Immediate effects of transcutaneous electrical nerve stimulation on gait patterns in chronic stroke survivors: A single group, pretest-posttest clinical trial.

BACKGROUND: Transcutaneous electrical nerve stimulation (TENS) has been used to reduce muscle spasticity and improve locomotion in stroke survivors. We speculate that acute changes in gait performance after TENS mediate functional improvement in the long-term. However, no previous study has investigated the effect of TENS on ankle kinetics and kinematics during walking in stroke survivors. PURPOSE: We aimed to investigate whether TENS applied over the paretic leg could rapidly improve the plantar flexion moment and ankle kinematics in chronic stroke survivors with lower limb paresis. METHODS: Twenty chronic stroke survivors were recruited. They underwent 30 min of TENS over the area innervated by the common peroneal nerve on the paretic leg. Three-dimensional (3D) motion capture was performed and ankle plantar flexor spasticity was assessed before and immediately after stimulation. Ankle kinematics and kinetic and spatiotemporal data were collected using 3D motion capture. Ankle plantar flexor spasticity was assessed using the Modified Tardieu Scale. PRINCIPAL RESULTS: A significant increase in the ankle plantar flexion moment of the paretic side during the pre-swing phase was observed immediately after stimulation (p = 0.009, maximal mean difference = 0.035, 95%CI = 0.0125 to 0.0575). The step length of the paretic limb also increased significantly after stimulation (p = 0.023, mean difference = -0.02, 95%CI = -0.04 to -0.004). TENS had no immediate effect on paretic ankle spasticity, as measured by the Modified Tardieu Scale, or on other temporo-spatial parameters. CONCLUSION: The findings support the use of TENS to improve the motor function and gait pattern in chronic stroke survivors. The study indicated that the application of TENS to the paretic leg before gait training might improve rehabilitation outcomes. Future studies investigating the effects of TENS on functional outcomes, the optimal stimulation duration, and assessing spasticity using more sensitive measures are warranted.

Maternal L-carnitine supplementation improves glucose and lipid profiles in female offspring of dams exposed to cigarette smoke.

Sex differences in disease susceptibility due to maternal programming have been reported. We previously observed that maternal smoking induced renal disease and neurological changes are restricted to males, while both male and female offspring develop metabolic disorders. We have also found that maternal L-carnitine supplementation during gestation and lactation can significantly improve glucose intolerance and hyperlipidaemia in male offspring. This study aimed to determine whether such beneficial effects can also occur in female offspring. Balb/c female mice were exposed to cigarette smoke (SE) 6 weeks prior to gestation, during gestation and lactation. A subgroup of the SE dams was given L-carnitine (1.5 mmol/L in drinking water) during gestation and lactation. Female offspring were studied at 20 days (weaning) and 13 weeks (adulthood). Maternal smoking increased liver weight (%) and blood glucose levels at 20 days, as well as glucose intolerance and plasma triglycerides levels at adulthood (P < .05). The hepatic lipid metabolic marker adipose triglyceride lipase was downregulated in the SE offspring at 20 days (P < .05). At 13 weeks, the hepatic pro-inflammatory markers IL-1ß and TNF-α mRNA expression were upregulated, while the anti-inflammatory marker IL-10 mRNA expression was downregulated in the SE offspring (P < .05). Liver fibrosis was apparent at 20 days and 13 weeks. Maternal L-carnitine supplementation either normalised or suppressed the detrimental effects induced by maternal smoke exposure (P < .05). We conclude that maternal L-carnitine supplementation improves metabolic parameters in the female offspring of SE dams.

Cutaneous stimulation improves function of a chronic patient with cerebellar damage.

The prognosis of cerebellar hemorrhage with brain stem compression is known to be poor, and patients who can usually survive are severely disabled with limited benefit from conventional rehabilitation. An innovative cutaneous stimulation was administered to a chronic patient (2 years after the incidence) who has severe ataxia, gait imbalance and limb spasticity caused by cerebellar hemorrhage. After 8 months of intervention, patient's function as evaluated by two functional measures has improved by 40%. In addition, the patient's ataxia and hypotonia have improved significantly in which he has regained the abilities to grasp objects, sit upright, control his equilibrium, and monitor an electric wheelchair. The present case study demonstrated a significant improvement of a chronic severely disabled patient who received the intervention 2 years after the accident, suggesting that the cutaneous stimulation may be a possible effective neurologic intervention.

Deferoxamine-induced dysplasia of the knee: sonographic features and diagnostic performance compared with magnetic resonance imaging.

OBJECTIVE: To evaluate the features and diagnostic performance of sonography in the assessment of deferoxamine-induced dysplasia of the knee. METHODS: The left knees of 32 patients with thalassemia who were receiving regular blood transfusions and chelation therapy were studied with sonography for signs of deferoxamine-induced bone dysplasia. Abnormal physeal and metaphyseal changes detected on sonography included notching at the metaphyseal corner, a blurred or irregular peripheral juxtaphyseal metaphyseal contour, and widening of the peripheral juxtaphyseal metaphyseal echogenic interface. The accuracy of sonography in diagnosing dysplasia was evaluated by using magnetic resonance imaging as the standard of reference. RESULTS: There were 14 true-positive findings, 10 true-negative findings, 7 false-negative findings, and 1 false-positive sonographic diagnosis of dysplasia, giving 67% sensitivity, 91% specificity, a 93% positive predictive value, and a 59% negative predictive value. CONCLUSION: Sonography was specific but only moderately sensitive in the diagnosis of deferoxamine-induced dysplasia at the knee when compared with magnetic resonance imaging.

Desferrioxamine-induced long bone changes in thalassaemic patients - radiographic features, prevalence and relations with growth.

AIM: To study the radiographic findings of desferrioxamine-induced bone dysplasia, its prevalence and relation to growth in thalassaemic patients. MATERIALS AND METHODS: A cross-sectional study was performed in 35 thalassaemic patients on a hypertransfusion scheme and chelation therapy at a dose not exceeding 50 mg/kg/day. Radiographs of the left hand taken for bone age assessment in consecutive patients over the past 12 months were evaluated for signs of desferrioxamine-induced bone dysplasia. The findings were correlated with data on growth, chelation and body iron content. RESULTS: Twelve of 35 patients had evidence of desferrioxamine-induced long bone dysplasia. There was no significant difference in the groups with and without radiographic evidence of bone dysplasia with respect to the height percentile at time of initiation of therapy, height percentile at time of radiography, skeletal age delay, age at starting chelation, chelation dose and duration, units of blood transfused, average chelation dose, and serum ferritin levels at time of radiography. Both groups showed a reduced percentile growth with a significantly greater reduction (P = 0.03) in the patients with dysplastic change. CONCLUSION: Desferrioxamine-induced bone dysplasia is associated with height reduction and can be seen in patients receiving desferrioxamine chelation therapy at doses of less than 50 mg/kg/day. Awareness of the diagnosis is of importance as reduction of the desferrioxamine dose may improve bone growth.

Magnetic resonance imaging evaluation of the pituitary gland and hypothalamus in thalassaemic children with elevated serum ferritin levels.

OBJECTIVE: Despite modern treatment with hypertransfusion and chelation therapy, growth retardation continues to be observed in a significant proportion of thalassaemic children. The underlying reason remains unclear, but hypothalamic-pituitary axis disorder has been implicated. We aimed to assess iron overloading in the hypothalamus and pituitary gland in thalassaemic children with elevated serum ferritin, with and without growth retardation. METHODOLOGY: Twelve thalassaemic children on hypertransfusion and chelation therapy with high serum ferritin were investigated with magnetic resonance imaging (MRI). Five children, all over 10 years of age, had growth retardation. Gradient recalled echo sequence was used to highlight any susceptibility effect that could be due to iron in the hypothalamus or pituitary gland. RESULT: There was no evidence of abnormal hypointense signal in the hypothalamus or pituitary gland in the patients studied, regardless of the presence of growth retardation. CONCLUSION: There was no apparent characteristic MRI appearances of iron deposition in the hypothalamus or pituitary gland in thalassaemic children with high serum ferritin.

The primary structure of rat ribosomal protein L6.

The amino acid sequence of the rat 60S ribosomal subunit protein L6 was deduced from the sequence of nucleotides in a recombinant cDNA and confirmed by determination of amino acid sequences in the protein. Ribosomal protein L6 has 296 amino acids (the NH2-terminal methionine is removed after translation of mRNA); the molecular weight is 33,417. Hybridization of the cDNA to digests of nuclear DNA suggests that there are 7 to 10 copies of the L6 gene. The mRNA for the protein is about 1,100 nucleotides in length. Rat L6 is related to ribosomal proteins from other eukaryotes and to histone H1.

The carboxyl extensions of two rat ubiquitin fusion proteins are ribosomal proteins S27a and L40.

Two rat recombinant cDNAs were characterized; they encode fusion proteins that have at their NH2 terminus the conserved 76 amino acid ubiquitin and at their carboxyl terminus the extension ribosomal proteins S27a (80 amino acids and a molecular weight of 9,397) or L40 (52 amino acids and a molecular weight of 6,177). The fusion proteins are processed in a reticulocyte lysate to ubiquitin and either S27a or L40. Hybridization of cDNAs to digests of nuclear DNA suggests that there are 14 to 19 copies of the S27a, and 6 to 10 of the L40, genes. The mRNA for ubiquitin-S27a has about 700 nucleotides and ubiquitin-L40 about 650. Ribosomal proteins S27a and L40 contain zinc finger motifs of the C2-C2 variety. S27a and L40 are related to ribosomal proteins from other species.

The primary structures of rat ribosomal proteins L4 and L41.

The amino acid sequences of the rat 60S ribosomal subunit proteins L4 and L41 were deduced from the sequences of nucleotides in recombinant cDNAs. Ribosomal protein L4 has 421 amino acids; the molecular weight is 47,280. L41 is the smallest ribosomal protein; it has 25 amino acids and a molecular weight of 3,454. Hybridization of the cDNAs to digests of nuclear DNA suggests that there are 7 to 8 copies of the L4, and 9 to 12 of the L41, genes. The mRNA for L4 is about 1,500 nucleotides in length and that for L41 about 500 nucleotides. The 5' noncoding sequence of the L4 cDNA is exceptional in that it has, in addition to a short polypyrimidine sequence at the 5' end, a second stretch of 15 consecutive pyrimidines near the site of initiation of translation. The 3' noncoding sequence of the L41 mRNA is unusual in that it is at least 246 nucleotides long. Rat L4 and L41 are related to ribosomal proteins from other eukaryotes.

The primary structure of rat ribosomal protein L7. The presence near the amino terminus of L7 of five tandem repeats of a sequence of 12 amino acids.

The covalent structure of rat ribosomal protein L7 was determined in part from the sequence of nucleotides in a recombinant cDNA and in part from the sequence of amino acids in portions of the protein. The complementary analyses supplemented and confirmed each other. Ribosomal protein L7 contains 258 amino acids and has a molecular weight of 30,040. The protein has an unusual and striking structural feature near the NH2 terminus: five tandem repeats of a sequence of 12 residues. Rat L7 appears to be related to ribosomal protein L7 from the moderate halophile Vibrio costicola and perhaps to L30 from Bacillus stearothermophilus, to L7 from the moderate halophile NRCC 41227, and to L22 from Nicotinia tobaccum chloroplast. In addition, there is a sequence of 24 amino acids in rat protein L7 that may be related to segments of the same number of residues in Escherichia coli ribosomal proteins S10, S15, L9, and L22.

The effects of discontinuation of aluminum exposure on aluminum-induced osteomalacia.

Studies in patients on dialysis have shown that aluminum (Al) accumulation in bone plays a major role in the pathogenesis of osteomalacia. It has been suggested that deferoxamine (DFO) may be beneficial in the treatment of aluminum-induced osteomalacia. The present studies were performed in four groups of uremic rats to determine if DFO and/or discontinuation of Al administration have an effect on bone histomorphometry and blood chemistries. The groups were: 1) uremic control 2) aluminum (0.75 to 1.0 mg/rat i.p., five times a week for twelve weeks): 3) aluminum + DFO, after twelve weeks Al was discontinued and the rats received DFO (75 mg/rat two times a week for nine weeks); 4) aluminum + time, after twelve weeks Al was discontinued and the rats were sacrificed after nine weeks. High levels of Al in serum and bone and low levels of PTH were seen in rats receiving Al. Bone histology revealed Al at the mineralization front, abnormal tetracycline uptake, and an increase in osteoid. DFO treatment did not significantly change the level of Al in bone, however both DFO treatment and discontinuation of Al reversed towards normal the above described lesions. In conclusion, these studies suggest that DFO and/or discontinuation of Al administration to rats with approximately 30% of renal function greatly improve aluminum-induced osteomalacia.

The effect of 1,25 dihydroxycholecalciferol on parathyroid hormone secretion by monolayer cultures of bovine parathyroid cells.

Controversy exists over a direct effect of 1,25(OH)2D3 on PTH secretion. To investigate the possibility that the suppressive effect of 1,25(OH)2D3 on PTH secretion may be demonstrable in 1,25(OH)2D3-depleted tissue and/or after prolonged periods of exposure to 1,25(OH)2D3, primary monolayer cultures of bovine parathyroid cells were established in 1:1 DMEM/Ham's F-12 media supplemented with 2% calf serum but not 1,25(OH)2D3. Ionized calcium was maintained at 1.0 mM. Experiments were performed on 4-day-old culture cells. PTH concentration was measured using both a mid-region/carboxyl and an amino-terminal PTH antisera. 1,25(OH)2D3 at a concentration of 0.1 ng/ml suppressed PTH secretion by 32 +/- 7% after 48 hours. High calcium concentration (2.0 mM) suppressed PTH secretion by 37 +/- 10% and this effect was not additive over that of 1,25(OH)2D3. PTH secretion rate recovered fully 48 hours after normalization of the external calcium concentration but not after the removal of 1,25(OH)2D3. It is concluded that 1,25(OH)2D3 directly suppresses PTH secretion by monolayer culture of bovine parathyroid cells.

Total parathyroidectomy and renal function in patients with chronic renal failure.

5 patients with nonterminal renal failure who underwent total parathyroidectomy at Sydney Hospital over a 4-year period showed significant postoperative deterioration in renal function. In 4 of these patients, this deterioration occurred at a time when they were receiving supplements of calcium and 1,25-dihydroxyvitamin D3 but when close monitoring failed to show any evidence of hypercalcemia. In 1 patient the deterioration in renal function was clearly associated with hypercalcemia. We suggest that parathyroidectomy in nondialyzed patients be reserved for those with severe symptomatic hyperparathyroidism and that wherever possible the need for large doses of calcium and vitamin D be avoided.