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Biomedical subjects

G Nicholson

Publications and source records attributed to G Nicholson.

At least 55 records · Page 3Linked to original sources
PubMed1998

Lifestyle factors fail to explain the variation in plasma leptin concentrations in women.

To assess the relationship between circulating leptin concentrations, metabolic parameters, and lifestyle factors such as alcohol intake, physical activity level, smoking habits, and reproductive history, a cohort of 359 women was drawn from a population-based study conducted in Victoria, Australia. The parameters measured included body mass index (BMI); waist and hip circumference; blood pressure; and fasting glucose, insulin, triacylglycerol, cholesterol, and leptin concentrations. In addition, a self-administered questionnaire was used to assess reproductive history, physical activity level, alcohol intake, and smoking habits. Our results demonstrated that BMI, body weight, waist circumference, and hip circumference were all strongly correlated with circulating leptin concentrations in this population (r > 0.56, P < 0.001 in all cases). Waist/hip ratio, triacylglycerols, insulin, glucose, and cholesterol were also associated with leptin (P < 0.05), but there was no association between leptin and age, height, or blood pressure. When these associations were adjusted for BMI, age, glucose, and waist circumference were significantly associated with leptin. The lifestyle factors examined did not help to explain the observed variation in leptin concentrations between individuals when results were adjusted for degree of adiposity and age.

Adult↗
PubMed1997

A multicenter, double-blind, one-year study comparing safety and efficacy of atorvastatin versus simvastatin in patients with hypercholesterolemia.

We directly compared the safety and efficacy of atorvastatin and simvastatin in hypercholesterolemic patients. This 1-year, randomized, double-blind study was performed at 9 community- and university-based research hospitals in Australia. One-hundred seventy-seven patients between the ages of 18 and 80 years with baseline low-density-lipoprotein (LDL) cholesterol > or = 4.14 and < or = 7.76 mmol/L (160 and 300 mg/dl, respectively) and triglycerides < or = 4.52 mmol/L (400 mg/dl) received once-daily dosing with atorvastatin (Lipitor) 10 mg or simvastatin (Zocor) 10 mg. At week 16, the dose of medication was titrated to atorvastatin 20 mg or simvastatin 20 mg if patients did not meet LDL cholesterol target of < or = 3.36 mmol/L (130 mg/dl). Efficacy was reported as percent change from baseline in LDL cholesterol, total cholesterol, very low density lipoprotein cholesterol, total triglycerides, high-density lipoprotein cholesterol, apolipoproteins AI and B, and lipoprotein(a). Atorvastatin caused significantly greater reductions from baseline than did simvastatin for LDL cholesterol, total cholesterol, very low density lipoprotein cholesterol, triglycerides, and apolipoprotein B (p <0.05). No patient in either treatment group had clinically important elevations in creatine phosphokinase, alanine aminotransaminase, or aspartate aminotransaminase. No serious adverse events were considered associated with treatment. With atorvastatin 10 mg, 46% of the patients achieved LDL cholesterol target goal by week 16, whereas only 27% of the simvastatin patients achieved the target goal at the 10-mg dose. This cholesterol-lowering profile affords utility in many patient types.

Adult↗
PubMed1997

K-ras mutation and loss of heterozygosity of chromosome 17p and survival in colorectal cancer.

BACKGROUND: The development of colorectal cancer (CRC) is thought to be a multistage process involving alterations to several types of genes, including oncogenes and tumour suppressor genes. This study examined the associations between allelic deletions of chromosome 17p in the region of the p53 gene and K-ras gene mutation and survival among CRC patients. METHODS: Resected specimens from 233 patients were examined. Point mutation of codon 12 of K-ras was assessed using a modified polymerase chain reaction method. Allelic deletion of 17p was demonstrated by loss of heterozygosity (LOH) with the marker Mfd144. RESULTS: Fifty-seven tumours (24%) showed somatic point mutation of codon 12 of K-ras and 86 tumours (37%) showed LOH of Mfd144. There were 107 tumours (46%) with either K-ras mutation or LOH and 18 tumours (8%) with both. Compared with patients with neither alteration, significantly poorer survival was experienced only by those with both alterations (P = 0.015). However, when this variable was introduced into a multivariate analysis controlling for the patient's age and tumour stage, it failed to show a statistically significant independent effect on survival. CONCLUSIONS: Point mutation of K-ras and LOH of Mfd144 in CRC does not add to the prognostic information already available from clinicopathological staging.

Adult↗
PubMed1996

A novel homozygous mutation of the myelin Po gene producing Dejerine-Sottas disease (hereditary motor and sensory neuropathy type III).

We have previously reported that heterozygosity for myelin Po gene mutations were associated with Charcot-Marie-Tooth disease type 1B (CMT1B) or Dejerine-Sottas disease. We investigated the Po gene in a family with clinical Dejerine-Sottas disease and found two children were homozygous for a deletion of Phe 64. The parents were heterozygous first cousins with subclinical CMT1B and slow nerve conduction velocities. These results suggest that the effect of homozygous Phe 64 deletion on impairment of myelination is dosage-dependent. Clinical phenotype and/or myelin impairment may be determined both by the type of mutation and by the dosage of mutated gene.

Base Sequence↗
PubMed1996

Slowing of central conduction in X-linked Charcot-Marie-Tooth neuropathy shown by brain stem auditory evoked responses.

BACKGROUND: The most common form of CMT with slow nerve conduction velocities (CMT type I) is CMT1A, caused by a submicroscopic duplication of a region of DNA on chromosome 17 including the PMP22 gene. This gene is expressed in peripheral nerve but not in the CNS. The second most common form is CMTX, caused by mutations in the connexin32 gene in the X chromosome. Connexin32 is expressed both in brain and in peripheral nerve. These molecular variants are difficult to distinguish clinically. METHODS: Brain stem auditory evoked responses (BAERs) were measured in patients with CTMX and CMT1A. RESULTS: BAERs showed central conduction slowing in male patients with CMTX which did not overlap the normal range. Patients with CMT1A had a delay in wave I latency but otherwise normal responses. These results are consistent with the pattern of expression of PMP22 in the peripheral portion of the eighth nerve (myelinated by Schwann cells) and of connexin32 in the central portion in the brainstem auditory pathways (myelinated by oligodendrocytes). This is the first evidence for central involvement in CMTX. CONCLUSION: BAERs are useful to distinguish CMTX from CMT1A and may assist selection of appropriate patients for connexin32 mutation analysis.

Adolescent↗
PubMed1996

Machado-Joseph disease in east Arnhem Land, Australia: chromosome 14q32.1 expanded repeat confirmed in four families.

Four kindreds of east Arnhem Land Australian aboriginal people from Groote Eylandt and adjacent communities display symptoms of a similar spinocerebellar degeneration (multiple-system degenerative disease). The familial pattern indicates an autosomal dominant inheritance, though with varying penetrance in different families. This condition is clinically and pathologically consistent with Machado-Joseph disease (MJD), and there is the possibility of Portuguese ancestry. These families exhibit anticipation, particularly in the case of paternal inheritance, with those with earlier age of onset presenting a clinical pattern consistent with MJD type I. There was no expansion of the CAG repeat region of the SCA1 gene in these families. The demonstration of expansion of the CAG repeat on chromosome 14q32.1 in all four families confirms the diagnosis of MJD.

Australia↗
PubMed1995

The efficacy of the disinfection of bronchoscopes contaminated in vitro with Mycobacterium tuberculosis and Mycobacterium avium-intracellulare in sputum: a comparison of Sactimed-I-Sinald and glutaraldehyde.

The efficacy of Sactimed-I-Sinald and glutaraldehyde was tested against clinical isolates of Mycobacterium tuberculosis (MTB) and Mycobacterium avium-intracellulare (MAI). An in-use method demonstrated that over 10 disinfection cycles, using an auto-disinfector and a contact time of 60 min, MTB was eradicated in 10 out of 10 cycles with Sactimed-I-Sinald and five out of 10 cycles for glutaraldehyde. For MAI, Sactimed-I-Sinald showed a 5 log reduction at a 60 min contact time, which was not seen with glutaraldehyde. Although further evaluation is necessary, Sactimed-I-Sinald appears a promising alternative to glutaraldehyde.

Bronchoscopes↗
PubMed1995

The effect of mobilization on cervical headaches.

Headaches of cervical origin are often treated with mobilization. Mobilization of the upper cervical spine, occiput-C3, and effect on frequency, duration, and intensity of cervical headaches were studied utilizing an A-B-A single case design. Ten subjects who met the operational criteria of cervical headaches completed the study. A headache log was used to document headache frequency, duration, and intensity throughout all three phases (A-B-A). The baseline phase (A) lasted approximately 1 month, and no intervention was performed. The intervention phase (B) consisted of 9-12 treatment sessions, two times per week for 3-4 weeks. Visual analysis of data plots revealed a decrease in headache frequency, duration, and intensity from the baseline phase to the treatment phase. This improvement continued through the second A phase for frequency but leveled off for both duration and intensity. A one-way analysis of variance supported the findings from the visual analysis. In these 10 subjects, mobilization had a therapeutic effect on cervical headaches.

Adult↗
PubMed1995

Biosynthetic capacities of actinomycetes. 4. Echinoserine, a new member of the quinoxaline group, produced by Streptomyces tendae.

A new member of the quinoxaline group antibiotics has been detected by HPLC-diode-array screening. The main compound produced by Streptomyces tendae strain Tü 4031 showed a high degree of similarity in the UV-visible spectral region with echinomycin and their structural similarity was confirmed by structure elucidation using electron tandem mass spectrometry and 2D nuclear magnetic resonance. The new compound, named echinoserine, is a non-cyclic form of echinomycin, but it is not a biosynthetic precursor. Echinoserine is less antibiotically active than echinomycin.

Antibiotics, Antineoplastic↗
PubMed1994

Evidence for expression of the Joa blood group antigen on the Gya/Hy-active glycoprotein.

The phenotypic association between the non-assigned high-incidence antigen Joa and the Gya collection antigens Gya and Hy was investigated by haemagglutination studies, flow cytometric analysis, immune precipitation and immunoblotting experiments. In haemagglutination tests anti-Joa gave the same pattern of reactivity with erythrocytes pre-treated with pronase, trypsin, alpha-chymotrypsin and thiol reducing agents as did anti-Gya and anti-Hy. In addition, similar to that found for anti-Gya and anti-Hy, anti Joa also showed reduced binding, as determined by haemagglutination and flow cytometric analysis, to erythrocytes from patients with paroxysmal nocturnal haemoglobinuria. Immune precipitates prepared from radio-iodinated antigen-positive red cells with anti-Joa, anti-Gya and anti-Hy gave similar results--a major component of M(r) 49,000-60,000 (the Gya/Hy-active glycoprotein) and a second component of M(r) 85,000-92,000 (this may be a dimer of the Gya/Hy-active glycoprotein, or a coprecipitated protein). These immune precipitates, when probed with both anti-Gya and anti-Hy under non-reducing conditions, gave a positive immunoblotting reaction to both the M(r) 49,000-60,000 and the M(r) 85,000-92,000 components. These results strongly suggest that the Joa antigen is expressed on the same glycoprotein that carries the Gya and Hy antigens.

Blood Group Antigens↗