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Biomedical subjects

C S Tam

Publications and source records attributed to C S Tam.

At least 19 recordsLinked to original sources
PubMed2006

Soft drink consumption and excess weight gain in Australian school students: results from the Nepean study.

We studied the relation between soft drink/cordial (a sweet, flavoured, concentrated syrup that is mixed with water to taste), fruit juice/drink and milk consumption in mid-childhood, and body mass index (BMI) status in early adolescence in a contemporary Australian cohort. In 1996/7, 268 children (136 males) were recruited from western Sydney at baseline (mean+/-s.d.: 7.7+/-0.6 years), and at follow-up 5 years later (13.0+/-0.2 years). Height and weight were measured at both time periods and overweight and obesity defined using the International Obesity TaskForce criteria. Beverage consumption was calculated from a 3-day food record at baseline. Median carbohydrate intake from soft drink/cordial was 10 g higher (P=0.002) per day in children who were overweight/obese at follow-up compared to those who had an acceptable BMI at both baseline and follow-up. Intakes of soft drink/cordial in mid-childhood, but not fruit juice/fruit drink and milk, were associated with excess weight gain in early adolescence.

Animals↗
PubMed2004

Reversible posterior leukoencephalopathy syndrome complicating cytotoxic chemotherapy for hematologic malignancies.

Reversible posterior leukoencephalopathy syndrome (RPLS) is an uncommon but distinctive clinicoradiological entity comprising of headache, seizures, visual disturbance, and altered mental function, in association with posterior cerebral white matter edema. With appropriate management, RPLS is reversible in the majority of cases. Previous reported associations of RPLS include hypertension, eclampsia, renal failure, and use of immunosuppressive drugs; reports in the adult hematology setting are rare. We report two cases of adults undergoing treatment for hematological malignancies who developed RPLS, and we emphasize the importance of early recognition and institution of appropriate management in reducing the risk of development of permanent neurological disability.

Aged↗
PubMed2000

Erect bipedal stance exercise partially prevents orchidectomy-induced bone loss in the lumbar vertebrae of rats.

This study investigates the responses of the fourth and fifth lumbar vertebral bodies of 6-month-old male Sprague-Dawley (SD) rats to orchidectomy (orx) and to erect bipedal stance for feeding for 12 weeks in specially designed raised cages (RC) for which the heights were raised from 20 cm to 35.5 cm. A total of 30 rats were divided into groups of: baseline; sham + housed in normal height cage (NC); orx + NC; sham + RC; and orx + RC. Bone histomorphometry was performed on the triple-labeled undecalcified fourth sagittal (LVL-4) and fifth transverse (LVX-5) sections. We found that orchidectomy induced high-turnover trabecular and cortical bone loss in the lumbar vertebrae. Forcing the rats to rise to erect stance for feeding reduced trabecular and cortical bone loss caused by orx. Apparently, depressing the elevated bone resorption next to the marrow induced by orx, and stimulating bone formation at the ventral periosteal surfaces, caused these effects. Orchidectomy and raised cage had similar effects on the two vertebrae except that the percentage of trabecular bone loss was greater in the LVL-4 than in LVX-5, and that bipedal stance exercise increased the total tissue area and mineral apposition rates (0-80 day interval) of ventral periosteal and dorsal endocortical surfaces of LVX-5 to a greater extent than it did in LVL-4. Such findings suggest that forcing rats to rise to an erect bipedal stance for feeding helps prevent loss of trabecular and cortical bone "mass," and presumably bone strength, in orchidectomized rats. This method also provides an inexpensive, noninvasive, reliable model to increase in vivo vertebral loading in rats that is similar in humans.

Animals↗
PubMed2000

Making rats rise to erect bipedal stance for feeding partially prevented orchidectomy-induced bone loss and added bone to intact rats.

The objectives of this study were to investigate the different effects on muscle mass and cancellous (proximal tibial metaphysis [PTM]) and cortical (tibial shaft [TX]) bone mass of sham-operated and orchidectomized (ORX) male rats by making rats rise to erect bipedal stance for feeding. Specially designed raised cages (RC) were used so that the rats had to rise to erect bipedal stance to eat and drink for 12 weeks. Dual-energy X-ray absorptiometry (DEXA) and peripheral quantitative computerized tomography (pQCT) were used to estimate the lean leg mass and bone mineral. Static and dynamic histomorphometry were performed on the triple-labeled undecalcified sections. We found that making the intact rats rise to erect bipedal stance for feeding increased muscle mass, cortical bone volume, and periosteal bone formation. Orchidectomy increased net losses of bone next to the marrow by increasing bone turnover. Making the ORX rats rise to erect bipedal stance increased muscle mass, partially prevented cancellous bone loss in the PTM, and prevented net cortical bone loss in TX induced by ORX by depressing cancellous and endocortical high bone turnover and stimulating periosteal bone formation. The bone-anabolic effects were achieved mainly in the first 4 weeks in the PTM and by 8 weeks in the TX. These findings suggested that making the rats rise to erect bipedal stance for feeding helped to increase muscle mass and cortical bone mass in the tibias of intact rats, increase muscle mass, and partially prevented cancellous and net cortical bone loss in ORX rats.

Animals↗
PubMed1993

Pseudohypoparathyroidism with osteitis fibrosa cystica: direct demonstration of skeletal responsiveness to parathyroid hormone in cells cultured from bone.

A young girl had tibial osteotomies at age 14 for genu valgum and then had recurrent tibial cysts over a number of years. Hypocalcemia and hyperphosphatemia were first noted at age 21. The diagnosis of pseudohypoparathyroidism was made at age 28, when elevated plasma PTH was detected. Clinical and biochemical features, including a PTH response test and assay of RBC Gs, established the diagnosis of pseudohypoparathyroidism type 1b. Failure to suppress plasma PTH with vitamin D therapy led to an exacerbation of her cystic bone disease; there were widespread lytic lesions radiologically, most of which took up [99mTc]diphosphonate on bone scan. Microradioscopy revealed evidence of resorption of phalangeal tufts. Bone biopsy showed osteitis fibrosa cystica. During an orthopedic procedure, trabecular bone fragments were taken from her right humerus, and bone-derived cells cultured using an explant technique. The cultured cells were osteoblast-like in morphology, fully responsive to PTH, cholera toxin, forskolin, and PGE1 in vitro, and had an alkaline phosphatase and osteocalcin response to 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. Following this examination of skeletal responsiveness, attempts were made to suppress the elevated plasma PTH levels and symptomatic bone disease by optimizing therapy with oral 1,25-(OH)2D3. When bone pain associated with the cystic bone disease failed to resolve, the patient underwent total parathyroidectomy, following which the bone pain gradually resolved. This is the first direct demonstration of PTH responsiveness in cultured bone cells in the syndrome of pseudohypoparathyroidism with osteitis fibrosa cystica.

Adenylyl Cyclases↗
PubMed1988

Recombinant human parathyroid hormone synthesized in Escherichia coli. Purification and characterization.

Recombinant human parathyroid hormone (hPTH) was expressed in Escherichia coli harboring a plasmid containing a synthetic human parathyroid hormone gene under the control of the E. coli lac promoter. Three major forms of the hormone were isolated by acid extraction and purified to homogeneity by high performance liquid chromatography. By amino acid analysis and NH2-terminal sequencing, these were identified as hPTH-(1-84), formyl-methionyl-hPTH-(1-84), and hPTH-(8-84). The recombinant hPTH-(1-84) was immunologically indistinguishable from a World Health Organization standard of extracted native hPTH-(1-84). Recombinant hPTH-(1-84) was also bioactive in renal and skeletal adenylate cyclase assays. In the skeletal bioassay performed in UMR 108 osteosarcoma cells its activity was identical to that of an hPTH-(1-84) standard. In this bioassay, formyl-methionyl-hPTH-(1-84) had 10% of the activity of hPTH-(1-84) and hPTH-(8-84) was inactive. The results demonstrate the importance of isolating hPTH-(1-84) from other recombinant forms and metabolites to achieve full hormonal bioactivity and indicate that purified recombinant hPTH-(1-84) can thereby be obtained which should be a useful source of hormone for both basic and clinical studies.

Adenylyl Cyclases↗
PubMed1986

The relationship between bone apposition rate and vitamin D activity in phosphate-deficient rats.

In rats, phosphorus deficiency (P-) has been shown previously to stimulate the linear bone apposition rate (BAR) and this P- effect is dependent on adequate intake of vitamin D. To investigate further the relative importance of the vitamin D3 metabolites, 1,25(OH)2D3, 24,25(OH)2D3, and 25(OH)D3, in BAR stimulation, we studied, in P- rats, the relationships between BAR and plasma levels of these three vitamin D3 metabolites following vitamin D3 deprivation. Three groups of rats were placed on diets differing only in phosphorus (P) and vitamin D3(D3) content, with one group diet deficient in both P and D3, one diet, P-, D3 replete, and one diet both P and D3 replete. Plasma levels of the three vitamin D3 metabolites, plasma Ca and P, isotopic Ca absorption and BAR measurements were carried out at 1, 3, and 5 weeks after onset of the test diets. In P-, D3 replete rats, both plasma levels of 1,25(OH)2D3 and BAR were increased throughout the 1 to 5 week study period, while 25(OH)D3 and 24,25(OH)2D3 levels were not significantly different from P and D3 replete controls. In P-, D3 restricted rats, BAR was decreased by one week, prior to any reduction in plasma levels of 25(OH)D3 and 24,25(OH)2D3 and while plasma 1,25(OH)2D3 levels were still well above control values. In this P- rat model, the vitamin D dependent BAR stimulation does not appear to be directly related to alterations in the plasma levels of 1,25(OH)2D3, 24,25(OH)2D3, or 25(OH)D3.

24,25-Dihydroxyvitamin D 3↗
PubMed1986

Synthesis of mutant parathyroid hormone genes via site-specific recombination directed by crossover linkers.

A synthetic 'crossover linker' technique has been designed for gene modification. The linker has a restriction end for an initial 'cohesive end' ligation with one terminus of a linearized plasmid, a middle section carrying modified sequence information, and an 'homology-searching' sequence of 20 bp at its other end, that is homologous to a specific region in the opposite terminus of the plasmid. Inside the Escherichia coli transformation host, intramolecular recombination between the homologous ends of the resultant plasmid intermediate completes the integration of the linker. Using different crossover linkers, a human parathyroid hormone gene which had previously been cloned into plasmid pUC8 was converted to mutant coding sequences via specific base substitution, sequence deletion and sequence insertion.

Base Sequence↗
PubMed1986

Hybrid gene synthesis: its application to the assembly of DNA sequences encoding the human parathyroid hormones and analogues.

Bypassing any intermediate steps of purification and gene assembly, several synthetic oligonucleotides constituting a DNA duplex with a small base-mismatching region were phosphorylated, annealed, and ligated directly into a linearized plasmid vector. After transformation in bacteria, the two plasmid strands individually yielded two different plasmids bearing altered versions of the same gene. Via this approach, DNA coding sequences of the human parathyroid hormone and analogues were synthesized and cloned in Escherichia coli.

Amino Acid Sequence↗
PubMed1986

The effect of vitamin D on bone in vivo.

The linear rate of bone mineral apposition (BMAR) was measured in vitamin D-deficient and vitamin D-sufficient adult rats before and during treatment with either 25-hydroxyvitamin D3 (25OHD3), 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], or 24,25-dihydroxyvitamin D3 [24,25-(OH)2D3]. Dietary vitamin D restriction caused a fall in BMAR which began after 1 week and fell progressively to a value of 35-50% of control values by 4 weeks. The fall in BMAR was related to a fall in the serum concentrations of 25(OH)D3 and 24,25-(OH)2D3, without a fall in the 1,25-(OH)2D3 concentration. Dietary supplementation of the D-deficient animals with either 25OHD3 or 24,25-(OH)2D3 at doses of 200 ng/day restored BMAR. If vitamin D-deficient animals were thyroparathyroid-ectomized before supplementation with vitamin D metabolites, 24,25-(OH)2D3 administration was without effect on BMAR. The combined administration of PTH and 24,25-(OH)2D3 to such animals led to a restoration of the BMAR to normal. In vitamin D-sufficient animals, parathyroidectomy led to a 50% reduction in BMAR, which could be restored by treatment with PTH alone but not with 24,25-(OH)2D3. Simultaneous treatment of these animals with PTH and 24,25-(OH)2D3 led to a greater than normal increase in BMAR (130% of control) in these animals. These data support the concept that 24,25-(OH)2D3 has a role in the regulation of bone formation and/or mineralization, and demonstrate the interrelation between the effects of PTH and 24,25-(OH)2D3 on bone.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

The effect of fluoride on nephrocalcinosis in rats.

To investigate the effects of fluoride on soft tissue calcification, female weanling rats were fed a nephrocalcinogenic diet and NaF in drinking water over a 4 week period. The diet contained adequate Ca (0.5%) and high phosphorus (1.0%, P). The nephrocalcinosis is attributed to the relatively low dietary Ca/P ratio since addition of Ca to provide a Ca/P ratio of 2.0 prevents kidney calcification. With NaF in drinking water at levels of 1.19 to 4.76 mmol/L kidney calcification was decreased from 127 +/- 24 to 17.3 +/- 1.7 mumol/g wet weight, with no significant differences over this dose range. With the increasing NaF doses, serum F, at 4 weeks, increased from 4.4 +/- 0.8 to 36.5 +/- 6.0 mumol/L compared to untreated F levels of 1.2 +/- 0.1 mumol/L. Bone histology showed no evidence of F stimulation with any of these NaF doses. Previously reported work has shown that, for weanling rats on this diet, greater than 4.8 mumol/L NaF in drinking water is required to produce histological fluorosis within 5 weeks. To inhibit kidney calcification, NaF treatment must be maintained throughout the 4-week study period since calcification occurred if NaF was withheld over either the initial or final 2-week period. These findings indicate a possible therapeutic value of NaF, clinically, in the prevention of soft tissue calcification.

Animals↗
PubMed1984

Skeletal response in rats following the implantation of hypercalcemia-producing Leydig cell tumors.

The effect of Rice H-500 Leydig cell tumor tissue on bone in rats was assessed by morphometric analysis and tetracycline labeling of the lower femoral metaphyses. The rats in which tumor was implanted showed hypercalcemia, increased osteoclastic bone resorption, inhibition of bone formation with reduction in the bone apposition rate, and a loss in trabecular volume compared with the control rats. There was no evidence of tumor metastasis to bone. The results are consistent with the hypothesis that the Leydig cell tumor secretes a humoral factor capable of causing systemic bone resorption.

Animals↗
PubMed1984

The effect of diet calcium on fluoride toxicity in growing rats.

The effect of dietary Ca in response to fluoride (F) treatment was investigated in rats. Rats were maintained on either adequate (0.5%) or high (2.0%) dietary Ca and given for 5 weeks, NaF in drinking water. The minimum NaF levels that inhibited body growth and reduced survival were 300 mg/L with 0.5% diet Ca and 550 mg/L with 2.0% diet Ca. With these toxic F doses, bone histology showed increased formation surfaces and thickened osteoid seams (osteoid index 6-7%). Fluoride doses 30% below toxic levels (200 and 350 mg/L for 0.5 and 2.0% diet Ca, respectively) had no demonstrable effect on bone. Additional diet Ca reduced F absorption from 76 +/- 3 to 47 +/- 3% for 0.5 and 2.0% diet Ca, respectively. Comparable absorbed doses of F produced comparable effects on bone and body growth but, with additional dietary Ca, these effects were observed with 50% lower serum and bone F levels. Variable response to NaF therapy can be produced in rats by alterations in dietary Ca alone. Results indicate that for clinical treatment the NaF dose needs to be adjusted on an individual basis but neither serum nor bone F levels can be used reliably to establish optimal doses.

Animals↗
PubMed1982

Increased bone apposition in primary hyperparathyroidism: measurements based on short interval tetracycline labeling of bone.

Bone biopsies of 23 subjects suffering from primary hyperparathyroidism, which was proven by the demonstration of parathyroid pathology during neck surgery, were studied by morphometric analysis and short interval sequential tetracycline labelling and compared with those of 13 patients without metabolic bone disease. In 19 of these patients, abnormalities were found in the trabecular volume, resorption surface, formation surface, or in various combinations. However, no constant pattern of bone changes was observed. In 4 patients, the bone morphometric parameters were normal. The bone apposition rate, on the other hand, was elevated in all 23 subjects. The rate was re-evaluated in 4 patients 6 wk to 3 mo following successful parathyroid surgery. It fell back within the control range. These findings confirm the observation in experimental animals that parathyroid hormone stimulates bone apposition in vivo and give support to the rationale of using this hormone in the treatment of osteoporosis.

Adolescent↗
PubMed1982

Plasma vitamin D metabolite levels in phosphorus deficient rats during the development of vitamin D deficient rickets.

Plasma levels of the vitamin D metabolites were related to changes in bone morphology during the development of rickets in rats deprived of phosphorus and vitamin D. Weanling rats were studied at 1, 3, and 5 wk after onset of diets deficient in phosphorus or in both phosphorus and vitamin D. Bone histology and morphometry were carried out and measurements were made of 45Ca and 32P absorption, serum Ca and P, and plasma 25(OH)D3, 24,25(OH)2D3 and 1,25(OH)2D3. After 1 wk of vitamin D restriction, the plasma levels of 25(OH)D3 and 24,25(OH)2D3 were non-detectable (less than 0.5 and less than 0.8 ng/ml). The plasma 1,25(OH)2D3 level was elevated at 1 wk (105.5 pg/ml) and fell to 19 pg/ml by 5 wk. At 1 wk mild rachitic lesions in epiphyseal cartilage were observed despite the elevated 1,25(Oh)D3 level. Serum Ca and P levels and values for 45CA and 32P absorption decreased and the severity of the rickets increased with the fall in plasma levels of 1,25(OH)2D3. In Vitamin D replete, phosphate deficient rats the epiphyseal cartilage was normal throughout the 5 wk study period. Our results provide further evidence that physiological levels of 1,25 (OH)2 D3 will not prevent rickets without adequate plasma concentrations of either 25(OH)D3 or 24,25(OH)2D3.

Animals↗
PubMed1982

Parathyroid hormone stimulates the bone apposition rate independently of its resorptive action: differential effects of intermittent and continuous administration.

The deposition of mineralized bone matrix by differentiated osteoblasts was studied in rats in vivo by labeling the bone with three doses of tetracycline given at 48-h intervals. Only bone formation loci bearing all three tetracycline doses were measured, thus eliminating sites where bone formation was not continuous during the labeling period. Using this technique, the effects of intact bovine parathyroid hormone [bPTH-(1-84)] and of a synthetic amino-terminal fragment of human PTH [hPTH-(1-34)] were measured in thyroparathyroidectomized animals. bPTH-(1-84), administered sc, and hPTH-(1-34), administered iv, caused a dose-dependent increase in the bone apposition. Subcutaneous administration of hPTH-(1-34) in doses varying from 2.7-173.0 pmol/rat.day had no effect, probably due to the degradation of the hormone when administered this way. We also compared the effects of bPTH-(1-84) when administered by either daily sc injections or continuous infusion. Continuous infusion of bPTH-(1-84) resulted in an increased apposition rate. Using a morphometric technique, we also found an increase in both formation and resorption surfaces and a net decrease in the trabecular bone volume in this group. Daily injection of the hormone caused an increase in the bone apposition rate, accompanied by an increase in the formation surface without an increase in the resorption surface. This resulted in a net increase in trabecular bone volume. The results thus suggest that the resorptive effects of bPTH-(1-84) can be separated from the effects of the hormone on the apposition rate.

Animals↗