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Biomedical subjects

Y Segev

Publications and source records attributed to Y Segev.

At least 37 records · Page 2Linked to original sources
PubMed2000

Increasing chronic subdural hematoma after endoscopic III ventriculostomy.

OBJECT: Endoscopic III ventriculostomy (ETV) is an effective and a rather safe treatment for noncommunicating hydrocephalus secondary to aqueductal stenosis and other obstructive pathologies. Though not devoid of risk, ETV is increasingly replacing shunt operations, and it prevents related complications, including overdrainage. METHODS: We report a rare case of a large chronic subdural hematoma (ChSDH) after ETV in a patient with aqueductal stenosis. Three weeks after he was shunted elsewhere, he presented to us with clinical symptoms of intracranial hypotension and overdrainage. ETV was performed and the shunt removed uneventfully. On routine postoperative MRI a few weeks later, a large ChSDH was noted, the patient being totally asymptomatic. Since the ChSDH grew significantly, causing a mass effect on the follow-up MRI, it was finally drained. Large and increasing ChSDHs have previously been reported secondary to overdrainage after shunt placement, but not after ETV. CONCLUSIONS: We conclude that though rare, a ChSDH may evolve even after ETV, if there is a substantial decrease in previously elevated intracranial pressure.

Adult↗
PubMed2000

Changes in the growth hormone-IGF-I axis in non-obese diabetic mice.

We investigated the changes in GH-IGF-I axis in non-obese diabetic (NOD)-mice, a model of insulin-dependent diabetes mellitus. Diabetic female NOD mice and their age- and sex-matched controls were sacrificed at 4, 14, 21 and 30 days (30d DM) after the onset of glycosuria. Serum GH levels increased and serum IGF-I levels decreased in the 30d DM group (182 +/- 32% and 45 +/- 24% of age-matched controls respectively, p < 0.05). Another group (30d DM + I) was given SC insulin, and its serum IGF-I levels remained decreased. Liver GH receptor (GHR) and GH binding protein (GHBP) mRNA levels, as well as liver membrane GH binding assays were deeply decreased in the 30d DM group in comparison to controls. GHR message and binding capacity remained decreased in the 30d DM + I group. Renal GHR mRNA was decreased at 21d DM but not at 14d DM, whereas GHBP mRNA remained unchanged throughout the experiment. In conclusion, increased serum GH levels are documented in NOD diabetic mice, similarly to the changes described in humans. The decrease in GHR levels and decreased serum IGF-I in spite of increased circulating GH suggest a state of GH resistance.

Aging↗
PubMed1999

The effect of adenotonsillectomy on serum insulin-like growth factor-I and growth in children with obstructive sleep apnea syndrome.

OBJECTIVE: Obstructive sleep apnea syndrome (OSAS) in children is frequently associated with growth interruption. The objective of this study was to evaluate the effect of OSAS and adenotonsillectomy on the insulin-like growth factor-I (IGF-I) axis in children. STUDY DESIGN: Thirteen prepubertal children (mean age, 6.0 +/- 2.8 years) were studied before and after adenotonsillectomy (T&A). Weight, height, overnight polysomnography, and IGF-I and IGF-binding protein-3 levels were evaluated before and 3 to 12 months after T&A. The children's weights and heights were monitored for 18 months. RESULTS: The respiratory disturbance index improved from 7.8 +/- 9.1 events/h to 1.0 +/- 2.1 events/h after T&A (P <.02). Slow-wave sleep increased from 29.1% +/- 7.2% to 34.6% +/- 9.8% after T&A (P <.02). The weight standard deviation score increased from 0.86 +/- 1 to 1. 24 +/- 0.9, 18 months after T&A (P <.01). Serum IGF-I levels increased from 146.3 +/- 76.2 ng/mL before T&A to 210.3 +/- 112.5 ng/mL after surgery (P <.01), but IGF-binding protein-3 levels did not change significantly. CONCLUSION: The respiratory improvement after T&A in children with OSAS is associated with a significant increase in serum IGF-I levels and weight. We conclude that the IGF-I axis is affected in children with OSAS.

Adenoidectomy↗
PubMed1999

Zinc supplementation increases the level of serum insulin-like growth factor-I but does not promote growth in infants with nonorganic failure to thrive.

We investigated in a randomized double-blind placebo-controlled study the effects of zinc supplementation (2 mg/kg/day) for 12 weeks on growth, serum insulin-like growth factor-I (IGF-I) and insulin-like factor binding protein-3 (IGFBP-3) on 3- to 9-month-old infants with nonorganic failure to thrive (NOFTT). 25 infants completed the study, 14 received zinc supplementation (group A), and 11 received placebo (group B). The control group for baseline measurements was composed of 10 age-matched normal growing infants. There were no significant changes in weight for age, length for age, or weight for length during the entire study period in either group A or B. Serum IGF-I levels at baseline were similar in all the groups. After 12 weeks of therapy, serum IFG-I levels increased significantly only in the zinc-supplemented group, from 40.3 +/- 7 ng/ml at baseline to 65 +/- 8 ng/ml (p < 0.05). There was a marked difference in serum IGF-I levels between the zinc-supplemented group and the placebo group after 12 weeks: 65 +/- 8 vs. 49.4 +/- 5 ng/ml (p = 0.058, 95% CI of difference 9.88-21.31). No change was demonstrated in serum IGFBP-3 levels in either study group. We conclude that although zinc supplementation increased serum IGF-I levels, it did not improve the growth parameters of infants with NOFTT.

Dietary Supplements↗
PubMed1999

Testosterone stimulates insulin-like growth factor-I and insulin-like growth factor-I-receptor gene expression in the mandibular condyle--a model of endochondral ossification.

Puberty is associated with an increase in the plasma concentration of sex steroids, GH, and insulin-like growth factor-I (IGF-I). Gonadal steroid hormones are important for the normal pubertal growth spurt and skeletal growth. The mechanism by which gonadal steroids induce skeletal growth is still not fully understood. To better understand the direct effect sex steroids have on bone growth, we studied an isolated organ culture system of the mandibular condyle, derived from 3.5-5.5-week-old male and female mice. We found that testosterone 10(-6) M, but not estradiol, stimulated thymidine incorporation into the DNA of male-derived condyle. Three days of testosterone treatment doubled the condyle size and increased the chondroprogenitor zone, while maintaining the normal gradient of the developing chondrocytes. Immunohistochemistry and in situ hybridization techniques showed that testosterone stimulated IGF-I and IGF-I-R and their messenger RNAs (mRNAs) mainly in the mature chondrocyte layer. Immunoneutralization of IGF-I in the testosterone-treated condyle caused the disappearance of the chondroblast and young chondrocyte layers, though the progenitor cell layer remained almost unaffected. Overtreatment with testosterone (dose or duration) accelerated condylar ossification. In the presence of testosterone 10(-5) M (high dose), calcification "climbs" up to the chondroprogenitor zone, and most of the condylar chondrocytes are replaced by bone tissue. Similar changes occurred after 7 days of testosterone treatment (long duration) with 10(-6) M. In conclusion, testosterone stimulates growth and local production of IGF-I and IGF-I-R in chondrocyte cell layers of an isolated organ culture of mice mandibular condyle. Part of the effect testosterone has on condylar growth is mediated by IGF-I.

Animals↗
PubMed1999

Growth hormone receptor antagonism prevents early renal changes in nonobese diabetic mice.

The growth hormone (GH)/insulin-like growth factor (IGF) axis is involved in diabetic renal disease. The role of a specific GH receptor (GHR) antagonist in the development of early renal changes in nonobese diabetic (NOD) mice was investigated. Female diabetic (nonketotic) NOD mice treated with a polyethylene glycol-treated GHR antagonist (2 mg/kg, every other day) (DA group) or saline (D group) and their nonhyperglycemic age-matched littermates (control animals) were euthanized 3 wk after the onset of diabetes. Body weights at euthanasia were similar among the groups. Serum GH levels were markedly elevated, and serum IGF-I levels were significantly decreased in D and DA animals, compared with controls. The increases in kidney weights and glomerular volumes observed for the D group were absent in the DA group. Albuminuria was increased in the D group but was normalized in the DA group. Extractable renal IGF-I protein levels were increased in the D group but were partially normalized in the DA group. Renal IGF-binding protein 1 mRNA levels were increased in the D group but returned to almost normal levels in the DA animals. Kidney IGF-I and GHR mRNA levels were decreased in both the D and DA groups. Renal GH-binding protein mRNA levels remained unchanged in both diabetic groups. GHR antagonism had a blunting effect on renal/glomerular hypertrophy and albuminuria in diabetic NOD mice. These salutary effects were associated with concomitant inhibition of increased renal IGF-I protein levels and were obtained without affecting either somatic growth or circulating GH and IGF-I levels. Therefore, modulation of GH effects may have beneficial therapeutic implications in diabetic nephropathy.

Animals↗
PubMed1998

Serum insulin-like growth factors I and II are not affected by undernutrition in children with nonorganic failure to thrive.

The aim of our study was to determine the serum levels of IGF-I, IGF-II, and their binding proteins IGFBP-1 and IGFBP-3 in young children 3 months to 2 years of age with nonorganic failure to thrive (NOFTT). 29 children with NOFTT and 32 normal controls were recruited and studied for auxologic and hormonal parameters. The NOFTT group had significantly higher serum concentrations of IGFBP-1 than the control group: 57.7+/-18 vs. 48+/-19 microg/l (p < 0.05). IGF-I and IGF-II serum levels were highly correlated to serum IGFBP-3 but there were no differences in the serum IGF-I, IGF-II and IGFBP-3 levels between the groups. We conclude that IGF-I, IGF-II, and IGFBP-3 are not useful for the evaluation of nutritional status in children, under the age of 2 years, with NOFTT.

Child, Preschool↗
PubMed1998

Normal melatonin levels in patients with fibromyalgia syndrome.

OBJECTIVE: To assess urine levels of melatonin measured by 6-sulphatoxymelatonin (aMT6s) in patients with fibromyalgia (FM). METHODS: Nocturnal aMT6s urine levels were measured by ELISA, in a sample of urine collected from 10 PM to 7 AM from 39 female patients with FM and 39 age matched healthy female controls. All subjects were interviewed and assessed for nonarticular tenderness, FM symptoms, quality of life, and physical functioning. RESULTS: Nocturnal aMT6s levels of patients with FM were not statistically different from those of controls: 16.7+/-9.2 vs 16.0+/-11.3 microg, respectively. No association was observed between aMT6s levels of patients with FM and disease duration, reproductive status, sleep and mood disturbances. CONCLUSION: Nocturnal urine aMT6s levels were similar in patients with FM and controls. Studies are needed to elucidate the possible role of melatonin in FM and should include larger samples of newly diagnosed untreated patients with FM.

Adult↗
PubMed1997

Renal hypertrophy in hyperglycemic non-obese diabetic mice is associated with persistent renal accumulation of insulin-like growth factor I.

The non-obese diabetic mouse is a model of spontaneous insulin-dependent diabetes as a result of autoimmune destruction of pancreatic beta cells, similar to the disease seen in human Type I diabetes. This mouse strain develops glomerular lesions reminiscent of those seen in human disease. The study presented here investigated the changes in renal insulin-like growth factor (IGF) system in hyperglycemic non-obese diabetic mice. Female non-obese diabetic mice and their age- and sex-matched controls were euthanized 4 days, 2 wk, and 4 wk after the onset of glycosuria. Kidney weight increased in diabetic mice, beginning at 2 wk after the onset of glycosuria. This renal hypertrophy was associated with an increase in renal extractable IGF-I protein. However, a decrease in IGF-I mRNA was observed at the same time. Serum IGF-I levels remained stable after 2 wk of diabetes and decreased at 1 month. No change was detected in renal IGF-I receptor mRNA levels. Renal cortical IGF binding protein (IGFBP)-1 mRNA levels were increased. Ligand blot analysis revealed a significant increase in serum and renal 30-kd IGFBP and a decrease in serum and kidney IGFBP-3 and IGFBP-4 at 30 days of diabetes. Insulin therapy prevented the increases in kidney weight, renal IGF-I, and 30-kd IGFBP, but did not reverse the decreased serum IGF-I levels observed at 1 month of diabetes. In summary, renal hypertrophy in non-obese diabetic mice is associated with a persistent accumulation of renal IGF-I and, IGFBP-1. These changes were partially reversed with insulin therapy, which did not correct the hyperglycemia, suggesting an important role for insulin deficiency in mediating these changes in the IGF system. These findings suggest that the IGF system may play a potential role in the development of diabetic nephropathy.

Animals↗
PubMed1995

Tyrosine phosphorylation of measles virus nucleocapsid protein in persistently infected neuroblastoma cells.

Subacute sclerosing panencephalitis is a slowly progressing fatal human disease of the central nervous system which is a delayed sequel of measles virus (MV) infection. A typical pathological feature of this disease is the presence of viral ribonucleocapsid structures in the form of inclusion bodies and the absence of infectious virus or budding viral particles. The mechanisms governing the establishment and maintenance of a persistent MV infection in brain cells are still largely unknown. To understand the mechanisms underlying MV persistence in neuronal cells, a tissue culture model was studied. Clone NS20Y/MS of the murine neuroblastoma C1300 persistently infected with the wild-type Edmonston strain of MV secretes relatively high levels of alpha/beta interferon (IFN). As shown previously, treatment of the persistently infected cultures with anti-IFN serum converted the persistent state into a productive infection indicated by the appearance of multinucleated giant cells. In this study, we have investigated whether alpha/beta IFN produced by NS20Y/MS cells activates cellular protein tyrosine kinases which will induce tyrosine phosphorylating activity specific to virus-infected cells. We present data to show augmented protein tyrosine kinase activity in the persistently infected cells. We demonstrate that the MV N protein is phosphorylated on tyrosine in addition to serine and threonine in the persistent state but not in NS20Y cells acutely infected with MV.

2',5'-Oligoadenylate Synthetase↗
PubMed1995

Modulation of insulin-like growth factor I (IGF-I) receptors and membrane-associated IGF-binding proteins in endometrial cancer cells by estradiol.

Insulin-like growth factor I (IGF-I) receptors and membrane-associated IGF-binding proteins (IGFBPs) were examined in Ishikawa endometrial cancer cells. Our findings suggest that about 95% of [125I]IGF-I is bound to membrane-associated IGFBPs rather than to IGF-I receptors. Specifically, [125I]IGF-I binding to cell membranes could be completely displaced by cold IGF-I or IGF-II, but not by insulin, suggesting that binding was primarily due to IGFBPs. This was confirmed by using [125I]des-(1-3)IGF-I as the ligand. Des-(1-3) IGF-I binds with high affinity to IGF-I receptors, but with markedly lower affinity to IGFBPs. [125I]Des-(1-3)IGF-I bound to Ishikawa cells was displaced by IGF-I, IGF-II, and insulin. These results suggest that measuring IGF-I receptor levels using labeled IGF-I may be misleading. Accordingly, we evaluated the differential binding of [125I]IGF-I and [125I]des-(1-3)IGF-I to study the involvement of the IGF system in the stimulation of Ishikawa cell growth by estradiol. IGF-I stimulates Ishikawa cell proliferation, but at low concentrations, and this stimulation is largely dependent on the presence of estradiol. Estradiol caused a 2.5-fold increase in IGF-I receptor levels. Moreover, estradiol reduced soluble IGFBP levels, presumably increasing the availability of IGFs for their receptors. This elevation in IGF-I receptor levels and the decrease in IGFBP levels were accompanied by a 3.5-fold increase in IGF-I receptor messenger RNA and a 2.5-fold decrease in IGFBP messenger RNAs. These experiments suggest that estradiol sensitizes endometrial cancer cells to the effects of IGFs by simultaneously elevating receptor levels and decreasing (potentially inhibitory) IGFBP levels.

Binding, Competitive↗
PubMed1995

CT appearance of a traumatic cataract.

We describe a case of a traumatic cataract that presented on CT as a hypodense lens with a hyderdense rim. The finding reflects the pathogenesis of this entity: a capsular tear and consequent entry of fluid into the lens.

Cataract↗
PubMed1994

Reversal of the measles virus-mediated increase of phosphorylating activity in persistently infected mouse neuroblastoma cells by anti-measles virus antibodies.

To investigate the effect of persistent measles virus infection on signal transduction in cells of neuronal origin, the mouse neuroblastoma cell line NS20Y/MS, which is persistently infected with measles virus, was used. The results demonstrate an approximate 50% increase in total phosphorylation and a similar increase in protein kinase C (PKC) activity. Western blot analysis with anti-total PKC or anti-PKC-alpha antibodies revealed a significant increase in the level of an 80K immunoreactive PKC in NS20Y/MS cells. Following incubation of NS20Y/MS cells with polyclonal anti-measles virus antibodies, which down-regulate the level of measles virus proteins, total and PKC-mediated phosphorylation returned to the basal level of uninfected cells. This effect was reversible and removal of the antibodies resulted in restoration of the high level of total and PKC-mediated phosphorylation. The release of infectious measles virus was strongly inhibited by incubation of NS20Y/MS cells with the PKC inhibitor, 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7). These results demonstrate that measles virus induces elevation in cellular phosphorylation which is essential for measles virus production.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗