Young adult cancer survivors' experience of taking part in a 12-week exercise referral programme: a qualitative study of the Trekstock RENEW initiative.

PURPOSE: There is emerging evidence that physical activity interventions have the potential to improve the physical function and psychosocial well-being of young adult cancer survivors. However, most existing interventions for young adult cancer survivors have been delivered in an in-patient hospital setting. The purpose of this study is to explore young adult cancer survivors' (YACS) experiences of the RENEW programme, a 12-week community-based exercise referral scheme delivered by Trekstock, a UK-based cancer charity. METHODS: Sixteen semi-structured interviews were conducted with YACS (mean age, 33 years; 87.5% female) who participated in the RENEW exercise referral programme. Each interview followed the same semi-structured interview guide which asked participants about their experiences of the RENEW programme and their ideas for the future development of the scheme. Data was audio-recorded, transcribed full verbatim and analysed using framework analysis. RESULTS: YACs predominantly chose to take part in the RENEW programme as a means to improve their health and overcome cancer related impairments (e.g. fatigue, loss of strength, low body confidence). The offer of one-to-one tailored support and unlimited gym access was often cited as a factor which motivated enrolment. Overall, YACS experience of the programme was positive with many describing improvements in physical function and general well-being. Barriers to participating in the programme included sign-off from clinicians prior to enrolment, travelling to the gym and fear of exercising alone. CONCLUSIONS: Exercise referral schemes are acceptable to YACS and provide a promising opportunity for young people with cancer to improve their physical and psychosocial health through physical activity.

The health behaviour status of teenage and young adult cancer patients and survivors in the United Kingdom.

PURPOSE: The primary aim of this study was to investigate the health behaviour status of teenage and young adult (TYA) cancer patients and survivors; the secondary aim was to determine if TYA cancer patients and survivors health behaviour differs to general population controls. METHODS: Two hundred sixty-seven young people with cancer (n =83 cancer patients receiving active treatment: n =174 cancer survivors, 57.1% >1 year since treatment completion) and 321 controls completed a health and lifestyle questionnaire which included validated measures of physical activity (PA) (Godin Leisure Time Exercise Questionnaire), diet (Dietary Instrument for Nutrition Education, DINE), smoking status, and alcohol consumption (AUDIT-C). RESULTS: General population controls and cancer survivors were more likely to meet current (PA) recommendations (p <0.001) than TYA cancer patients undergoing treatment (54.8% vs 52.3% vs 30.1%, respectively). Less than 40% of young people with cancer and controls met fat intake, sugar intake, fibre intake or current fruit and vegetable recommendations. TYA cancer survivors were more likely to report binge drinking than controls (OR=3.26, 95% CI 2.12-5.02, p <0.001). Very few young people with in the study were current smokers. The majority of TYA cancer patients and survivors reported a desire to make positive changes to their health behaviour. CONCLUSION: Consideration should be given to whether existing health behaviour change interventions which have demonstrated positive effects among the general TYA population could be adapted for young people with cancer.

Trekstock RENEW: evaluation of a 12-week exercise referral programme for young adult cancer survivors delivered by a cancer charity.

PURPOSE: To evaluate the uptake and effect of RENEW, a 12-week exercise referral programme for young adult cancer survivors delivered by Trekstock, a UK-based cancer charity. METHODS: The RENEW programme provides one-to-one individually tailored support from a level-4 cancer-rehabilitation-qualified gym instructor, free gym membership and access to information resources online. Objective and self-report data on cardiorespiratory function, strength, body composition, fatigue, sleep quality and general health-related quality of life (HRQoL) was collected from participants before the programme (week 0), immediately after (week 12) and 1 month later (week 16). RESULTS: Forty-eight young adults (83% female; mean age, 29 years) with a history of cancer took part within the 12-week programme and completed the evaluation measures. Physical activity (PA) levels significantly increased following the programme and remained raised at follow-up. Improvements in physical function were significant: peak expiratory flow (mean change, 30.96, p = 0.003), sit-and-reach test (mean change, 6.55 ± 4.54, p < 0.0001), and 6-mine-walk test (mean change, 0.12 ± 0.04, p < 0.0001). No significant changes in BMI, weight or muscle mass were observed. Improvements in fatigue, sleep and HRQoL were observed across the programme and at follow-up (mean change, weeks 0-16; 8.04 ± 1.49 p < 0.01; 1.05 ± 0.49 p < 0.05; and - 0.9 ± 0.46 p = 0.051, respectively). Changes in self-efficacy to exercise and motivations to exercise were not observed at 12 weeks or at follow-up. CONCLUSIONS: Results suggest that the RENEW exercise referral programme has a positive impact upon some domains of physical function and well-being among young adult cancer survivors. IMPLICATION FOR CANCER SURVIVORS: Exercise referral programmes delivered by charity organisations are one means by which PA behaviour change support may be widely disseminated to young adult cancer survivors. Health professionals and charitable bodies specialising in the care of young adults with cancer should look to address factors which prevent engagement and uptake of 'real-world' PA interventions such as the RENEW programme.

Childhood cancer incidence & survival in Aotearoa, New Zealand 2010-2019.

OBJECTIVE: To provide updated estimates of childhood cancer incidence and survival in Aotearoa, New Zealand. METHOD: Registrations for children under the age of 15 years diagnosed with cancer between 2010 and 2019 were extracted from the New Zealand Children's Cancer Registry. Cases were stratified by age, sex, prioritised ethnicity (Maori, Pacific peoples, and non-Maori) and cancer type. Age-standardised incidence rates (ASRs) per million person years and observed survival rates were calculated. RESULTS: During the study period, 1522 children were diagnosed with cancer providing an ASR of 169.1 per million per year (95 % Confidence Interval, CI: 157.0-181.2). For all childhood cancers combined, survival at 5-years was 85.6 % (95 % CI 83.7-87.3). There was a gap in 5-year survival between Maori (80.9 %, 95 % CI 76.5-84.6), Pacific peoples (82.6 %, 95 % CI 75.6-87,7) and Non-Maori (87.8 %, 95 % CI 85.6-89.7) In both adjusted and unadjusted models, this difference in survival was most marked (p < 0.05) among children who were 10-14 years of age at diagnosis. CONCLUSION: Childhood cancer incidence and survival rates in Aotearoa, New Zealand remain comparable to other high-income countries. Further research is required to understand the survival difference between ethnic groups.

Interaction of the Escherichia coli DEAD box protein DbpA with 23 S ribosomal RNA.

The Escherichia coli DEAD box protein DbpA is unique among the DEAD box family in that its ATPase activity is specifically stimulated by bacterial 23 S ribosomal RNA. We have analysed the interaction between DbpA and a specific region within 23 S rRNA (namely nucleotides 2508-2580) which stimulates full ATPase activity. Using electrophoretic mobility shift assays we show that DbpA binds to this "specific" region with greater efficiency than to other regions of 23 S rRNA, and is not competed off by a non-specific RNA or a mutant RNA in which one of the stem-loops has been disrupted. These data suggest that the secondary structure within this region of 23 S rRNA is important for its recognition and binding by DbpA. We have also examined the ability of DbpA to unwind RNA and show that the purified protein does not behave as an RNA helicase in vitro with the substrates tested.

Thoracoscopic pulmonary lobectomy. Early operative experience and preliminary clinical results.

Thoracoscopic video-assisted lobectomy procedures were performed in 11 patients (7 men, 4 women; age range 40 to 74 years, mean 66 years). Ten patients had peripheral pulmonary opacities: eight of these were bronchogenic carcinomas, one was an atypical carcinoid lesion, and one was a pulmonary infarct. All of these cases had preoperative evaluation by computed tomographic scanning to exclude mediastinal lymphadenopathy. The remaining patient had preoperatively diagnosed lobar bronchiectasis. Surgical access was gained via three stab (1 cm) incisions and one short (7 cm) submammary incision, which was made without rib separation and was used for specimen delivery. Lobes resected were the left upper (n = 4), left lower (n = 2), right upper (n = 2), and right lower (n = 3). All patients survived. Overall mean operative time was 3.3 hours and blood loss 263 ml. For the latter five cases, however, these figures were reduced to 2.3 hours and 100 ml, respectively, indicating improvement with experience. In no cases was ventilatory assistance required. Mean high-dependency unit time was 41 hours. In each case, it was possible to perform a standard dissectional lobectomy with lobar lymph node clearance equal to that obtained at open thoracotomy. Comparison with a series of 33 open lobectomy procedures demonstrated reduced postoperative pain, morphine consumption, and high-dependency unit stay. This preliminary experience supports the development of video-assisted thoracoscopic pulmonary lobectomy for patients with small peripheral opacities or known benign disease.

Reversibility and persistence of di-2-ethylhexyl phthalate (DEHP)- and phenobarbital-induced hepatocellular changes in rodents.

The tumor promotion stage of chemical carcinogenesis has been shown to exhibit a persistence of cellular effects during treatment and the reversibility of these changes upon cessation of treatment. Inhibition of gap-junctional intercellular communication and increased replicative DNA synthesis appear to be important in this process. The present study assessed the persistence and reversibility of gap-junctional intercellular communication inhibition, peroxisomal proliferation, and replicative DNA synthesis in livers from male F344 rats and B6C3F1 mice. Dietary administration of 20,000 mg/kg DEHP to male rats for 2 weeks decreased intercellular communication (67% of control) and enhanced replicative DNA synthesis (4.8-fold over control). Elevation of the relative liver weight and the induction of peroxisomal beta oxidation were also observed following treatment with 20,000 mg/Kg DEHP for 2 weeks. Following DEHP administration at a dose of 6000 mg/kg for 18 months, inhibition of gap-junctional intercellular communication persisted, and the relative liver weight and induction of peroxisomal beta oxidation remained elevated in both rats and male B6C3F1 mice. Treatment of rats and mice with phenobarbital for 18 months (500-mg/kg diet) also produced an increase in relative liver weight and a decrease in cell-to-cell communication. In recovery studies in which DEHP was administered to male F344 rats for 2 weeks and then withdrawn, the relative liver weight, rate of peroxisomal beta oxidation, increase in replicative DNA synthesis, and inhibition of gap-junctional intercellular communication returned to control values within 2 to 4 weeks after DEHP treatment ceased. Recovery studies with phenobarbital produced similar results. The primary active metabolite of DEHP, mono-2-ethylhexyl phthalate (MEHP), was detected in the livers of animals treated with DEHP for greater than 2 weeks. However, it could not be detected after removal of DEHP from the diet for 2 weeks. This study demonstrated that inhibition of gap-junctional intercellular communication, along with indicators of peroxisomal proliferation, including increased relative liver weight and enhanced peroxisomal beta oxidation, persist while DEHP treatment continues but reverses when treatment is stopped. Studies with phenobarbital produced a similar pattern of response.

Comparative in vivo hepatic effects of Di-isononyl phthalate (DINP) and related C7-C11 dialkyl phthalates on gap junctional intercellular communication (GJIC), peroxisomal beta-oxidation (PBOX), and DNA synthesis in rat and mouse liver.

The short-term hepatic effects of DINP (CAS 68515-48-0, designated DINP-1) in rats and mice were evaluated at tumorigenic and nontumorigenic doses from previous chronic studies. Groups of male F344 rats were fed diets with DINP-1 at concentrations of 0, 1000, or 12,000 ppm and male B6C3F1 mice at 0, 500, or 6000 ppm DINP-1. After 2 or 4 weeks of treatment, changes in liver weight, gap junctional intercellular communication (GJIC), peroxisomal beta-oxidation (PBOX), and replicative DNA synthesis were examined. In addition, hepatic and serum concentrations of the parent compound and major metabolites were determined. Relative to controls in both species, increased liver weight and PBOX at the high dose of DINP-1 were consistent with peroxisomal proliferation. Hepatic GJIC was inhibited and DNA synthesis was increased at the high dose of DINP-1, which is also consistent with the tumorigenic response in rats and mice reported in other chronic studies at these doses. These hepatic effects were not observed at the low doses of DINP-1. At comparable low doses of DINP-1 in other chronic studies, no liver tumors were observed in rats and mice. The monoester metabolite (MINP-1) was detected in the liver at greater concentrations in mice than rats. This result is also consistent with the dose-response observations in rat and mouse chronic studies. Additionally, other structurally similar dialkyl phthalate esters ranging from C7 to C11 were evaluated using a similar protocol for comparison to DINP-1; these included an alternative isomeric form of DINP (DINP-A), di-isodecyl phthalate (DIDP), di-isoheptyl phthalate (DIHP), di-heptyl, nonyl undecyl phthalate (D711P), and di-n-octyl phthalate (DNOP). Collectively, these data indicate that in rats and mice, DINP-1 and other C7-C11 phthalates exhibit a threshold for inducing hepatic cellular events. Further, where previous chronic data were available for these compounds, these phthalates elicited hepatic effects at doses that correlated with the tumorigenic response. Overall, these studies suggest a good correlation between the inhibition of GJIC when compared with the data on production of liver tumors in chronic studies.

Effects of Di-2-ethylhexyl phthalate (DEHP) on gap-junctional intercellular communication (GJIC), DNA synthesis, and peroxisomal beta oxidation (PBOX) in rat, mouse, and hamster liver.

The present study evaluated the effect of di-2-ethylhexyl phthalate (DEHP) on gap-junctional intercellular communication (GJIC), peroxisomal beta-oxidation (PBOX) activity, and replicative DNA synthesis in several rodent species with differing susceptibilities to peroxisome proliferator-induced hepatic tumorigenesis. A low (non-tumorigenic) and high (tumorigenic) dietary concentration of DEHP was administered to male F344 rats for 1, 2, 4, and 6 weeks. Additionally, a previously non-tumorigenic dose (1000 ppm) and tumorigenic dose of DEHP (12,000 ppm), as determined by chronic bioassay data, were examined following 2 weeks dietary administration. Male B6C3F1 mice were fed the non-tumorigenic concentration, 500 ppm, and the tumorigenic concentration, 6000 ppm, of DEHP for two and four weeks. The hepatic effects of low and high concentrations of DEHP, 1000 and 6000 ppm, were also examined in male Syrian Golden hamsters (refractory to peroxisome proliferator-induced tumorigenicity). In rat and mouse liver, a concentration-dependent increase in the relative liver weight, PBOX activity, and replicative DNA synthesis was observed at the earliest time point examined. Concurrent to these observations was an inhibition of GJIC. In hamster liver, a slight increase in the relative liver weight, PBOX activity, and replicative DNA synthesis was observed. However, these effects were not of the same magnitude or consistency as those observed in rats or mice. Furthermore, DEHP had no effect on GJIC in hamster liver at any of the time points examined (2 and 4 weeks). HPLC analysis of DEHP and its primary metabolites, mono-2-ethylhexyl phthalate (MEHP), and phthalate acid (PA), indicated a time- and concentration-dependent increase in the hepatic concentration of MEHP. At equivalent dietary concentrations and time points, the presence of MEHP, the primary metabolite responsible for the hepatic effects of DEHP, demonstrated a species-specific response. The largest increase in the hepatic concentration of MEHP was observed in mice, which was greater than the concentration observed in rats. The hepatic concentration of MEHP was lowest in hamsters. Hepatic concentrations of DEHP and phthalic acid were minimal and did not correlate with concentration and time. Collectively, these data demonstrate the inhibition of hepatic GJIC and increased replicative DNA synthesis correlated with the observed dose- and species-specific tumorigenicity of DEHP and may be predictive indicators of the nongenotoxic carcinogenic potential of phthalate esters.

Effects of di-isononyl phthalate, di-2-ethylhexyl phthalate, and clofibrate in cynomolgus monkeys.

The effects of the peroxisome proliferators di-isononyl phthalate (DINP) and di-2-ethylhexyl phthalate (DEHP) were evaluated in young adult male cynomolgus monkeys after 14 days of treatment, with emphasis on detecting hepatic and other effects seen in rats and mice after treatment with high doses of phthalates. Groups of 4 monkeys received DINP (500 mg/kg/day), DEHP (500 mg/kg/day), or vehicle (0.5% methyl cellulose, 10 ml/kg) by intragastric intubation for 14 consecutive days. Clofibrate (250 mg/kg/day), a hypolipidemic drug used for cholesterol reduction in human patients was used as a reference substance. None of the test substances had any effect on body weight or liver weights. Histopathological examination of tissues from these animals revealed no distinctive treatment-related effects in the liver, kidney, or testes. There were also no changes in any of the hepatic markers for peroxisomal proliferation, including peroxisomal beta-oxidation (PBOX) or replicative DNA synthesis. Additionally, in situ dye transfer studies using fresh liver slices revealed that DINP, DEHP, and clofibrate had no effect on gap junctional intercellular communication (GJIC). None of the test substances produced any toxicologically important changes in urinalysis, hematology, or clinical chemistry; however, clofibrate produced some emesis, small increases in serum triglyceride, decreased calcium, and decreased weights of testes/epididymides and thyroid/parathyroid. The toxicological significance of these small changes is questionable. The absence of observable hepatic effects in monkeys at doses that produce hepatic effects in rodents suggests that DINP, DEHP, and clofibrate would also not elicit in primates other effects such as liver cancer. These data, along with results from in vitro hepatocyte studies, indicate that rodents are not good animal models for predicting the hepatic effects of phthalates in primates, including humans.

Antisense oligodeoxynucleotides to the kappa-1 receptor block the antinociceptive effects of delta 9-THC in the spinal cord.

Intrathecal pretreatment of mice with an antisense oligodeoxynucleotide directed against the kappa-1 receptor significantly reduced the antinociceptive effects of the kappa receptor agonist U50,488 as well as delta 9-THC, the major psychoactive ingredient found in cannabis. A mismatched oligodeoxynucleotide which contained four switched bases did not block the antinociception produced by U50,488 or delta 9-THC. Furthermore, kappa-1 antisense did not alter the antinociceptive effects of either the mu receptor-selective opioid DAMGO, or the delta receptor-selective opioid DPDPE. By using kappa-1 antisense, we were able to demonstrate that an interaction occurs between the cannabinoids and opioids in the spinal cord.

Effect of Brucella abortus transfer factor in preventing murine brucellosis.

Mice vaccinated with a protein extract of attenuated Brucella abortus strain 19 had increased resistance to infection with virulent B. abortus strain 2308 and had increased antibody responses to strain 2308. However, resistance to infection and antibody responses were not increased when nonvaccinated recipient mice were given transfer factor preparations that were obtained from either vaccinated donor mice or strain 2308-infected donor mice. Vaccination of mice with the strain 19 extract plus treatment with each transfer factor preparation also did not further increase resistance to infection or antibody responses when compared with mice that received the vaccine alone. These results suggest that transfer factor from mice that have either vaccine-induced protective immunity to B. abortus or active B. abortus infections does not enhance antibody responses and resistance to infection with B. abortus.

Unresponsiveness of vaccinated BALB/c mice to a second inoculation of lipopolysaccharide from Brucella abortus strain 2308.

A study was conducted to determine whether the protection induced in mice by a primary inoculation of lipopolysaccharide from Brucella abortus would be enhanced by a second inoculation given at different time intervals. Protection was challenged by exposure of the mice to a virulent culture of B. abortus strain 2308. Reduced mean viable count and/or splenic weights were the criteria of protection. There was no significant difference (P greater than 0.05) in the protective responses among mice given a single inoculation. Vaccinated mice were significantly (P less than 0.05) better protected than were nonvaccinated mice. Mice given vaccinal inoculations simultaneous with challenge exposure were less protected (P less than 0.001) than were mice vaccinated prior to challenge, but were better protected (P less than 0.010) than were nonvaccinated mice.

Role of immune responses to a GroEL heat shock protein in preventing brucellosis in mice vaccinated with Brucella abortus strain RB51.

Resistance to infection with virulent Brucella abortus strain 2308 and antibody and lymphocyte proliferative responses to a recombinant 60 kDa B. abortus GroEL heat shock protein were measured in mice vaccinated with attenuated B. abortus strain RB51. Mice at 12-20 weeks after vaccination with 5 x 10(8) colony forming units (CFU) of strain RB51 had increased resistance to infection with strain 2308 and increased antibody and lymphocyte proliferative responses to GroEL following challenge infection with 2308. However, these mice at 12-20 weeks after vaccination did not have greater resistance to infection than mice vaccinated with 5 x 10(6) CFU of strain RB51, which had no increased antibody or lymphocyte proliferative response to GroEL. These results indicate that mice vaccinated with strain RB51 can have antibody and cell-mediated immune responses to GroEL during infection with virulent strain 2308, although neither response appeared to have an essential role in vaccine-induced immunity to brucellosis.

Modulation of free intracellular calcium and cAMP by morphine and cannabinoids, alone and in combination in mouse brain and spinal cord synaptosomes.

Changes in [Ca++]i and cAMP were evaluated as possible mechanisms by which the cannabinoids enhance the antinociception of morphine. The addition of subactive concentrations of delta 9-(THC) and morphine in combination to brain synaptosomes did not result in an enhanced decrease in [Ca++]i; however, this drug combination enhanced decreases in [Ca++]i in spinal cord synaptosomes. The combination of CP55,940 and morphine produced enhanced decreases in [Ca++]i in both brain and spinal cord synaptosomes. In brain synaptosomes, the combination of delta 9-THC and morphine produced an additive decrease in cAMP accumulation, whereas no significant change was observed with this combination in the spinal cord. Thus, the difference in the modulation of [Ca++]i but not cAMP in the brain in vitro may be a predictor of the greater-than-additive antinociceptive effects observe in vivo.

Morphine-induced modulation of calcitonin gene-related peptide levels.

Calcitonin gene-related peptide (CGRP) is a novel calcium-modulatory product of the gene that encodes for calcitonin. Acute administration of morphine decreases levels of CGRP in rat corpus striatum. Tolerance to morphine did not alter the levels of CGRP in any brain region or in the spinal cord of the rat. CGRP did not alter the tolerance to the antinociceptive effects of morphine. Chronic naltrexone increased the levels of CGRP in the hypothalamus. Concurrent chronic administration of naltrexone plus morphine raised the levels of CGRP in the medulla, midbrain, and spinal cord. CGRP enhances naloxone-precipitated withdrawal jumping in mice. In rats, during withdrawal the levels of CGRP were tripled in the corpus striatum and significantly reduced in the hippocampus and hypothalamus. In the corpus striatum, CGRP enhances forskolin-stimulated cyclic adenosine monophosphate (cAMP) accumulation when such accumulation is suppressed (as with the chronic opiate administration), but conversely depresses forskolin-stimulated cAMP accumulation under normal conditions (as with chronic vehicle administration). These data are consistent with the hypothesis that CGRP acts as a modulatory peptide in opiate-sensitive systems and tonic opioid control of CGRP levels exists in brain.

Clinical results of thoracoscopic Heller's myotomy in the treatment of achalasia.

OBJECTIVES: Ideal treatment for achalasia permanently eliminates the dysfunctional lower oesophageal sphincter, relieving dysphagia and regurgitation. The aim of this study was to review the results in a series of patients undergoing video-imaged thoracoscopic Heller's myotomy (THM). METHODS: Records of all patients undergoing THM by a single surgeon at one institution were analysed. Follow-up was conducted using a structured questionnaire together with oesophageal manometry and/or 24 h pH monitoring when clinically indicated. RESULTS: Twenty-five consecutive patients (13 males, 12 females, mean age 40.3+/-19.9 years) suffering from grade 4 dysphagia underwent THM between 1993 and 2001. Preoperative mean lower oesophageal sphincter (LOS) pressure was 42.6+/-6.3 mmHg. Seven patients (28%) had undergone previous pneumatic dilatations. There were no hospital deaths and no oesophageal perforations. Length of hospital stay was 4.3+/-1.8 days. One patient died 3 years after surgery from unrelated causes. At follow-up of 5.4+/-2.1 years, freedom from any reintervention was 95.8% (23/24). Eleven patients (45.8%) were asymptomatic. In patients with residual or recurrent symptoms (n=13), their severity was significantly reduced from the preoperative period (dysphagia score 1.7+/-0.8 versus 4+/-0; P

Acute phase responses following minimal access and conventional thoracic surgery.

OBJECTIVES: Major thoracic surgery is associated with trauma-related immunological changes. These may impair anti-tumour immunity. We hypothesize that the reduced operative trauma associated with a video-assisted thoracic surgery (VATS) approach may decrease acute phase responses and, consequently, lead to better preservation of immune function. This prospective randomized study compared the effects of conventional open thoracic surgery and VATS on acute phase responses in patients undergoing pulmonary lobectomy. METHODS: Acute phase indicators were analyzed in patients undergoing lobectomy for suspected bronchogenic carcinoma. Surgery was prospectively randomized to pulmonary lobectomy by VATS or limited postero-lateral thoracotomy. Blood was taken pre-operatively and at 4, 24, 48, 72, 120 and 168 h post-operatively for analysis of C-reactive protein (CRP; 41 patients: open, n=22; VATS, n=19) interleukin (IL)-6, tumour necrosis factor (TNF) receptors (TNF-sR55, TNF-sR75) and P-selectin (24 patients: open, n=12; VATS, n=12). Samples taken at 48 and 168 h were also analyzed for phagocyte reactive oxygen species (ROS) production (25 patients: open, n=16; VATS, n=19). RESULTS: Surgery increased acute phase responses. VATS was associated with lower CRP and IL-6 levels. In the open surgery group, significant increases in ROS in neutrophils (up to 36% greater than before surgery, n=12, P<0.02-0.05) were detected at 2 days after surgery, but in the VATS group, the increase after surgery (of up to 17%, n=18) did not reach significance. Similarly, monocyte ROS increases of up to 25% in the mean ROS in the open surgery group and of up to 17% in the VATS group were detected on days 2 and 7 after surgery. CONCLUSIONS: VATS pulmonary lobectomy is associated with reduced peri-operative changes in acute phase responses. This finding may have implications for peri-operative tumour immuno-surveillance in lung cancer patients.

Computerized databases for emergency care: what impact on patient care?

A field-based evaluation is conducted of a Clinical Computerized Information System (CCIS). Following training, the use of the CCIS database, word processing and other programs by thirteen full-time practicing emergency physicians in two urban emergency departments of a University-associated teaching hospital was studied over a one-year period. A tracking program automatically logged frequency and duration of use by the physicians, and user satisfaction was assessed by a reliable and validated questionnaire instrument. Based on utilization data and verbal reports of these physicians, CCIS database searching was not only found to be easy-to-learn but was readily accessible during emergency shifts. Individual physicians were found to perform an average of 3.5 searches per month lasting a mean search time of 8 min. Positive notes about the CCIS system included ease-of-use, accuracy of data, accessibility of system, and value of output while negative perceptions included a lack of integration with other systems, a lack of system completeness, and a high subscription cost. It was suggested that a less costly telephone link to a high-volume Centre would be desirable in actual implementation of the system.

Infectious bovine keratoconjunctivitis: comparison of infection, signs of disease and weight gain in vaccinated versus nonvaccinated purebred Hereford heifer calves.

To determine whether the carrier state of Moraxella bovis could be prevented under natural conditions of exposure by vaccination, purebred Hereford calves were vaccinated twice; once in June 1982, and again in September 1982. Eyes of calves were examined for signs of infectious bovine keratoconjunctivitis (IBK) and cultured for M. bovis in June 1982, September 1982, January 1983 and June 1983. When calves were compared on the basis of selection lines (four genetic groups), there were significant (P less than 0.05) differences in the percentages of infection, disease and weight gain between selection line calves, regardless of their vaccination status. Results suggest that vaccination, in conjunction with clinical infectious, bovine keratoconjunctivitis, reduces the carrier state of M. bovis in the herd but the immunity lasted less than 9 months. The disproportionate representation of the most genetically resistant calves among nonvaccinated calves probably accounted for the equivocal results between vaccinated and nonvaccinated calves.