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Biomedical subjects

Ze'ev Hochberg

Publications and source records attributed to Ze'ev Hochberg.

At least 19 recordsLinked to original sources
PubMed2007

Nocturnal calcium, phosphorus and parathyroid hormone in the diagnosis of concealed and subclinical hypoparathyroidism.

CONTEXT: Circadian rhythms of plasma parathyroid hormone (PTH) show peak values at night, whereas serum calcium levels peak in the evening and display a nadir at night. HYPOTHESES: Subclinical hypoparathyroidism (HPT) can be detected by utilizing the knowledge of diurnal variations. Thalassemia major (TM) may provide a model system of subclinical HPT. DESIGN: Nocturnal plasma PTH and serum calcium values were determined in 13 TM patients with normal morning serum calcium levels as compared with the corresponding values in eight healthy control subjects. RESULTS: Six patients with TM presented a nadir serum calcium level of 8.3 mg/dl or lower (hypoCa TM) at 0200 h, whereas the remaining seven showed nadir levels of 8.4 mg/dl or higher (normoCa TM). Patients with hypoCa TM displayed a drop between peak and nadir of 1.2 +/- 0.5 mg/dl as compared with a considerably smaller fall of 0.3 +/- 0.7 mg/dl in control subjects (P < 0.05). NormoCa TM patients experienced comparable nocturnal variation to that of control subjects. Patients from both the hypoCa and normoCa TM groups presented significantly lower nocturnal PTH levels than those of control subjects and lost the nocturnal PTH variation characteristic of healthy subjects. A plot of all serum calcium against plasma PTH levels provides a clear distinction of the three groups. CONCLUSIONS: All 13 daytime normocalcemic TM patients presented a certain degree of HPT. The hypoCa TM group displayed a concealed HPT detected in all, except the morning sampling, whereas normoCa TM patients experienced sub clinical HPT observed in the absence of nocturnal HPT variation. Nocturnal measurements of serum minerals thus enhance the sensitivity of HPT diagnosis.

Adolescent↗
PubMed2006

Clinical significance of the parental origin of the X chromosome in turner syndrome.

CONTEXT: The phenotype in Turner syndrome (TS) is variable, even in patients with a supposedly nonmosaic karyotype. Previous work suggested that there were X-linked parent-of-origin effects on the phenotype. HYPOTHESIS: The TS phenotype is influenced by the parental origin of the missed X chromosome. DESIGN: This was a multicenter prospective study of TS patients and both their parents, determining parental origin of the X-chromosome, and characterizing the clinical phenotype. PATIENTS AND METHODS: Eighty-three TS patients and their parents were studied. Inclusion criteria were TS with karyotype 45,X or 46Xi(Xq). Four highly polymorphic microsatellite markers on the X-chromosome DMD49, DYSII, DXS1283, and the androgen receptor gene and three Y chromosome markers, SRY, DYZ1, and DYZ3. OUTCOME MEASURES: The study determined the correlation between the parental origin of the X chromosome and the unique phenotypic traits of TS including congenital malformations, anthropometry and growth pattern, skeletal defects, endocrine traits, education, and vocation. RESULTS: Eighty-three percent of 45,X retained their maternal X (X(m)), whereas 64% 46Xi(Xq) retained their paternal X (X(p), P < 0.001). Kidney malformations were exclusively found in X(m) patients (P = 0.030). The X(m) group had lower total and low-density lipoprotein cholesterol (P < 0.003), and higher body mass index sd score (P = 0.030) that was not maintained after GH treatment. Response to GH therapy was comparable. Ocular abnormalities were more common in the paternal X group (P = 0.017), who also had higher academic achievement. CONCLUSIONS: The parental origin of the missing short arm of the X chromosome has an impact on overweight, kidney, eye, and lipids, which suggests a potential effect of an as-yet-undetermined X chromosome gene imprinting.

Adolescent↗
PubMed2006

Parturition itself is the basis for fetal adrenal involution.

CONTEXT: Newborn infants show a postnatal decline in androgen levels as the fetal adrenal glands involute. HYPOTHESIS: Placental factors up-regulate dehydroepiandrosterone sulfate (DHEA-S) generation. Hence, regardless of age, parturition will result in fetal adrenal involution and decline in DHEA-S levels. SUBJECTS AND METHODS: Premature neonates (n = 30) with gestational age 26-35 wk were studied. Adrenal volume by ultrasonography and serum DHEA-S, cortisol, and androstendione levels were followed weekly between d 1 and 28 of life. RESULTS: Serum DHEA-S was high on d 1 of life, declining rapidly regardless of gestational age during the first week of life (P < 0.001), and serum androstenedione and cortisol levels followed a similar pattern. Androstenedione levels showed a rise as of d 21 of life in boys but not in girls. The adrenals decreased in ultrasonographic volume from d 1 to 14 of life (P < 0.001), regardless of gestational age. CONCLUSIONS: Involution of the adrenal is faster than previously reported and, regardless of gestational age, occurs within the first week of life in terms of hormone secretion and within 2 wk in adrenal size. Involution involves a decline in DHEA-S but also in androstenedione and cortisol secretion, with a change in enzymatic activity. Males and females differ in their androstenedione levels and enzymatic activity. Parturition itself is the basis for fetal adrenal involution, supporting a key role for placental factors in maintaining the fetal adrenal and generating adrenal androgens.

Adrenal Glands↗
PubMed2006

Physiological and catecholamine response to sympathetic stimulation in turner syndrome.

OBJECTIVE: Women with Turner syndrome have increased heart rate and high blood pressure (BP), and have been described as having high tolerance for emotional stress. We hypothesized that women with Turner syndrome have reduced catecholaminergic and physiological response to sympathetic stimulation, and that changes in BP and heart rate are related to their catecholamine response to sympathetic stimulation. DESIGN AND PATIENTS: Ten young women with Turner syndrome, age 17-34 years were the subjects of this study. Their response to sympathetic stimulation was compared to a group of 10 age-matched healthy women. MEASUREMENTS: After a period of 30 min resting, subjects and controls were subjected to an escalating series of sympathetic stimulation: orthostatic, cold pressor and exercise, and their plasma catecholamines and haemodynamic response were monitored and compared to resting levels. RESULTS: Resting heart rate was higher in Turner syndrome patients at 83 +/- 9 beats per min (bpm, mean +/- SD), as compared to controls (74 +/- 10 bpm, P < 0.05). Their supine BP was also higher at 122 +/- 9/84 +/- 6 vs. 106 +/- 11/70 +/- 9 mmHg (P < 0.02/< 0.02). The corresponding resting norepinephrine, but not epinephrine, was higher in Turner syndrome patients (2.54 +/- 1.09 nmol/l) as compared to controls (1.69 +/- 0.55 nmol/l, P < 0.02). In response to orthostatic stimulation and cold pressor test the systolic, but not the diastolic BP or heart rate, increased in Turner syndrome patients but not in the control group (P < 0.01). The change in blood catecholamine levels was comparable in both groups. Their physiological response to exercise was normal. Yet, the exercise-induced surge of norepinephrine and epinephrine in Turner syndrome patients was lower (P < 0.02). CONCLUSIONS: Turner syndrome is associated with dysregulation of the sympathetic nervous system (SNS), leading to tachycardia and high BP, increased resting norepinephrine levels, and a greater tolerance of the cathecholamine response to exercise.

Adolescent↗
PubMed2005

Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3.

Hypophosphatemia due to isolated renal phosphate wasting results from a heterogeneous group of disorders. Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is an autosomal recessive form that is characterized by reduced renal phosphate reabsorption, hypophosphatemia, and rickets. It can be distinguished from other forms of hypophosphatemia by increased serum levels of 1,25-dihydroxyvitamin D resulting in hypercalciuria. Using SNP array genotyping, we mapped the disease locus in two consanguineous families to the end of the long arm of chromosome 9. The candidate region contained a sodium-phosphate cotransporter gene, SLC34A3, which has been shown to be expressed in proximal tubulus cells. Sequencing of this gene revealed disease-associated mutations in five families, including two frameshift and one splice-site mutation. Loss of function of the SLC34A3 protein presumably results in a primary renal tubular defect and is compatible with the HHRH phenotype. We also show that the phosphaturic factor FGF23 (fibroblast growth factor 23), which is increased in X-linked hypophosphatemic rickets and carries activating mutations in autosomal dominant hypophosphatemic rickets, is at normal or low-normal serum levels in the patients with HHRH, further supporting a primary renal defect. Identification of the gene mutated in a further form of hypophosphatemia adds to the understanding of phosphate homeostasis and may help to elucidate the interaction of the proteins involved in this pathway.

Animals↗
PubMed2005

Mutations in CYP11B1 and congenital adrenal hyperplasia in Moroccan Jews.

CONTEXT: In Jews of Moroccan descent (MJ), the prevalence of steroid 11beta-hydroxylase deficiency (11-OHD) is relatively high, with a carrier rate estimated as approximately one in 40. A single mutation in the CYP11B1 gene (encoding 11beta-hydroxylase), R448H, was suggested to account for the disease alleles in this population. STUDY SUBJECTS: We screened 236 healthy MJ for R448H. RESULTS: Only two of the subjects screened were found to be carriers, suggesting that the R448H allele frequency is lower than was assumed previously. An R448H/R448C compound heterozygote patient, diagnosed with 11-OHD, was identified. However, a subsequent screen of MJ subjects for R448C failed to detect any carriers, suggesting that this was a private mutation of this family. CONCLUSION: The high incidence of 11-OHD in MJ, therefore, is only partially explained by the presence of R448H as a founder mutation.

Adrenal Hyperplasia, Congenital↗
PubMed2005

The human glucocorticoid receptor (GR) isoform {beta} differentially suppresses GR{alpha}-induced transactivation stimulated by synthetic glucocorticoids.

The beta-isoform of human glucocorticoid receptor beta (hGRbeta) acts as a natural dominant negative inhibitor of hGRalpha-induced transactivation of glucocorticoid-responsive genes. We determined hGRbeta ability to suppress hGRalpha transactivation that was induced by commonly used synthetic glucocorticoids. HepG2/C3A cells were transiently cotransfected with GR cDNA and a glucocorticoid-responsive promoter, luciferase (MMTV-luc). Transfected cells were incubated for 16 h with glucocorticoid and luciferase. For each compound, a dose-response curve was constructed, and half-maximal effective concentrations and maximal transcriptional activities were compared. hGRbeta, at a 1:1 ratio to hGRalpha, differentially suppressed hGRalpha-induced maximal transcriptional activity stimulated by triamcinolone, dexamethasone, hydrocortisone, and betamethasone (by 96, 68, 62, and 49%, respectively) but not by methylprednisolone. The suppressive effect of hGRbeta on hGRalpha-induced transactivation was stronger at lower concentrations of all tested glucocorticoids, whereas it was blunted at higher concentrations. We conclude that the potency of the dominant negative effect of hGRbeta on hGRalpha-induced transactivation depends on both the type and the dose of the synthetic glucocorticoids in use. These results may provide helpful information concerning the selection of synthetic glucocorticoids for treatment of pathological conditions in which hGRbeta modulates the sensitivity of tissues to glucocorticoids.

Carcinoma, Hepatocellular↗
PubMed2004

A novel C-terminal growth hormone receptor (GHR) mutation results in impaired GHR-STAT5 but normal STAT-3 signaling.

GH insensitivity (GHI) is an autosomal recessive disorder caused by defects in the GH receptor (GHR). In a 17-yr-old female with severe short stature and biochemical features of GHI, sequencing of GHR gene revealed a compound heterozygosity for two novel mutations: C83X and a G deletion at position 1776 (1776del). 1776del is predicted to result in GHR truncation to 581 amino acids with a nonsense sequence of residues 560-581. To clarify the effect of 1776del on GHR function, wild-type GHR, GHR-1776del, and two additional GHR mutants, GHR-L561X (stop codon at site of the 1776del) and GHR-I582X (translation termination in GHR-1776del) were transiently expressed in CHO cells. After incubation with recombinant human GH, GHR-1776del showed lower signal transducer and activator of transcription 5 (STAT5)-mediated transcriptional activation ( approximately 50%, P < 0.05), as well as STAT5 Tyr694 phosphorylation (P < 0.05) compared with wild-type GHR, whereas GHR-L561X and GHR-I582X showed normal STAT5 phosphorylation and transcriptional activity. In contrast, all vectors produced similar effects on STAT3-mediated transcriptional activation. In conclusion, this novel GHR-1776del mutation in a classical GHI patient illustrates an important mechanism of impaired GHR-STAT5 but intact GHR-STAT3 signaling. This effect might result from interference of C-terminal nonsense sequence in mutated GHR with STAT5 docking to upstream tyrosine residues.

Adolescent↗
PubMed2003

Clinical and pathologic correlations in genetically distinct forms of atrichia.

BACKGROUND: The genetic basis of 2 distinct forms of atrichia with papules has recently been defined at the molecular level. In atrichia with papular lesions (APL; Online Mendelian Inheritance in Man [OMIM] 209500), mutations in the hairless gene on chromosome 8p21 have recently been identified. Atrichia with papules also occurs in the clinical setting of vitamin D-dependent rickets type IIA (VDDR IIA; OMIM 277440), resulting from mutations in the vitamin D receptor gene on chromosome 12q12-q14. Despite the distinct genetic basis for both forms of atrichia, the clinical findings are strikingly similar and exhibit classic pathognomonic features unique to this phenotype. We sought to document the clinical and molecular features of APL and VDDR IIA. OBSERVATIONS: Molecular analysis of the hairless and vitamin D receptor genes was performed on genomic DNA from probands and family members from 3 families with APL and 2 with VDDR IIA. We present a clinical and histologic comparison of atrichia in patients with APL and VDDR IIA and highlight the genetically heterogeneous basis of atrichia by identification of pathogenetic mutations. CONCLUSIONS: Increased awareness of these diseases will allow early diagnosis and potential therapeutic intervention for the rickets in VDDR IIA and avoidance of treatment of the atrichia in both APL and VDDR IIA. Their phenotype similarities suggest the possibility of a functional relationship between HR and VDR.

Adolescent↗
PubMed2003

Maternal hypothyroidism may affect fetal growth and neonatal thyroid function.

OBJECTIVE: To investigate the pituitary-thyroid axis function in the early neonatal period of newborns to hypothyroid mothers who have been apparently adequately treated. METHODS: Among the 27,386 full-term newborns delivered over a 6-year period, 259 were born to 250 treated hypothyroid mothers (0.9%); 246 of these newborns constituted the study group. Controls were 139 term healthy neonates from healthy group-matched mothers. The study infants and controls underwent thyroid function tests in a prospective design. A single blood sample was collected from each infant at 25-120 hours of life. RESULTS: Compared with the controls, serum thyroid-stimulating hormone (TSH) levels were higher in the study neonates (P <.005), as were those of serum free thyroxine (T4) (P <.03), particularly at 49 hours of life or older (P <.001). At 49-120 hours, 44.7% of the study group newborns had serum free T4 levels greater than the 95th percentile of the controls (P <.001), and 16.8% had significantly higher TSH levels (P <.001). Serum free T4 correlated positively with TSH in the controls (r =.316) but not in the study newborns (r =.062, P =.36). Neonatal TSH at 49 hours or older correlated positively with maternal TSH during pregnancy in the 18 cases where maternal TSH values during pregnancy were available (r =.751, P <.001). Birth weight and head circumference were significantly lesser in the study group (P <.001). CONCLUSION: The impaired intrauterine growth and the unduly elevated serum values of TSH and serum free T4 found in a substantial fraction of the study newborns might reflect an insufficient level of hormone replacement therapy of their hypothyroid mothers during pregnancy, despite an assumed adequate management. Gestational hypothyroidism requires close monitoring.

Case-Control Studies↗
PubMed2003

Androgen therapy in constitutional delay of growth.

BACKGROUND/AIMS: Two modalities of androgen therapy prevail in the treatment of constitutional delay of growth (CDG): monthly injections of testosterone or daily tablets of the non-aromatizable oxandrolone. The present study was undertaken to prospectively compare both compounds and dose. METHODS: Thirty patients with CDG were the subjects of this study. The protocol required that they all be at age 12-14 years with a bone age delay of more than 2 'years', height less than -2 SDS and growth velocity less than -0.5 SDS. The subjects were at a Tanner stage 1 or 2 and testicular volume were no larger than 4 ml. They were randomly assigned into 3 treatment groups: group 1 patients received monthly injections of 25 mg testosterone propionate-enanthate; group 2 patients received monthly injections of 50 mg testosterone propionate-enanthate; group 3 patients received oral oxandrolone at a weekly dose of 0.7 mg/kg. Treatment was given for a period of 6 months and follow-up commenced 6 months later and yearly thereafter for 2 years. RESULTS: Height velocity and height increased significantly only in groups 2 and 3. Bone age advanced most in group 2. Puberty progressed faster in that group as compared with group 3. The predicted adult height before and 2 years after completion of treatment remained unchanged in the two testosterone groups. It increased significantly in the oxandrolone group from a mean 169.8 cm before therapy to a mean 177.5 cm 2 years after completion of therapy. Peak GH levels were significantly higher on both testosterone 50 mg and oxandrolone, as compared to pretreatment levels. The increment was significantly greater in group 2 as was the increment in serum IGF-1 and IGFBP3. CONCLUSIONS: These results imply that 6 months of testosterone injections at a dose of 50 mg, but not 25 mg, is an effective and safe treatment for patients with CDG, with no considerable impact on final height prediction. On the other hand, daily oxandrolone treatment, starting at age 12-14 years, may increase the predicted final adult height.

Adolescent↗
PubMed2003

Endocrine withdrawal syndromes.

Hypersecretion of endogenous hormones or chronic administration of high doses of the same hormones induces varying degrees of tolerance and dependence. Elimination of hormone hypersecretion or discontinuation of hormone therapy may result in a mixed picture of two syndromes: a typical hormone deficiency syndrome and a generic withdrawal syndrome. Thus, hormones with completely different physiological effects may produce similar withdrawal syndromes, with symptoms and signs reminiscent of those observed with drugs of abuse, suggesting shared mechanisms. This review postulates a unified endocrine withdrawal syndrome, with changes in the hypothalamic-pituitary-adrenal axis and the central opioid peptide, in which noradrenergic and dopaminergic systems of the brain act as common links in its pathogenesis. Long-term adaptations to hormones may involve relatively persistent changes in molecular switches, including common intracellular signaling systems, from membrane receptors to transcription factors. The goals of therapy are to ease withdrawal symptoms and to expedite weaning of the patient from the hormonal excess state. Clinicians should resort to the fundamentals of tapering hormones down over time, even in the case of abrupt removal of a hormone-producing tumor. In addition, the prevention of stress and concurrent administration of antidepressants may ameliorate symptoms and signs of an endocrine withdrawal syndrome.

Androgens↗
PubMed2003

Modulation of 11 beta-hydroxysteroid dehydrogenase type 1 in mature human subcutaneous adipocytes by hypothalamic messengers.

Glucocorticoids are regulated at the prereceptor level by 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), which interconverts inactive cortisone and active cortisol. In a previous study, we noted that patients with hypothalamic obesity had an increased ratio of cortisol/cortisone metabolites, suggesting enhanced 11 beta-HSD-1 activity. In this in vitro study, we tested the hypothesis that adipose 11 beta-HSD-1 is regulated by the hypothalamus via circulating hormones, sympathetic nervous system innervation, and/or cytokines. Preadipocytes were retrieved from sc fat from healthy nonobese individuals and differentiated in vitro to mature adipocytes. Cells were incubated with several potential effectors, and the activity of 11 beta-HSD-1 was assayed by measuring conversion of added 500 nM cortisone to cortisol. Expression of 11 beta-HSD-1 mRNA was determined by real-time PCR, whereas lipolytic effects were determined by measuring glycerol concentration in the culture medium. CRH down-regulated 11 beta-HSD-1 activity with maximal effect at 10(-9)M (65 +/- 10% of control; P < 0.001) and caused a reduction in lipolysis. Likewise, ACTH down-regulated 11 beta-HSD-1 activity with maximal effect at 10(-9) M (65 +/- 20%; P < 0.05) and reduced medium glycerol. Neither CRH nor ACTH affected 11 beta-HSD-1 mRNA expression. TNF alpha up-regulated 11 beta-HSD-1 activity maximally at 0.6 x 10(-9) M (140 +/- 20%; P < 0.001); the same cytokine increased 11 beta-HSD-1 mRNA levels to 3-fold of control (P < 0.05) and increased medium glycerol levels to 165 +/- 14% of control (P < 0.01). IL-1 beta also up-regulated 11 beta-HSD-1 activity maximally at 0.6 x 10(-9) M (160 +/- 33%; P < 0.001) and caused an increase in glycerol levels (159 +/- 11% of control; P < 0.001). Of the adrenergic agonists, salbutamol up-regulated 11 beta-HSD-1 activity maximally at 10(-7) M (162 +/- 46%; P < 0.02), and clonidine down-regulated it at 10(-7) M (82 +/- 15%; P < 0.005). We conclude that possible distinct hypothalamic mediators regulating adipose tissue 11 beta-HSD-1 might include down-regulation of 11 beta-HSD-1 activity by CRH, ACTH, and alpha 2 sympathetic stimulation, and up-regulation of the enzyme by beta 2 sympathetic stimulation and by the cytokines TNFalpha and IL-1 beta.

11-beta-Hydroxysteroid Dehydrogenase Type 1↗
PubMed2003

11 beta-Hydroxysteroid dehydrogenase activity in hypothalamic obesity.

After extensive suprasellar operations for hypothalamic tumor removal, some patients develop Cushing-like morbid obesity while they receive replacement doses of glucocorticoids. In this study, we examined the hypothesis that target tissue conversion of inactive 11-ketosteroids to active 11 beta-OH glucocorticoids might explain the obesity of some patients with hypothalamic lesions. Toward this aim, we studied 10 patients with hypothalamic obesity and secondary adrenal insufficiency and 6 control Addisonian patients while they were on glucocorticoid replacement therapy. Pituitary hormone deficiencies were replaced when medically indicated. Twenty-four-hour urine was collected after a single oral dose of 12 mg/m(2) hydrocortisone acetate. The ratios of free and conjugated cortisol (F) to cortisone (E) and their metabolites, [tetrahydrocortisol (THF)+5 alpha THF]/tetrahyrdocortisone (THE), dihydrocortisols/dihydrocortisones, cortols/cortolones, and (F+E)/(THF+THE+5 alpha THF), were considered to represent 11 beta-hydroxysteroid dehydrogenase (HSD) activity. The 11-OH/11-oxo ratios were significantly higher in the urine of patients with hypothalamic obesity. The 11-OH/11-oxo ratios, however, did not correlate with the degree of obesity, yet a significant correlation was found between conjugated F/E and the ratio of visceral fat to sc fat measured by computerized tomography at the umbilical level. The consequence of increased 11 beta-HSD1 activity and the shift of the interconversion toward cortisol may contribute to the effects of the latter in adipose tissue. We propose that deficiency of hypothalamic messengers after surgical injury induces a paracrine/autocrine effect of enhanced glucocorticoid activity due to up-regulated 11 beta-HSD1 activity.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed2002

Clinical physiology and pathology of the growth plate.

This chapter reviews the unique anatomical and histological maturation of long bones and cuboid bones with emphasis on the means available to evaluate them in the clinical setting as they are represented in the hand and wrist radiogram. It summarizes the endocrine regulation of these maturational processes and attempts to uncover endocrine function and malfunctions as they unfold in the radiogram.

Animals↗
PubMed2002

Ultrasonographic assessment of bone maturity in newborns.

BACKGROUND: Traditionally, the bone maturity at birth has been estimated from the radiological presence and size of the ossified distal femoral epiphysis. This study was conducted in a search for a sonographic tool for the evaluation of neonatal bone maturity. METHODS: We examined sonographically 256 neonates within 24 h of birth. Gestational ages ranged from 36 to 42 weeks (mean: 39.4; median: 40). Birth weights ranged from 1,945 to 5,000 g (mean: 3,175; median: 3,180). The distal femoral epiphysis was imaged on the coronal plane sonogram of the distal femur with the knee at 90 degrees flexion and the distal femoral epiphysis maximal height was recorded. The acetabulum was imaged using Graf's method in the coronal plane image and the acetabular diameter recorded. RESULTS: It was found that plotting the distal femoral epiphysis against neonatal birth weight and gestational age provided a simple method for assessing the bone maturity. According to our study, a neonate can be regarded as bone maturity percentile X when plotting distal femoral epiphysis height or acetabulum diameter against birth weight and gestational age or when averaging the four readings. CONCLUSIONS: We suggest performing sonography of the distal femoral epiphysis as a bedside tool for the assessment of skeletal maturity in newborns.

Acetabulum↗