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Biomedical subjects

L Parry

Publications and source records attributed to L Parry.

17 recordsLinked to original sources
PubMed2004

Anal function following third degree tears.

OBJECTIVE: To assess the anal function of women who have suffered a third degree perineal tear during parturition. PATIENTS: Fifty-three consecutive women who sustained a third degree tear, between January 1998 and March 2000, at the Princess Anne Maternity Unit, Royal Bolton Hospital were assessed. METHODS: Women were assessed at 3 months post partum using the Cleveland Clinic Incontinence Score, digital assessment of anal sphincter and endo-anal ultrasound scan. RESULTS: At 3 months post partum 75% of the participants had no symptoms of anal incontinence, 18% had mild symptoms and 7% had more severe symptoms. Anal endosonography demonstrated normal anal sphincters in 66% of participants, an abnormality in the external sphincter in 29% and a defect in both sphincters in 2%. There was poor correlation between symptoms and scan defects. CONCLUSION: The incidence of anal incontinence following repair of a third degree tear was not high and it is unlikely that we are missing a hidden pool of symptomatic women. No major change in management policy is required. The routine assessment of anal function in women who had sustained a third degree tear was appreciated by the women and enabled us to identify the small portion of women with significant symptoms.

Anal Canal↗
PubMed2003

Four years of monitoring for viral haemorrhagic septicaemia virus in marine waters around the United Kingdom.

Between 1995 and 1998, marine fish from around the coast of the UK were collected and samples analysed for viral haemorrhagic septicaemia virus (VHSV) using cell culture isolation methods. In 1997 and 1998 the samples were also analysed for VHSV by reverse transcription PCR (RT-PCR). A total of 1867 fish of 11 species were tested, but VHSV was isolated on only 1 occasion, from herring Clupea harengus, in 1996. However, despite VHSV not being isolated in 1997 and 1998, in both years samples of herring from the west and south coasts of England produced positive signals in the RT-PCR, and in 1997 cod from the east coast of England also produced positive signals in the RT-PCR. These results are believed to be true indications of the presence of VHSV nucleic acid in the fish. In 1997, birnaviruses from Serogroup B1 were isolated from herring (a previously unrecorded host for the virus) and cod Gadus morhua, and a birnavirus from Serogroup A2 was also isolated from cod. In 1998, an aquareovirus was isolated from haddock Melanogrammus aeglefinus, a previously unrecorded host for the virus.

Animals↗
PubMed2001

Pathological mutations in TSC1 and TSC2 disrupt the interaction between hamartin and tuberin.

Critical functions of hamartin and tuberin, encoded by the TSC1 and TSC2 genes, are likely to be closely linked. The proteins interact directly with one another and mutations affecting either gene result in the tuberous sclerosis phenotype. However, the regions of hamartin and tuberin that interact have not been well defined, and the relationship between their interaction and the pathogenesis of tuberous sclerosis has not been explored. To address these issues a series of hamartin and tuberin constructs were used to assay for interaction in the yeast two-hybrid system. Hamartin (amino acids 302-430) and tuberin (amino acids 1-418) interacted strongly with one another. A region of tuberin encoding a putative coiled-coil (amino acids 346-371) was necessary but not sufficient to mediate the interaction with hamartin, as more N-terminal residues were also required. A region of hamartin (amino acids 719-998) predicted to encode coiled-coils was capable of oligermerization but was not important for the interaction with tuberin. Subtle, non-truncating mutations identified in patients with tuberous sclerosis and located within the putative binding regions of hamartin (N198_F199delinsI;593-595delACT) or tuberin (G294E and I365del), abolished or dramatically reduced interaction of the proteins as assessed by yeast two-hybrid assays and by co-immunoprecipitation of the full-length proteins from Cos7 cells. In contrast, three non-pathogenic missense polymorphisms of tuberin (R261W, M286V, R367Q) in the same region as the disease-causing TSC2 mutations did not. These results indicate a requirement for interaction in critical growth suppressing functions of hamartin and tuberin.

Animals↗
PubMed2001

Analysis of the TSC1 and TSC2 genes in sporadic renal cell carcinomas.

The genetic events involved in the aetiology of non-clear-cell renal cell carcinoma (RCC) and a proportion of clear cell RCC remain to be defined. Germline mutations of the TSC1 and TSC2 genes cause tuberous sclerosis (TSC), a multi-system hamartoma syndrome that is also associated with RCC. We assessed 17 sporadic clear cell RCCs with a previously identified VHL mutation, 15 clear-cell RCCs without an identified VHL mutation and 15 non-clear-cell RCCs for loss of heterozygosity (LOH) at chromosomes 9q34 and 16p13.3, the chromosomal locations of TSC1 and TSC2. LOH was detected in 4/9, 1/11 and 3/13 cases informative at both loci. SSCP analysis of the whole coding region of the retained allele did not reveal any cases with a detectable intragenic second somatic mutation. Furthermore, RT-PCR analysis of TSC1 and TSC2 on total RNA from 8 clear-cell RCC cell lines confirmed expression of both TSC genes. These data indicate that biallelic inactivation of TSC1 or TSC2 is not frequent in sporadic RCC and suggests that the molecular mechanisms of renal carcinogenesis in TSC are likely to be distinct.

Alleles↗
PubMed2000

Molecular analysis of the TSC1 and TSC2 tumour suppressor genes in sporadic glial and glioneuronal tumours.

Reduced expression of the TSC2 tumour suppressor gene product, tuberin, has been reported in sporadic astrocytomas, suggesting that the TSC genes may play a role in formation of sporadic glial or glioneuronal tumours. We studied paired constitutional and tumour DNA samples from 100 patients with sporadic glial and glioneuronal tumours for loss of heterozygosity (LOH) at the TSC1 and TSC2 loci using a combination of seven previously reported and seven novel polymorphic markers. LOH was seen in 1/16 astrocytomas, 3/15 ependymomas, 5/16 gangliogliomas, 2/14 glioblastoma multiforme, 0/7 oligodendrogliomas, 0/7 tumours of mixed oligodendrocytic/astrocytic histology, 2/11 pilocytic astrocytomas and 0/1 subependymal giant cell astrocytomas informative at both loci. However, SSCP screening of all coding exons of the TSC1 or TSC2 genes in the tumours displaying LOH, and of both genes in 21 gangliogliomas, revealed no intragenic mutations. The lack of demonstrable inactivation of both alleles of either TSC gene in any of the tumours investigated suggests that they do not play a frequent role in the aetiology of sporadic glial or glioneuronal tumours.

Alleles↗
PubMed2000

A pilot project to determine the demand for and utility of an out-of-hours psychiatric service run by on-call psychiatric nurses in an A&E department.

This paper presents the results of a 12-week pilot project that studied the demand for and utility of an out-of-hours on-call psychiatric service delivered by two experienced psychiatric nurses in an A&E department. It also considers some of the implications for a possible permanent, substantive service. An initiative to reduce the on-call hours worked by junior medical staff harked back to literature which has long suggested that health professionals, other than medical staff, can competently perform risk assessments and determine the immediate needs of patients who self-harm. The project's aims were to determine: (i) whether an on-call psychiatric nurse could satisfactorily reduce the pressures on on-call junior doctors; and (ii) the absolute demand for and nature of requested out-of-hours psychiatric assistance. Summarized details of referred patients include data on time and duration of contact, reasons for referral, outcome and other professionals involved. Of the 88 patients referred during the pilot period, 33 (37.5% of the total) were admitted to psychiatric wards and four to medical wards. Although a range of professionals was needed during the 12-week period, the nurses dealt with 42 (47.7%) of the referrals without any other professional involvement.

Adolescent↗
PubMed1999

Structure and expression of the rat relaxin-like factor (RLF) gene.

The relaxin-like factor (RLF) is a novel member of the insulin-IGF-relaxin family of growth factors and hormones, and its mRNA is expressed very specifically in the Leydig cells of the testis and in the theca and luteal cells of the ovary. Here we report the cloning of the RLF gene and cDNA from the rat. The 0.8kb mRNA is produced from a small gene comprising two exons situated less than 1 kb downstream of the gene for the signalling factor JAK3. Northern hybridization confirms high RLF mRNA expression in the adult rat testis, and low expression in the ovary, but in no other tissues examined. Northern analysis of fetal and neonatal gonadal tissues showed that RLF mRNA is highly upregulated in the testes of day 19 embryos, but not in later neonatal stages, nor in any ovarian tissue from this period. This would indicate that RLF is a marker for the mature fetal as well as the adult-type Leydig cell, but is not expressed in premature, precursor, or dedifferentiated Leydig cells of either cell type. Finally, RNA was analysed from the testes of rats which had been treated with ethylene dimethane sulfonate (EDS), an alkylating agent that specifically destroys rat Leydig cells. RLF mRNA was absent from the acutely treated testes, but became detectable between 15 and 20 days post-treatment, concomitant with the repopulation of the testes by new Leydig cells. Continuous testosterone substitution of EDS-treated rats suppressed the production of gonadotropins, and LH-dependent Leydig cell differentiation, with the result that RLF mRNA remained undetectable throughout the study period. In conclusion, RLF is a very specific marker for the mature Leydig cell phenotype in both the adult-type and fetal Leydig cell populations of the rat testis.

Amino Acid Sequence↗
PubMed1999

Comparison of lung function in infants exposed to maternal smoking and in infants with a family history of asthma.

STUDY OBJECTIVE: To compare lung function in infants exposed to maternal smoking with lung function in infants with a family history of asthma. There are no published studies comparing lung function in both groups. DESIGN: Cross-sectional study. SETTING: A tertiary pulmonary care center at a children's hospital. PATIENTS: One hundred five infants with daily wheezing. Thirty-five infants had persistent exposure to maternal smoking, and 70 had a family history of asthma in parents or siblings. MEASUREMENTS: Infant pulmonary function tests were compared between the two groups. The ratio of terminal to peak expiratory flow at tidal breathing at 25% of the previous expiration remaining and the ratio of terminal to peak expiratory flow with forced expiration at 25% of the previous expiration remaining (FEF25/PFEF) were used to evaluate peripheral airflow. A > 25% improvement in FEF25/PFEF after a bronchodilator challenge test was considered a positive response. RESULTS: Most infants in both groups had evidence of peripheral airflow obstruction with forced expiration. In infants exposed to maternal smoking, only 4 of 35 (11.4%) responded to a bronchodilator, compared to 51 of 70 (72.9%) in the group with a family history of asthma (p < 0.0005). There was no statistically significant difference in total respiratory system compliance, total respiratory system resistance, tidal volume, and degree of peripheral airflow obstruction at tidal breathing or after forced expiration in both groups. CONCLUSION: Infants with exposure to maternal smoking and infants with a family history of asthma have altered lung function, and a positive response to a bronchodilator is one variable that seems to differentiate the two groups.

Airway Resistance↗
PubMed1995

Effect of expression of human spermidine/spermine N1-acetyltransferase in Escherichia coli.

A plasmid expression vector, pINSAT2, was constructed in order to express spermidine/spermine N1-acetyltransferase (SSAT) in Escherichia coli. Cells transfected with this vector produced large amounts of SSAT, amounting to up to 2% of the soluble protein when isopropyl beta-D-thiogalactopyranoside (IPTG) was added and 0.3% of the soluble protein in the absence of inducer. The growth rate of cells expressing SSAT was reduced, and all of the cellular spermidine was converted to N1-acetylspermidine, much of which was excreted. Putrescine and 1-methylspermidine, which is not a substrate for SSAT, could reverse the effects of SSAT expression on growth, but spermidine was only effective when the amount of SSAT expression was limited by omitting the IPTG inducer. The lack of stimulation of growth by spermidine correlated with its complete conversion to N1-acetylspermidine. These results show that N1-acetylspermine is not able to substitute for the unmodified polyamines in supporting growth and suggest that acetylation is a physiological response to convert excess polyamines to a physiologically inert form which is readily excreted. Cells expressing large amounts of SSAT were much more sensitive to the growth inhibitory action of the antitumor agent N1,N12-bis(ethyl)spermine, supporting the hypothesis that the ability of such bis(ethyl) polyamines to induce SSAT contributes to their antiproliferative actions. SSAT was readily purified to homogeneity from extracts of DH5 alpha cells containing pINSAT2. The purified enzyme had a similar specific activity and Km values for spermine and spermidine as the enzyme purified from human colon cancer cells, suggesting that posttranslational modifications specific to eukaryotes are not needed for enzymatic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetyltransferases↗
PubMed1995

Post-transcriptional regulation of the content of spermidine/spermine N1-acetyltransferase by N1N12-bis(ethyl)spermine.

Spermidine/spermine N1-acetyltransferase (SSAT) is the rate-limiting enzyme for the degradation and excretion of polyamines in mammalian cells, and its activity is known to be increased enormously on exposure to polyamines and polyamine analogues. The mechanism by which such an analogue, BESM [N1N12-bis(ethyl)spermine], increases the content of SSAT was investigated by transfecting COS-7 cells with plasmids containing SSAT cDNA in the pEUK expression vector. Despite a large increase in mRNA production, there was only a very small increase in SSAT activity in the transfected cells. When BESM was added at 36 h after transfection, there was a large and very rapid increase in SSAT protein amounting to 380-fold in 12 h without any increase in the mRNA. SSAT protein turned over very rapidly, with a half-life of about 20 min. In the presence of BESM, this turnover was greatly reduced, and the half-life increased to more than 13 h. However, this increase was not sufficient to account for all of the increase in SSAT protein, suggesting that there is also regulation of the translation of the mRNA by BESM. Further evidence for such translation regulation was obtained by studying the polysomal distribution of the SSAT mRNA. In the absence of BESM, most of the mRNA was present in fractions which sedimented more slowly than the monoribosome peak. In BESM-treated cells, a significant proportion of the SSAT mRNA was moved into the small-polysome region of the gradient. The expression of SSAT and the effects of BESM on the polysomal distribution of SSAT mRNA were not affected by the 5'- or 3'-untranslated regions of the mRNA, since constructs which lacked all of these regions gave similar results to constructs containing the entire mRNA sequence. These results show that the increased transcription of the SSAT gene that occurs in the presence of polyamine analogues such as BESM is not sufficient for SSAT expression and that post-transcriptional regulation is critical for the control of SSAT content.

Acetyltransferases↗
PubMed1986

Surgery for thoracic outlet syndrome may be hazardous to your health.

We are reporting five patients who suffered serious injuries from surgery for thoracic outlet syndrome, which has been a controversial subject from many aspects. Many argue that it is much overdiagnosed and overtreated. The term "disputed thoracic outlet syndrome" has recently been applied to the majority of cases in which there are little or no clinical findings. The much more rare true neurogenic thoracic outlet syndrome does have associated neurologic and electrical findings. Recently, the use and misuse of electrodiagnostic studies in the diagnosis of disputed thoracic outlet syndrome has been discussed in the literature. The cases that we are reporting are especially tragic because the elective surgeries were performed in patients who had little or no clinical abnormalities on examination prior to the surgery.

Adult↗
PubMed1980

Nutritional consequences of low dose milk supplements consumed by lactose-malabsorbing children.

The nutritional consequences of supplementary milk consumption by lactose-malabsorbing children were determined by nutrient balance studies. Twelve subjects received a marginally adequate rice and vegetable base-line diet alone and with simulated milk supplements containing either glucose or lactose during three separate balance periods. The diets were equally well accepted and tolerated. The children gained significantly more weight and had improved apparent nitrogen absorption and retention on the milk supplemented diets (P less than 0.001), and there was no difference between the effects of glucose milk and lactose milk. Fecal wet weights and energy and carbohydrate excretions were modestly increased with the lactose-containing diet, but not significantly so. It is suggested that low dose milk supplements can be well utilized when consumed by lactose malabsorbers in conjunction with other foods. Milk consumption need not be discouraged for populations among whom lactose malabsorption is widely prevalent, but milk should be provided in relatively low doses and the clinical responses to its consumption should be monitored.

Animals↗
PubMed1979

Lactose malabsorption in Bangladeshi village children: relation with age, history of recent diarrhea, nutritional status, and breast feeding.

The prevalence of lactose malabsorption (LM) among Bangladeshi village children has been determined using the recent developed breath hydrogen test. Initial hospital-based comparison studies showed general agreement between the breath hydrogen test and a modified lactose tolerance test. Two hundred thirty-four children, stratified by age, nutritional status, and history of recent diarrhea then participated in the field study. LM was diagnosed in more than 80% of children over 36 months of age but in none of the children under 6 months. Rates of LM were significantly increased in children with a history of recent diarrhea and a greater proportion of children in some age groups evidenced malabsorption in association with acute undernutrition. In the weanling age group children who were still breast feeding had a lower rate of LM than fully weaned subjects.

Adolescent↗