We suggest these kinds of physiological indices should be used to monitor the possible effects of spatial and temporal variation in population density and to evaluate changes in herding practices.

scholarly journals OCT-Angiography Findings in Patients with Amblyopia: Comparison between Healthy Controls, Treatment-Responsive, and Treatment-Unresponsive Amblyopic Patients

Diagnostics ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1751
Author(s):  
Annabella Salerni ◽  
Gloria Gambini ◽  
Chiara Fedeli ◽  
Ludovica Paris ◽  
Emanuele Crincoli ◽  
...  
Keyword(s):  
Linear Regression Analysis ◽  
Vascular Density ◽  
Ocular Motility ◽  
Ophthalmological Examination ◽  
Light Stimulation ◽  
Cross Sectional ◽  
Vascular Plexus ◽  
The Mean ◽  
Normal Controls ◽  
Expert Physician

There is no consensus on whether amblyopia affects the retinal vascular plexus and morphology. Previous studies focused on the differences between amblyopic patients and normal controls without evaluating amblyopic eyes after patching. To evaluate differences in the superficial vascular density of amblyopic eyes, normal eyes, and amblyopic eyes reaching normal BCVA after patch therapy, OCTA was used. All patients underwent a comprehensive ophthalmological examination, including visual acuity, refraction, ocular motility tests, and anterior and posterior segment examination. OCTA was performed by an expert physician using the Zeiss Cirrus 5000-HD-OCT Angioplex (Carl Zeiss, Meditec, Inc., Dublin, OH, USA). OCTA scans were performed using a 3 × 3 mm2 and 6 × 6 mm2 fovea-centered image setting. The mean outer macular vessel density in the previously amblyopic group was 19.15 ± 0.51%. This was statistically significantly higher than in both the amblyopic group (18.70 ± 1.14%) and the normal controls (18.18 ± 1.40%) (p = 0.014). The previously amblyopic group also significantly differed from both normal controls and amblyopic eyes with regards to the inner (p = 0.011), outer (p = 0.006), and full (p = 0.003) macular perfusion. Finally, linear regression analysis revealed that BCVA was linearly correlated to outer perfusion in amblyopic (p = 0.003) and ex amblyopic eyes (p < 0.001). Considering the cross-sectional nature of our study, from our results, we can only hypothesize a possible correlation between light stimulation and retinal vasculature development. However, further longitudinal studies are needed to support this hypothesis.

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