Correction to: Lower grip strength and dynamic body balance in women with distal radial fractures.

The article Lower grip strength and dynamic body balance in women with distal radial fractures, written by. K. Fujita, H. Kaburagi, A. Nimura, T. Miyamoto, Y. Wakabayashi, Y. Seki, H. Aoyama, H. Shimura, R. Kato, A. Okawa was originally published electronically on the publisher's internet portal.

Lower grip strength and dynamic body balance in women with distal radial fractures.

In this case-control study, we concluded that women with distal radial fractures who were surgically treated showed lower grip strength and dynamic body balancing than those of controls. These results suggest that measurements of grip strength and dynamic body balance may be useful screening tools to assess future fracture risk. INTRODUCTION: Patients with distal radial fractures (DRFs) are at risk of future fragility fractures. However, their physical characteristics and tendencies for falls remain unclear. We aimed to compare the physical characteristics of women with and without distal radial fractures. METHODS: We included 128 women with a DRF as their first fragility fracture (fracture group) who underwent surgical treatment. Concurrently, 128 age- and sex-matched participants without a history of fragility fractures were selected as controls (control group). The participants underwent assessments of grip strength and the body balancing ability test. Measurements were taken twice in the fracture group, at 2 weeks and 6 months postoperatively, and once in the control group. The body balancing ability test included the Functional Reach Test, Timed Up and Go test (TUG), 2-Step test (2ST), and Timed Uni-pedal Stance test. The participants also completed questionnaires about their health. RESULTS: There were no significant differences (p > 0.05) in patient characteristics between the groups. The fracture group showed lower grip strength across all age groups. In the DRF group, prolonged TUG time was observed at 2 weeks postoperatively in all age groups and at 6 months in participants aged 55-74 years; the 2ST score was significantly lower in participants aged between 65 and 74 years. CONCLUSIONS: Women with DRF demonstrated lower grip strength and dynamic body balancing ability. Lower grip strength and dynamic body balancing ability were identified as significant risk factors in women with DRF, suggesting that these may be useful screening tools to assess fracture risk.

Distribution of the axillary nerve to the subacromial bursa and the area around the long head of the biceps tendon.

PURPOSE: Patients with a shoulder disorder often complain of pain on the anterior or lateral aspect of the shoulder. Such pain has been thought to originate from the suprascapular nerve. However, taking into consideration the distinctive course of the axillary nerve, the axillary nerve is likely to supply branches to the structure around the shoulder joint. This study was conducted to clarify the division, course, and distribution of the branches which originate from the axillary nerve and innervate structures around the shoulder joint. METHODS: The division, course, and distribution of the branches which originate from the axillary nerve and innervate structures around the shoulder joint were examined macroscopically by dissecting 20 shoulders of 10 adult Japanese cadavers. RESULTS: The thin branches from the anterior branch of the axillary nerve were distributed to the subacromial bursa and the area around the long head of the biceps tendon. The branches from the main trunk of the axillary nerve or the branch to the teres minor muscle were distributed to the infero-posterior part of the shoulder joint. CONCLUSION: The pain on the anterior or lateral aspect of the shoulder, which has been thought to originate from the suprascapular nerve, might be related to the thin branches which originate from the axillary nerve and innervate the subacromial bursa and the area around the long head of the biceps tendon. CLINICAL RELEVANCE: These results would be useful to consider the cause of the shoulder pain or to prevent the residual pain after the biceps tenodesis.

An anatomic study of structure and innervation of the serratus anterior muscle.

BACKGROUND: The structure and function of the serratus anterior muscle are partitioned into three parts. If the morphological characteristics in each part can be demonstrated in more detail, the cause of dysfunction will probably be identifiable more accurately. The purpose of this study was to demonstrate the details of the structure and innervation in each part of the serratus anterior muscle. MATERIALS AND METHODS: This macroscopic anatomic study was conducted using ten sides from five cadavers. The structure and innervation in each part of this muscle were examined. RESULTS: In the superior part, the independent branch was divided from a branch innervating the levator scapulae muscle. In the middle part, the long thoracic nerve descended on one-third of the anterior region between the origin and insertion. In the inferior part, the long thoracic nerve which ramified into many branches and branches from the intercostal nerves were distributed on all sides. CONCLUSION: This study demonstrated that the innervation of the serratus anterior muscle was different in each part. The difference indicates that the superior part has an intimate relation with the levator scapulae muscle while the middle and inferior parts could be the actual serratus anterior muscle. Moreover, the distribution of branches from the intercostal nerves shows that the inferior part has a connection with some trunk elements. Understanding these characteristics of innervation is useful to identify the cause of dysfunction. In addition, we assert that the constant distribution of branches from the intercostal nerves is significant for the morphology.

A novel specific bioassay for serum human growth hormone.

Human GH receptor (hGHR) was recently expressed on a Ba/F3 cell line, which is a mouse pro-B cell lymphoma that has been induced to become a cloned cell line (Ba/F3-hGHR). Using a Ba/F3-hGHR cell line, we have established a bioassay for serum hGH. hGH stimulated cell proliferation in a dose-dependent manner in concentrations ranging from 1 ng to 100 ng/mL. Cell proliferation was not influenced by other hormones or growth factors in the bioassay, with the exception of insulin-like growth factor I (IGF-I) and GH binding protein. Free IGF-I significantly stimulated the proliferation of Ba/F3-hGHR cells at concentrations over 25.85 ng/mL in this bioassay system, but serum IGF-I did not stimulate cell proliferation because the sensitivity of cell proliferation was insufficient for free IGF-I in serum. GH binding protein, however, did suppress cell proliferation at the highest concentration (100 ng/mL), but did not at the average concentration (20 ng/mL). Human serum stimulated cell proliferation, which was completely suppressed by anti-GH antibody. The GH bioactivity of serum samples from normal children and patients with non-GH deficient short stature correlated strongly with the serum hGH concentration determined by immunoradiometric assay (IRMA) (r = 0.967, r = 0.924, P < 0.0001, respectively). The ratio of bioactivity/IRMA was 1.01+/-0.26 in sera from normal children and 1.18+/-0.24 and 1.00+/-0.29 at basal values and peak values in GH stimulation tests, respectively, in sera from patients with non-GH deficient short stature. The bioactivity/IRMA ratio for the serum GH bioactivity of a patient who had biologically inactive GH caused by an amino acid substitution was 0.333+/-0.056 (mean +/- SD). In conclusion, we established a new sensitive bioassay for hGH that is specific for hGH somatogenic action and is useful for screening of patients with short stature caused by biologically inactive hGH.

Acid-labile subunit (ALS) measurements in children.

Almost all of the serum IGFs are found in a ternary complex composed of IGF, IGFBP-3 and acid-labile subunit (ALS). It was reported that ALS levels were age- and sex-dependent. In the present study we measured serum ALS levels in 264 normal children (145 boys and 119 girls) aged from 5 days to 16 years, and 15 patients with growth hormone deficiency (GHD) aged from 11 months to 13 years. Serum ALS levels increased during childhood, and reached peak values in mid to late puberty. ALS levels reached their highest levels 2 years earlier in girls than in boys. Serum ALS levels were significantly correlated with serum IGF-I levels and IGFBP-3 levels. Serum ALS levels were below -2SD in 6 out of 7 children with complete GHD (CGHD), while serum ALS levels were below -2SD in 1 out of 8 patients with partial GHD (PGHD). These results indicate that serum ALS levels are regulated by GH, and that the measurement of ALS is useful for the diagnosis of CGHD in children.

Bone mineral density in Turner syndrome: relation to GH treatment and estrogen treatment.

The bone mineral density (BMD) of the second metacarpal bone of the left hand was measured in 57 patients with Turner syndrome by the digital image processing (DIP) method to study the relations between the treatment regimen and their bone mineral density. BMD SD score in the patients who had started the GH treatment before 10 years old was within +/-2SD of the standard before 14 years, but the score decreased to below -2SD after 14 years. In the patients who had started GH treatment after 10 years old, BMD score were significantly lower than -2SD, although there was tendency to increased. In the patients who had estrogen after 15 years old, BMD did not increase with GH alone and slowly increased after estrogen replacement. In the other two patients who had started sex steroid hormone replacement treatment before 15 years old, BMD maintained +/-2SD. In patients who received combined GH and LH-RH analog treatment, their BMD score did not increase during LH-RH analog treatment. It slowly increased but was still below -3SD after stop of LH-RH analog and start of estrogen treatment. In Turner syndrome, GH may play a role in maintaining prepubertal BMD levels [4], and estrogen plays an important role in pubertal BMD increment. It is recommended that estrogen treatment is started before 15 years of age for maintenance of normal BMD level.

Analysis of the FGFR3 gene in Japanese patients with achondroplasia and hypochondroplasia.

It has been reported that mutations in the FGFR3 gene cause autosomal dominant forms of dwarfism, achondroplasia (ACH) and hypochondroplasia (HCH). In the present study, we analyzed the FGFR3 gene in 26 Japanese patients with ACH and 14 with HCH. Genomic DNAs of the patients were isolated from whole blood. For the ACH patients, a 164-bp fragment of the FGFR3 gene that spans the entire transmembrane domain was amplified by polymerase chain reaction (PCR), and the PCR products were analyzed by direct sequencing of the PCR products and by digestion of the PCR products with restriction enzymes. For the HCH patients, a 206-bp fragment of the FGFR3 gene which encodes a part of the TK1 domain was amplified, and the PCR products were directly sequenced. The heterozygous G380R mutations were identified in all of the 26 ACH patients, whereas the heterozygous N540K mutations were identified in 8 out of 14 HCH patients. These results were consistent with previous reports from abroad.

A novel compound heterozygous mutation in the steroidogenic acute regulatory protein gene in a patient with congenital lipoid adrenal hyperplasia.

Congenital lipoid adrenal hyperplasia (CLAH) is an autosomal recessive disorder characterized by impaired synthesis of all adrenal and gonadal steroid hormones. Recently, it was reported that mutations in the steroidogenic acute regulatory protein (StAR) gene cause CLAH. In the present study, we have analyzed the StAR gene of a Japanese patient with CLAH. PCR amplification and subsequent nucleotide sequencing of the StAR gene and those of her parents revealed that the patient has a compound heterozygous mutation of this gene. In one allele, an undescribed G to C transversion in codon 217, which occurred at the last base of exon 5 and thus altered the splice donor site sequence, apparently resulted in a substitution of Arg to Thr (AGG to ACG: R217T), and in the other allele, a C to T transition in codon 218 caused a substitution of Ala to Val (GCG to GTG: A218V), which has been previously shown to abolish StAR activity. In vitro expression analysis of an allelic minigene that consists of exons 4-6 of the R217T mutant StAR gene showed that the G to C transversion in the splice donor site of exon 5 caused by the R217T mutation disrupts normal splicing, resulting in the complete skipping of exon 5, which alters the translation reading frame of exon 6, introduces a stop codon at amino acid position 174, and thus impairs the activity. A functional expression study of the R217T replacement mutant revealed that the mutant has no steroidogenesis-enhancing activity if the transcript of the R217T mutant allele is ever spliced normally and translated into the protein. From the genetic analysis of 50 healthy subjects, the novel R217T mutation was unlikely to be due to polymorphism. Together, these results indicate that this patient is a compound heterozygote for the mutation in the StAR gene (T217R and A218V) and that these mutations inactivate the StAR function and give rise to clinically manifest CLAH.

Setting up an automated system for evaluation of bone age.

The "Tanner-Whitehouse 2" method is the most popular in evaluating skeletal maturation, but this method has some inherent weak points. We therefore developed the new system to automatically evaluate the skeletal maturation of Japanese children by means of a personal computer. The subjects of this study were 318 healthy Japanese boys and 199 girls ranging from 2 to 15 years of age. The bone age was calculated by multiple regression analysis with parameters for the epiphysis and metaphysis. Successful automatic evaluation was about 80-90% on each phalanx. There was a significant correlation between chronological age and the ratio of epiphyseal width to metaphyseal width. The system developed in this study was useful for evaluating the skeletal maturation.

G370C mutation in the FGFR3 gene in a Japanese patient with thanatophoric dysplasia.

Thanatophoric dysplasia (TD) is a sporadic lethal skeletal dysplasia with micromelic shortening of the limbs, relative macrocephaly, platyspondyly and reduced thoracic cavity. It has recently been reported that TD is caused by mutations in the FGFR3 gene. In the present study, we report a missense mutation in the FGFR3 gene in a Japanese patient with TD. The patient was noticed to have typical features of TD type 1 (TD1) at birth. The genomic DNAs of the patient and his parents were isolated from whole blood. DNA fragments of the FGFR3 gene were amplified by polymerase chain reaction, and directly sequenced. The patient was revealed to be heterozygous for a missense mutation G370C, changing codon 370 (GGC) encoding Gly to TGC encoding Cys, but his parents did not have the G370C mutation. The G370C mutation introduces an unpaired cysteine residue in the extracellular domain of FGFR3, which may result in formation of an intermolecular disulfide bond between two mutant FGFR3 monomers and their constitutive activation. In conclusion, we have identified the G370C mutation in the FGFR3 gene in a Japanese TD1 patient.

[Gastric juice secretion increases during extracorporeal circulation employed in cardiac surgery].

We evaluated gastric juice secretion during extracorporeal circulation (ECC) in cardiac surgery. The effect of pirenzepine, a muscarine receptor blocker, was also tested to clarify the mechanism involved. Gastric juice secretion increased significantly from pre ECC value of 3.8 +/- 1.3 ml.h-1 to 12.4 +/- 4.0 ml.h-1 during ECC. It decreased to 5.0 +/- 1.4 ml.h-1 (mean +/- SE) after ECC. Pirenzepine premedication reduced serum gastrin level. However, it did not suppress the increase of gastric juice secretion. There is no significant correlation between serum gastrin level and gastric juice secretion. ECC is a major stress and increases gastric juice secretion. This phenomenon is probably activated via sympathetic and hypophysis-adrenal gland system.

Syntheses of oligonucleotide derivatives with P(V) porphyrin and their properties.

Two types of oligonucleotide derivatives which are substituted by P(V) porphyrin at the phosphorus atom of an internucleotidic linkage and at the 5'-terminal internucleotidic linkage via a spacer were synthesized (Fig. 1), and hybridization capabilities of them with complementary oligonucleotides were evaluated. A novel method for a sensing of oligonucleotide by the fluorescence quenching via photo-induced electron transfer between the P(V) porphyrin labeled oligonucleotide and pyrene-labeled one on the oligonucleotide template is reported.

Synthesis and properties of oligonucleotide derivative with P(V) porphyrin.

Oligonucleotide derivatives with a P(V)tetraphenylporphyrin at the internucleotidic phosphodiester linkage were synthesized. Their interactions with the complementary oligonucleotide and pyrene-labeled oligonucleotide were investigated. Fluorescence from the porphyrin moiety was strongly quenched by the addition of the pyrene-labeled oligonucleotide and the template oligonucleotide.

Oligonucleotides with bis-pyrene adduct in the backbone: syntheses and properties of intramolecular excimer forming probe.

2-(N-bis(2-pyrenylethyl)methyl-amino)ethanol (BPAE) was synthesized and its interaction with DNA was examined to explore the efficiency of intramolecular excimer forming probe. As a result the fluorescence of intramolecular excimer of BPAE disappeared with the addition of poly(dA)-poly(dT). This result suggests an unique type of probe with its introduction to oligonucleotide.