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Biomedical subjects

R Lynch

Publications and source records attributed to R Lynch.

At least 19 recordsLinked to original sources
PubMed2006

Validation of a self-completion measure of breakfast foods, snacks and fruits and vegetables consumed by 9- to 11-year-old schoolchildren.

OBJECTIVE: To evaluate the validity and reliability of a dietary recall questionnaire, designed for group-level comparisons of foods eaten at breakfast and intake of fruits, vegetables, sweet items and crisps. DESIGN: Validity was assessed relative to 24-h dietary recall interviews, and reliability by comparing the baseline data with 4-month follow-up data. SUBJECTS AND SETTING: Fifty-eight schools took part in the validity assessments, with 374 children completing both measures. Reliability was assessed using 29 schools, with 1233 children at baseline and 1033 at follow-up. Children were aged 9-11 years and schools were located in socio-economically deprived areas of Wales. RESULTS: Results indicated moderate to substantial agreements for most foods eaten at breakfast on the day of reporting and fair to moderate agreements for breakfast foods the previous day. For items throughout the rest of the previous day, agreement was fair to substantial during school hours, but slight after school. Correlations were moderate in terms of 'healthy' items and 'unhealthy' items consumed at breakfast on the day of reporting, but weaker for the previous breakfast. Correlations between measures in terms of fruits, vegetables, sweet items and crisps throughout the rest of the previous day were fair to moderate. The measure demonstrated fair to substantial group-level reliability. CONCLUSIONS: The questionnaire, while subject to a number of limitations, gives an adequately valid and reliable overview of selected aspects of children's diet. It is likely to be of value at group-level in randomized controlled trials of school-based interventions.

Child↗
PubMed2004

Reducing medication errors in the neonatal intensive care unit.

BACKGROUND: Medication errors are common in the neonatal intensive care unit (NICU). Various strategies to reduce errors have been described in adult and paediatric patients but there are few published data on their effect in the NICU. AIM: To describe the medication errors occurring within an NICU, and assess the impact of a combined risk management/clinical pharmacist led education programme on these errors. METHODS: Medication errors were identified prospectively over one year by critical incident reporting. Four months into the study, a pharmacist led education programme was instituted. This involved a daily, cot side, pharmacist led review of medication orders. Each new member of pharmacy, nursing, or medical staff was also required to successfully complete a series of dose calculations. In addition, a risk management approach was used to make several changes in practice during the study period. RESULTS: A total of 105 errors were identified, four serious, 45 potentially serious, and 56 minor. The four serious errors included two tenfold dose miscalculations. Most (71%) of the errors were due to poor prescribing. After the introduction of our interventions, monthly medication errors fell from a mean (SD) of 24.1 (1.7) per 1000 neonatal activity days to 5.1 (3.6) per 1000 days (p < 0.001) in the following three months. The subsequent change over of junior medical staff was associated with a significant increase in medication errors to 12.2 (3.6) per 1000 neonatal activity days (p = 0.037). However, the number remained significantly less than before our interventions (p < 0.001). Three serious errors occurred in the first four months compared with one in the second eight month period, the latter corresponding to the six monthly change over of junior medical staff. CONCLUSIONS: Medication errors are common in NICUs. Fortunately, actual harm to an infant is rare. Interventions to reduce errors, particularly within the context of a risk management programme, are effective.

Drug Prescriptions↗
PubMed2001

Carbon monoxide poisoning: correlation of neurological findings between accident and emergency departments and a hyperbaric unit.

OBJECTIVES: To investigate and quantify the differences in neurological examination findings in patients acutely poisoned with carbon monoxide, between initial assessment at accident and emergency (A&E) departments and subsequently at a hyperbaric unit. METHODS: Retrospective case note review of all patients referred to the Hull Hyperbaric Unit for treatment of acute carbon monoxide poisoning between August 1998 and August 1999. Patients who were ventilated or less than 16 years old were excluded because of difficulty in assessing their neurological status. RESULTS: Thirty patients were included for analysis. The mean duration from exposure to assessment in A&E was four hours while patients were reviewed on average three hours later at the hyperbaric unit. Referrals came from 14 different hospitals. A history of loss of consciousness accounted for 70% of referrals. A mean of 3.2 neurological signs per patient was documented in A&E compared with 9.2 at the hyperbaric unit. Seventy nine per cent of abnormal neurological signs were not detected at A&E departments compared with 3% at the hyperbaric unit. The major source of discrepancy was in sharpened Rhomberg's test and heel-toe gait, in 13% of patients examined in A&E departments these signs were recorded as abnormal compared with 90% at the hyperbaric unit. CONCLUSION: There is a large discrepancy in neurological findings between assessment in A&E departments and the Hull Hyperbaric Unit. A number of factors may account for this including interobserver variation, patient deterioration during transfer, poor documentation, lack of understanding of the sequelae of carbon monoxide poisoning and inadequate examinations. Further research is required to quantify the impact of the various factors that may contribute to the differences in neurological findings.

Adolescent↗
PubMed2000

Cytologic atypia in a 53-year-old man with finasteride-induced gynecomastia.

Finasteride has been associated with the development of gynecomastia. Although cytoplasmic vacuolization has been noted in prostatic epithelium in men taking this drug, we found no documentation of the cytologic changes in finasteride-associated gynecomastia. We present the case of a 53-year-old man who developed unilateral gynecomastia following finasteride therapy for alopecia. A fine-needle aspiration biopsy of the mass was diagnosed as adenocarcinoma on the basis of nuclear atypia and particularly because of cytoplasmic vacuolization. Subsequent excisional biopsy revealed benign gynecomastia with no evidence of malignant change. The ductal epithelium did exhibit cytoplasmic vacuolization similar to that described in the prostate following finasteride therapy. We believe this is the first reported case documenting the cytologic changes seen in gynecomastia secondary to finasteride therapy. Cytoplasmic vacuolization in this setting should not be considered evidence of malignancy in men with gynecomastia. As with gynecomastia in general, extreme caution should be used before rendering a cytologic diagnosis of malignancy.

Alopecia↗
PubMed1999

Reconstructive surgery in children after meningococcal purpura fulminans.

BACKGROUND/PURPOSE: Purpura fulminans (PF) is a serious, often life-threatening disease. As more children are surviving their disease, surgeons are presented with increasing numbers of multiple and complicated wounds as sequelae of PF. The purpose of this paper is to review the management of nine cases of PF, and present the reconstruction method in treating bilateral exposed elbow and knee joints. METHODS: All cases of pediatric patients with PF and treated by the division of plastic and reconstructive surgery between 1986 and 1998 were reviewed. RESULTS: Seven children (78%) had meningococcal PF, and one (11%) had PF after Haemophilus influenza septicemia. PF developed in one (11%) but with no growth in either blood or cerebrospinal fluid cultures. Five children (56%) required amputation procedures. Two children (22%) required knee disarticulation. Two patients (22%) had free myocutaneous flap transfers for bone coverage. One (11%) had PF involving the face. CONCLUSIONS: Meningococcal PF is a rare, often life-threatening disease generally of childhood. More children are surviving their diseases but with devastating sequelae. Successful reconstructive treatment outcome of these children requires a multidisciplinary team approach involving multiple specialties. The goal is to preserve function, maintain maximal length, and salvage limbs when possible. Flexibility and innovation are necessary in treating these multiple and complicated wounds.

Amputation, Surgical↗
PubMed1999

Pharmacokinetic and glucodynamic comparisons of recombinant and animal-source glucagon after IV, IM, and SC injection in healthy volunteers.

The structure of the hormone glucagon is identical among humans and several species of other mammals. Equivalence of recombinant glucagon (rG) to animal-source glucagon (aG) was assessed in this two-part, open-label, randomized study. Part I was a four-way crossover intravenous dose-ranging study of rG (pH 2.8) involving 12 subjects. Part II was a six-way crossover study of 29 subjects comparing rG (diluent pH 2.0 and 2.8) with aG administered subcutaneously (sc) and intramuscularly (im). Maximum glucagon plasma concentrations (C(max)) and area under the glucagon concentration curve (AUC) were calculated. Additionally, maximum blood glucose concentrations (BG(max)), maximum absolute BG excursion (MAE), and area under the glucose concentration curve from time of dosing to return to baseline (AUC(rtb)) were calculated. The primary focus was equivalence of the formulation intended for marketing (rG pH 2.0) to aG. Administration of rG pH 2.0 through the im route demonstrated equivalence to aG for all pharmacokinetic and glucodynamic comparisons. Subcutaneous administration of rG pH 2.0 demonstrated standard bioequivalence for AUC (5.87 versus 6.63 ng x h/mL; NS) and near equivalence for C(max) (7.94 versus 9.12 ng/mL; p < 0.05). rG pH 2.0 showed glucodynamic equivalence to aG (BG(max), 136 versus 133 mg/dL; MAE, 50.0 versus 47.4 mg/dL, respectively) and statistically greater AUC(rtb) values (151 versus 126 mg x h/dL, p < 0. 05). rG and aG were equally safe and well tolerated. In conclusion, rG provides equivalent safety and efficacy to aG.

Adult↗
PubMed1998

Localization and regulation of IFN-gamma production within the granulomas of murine schistosomiasis in IL-4-deficient and control mice.

Schistosome granulomas from normal or IL-4-deficient C57BL/6 mice make little IFN-gamma and show no Th1 polarization. This could signify that these granulomas have few cells capable of IFN-gamma synthesis or that such cells are under tight control. Granulomas can make IL-10 and TGF-beta, which can regulate IFN-gamma synthesis. Using FACS analysis and ELISA, we explored the origin and regulation of IFN-gamma in schistosome granulomas from both IL-4(-/-) and IL-4(+/+) mice. FACS analysis of intracytoplasmic IFN-gamma staining showed that some granuloma Thy1.2+ T cells (CD8+ and CD4+) express IFN-gamma. Granulomas had NK1.1+ cells, but they appeared to produce little or no IFN-gamma. Purified granuloma Thy1.2+ cells made IFN-gamma in vitro, whereas isolated NK1.1+ lymphocytes secreted little even with rIL-12 stimulation. Culture of granuloma cells with blocking anti-IL-10 or anti-TGF-beta mAb or with rIL-12 substantially increased T cell IFN-gamma synthesis, particularly in the IL-4(-/-) animals. Cultured granuloma cells depleted of Thy1.2+ lymphocytes by Ab and C released no IFN-gamma. It is concluded that granuloma IFN-gamma comes from T cells, not NK cells. Also, this T cell-derived IFN-gamma is subject to IL-10 and TGF-beta regulation, which is particularly evident in IL-4(-/-) mice. Thus, the Th2 granuloma of schistosomiasis has large numbers of activated Th1 or Th0 lymphocytes that are under tight restraint.

Animals↗
PubMed1996

The granulomatous response in murine Schistosomiasis mansoni does not switch to Th1 in IL-4-deficient C57BL/6 mice.

IL-4 plays an important role in polarizing inflammation toward a Th2 response. It remains uncertain, however, whether IL-4 also serves to prevent expression of Th1 inflammation. Therefore, using a genetically pure C57BL/6 IL-4-deficient mouse, we studied the role of IL-4 in regulating the production of IFN-gamma and Th1 inflammation in the granulomas of mice infected with Schistosoma mansoni. In contrast to normal animals, IL-4 mutant mice generated smaller liver granulomas that contained fewer eosinophils and no mast cells. Collagenase-dispersed granuloma cells were analyzed by flow cytometry and cultured in vitro to measure cytokine and Ig production. Compared with control granuloma cells, IL-4-/- cells secreted only small quantities of IL-5 and IL-10. Also, there was impaired expression of the IL-4-dependent molecules IgE and IgG1 as well as B cell surface class II and CD23. Yet the granulomas of IL-4 -/- animals produced little IFN-gamma, IgG2a, or other molecules associated with Th1 inflammation even after Ag or anti-CD3 stimulation. Splenocytes from IL-4 -/- animals stimulated with schistosome Ag also failed to produce a Th1 response. Our data show that most aspects of the Th2 response in murine schistosomiasis are highly dependent on IL-4 production. But in the absence of IL-4, neither the natural local granulomatous response to schistosome ova nor the systemic response to soluble egg Ag switches to the type 1 phenotype. Thus the production of IL-4 early in the inflammatory response is not the only factor preventing Th1 expression in inflammation.

Animals↗
PubMed1996

Substance P receptor antagonist inhibits murine IgM expression in developing schistosome granulomas by blocking the terminal differentiation of intragranuloma B cells.

Schistosome granulomas make substance P (SP). CP96,345 is a nonpeptide SP receptor antagonist active in vivo. Granulomas that form in the presence of SP receptor blockade produce little IgM as compared to normal lesions. The objective of this study was to determine how CP96,345 modulates granuloma IgM production. Schistosome ova were embolized to the lungs of infected mice to induce granulomas of synchronous age. Animals received CP96,345 (50 mg/kg/day) for 4 days following egg embolization. Then granulomas were isolated from tissue and dispersed into single-cell preparations. The dispersed granuloma cells were cultured in vitro to measure IgM and cytokine secretion. Also, granuloma B cells were studied using an IgM ELISPOT assay and flow cytometry. As expected, mice treated with CP96,345 formed granulomas that secreted little IgM. Granulomas from CP96,345-treated mice, as compared to buffer-treated animals, contained few IgM-secreting B lymphocytes, but had appropriate numbers of B cells expressing surface IgM. Also decreased was the capacity of the granulomas to make IFN-gamma, IL-4, IL-5 and IL-6. CP96,345 treatment did not affect splenocyte IgM or cytokine synthesis. These data suggest that CP96,345 inhibits granuloma IgM secretion by blocking intragranuloma B cell maturation at a terminal stage of B cell differentiation. Moreover, SP receptor antagonist affects a variety of cytokine circuits that could influence IgM B cell maturation in vivo.

Animals↗
PubMed1995

Precise mapping of t(12;14) leiomyoma breakpoint on chromosome 14 between D14S298 and D14S540.

Uterine leiomyoma is a common tumor of smooth muscle cell origin often characterized by the presence of a balanced t(12;14)(q13-15;q24.1) chromosomal translocation. This breakpoint on chromosome 14 had previously been placed between the markers SPTB and D14S77, a region estimated to span 7 cM. In this study we have used a meiotic breakpoint mapping panel to construct a high resolution genetic map of this interval. Markers that mapped within this interval were used to analyze DNA from a somatic cell hybrid containing the t(12;14) translocated chromosome. The results of this analysis localize the t(12;14) breakpoint on chromosome 14 between D14S298 and D14S540, between which no meiotic recombination was detected. This sets the stage for identifying the gene(s) disrupted by the chromosomal translocation by defining the markers that flank the translocation breakpoint.

Base Sequence↗
PubMed1994

T lymphocytes isolated from the hepatic granulomas of schistosome-infected mice express somatostatin receptor subtype II (SSTR2) messenger RNA.

Schistosomiasis mansoni is a disease characterized by liver and intestinal granulomas. Previous investigations in our laboratory showed that nylon wool-adherent CD4+ T lymphocytes isolated from murine hepatic schistosome granulomas express receptors for somatostatin 1-14. Moreover, somatostatin 1-14 substantially decreased IFN-gamma and IgG2a, but not IL-5 secretion by dispersed granuloma cells. This paper extends these observations by defining the somatostatin receptor (SSTR) isoform most likely expressed by granuloma inflammatory lymphocytes. Amplification of mRNA by reverse transcription PCR shows SSTR1, SSTR2, and SSTR3 mRNA in normal mouse brain and other tissues. Nevertheless, only the SSTR2 PCR product was amplified from granuloma cell RNA. The nucleotide sequence of the granuloma SSTR2 PCR product from inflammatory cells is identical to the CBA murine brain SSTR2 cDNA sequence. Granuloma-derived T cell lines, FACS-isolated granuloma CD4+ T cells, thymocytes, splenocytes, and cloned T cell lines all contain mRNA for SSTR2 by reverse transcription PCR. Moreover, both SSTR2A and the splice variant SSTR2B can be amplified from dispersed granuloma cells, granuloma T cell lines, thymocytes, and splenocytes. This is the first demonstration that inflammatory cells produce mRNA for an authentic somatostatin receptor. It is probable that the lymphocyte SSTR2 receptor mediates somatostatin-induced modulation of IFN-gamma secretion.

Animals↗
PubMed1994

Molecular evidence that granuloma T lymphocytes in murine schistosomiasis mansoni express an authentic substance P (NK-1) receptor.

Murine Schistosomiasis mansoni is a parasitic disease in which granulomas develop around the schistosome ova that lodge in the liver and intestines of the host. The granuloma eosinophils make substance P (SP), a cytokine with immunoregulatory properties. Within the granuloma SP can modulate IFN-gamma production through interaction with a substance P-like receptor. SP belongs to a family of hormones called tachykinins. Three mammalian tachykinins are SP, neurokinin A (substance K), and neurokinin B (neuromedin K). In humans and rats, there are at least three distinct tachykinin receptors designated NK-1, NK-2, and NK-3. The NK-1 receptor binds only SP with high affinity. Using reverse transcription-PCR, cDNA cloning, and sequence analysis, we showed that granulomas isolated from the liver of infected mice express an authentic SP (NK-1) receptor but have no detectable neurokinin A (NK-2) and neurokinin B (NK-3) receptor mRNA, as determined by PCR. CD4+ granuloma T lymphocytes, purified by FACS, express NK-1 receptor mRNA. Normal liver devoid of granulomas exhibited none of the three tachykinin receptor subclasses.

Amino Acid Sequence↗