Electron spin resonance of particulate soot samples from automobiles to help environmental studies.

The application of electron spin resonance (ESR) was studied for diesel soot samples and suspended particulate matter (SPM) from automobile engines. Soot samples or diesel exhaust particles (DEP) were recovered at various points: in the exhaust pipe of a diesel engine, at the dust sampler of a highway tunnel (standard DEP), on the soundproofing wall alongside a heavy traffic road, and on the filters of a dust sampler for SPM. The diesel soot samples apparently showed two ESR spectra: one was a broad spectrum at g=2.1 with a line width of ca. 80-120 mT and the other was a sharp signal of a carbon radical at g=2.003 with a line width of 0.4 mT. Annealing experiments with a DEP sample at 250 degrees C revealed drastic enhancement of the sharp ESR signal, which suggested a thermal process of carbonization of remnant organics. An oximetric study by ESR showed an enhancement of the broad signal in the diesel soot sample as well as in the sharp ESR signal. Therefore, the main part of the broad ESR signal would be attributed to carbon radicals, which form a different configuration, probably closely interacting aggregates. Enhancement of the sharp ESR signal was not observed in the standard DEP sample under vacuum condition, which suggested less adsorption sites on the surface of DEP samples.

[Hemodynamic effects of STA-MCA anastomosis on patients with occlusion of the main cerebral artery].

PURPOSE: We studied cerebral circulation in patients with occlusion of the main cerebral artery and investigated the efficacy of STA-MCA anastomosis. PATIENTS AND METHODS: Thirty-six patients with occlusion of the main cerebral artery were studied. Twenty-three patients had occlusion of the internal carotid artery and 13 had occlusion of the middle cerebral artery. The mean age was 62 years. Cerebral blood flow (CBF) was measured in all patients and cerebrovascular reactivity (CVR) was examined in 11 patients by xenon enhanced CT. Intraoperatively, cortical arterial pressure and anastomotic flow were measured. RESULTS: There was no perioperative mortality or morbidity. There was no ipsilateral stroke recurrence during the follow-up period averaging 35.1 months. Patency of the anastomosis was verified in 91% of the patients by magnetic resonance angiography. Twenty-three (64%) patients showed decreased CBF before the operation and 57% of these patients showed improvement to the normal range after STA-MCA anastomosis. All of the eight patients with decreased CVR showed improvement after the operation. Anastomotic flow correlated significantly with the cortical arterial pressure. CONCLUSION: STA-MCA anastomosis could improve cerebral circulation of patients with low CBF or low CVR due to occlusion of the main cerebral arterial. It was concluded that STA-MCA anastomosis may contribute to the reduction of stroke recurrence, if perioperative complications are reduced.

Successful surgical treatment of a large mixed pial-dural arteriovenous malformation.

A large mixed pial-dural arteriovenous malformation was successfully treated by surgical resection and occlusion of the draining veins. Treatment of this type of malformation is discussed.

Strategy for finding new materials for ESR dosimeters

The right strategy for finding a new ESR dosimetric material sensitive to radiation is to follow the orthodox procedures used in the development of thermoluminescence dosimeters (TLD) and phosphorescence studies. Modern procedures used in materials sciences, such as computer calculation of molecular orbitals (MO), should be employed to estimate the ESR and optical properties of prospective materials. Radiation effects in lithium and magnesium sulfates and metal salts of organic acids, such as lithium and magnesium lactates, have been investigated in search for tissue-equivalent dosimeter with a large G value.

Changes in cerebral blood flow after carotid endarterectomy.

We evaluated changes in cerebral blood flow (CBF) after carotid endarterectomy (CEA) in patients with internal carotid (ICA) stenosis. We studied 46 patients with ICA stenosis who underwent CEA. The mean age of the patients was 63 years, and their mean ICA stenosis was 73%. CBF in the middle cerebral artery territory was measured with xenon-enhanced CT tomography (Xe-CT) before and 3 weeks after CEA. In addition, cerebrovascular reactivity (CVR) was measured after intravenous administration of acetazolamide (ACZ) in 16 patients. There was no significant relationship between the degree of stenosis and CBF. Ten patients had decreased CBF before CEA, and CBF improved in nine of these after CEA. The CVR in 6 of 7 patients with impaired CVR before CEA improved to varying degrees after CEA. The CBF in patients with ICA stenosis varied according to the degree of collateral circulation. In conclusion, CEA can increase CBF and improve CVR in patients with low CBF or low CVR by restoring blood flow through the ICA.

Comparison of transcranial Doppler investigation of aneurysmal vasospasm with digital subtraction angiographic and clinical findings.

OBJECTIVE: Transcranial Doppler (TCD) findings for evaluation of the severity of vasospasm (VSP) in patients with ruptured aneurysmal subarachnoid hemorrhage are controversial. To clarify these TCD findings, intra-arterial digital subtraction angiography was used to simultaneously investigate the angiographic features of cerebral vessels and the cerebral circulation time (CCT). METHODS: Fifty patients with ruptured aneurysms, for whom computed tomographic scans indicated Fisher Grade III subarachnoid hemorrhage, were investigated. Aneurysmal neck clipping was performed in the acute stage. The mean flow velocity (MFV) at the M1 segment was measured using TCD ultrasonography. Intra-arterial digital subtraction angiography was used to simultaneously investigate angiographic features and CCTs on Days 7 to 13. The CCT was defined as the time difference between the two peaks in optical density curves recorded at the carotid artery (C3-C4 portion) and the ascending vein, after contrast material injection. Angiographic VSP was categorized using a modification of the Fisher classification. RESULTS: Angiograms for 9, 25, and 16 patients showed no, slight to moderate, and severe VSP, respectively. The MFVs of the patients with no, slight to moderate, and severe VSP were 70, 115, and 116 cm/s, respectively. No significant difference among the three groups could be observed. The mean CCTs of the patients with no, slight to moderate, and severe VSP were 4.1, 4.6, and 6.5 seconds, respectively. The CCTs of the patients with severe VSP differed significantly from those of the patients with no or slight to moderate VSP. The patients with severe VSP were divided into two groups. One group included eight patients with severe VSP at proximal sites (the internal carotid artery to the M1 segment), and the other included eight patients with severe VSP extending to the M2 segment and more peripheral sites. The mean CCT of the former group (5.3 s) was significantly different from that of the latter (7.5 s), and the MFV of the former group (128 cm/s) was significantly higher than that of the latter (81 cm/s). The clinical outcomes for the latter patients were more serious than those for the former patients. CONCLUSION: This study suggests that the MFV at the M1 segment is inadequate for estimation of the severity of VSP extending to vessels more peripheral than the M1 segment. Furthermore, severe VSP extending to more peripheral sites can produce more serious ischemic insults, compared with that localized to basal vessels. Patients with negative TCD results and clinical features suggesting the development of VSP should undergo quantitative investigation of cerebral circulatory parameters, such as the CCT, using intra-arterial digital subtraction angiography.

Early prepubertal ontogeny of pulsatile gonadotropin-releasing hormone (GnRH) secretion: I. Inhibitory autofeedback control through prolyl endopeptidase degradation of GnRH.

GnRH[1-5], a subproduct resulting from degradation of GnRH by prolyl endopeptidase (PEP) and endopeptidase 24.15 (EP24.15) was known to account for an inhibitory autofeedback of GnRH secretion through an effect at the N-methyl-D-aspartate (NMDA) receptors. This study aimed at determining the possible role of such a mechanism in the early developmental changes in frequency of pulsatile GnRH secretion. Using retrochiasmatic explants from fetal male rats (day 20-21 of gestation), no GnRH pulses could be observed in vitro, whereas pulses occurred at a mean interval of 86 min from the day of birth onwards. This interval decreased steadily until day 25 (39 min), during the period preceding the onset of puberty. Based on GnRH[1-10] or GnRH[1-9] degradation and GnRH[1-5] generation after incubation with hypothalamic extracts, EP24.15 activity did not change with age, whereas PEP activity was maximal at days 5-10 and decreased subsequently until day 50. These changes were consistent with the ontogenetic variations in PEP messenger RNAs (mRNAs) quantitated using RT-PCR. Using fetal explants, the NMDA-evoked release of GnRH was potentiated in a dose-dependent manner by bacitracin, a competitive PEP inhibitor and the desensitization to the NMDA effect was prevented using 2 mM of bacitracin. At day 5, a higher bacitracin concentration of 20 mM was required for a similar effect. Pulsatile GnRH secretion from fetal explants was not caused to occur using bacitracin or Fmoc-Prolyl-Pyrrolidine-2-nitrile (Fmoc-Pro-PyrrCN), a noncompetitive PEP inhibitor. At postnatal days 5 and 15, a significant acceleration of pulsatility was obtained using 1 microM of Fmoc-Pro-PyrrCN or 2 mM of bacitracin. At 25 and 50 days, a lower bacitracin concentration of 20 microM was effective as well in increasing the frequency of GnRH pulsatility. We conclude that the GnRH inhibitory autofeedback resulting from degradation of the peptide is operational in the fetal hypothalamus but does not explain the absence of pulsatile GnRH secretion at that early age. After birth, PEP activity is high and may account for the low frequency of pulsatility. The potency of that effect decreases before the onset of puberty and may contribute to the acceleration of GnRH pulsatility.

Relatively longer hand in patients with Ullrich-Turner syndrome.

We analyzed the total hand length (HL) and length of noncarpal bones (NCL) in 50 Japanese patients with Ullrich-Turner syndrome (UTS) and in 443 other patients with short stature used as controls. In each patient group we calculated relative HL (RHL= HL/height) and relative NCL (RNCL= NCL/height). UTS patients had significantly greater RHL than controls. The greater RHL in UTS patients is mainly due to their longer, short tubular bones. The RHL is not affected by ages and karyotypes of UTS patients or growth hormone treatments given to them. We conclude that relatively longer hands are a common manifestation of UTS and that this parameter is useful for the diagnosis of the syndrome among short females, who usually need chromosome analysis.

Cylindrical or T-shaped silicone rubber stents for microanastomosis--technical note.

The ostium of the recipient artery and the orifice of the donor artery must be clearly visualized for the establishment of microvascular anastomosis. Specially designed colored flexible cylindrical or T-shaped silicone rubber stents were made in various sizes (400 or 500 microns diameter and 5 mm length) and applied to bypass surgery in patients with occlusive cerebrovascular disease such as moyamoya disease and internal carotid artery occlusion. The colored flexible stents facilitated confirmation of the ostium of the artery even in patients with moyamoya disease and allowed precise microvascular anastomosis without problems caused by the stent.

Trauma-induced linear scleroderma.

Linear scleroderma (linear morphea) is a form of localized scleroderma characterized by sclerotic lesions distributed in a linear, band-like pattern. Despite its benign course, the disease can cause severe cosmetic, orthopedic, and psychologic problems. The cause is unknown. Many cases are preceded by a history of trauma. We describe a case in which linear scleroderma occurred following a laceration to the affected site. We review the treatment options and discuss the current theories regarding the pathogenesis of the disease.

Uniparental and functional X disomy in Turner syndrome patients with unexplained mental retardation and X derived marker chromosomes.

We analysed parental origin and X inactivation status of X derived marker (mar(X)) or ring X (r(X)) chromosomes in six Turner syndrome patients. Two of these patients had mental retardation of unknown cause in addition to the usual Turner syndrome phenotype. By FISH analysis, the mar(X)/r(X) chromosomes of all patients retained the X centromere and the XIST locus at Xq13.2. By polymorphic marker analysis, both patients with mental retardation were shown to have uniparental X disomy while the others had both a maternal and paternal contribution of X chromosomes. By RT-PCR analysis and the androgen receptor assay, it was shown that in one of these mentally retarded patients, the XIST on the mar(X) was not transcribed and consequently the mar(X) was not inactivated, leading to functional disomy X. In the other patient, the XIST was transcribed but the r(X) appeared to be active by the androgen receptor assay. Our results suggest that uniparental disomy X may not be uncommon in mentally retarded patients with Turner syndrome. Functional disomy X seems to be the cause of mental retardation in these patients, although the underlying molecular basis could be diverse. In addition, even without unusual dysmorphic features, Turner syndrome patients with unexplained mental retardation need to be investigated for possible mosaicism including these mar(X)/r(X) chromosomes.

Liver transplantation in a case of hypoproteinemia and coagulopathy.

A female infant with hypoproteinemia and coagulopathy associated with hypertyrosinemia was successfully treated with living-related liver transplantation (LRLT). On the 12th day of life plasma amino acid analysis revealed a marked elevation of tyrosine, so the patient was fed on a low-tyrosine and low-phenylalanine diet. However, hepatosplenomegaly, hypotonia, alopecia, eczema and psychomotor delay did not improve and recurrent episodes of disseminated intravascular coagulation (DIC) caused her condition to deteriorate. Liver biopsy on the 230th day revealed marked fatty change accompanied by mild to moderate cholestasis. Therefore, LRLT from her father was performed on the 286th day resulting in improvement of all the aforementioned signs and symptoms. Despite a thorough examination, no diagnosis of a known disorder could be established. However, her elder brother had also been born with severe hypoproteinemia and coagulopathy, and died of DIC on the second day of life. Thus, the disorder is designated as a new entity, namely 'congenital hypoproteinemia and coagulopathy associated with hypertyrosinemia'.

Combination therapy with GH and cyproterone acetate does not improve final height in boys with non-GH-deficient short stature.

BACKGROUND AND OBJECTIVE: Recently, we reported that GH therapy without gonadal suppression (GS) decreased the final height of boys with non-GH-deficient short stature by decreasing the height standard deviation score (SDS) for bone age (BA) during puberty. Combination therapy with GH and GS has been reported to suppress bone maturation and improve final height in some cases. We evaluated the effects of combination therapy with GH and GS using cyproterone acetate on the final height of boys with non-GH-deficient short stature. PATIENTS: Fifty nine boys with non-GH deficient short stature were observed retrospectively until they reached their final height. The boys were divided into 3 groups: Group A consisted of 26 boys who were not treated with GH, group B consisted of 13 boys who were treated with GH alone, and group C consisted of 20 boys who were treated with combination therapy with GH and GS using cyproterone acetate. At the start of observation, the height SDS for BA and projected height were matched among these three groups. RESULTS: The mean +/- SDS of the final height for groups A, B, and C were 162.7 +/- 5.3 cm, 155.4 +/- 4.9 cm, and 161.9 +/- 3.2 cm, respectively. GH therapy did not affect the height SDS for BA during the prepubertal period. GH therapy without GS decreased the height SDS for BA during puberty in group B. Combination therapy with GH and cyproterone acetate increased the height SDS for BA between 12 and 14 years BA in group C. However, after GS therapy was discontinued at 14 years BA, the height SDS for BA gradually decreased and eventually reached the same value as that in group A. CONCLUSIONS: GH therapy during the prepubertal period did not improve the final height of boys with non-GH-deficient short stature. GH therapy without GS decreased pubertal height gain, resulting in reduced final height. Combination therapy with GH and GS using cyproterone acetate decelerated the bone maturation during puberty which might be accelerated by GH therapy, but did not improve the final height which might have been attained without treatment.

Effectiveness of superficial temporal artery-middle cerebral artery anastomosis in adult moyamoya disease: cerebral hemodynamics and clinical course in ischemic and hemorrhagic varieties.

BACKGROUND AND PURPOSE: The efficacy of superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis in adult moyamoya disease was evaluated by clinicopathophysiological studies. METHODS: Fifteen patients with cerebral ischemic attacks (ischemia group) and 15 patients with intracranial hemorrhages (hemorrhage group) were investigated. Clinicoangiographic features and regional cerebral blood flow (rCBF) of the MCA territory were preoperatively and postoperatively investigated, and cortical arterial pressure (CAP) and anastomotic blood flow (AF) were intraoperatively measured. RESULTS: In the ischemia group, the preoperative rCBF of 38.4 mL/100 g per minute was significantly increased to 42.1 mL/100 g per minute with a diminution of angiographic moyamoya vessels in 67% of patients after surgery. The mean CAP and AF were 25.6 mm Hg and 34.7 mL/min, respectively. Proximal and distal cerebral vascular resistance (PCVR = [Mean Systemic Arterial Blood Pressure-Mean CAP]/rCBF and DCVR = [Mean CAP/rCBF]) were 1.78 and 0.68, respectively. One patient died perioperatively as a result of intracerebral hemorrhage. During follow-up (mean, 67 months), 12 of 14 patients recovered without neurological deficits, 1 was moderately disabled because of the initial insult, and another patient experienced an intracerebral hemorrhage but recovered fully. In the hemorrhage group, the preoperative rCBF of 38.0 mL/100 g per minute was significantly increased to 42.7 mL/100 g per minute with a diminution of moyamoya vessels in 60% after surgery. The mean CAP and AF were 29.1 mm Hg and 24.1 mL/min, respectively. PCVR and DCVR were 1.72 and 0.77, respectively. One patient became hemiparetic because of perioperative intracerebral hemorrhage. During follow-up (mean, 94 months), 3 patients had fatal intracranial hemorrhages, 10 had good recoveries, and 2 had moderate disabilities. CONCLUSIONS: This study revealed a high PCVR and a very low DCVR in both the ischemia and hemorrhage groups of patients. STA-MCA anastomosis partially normalized cerebral circulation and decreased moyamoya vessels but did not completely prevent rebleeding.

[Macroscopic and pathohistological investigation of endarterial plaque after intraoperative balloon dilatation of the carotid artery during carotid endarterectomy].

Twelve patients associated with stenosis of the extracranial carotid artery underwent intraluminal balloon dilatation during carotid endarterectomy (CEA). There were 11 men and 1 woman, and age ranged from 56 to 73 years old. The rate of stenosis, shown by angiography, in each patient was from 60 to 85% in width. After securing carotid blood flow by a T-shaped shunt tube, a balloon catheter was inserted from the exposed common carotid artery into the internal carotid artery. The balloon was inflated three or four times with 2.5-3.5 atm. for 30-40 seconds. Immediately after balloon dilatation, endoscopic investigation was performed (Wolf; hard type endoscope, 2.7 mm diameter). Then CEA was performed using the usual procedure. The removed endarterial plaque was investigated pathohistologically. In macroscopic and endoscopic findings, there were 6 patients with mural thrombosis, 4 patients with laceration of the intima, and one patient with outflow of atheroma from the intima. Only 3 patients had increase in lumen after balloon dilatation. In pathohistological appearance, all patients had a moderate degree of fibrosis, calcification, and atheroma in the cross section of the plaque. Ten patients had intramural hemorrhage. Three typical patients were revealed by the use of angiographical, ultrasonographical, endoscopic, and pathohistological presentation. Case 10 showed laceration of the intima by balloon dilatation, and had moderate increase in lumen size macroscopically and endoscopically. There were moderate cases of fibrosis, calcification, atheroma, and intramural hemorrhage. Dilatation of the lumen seemed to be accomplished by a decrease in thickness of the atheroma and intramural hemorrhage. Case 8 demonstrated an increase in lumen size, but also laceration of the intima and outflow of atheroma from the arterial wall. There were much atheroma and large intramural hemorrhage in the intima, which might become a source of enbolism. Case 7 revealed no laceration of the intima and no increase in lumen size. Preoperative ultrasonography showed hyperechoic finding and postoperative pathohistological findings showed severe fibrosis and calcification, which were thought to have interrupted balloon dilatation. There have been small numbers of reports about pathohistological presentation after percutaneous transluminal angioplasty (PTA), because it is very difficult to take a specimen after PTA. In this report we were able to present the necessity of preoperative investigations by angiography, ultrasonography, and 3D-CT.

Duality of glutamatergic and GABAergic control of pulsatile GnRH secretion by rat hypothalamic explants: I. Effects of antisense oligodeoxynucleotides using explants including or excluding the preoptic area.

Using antisense oligodeoxynucleotides we aimed to study the role of N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid (GABA) receptors in the mechanism of Gonadotrophin-releasing hormone (GnRH) secretion in vitro. Since GnRH cell bodies are located in the rat preoptic hypothalamus while most GnRH terminals are in the retrochiasmatic hypothalamus, we compared the effects of oligodeoxynucleotides on explants of the whole (preoptic area included) or retrochiasmatic hypothalamus. When GnRH secretion is evoked by muscimol and NMDA, a time-related reduction of GnRH secretion is caused by antisense oligodeoxynucleotides for the beta subunit of the GABAA receptor and the NR2A subunit of the NMDA receptor, respectively. After 6-7 h, binding studies of tritiated ligands show a decrease in GABA- and NMDA-receptor expression. While these antisense effects are observed using whole explants, no such effects are seen using retrochiasmatic explants, indicating that the facilitatory GABAA and NMDA receptors are encoded in the preoptic area. Using several missense oligodeoxynucleotides or antisense for the NR2B and NR2C subunits of the NMDA receptor, the muscimol- and NMDA-evoked release of GnRH is not affected. When spontaneous pulsatile GnRH secretion is studied, the NR2A antisense oligodeoxynucleotides cause an increase of the interpulse interval. This increase is seen using whole but not retrochiasmatic explants. In contrast, the GABAA and NR2C antisense oligodeoxynucleotides result in a reduction of GnRH interpulse interval. Such a reduction is seen using whole as well as retrochiasmatic explants, indicating that the GABAA and NMDA receptors which mediate inhibition of GnRH pulsatility are encoded in the retrochiasmatic hypothalamus. We conclude that NMDA receptors (NR2A subunit) encoded in the preoptic hypothalamus mediate a facilitatory effect on GnRH pulsatility while GABAA and NMDA (NR2C subunit) receptors encoded in the retrochiasmatic hypothalamus mediate an inhibition of GnRH pulsatility. Pulsatile GnRH secretion is affected differently than the agonist-evoked release of GnRH suggesting that the GnRH secretory neurons and the GnRH pulse generator consist of different cellular entities.

Duality of glutamatergic and GABAergic control of pulsatile GnRH secretion by rat hypothalamic explants: II. Reduced NR2C- and GABAA-receptor-mediated inhibition at initiation of sexual maturation.

N-methyl-D-aspartate (NMDA) receptors and gamma-aminobutyric acid (GABA) receptors are involved in the mechanism of pulsatile gonadotrophin-releasing hormone (GnRH) secretion. The aim of this study was to elucidate the role of those receptors in the acceleration of pulsatile GnRH secretion seen at onset of puberty. Using hypothalamic explants from prepubertal (15 days), early pubertal (25 days) and adult (50 days) male rats, we studied the effects of pharmacological antagonists and antisense oligodeoxynucleotides on GnRH release evoked by NMDA and GABA receptor agonists as well as the interval between spontaneous GnRH secretory pulses. At the three studied ages, the muscimol-evoked release of GnRh is similarly inhibited by the GABAA receptor antagonist bicuculline. In contrast, the frequency of pulsatility is stimulated by bicuculline as indicated by a reduction of the mean GnRh interpulse interval from 60 to 40 min and such an effect is seen at 15 days only. The GnRH interpulse interval is also reduced by GABAA receptor antisense oligodeoxynucleotides at 15 days while no effects are seen at 25 days. At the three studied ages, the NMDA-evoked release of GnRH and the GnRh interpulse interval are similarly inhibited by 100 or 500 microM of the NMDA receptor antagonist 7-chlorokynurenic acid (7CK). These effects are consistent with the increase of GnRH interpulse interval caused by NR2A antisense oligodeoxynucleotides at 15 days (86 vs 64 min in controls) as well as 25 days (44 vs 36 min). A low (5 microM) concentration of 7CK does not result in any effect except a reduction of GnRH interpulse interval which is seen at 15 days only. A similar reduction of GnRh interpulse interval is obtained using NR2C antisense oligodeoxynucleotides at 15 days (50 vs 64 min in controls) while no effects are seen at 25 days (35 vs 36 min). At 25 days, muscimol can prevent the developmental increase in frequency of pulsatile GnRH secretion. In summary, pulsatile GnRH secretion by the prepubertal hypothalamus characteristically involves an inhibition mediated through GABAA receptors and the NR2C subunit of NMDA receptors. Based on these data, we propose a model for the mechanism of the onset of puberty which involves the disappearance or inactivation of GABAergic neurons located in the retrochiasmatic hypothalamus and expressing the NR2C subtype of NMDA receptors.

Unfavorable effects of growth hormone therapy on the final height of boys with short stature not caused by growth hormone deficiency.

A group of 18 boys with non-growth hormone (GH)-deficient short stature without GH therapy (group A) and another group of 9 boys with non-GH-deficient short stature with GH therapy in doses of 0.5 IU (0.17 mg)/kg per week administered 5 to 6 times weekly (group B) were observed until they reached their final height. The mean duration of GH therapy was 4.2 years (range 3.2 to 5.0 years). These two groups were matched with respect to their standard deviation score (SDS) for bone age at the start of observation. Mean +/- SD of the final height for group A and group B was 162.0 +/- 5.4 cm and 154.2 +/- 4.2 cm, respectively. During the prepubertal period, height SDS for bone age of these two groups was not affected by GH therapy. During the pubertal period, however, height SDS for bone age remained constant for group A but decreased gradually for group B. Our observation indicates that for boys with non-GH-deficient short stature GH therapy does not improve height SDS for bone age during the prepubertal period, and in fact reduces it during the pubertal period, possibly resulting in a shorter final height than might have been attained naturally.