Two transects reveal remarkable variation in gene flow on opposite ends of a European toad hybrid zone.

Speciation entails a reduction in gene flow between lineages. The rates at which genomic regions become isolated varies across space and time. Barrier markers are linked to putative genes involved in (processes of) reproductive isolation, and, when observed over two transects, indicate species-wide processes. In contrast, transect-specific putative barrier markers suggest local processes. We studied two widely separated transects along the 900 km hybrid zone between Bufo bufo and B. spinosus, in northern and southern France, for ~1200 RADseq markers. We used genomic and geographic cline analyses to identify barrier markers based on their restricted introgression, and found that some markers are transect-specific, while others are shared between transects. Twenty-six barrier markers were shared across both transects, of which some are clustered in the same chromosomal region, suggesting that their associated genes are involved in reduced gene flow across the entire hybrid zone. Transect-specific barrier markers were twice as numerous in the southern than in the northern transect, suggesting that the overall barrier effect is weaker in northern France. We hypothesize that this is consistent with a longer period of secondary contact in southern France. The smaller number of introgressed genes in the northern transect shows considerably more gene flow towards the southern (B. spinosus) than the northern species (B. bufo). We hypothesize that hybrid zone movement in northern France and hybrid zone stability in southern France explain this pattern. The Bufo hybrid zone provides an excellent opportunity to separate a general barrier effect from localized gene flow-reducing conditions.

The sexuality of women with cervical cancer undergoing definitive radiotherapy in Ghana.

INTRODUCTION: The purpose of this study was to assess the sexuality of cervical cancer patients undergoing radiotherapy at a major cancer treatment center in Ghana. This is an area of interest as globally; cervical cancer kills approximately 342,000 people per annum with an estimated number of 604,000 new cases in 2020. Acknowledging the World Health Organization's definition of sexual health as a state of physical, mental and social well-being in relation to sexuality, this paper sheds light on how these dimensions affect the quality of life of cervical cancer patients. METHODS: This was a longitudinal study, which assessed the impact of radiotherapy on the sexuality of both premenopausal and postmenopausal cervical cancer patients presenting for primary treatment with chemoradiation from April to July, 2021 at a major cancer treatment centre in Ghana. The Female Sexual Function Index and Body Image Scale questionnaires were respectively used to evaluate the sexual functions scores among the cervical cancer patients, and to assess the impact of the treatment on their body image. MATLAB software was used for data analysis. RESULTS: Most of the cervical cancer patients sampled were postmenopausal (57 %). About 79 % premenopausal and 96 % postmenopausal cervical cancer patients were sexually inactive during radiotherapy (day 15). Also, 48 % premenopausal and 24 % postmenopausal patients were very dissatisfied with their bodies at the onset of treatment. The frequency of orgasm in cervical cancer patients declined after treatment causing a deterioration in their sexual function. The patients' sexuality was influenced by age and menopausal status. The decreased sexual desire of the patients resulted in emotional distancing from their partners, which invariably induced changes in their partners' level of sexual interest. This study established significant differences between premenopausal and postmenopausal cervical cancer patients who were generally very dissatisfied with their sexual relationships with their partners on day 1 (p = 0.02) and on day 15 (p = 0.00) of treatment. CONCLUSION: The majority of patients who presented for treatment for cervical cancer in this study were postmenopausal. Their interest in sexual activity was more influenced by their menopausal status than their antineoplastic treatment. This study indicates that cervical cancer patients are more likely to develop sexual health problems which could substantially worsen over the course of their treatment and beyond. IMPLICATION FOR PRACTICE: The study will contribute within the oncology team by assisting personnel in putting in place measures that will guide the treatment of cervical cancer patients and improve quality of care.

A nurse-led palpitations clinic: a 2-year experience.

OBJECTIVE: To investigate the role of a nurse-led clinic in the assessment of patients with palpitations. DESIGN: Prospective descriptive study. SETTING: Nurse-led palpitations clinic in a UK district general hospital. PARTICIPANTS: Patients referred from primary care or the emergency department with palpitations. METHODS: Referral letters were screened, and only patients without high-risk features or a documented arrhythmia were diverted to the palpitations clinic. Patients were evaluated using a protocol. All patients had an ECG and ambulatory ECG monitoring and were discussed with a cardiologist. RESULTS: Over 15 months, 389 patients were seen. The mean time from referral to assessment was 38 days (range 3-142). The most common diagnoses were symptomatic extrasystoles (42%) and sinus rhythm (22%). Significant arrhythmias were diagnosed in 15% (atrial fibrillation/flutter, 8%; supraventricular arrhythmias, 6%). Only 52 (13%) were subsequently referred to a cardiologist, including 20 with high-risk features. These 20 patients waited on average an additional 70 days to be seen by a cardiologist compared with patients who were seen directly by a cardiologist after referral by primary care or the emergency department. CONCLUSIONS: For low-risk patients, a nurse-led palpitations clinic may provide a viable alternative to the traditional cardiology outpatient service. Despite attempts to exclude them, some high-risk patients were seen. This was unforeseen and led to a clinically important delay in their appropriate assessment. Hence, before adopting a nurse-led palpitations service, a rigorous pathway for the early assessment of high-risk patients needs to be agreed.

Estimation of the requirement for implantable cardioverter defibrillators for the primary prevention of sudden cardiac death post-myocardial infarction based on UK national guidelines (2006).

AIMS: To assess the impact of the new UK National Institute for Health and Clinical Excellence (NICE) guidelines on the incidence of implantable cardioverter defibrillator (ICD) indications for the primary prevention of sudden cardiac death following myocardial infarction (MI). METHODS AND RESULTS: We performed a retrospective single centre study in a District General Hospital. The transthoracic echocardiogram reports of all patients with a discharge diagnosis of MI during a 6-month period were studied. We reviewed the notes of all patients with an estimated left ventricular ejection fraction (LVEF) of <35% and used UK national guidance to assess the incidence of potential ICD indications. Five hundred and forty-six patients had a discharge diagnosis of MI. Fifty had estimated LVEF <35% and 8-11 of these met the NICE post-MI primary prevention criteria for ICD implantation. This gives an estimated incidence based upon our local population of 29-39 patients/million/year. Most of these patients (64-88%) were identified purely by ECG criteria (QRS > 120 ms) and LVEF. CONCLUSION: The latest published UK ICD data give a new implantation rate of approximately 40/million/year. Combining our results with published data for NICE secondary prevention indications gives a combined ICD indication incidence of approximately 105-115/million/year. This suggests there is currently significant under-provision of ICD therapy in the UK.

Coronary spasm induced by capecitabine mimicks ST elevation myocardial infarction.

Capecitabine is a chemotherapeutic prodrug that is metabolised to 5-fluorouracil. Supported by the National Institute for Health and Clinical Excellence guidance it is now first-line adjuvant treatment for metastatic colorectal cancer in the UK. Although cardiac chest pain and myocardial ischaemia are well recognised side effects of 5-fluorouracil, their association with capecitabine is not widely appreciated. Two cases are described of coronary spasm secondary to capecitabine in patients referred for emergency invasive treatment of presumed ST elevation myocardial infarction (STEMI). The contemporary treatment of acute coronary syndromes involves aggressive antiplatelet therapy, anticoagulation and cardiac catheterisation. This treatment, although beneficial in most patients, is associated with a small but significant risk of bleeding complications. A wider appreciation of the potential for capecitabine to induce spasm mimicking STEMI is important in order to reduce the risk of the administration of thrombolytics and other potentially dangerous drugs and have a higher threshold for referral for emergency angiography.

Global inequality, and the challenge for ergonomics to take a more dynamic role to redress the situation.

This paper argues that ergonomics is more sorely needed, easier to implement, and potentially far more effective in industrially developing countries (IDCs) than where its efforts are presently most concentrated in the less populated, more affluent, technologically advanced world. The reasoning is a simple extension of the principle of diminishing returns in which the further from optimal a situation is, the greater the beneficial effect of any implemented improvement. The paper draws attention to the gap between 'have' and 'have not' cultures, plus the necessity for, and relative ease with which a sustainable ergonomics ethos can be engendered in IDCs. This requires a need to consider network causality, investigating both micro-problems (basic interaction between task and worker) and macro-conditions of the overall scenario (including managerial organisation, planning and responsibility). The two-pronged symbiosis of micro- and macro-ergonomics intervention has the potential to achieve both effective and sustainable development within small, medium and large enterprises.

Enhancement of tumor growth and vascular density by transfection of vascular endothelial cell growth factor into MCF-7 human breast carcinoma cells.

BACKGROUND: Vascular endothelial growth factor (VEGF) is a secreted endothelial-specific growth factor that is angiogenic in vivo. It is commonly expressed in a range of carcinomas. PURPOSE: The study was designed to investigate the effect of constitutive expression of VEGF on tumor formation by estrogen-dependent human MCF-7 breast carcinoma cells. METHODS: A full-length complementary DNA encoding the shortest isoform of VEGF (VEGF121) was stably transfected into MCF-7 cells. Transfected clones were screened for VEGF121 messenger RNA (mRNA) expression by ribonuclease protection analysis and for secretion of VEGF121 protein by Western blot analysis. Secretion of biologically active VEGF121 by transfectants was confirmed by 1) a competitive radioreceptor-binding assay, 2) stimulation of the growth of microvascular endothelial cells in vitro, and 3) potent angiogenic activity in the rabbit corneal assay. Tumor models were then established by subcutaneously implanting wild-type or VEGF121-transfected MCF-7 cells, together with either mouse BALB/3T3 clone A31 fibroblasts or human MDA-435S breast carcinoma cells, into ovariectomized nude mice either with or without a separately implanted slow-release estrogen pellet. Tumor vascularity was quantitatively assessed by capillary vessel counting after staining with the pan-endothelial marker CD31. RESULTS: Stable VEGF121-overexpressing MCF-7 cells were isolated and designated V12 cells. When implanted into the rabbit cornea, V12 cells elicited a strong directional outgrowth of capillaries. The growth rate of V12 cells in vitro was indistinguishable from that of MCF-7 wild-type cells. V12 cells formed faster growing tumors than did wild-type cells (P < .01) when xenografted subcutaneously into nude mice with either 3T3 fibroblasts or MDA-435S cells. Tumors formed from V12 cells were more vascular (P < .01) and showed a heterogeneous distribution of vessels when compared with the homogeneous distribution seen in tumors formed from wild-type cells. VEGF121 overexpression had no effect on hormone dependence or tamoxifen sensitivity of tumor formation by MCF-7 cells in mice. No macroscopic evidence for metastasis from subcutaneous implants was obtained. CONCLUSIONS: VEGF121 expression by breast carcinoma cells confers a growth advantage in vivo but not in vitro. Tumors formed by V12 transfectants were more vascular than those formed by wild-type MCF-7 cells, and we surmise that the growth advantage arises from increased tumor vascularization induced by VEGF121. IMPLICATIONS: Tumor formation by V12 cells could provide a useful model for the assessment of anti-angiogenic drugs.

Vascular endothelial growth factor-B and vascular endothelial growth factor-C expression in renal cell carcinomas: regulation by the von Hippel-Lindau gene and hypoxia.

Angiogenesis is essential for tumor growth and metastasis. It is regulated by numerous angiogenic factors, one of the most important being vascular endothelial growth factor (VEGF). Recently VEGF-B and VEGF-C, two new VEGF family members, have been identified that bind to the tyrosine kinase receptors flt-1 (VEGFR1), KDR (VEGFR2), and flt-4 (VEGFR3). Although the importance of VEGF-A has been shown in renal carcinomas, the contribution of these new ligands in kidney tumors is not clear. We have, therefore, measured the mRNA level of VEGF-B and VEGF-C together with their receptors by RNase protection assay (RPA) in 26 normal kidney samples and 45 renal cell cancers. We observed a significant up-regulation of VEGF-B (P = 0.002) but not VEGF-C (P = 0.3) in neoplastic kidney compared with normal tissues. In addition, although VEGF receptors were higher in tumors than normal kidney, there was a significant up-regulation of only flt-1 (P = 0.003) but not KDR (P = 0.12) or flt-4 (P = 0.09). There was also a significant correlation between VEGF-C and both of its receptors flt-4 (P = 0.006) and KDR (P = 0.03) but no association between VEGF-B and its receptor flt-1 (P = 0.23). A significant increase was observed in flt-1 (P < 0.001), KDR (P = 0.02), and flt-4 (P = 0.01) but not VEGF-B (P = 0.82) or VEGF-C (P = 0.52) expression in clear cell compared with chromophil (papillary) carcinomas. No significant association was demonstrated between VEGF-B, VEGF-C, flt-1, KDR, and flt-4 with patient sex, patient age, or tumor size (P > 0.05). The effect of von Hippel-Lindau (VHL) gene and hypoxia on VEGF-B and VEGF-C expression in the renal carcinoma cell line 786-0 transfected with wild-type and mutant VHL was determined by growing cells under 21% O2- and 0.1% O2. In wild-type VHL cells, whereas VEGF-A was significantly up-regulated under hypoxic compared with normoxic conditions (P < 0.001), expression of VEGF-C was reduced (P < 0.002). Nevertheless, the repression of VEGF-C was lost in mutant VHL cell lines under hypoxia. In contrast VEGF-B was not regulated by VHL despite clear up-regulation in vivo. These findings strongly support an enhanced role for this pathway in clear cell carcinomas by regulating angiogenesis and/or lymphangiogenesis. The study shows that clear cell tumors are able to up-regulate angiogenic growth factor receptors more efficiently than chromophil (papillary), that clear cell tumors can use pathways independent of VHL to regulate angiogenesis, and that this combined regulation may account for their more aggressive phenotype, which suggests that targeting VEGFR1 (flt-l) may be particularly effective in these tumor types.

Expression of the angiogenic factors vascular endothelial cell growth factor, acidic and basic fibroblast growth factor, tumor growth factor beta-1, platelet-derived endothelial cell growth factor, placenta growth factor, and pleiotrophin in human primary breast cancer and its relation to angiogenesis.

Angiogenesis is a significant prognostic factor in breast cancer, but the factors that control angiogenesis in vivo are not well defined. Multiple angiogenic polypeptides are known, and we have determined the expression of seven of these in primary human breast cancers; the relationship of expression to estrogen receptor and vascular density was also examined. Vascular endothelial growth factor (VEGF) and its four isoforms (121, 165, 189, and 206 amino acids), transforming growth factor (TGF)-beta1, pleiotrophin, acidic and basic fibroblast growth factor (FGF), placental growth factor, and thymidine phosphorylase (platelet-derived endothelial cell growth factor) were quantitated by RNase protection analysis. beta-FGF was also measured by ELISA. The estrogen receptor (ER), epidermal growth factor receptor, and vascular density were analyzed in 64 primary breast cancers. All tumors expressed at least six different vascular growth factors. VEGF was most abundant, and the transcript for the 121-amino acid form predominated. Other angiogenic factors expressed at high levels were thymidine phosphorylase and TGF-beta1. Expression of most of the angiogenic factors did not correlate with that of ER or vascular density. However, thymidine phosphorylase did, with a correlation coefficient of 0.3 (P = 0.03). There were significant associations of pleiotrophin with acidic FGF expression (P = 0.001) and TGF-beta with platelet-derived endothelial cell growth factor expression (P = 0.001). Thus, angiogenesis may involve a coordinate regulation of some vascular growth factors. High VEGF expression correlated with poor prognosis in univariate analysis (P = 0.03), as did ER and epidermal growth factor receptor expression. Basic FGF was also assessed by ELISA and was more highly expressed in tumors than normal breast tissues (median, 346 microg/ml cytosol; range, 54-1323 versus median, 149; range, 32-509; P = 0.01). Implications for therapy are that broad spectrum agents that block features common to these factors may be useful (e.g., antagonism of heparin-binding activity agents), because so many angiogenic factors are expressed. Inhibiting endothelial migration or agents directly toxic to endothelium would be of value in a combined approach to therapy.

Vascular endothelial growth factor, wild-type p53, and angiogenesis in early operable non-small cell lung cancer.

Vascular endothelial growth factor (VEGF) is a cytokine that is involved in tumor angiogenesis. Wild-type p53 (wt-p53) protein has been shown in cell lines to suppress angiogenesis through thrombospondin regulation. In this study, we immunohistochemically examined the expression of VEGF, nuclear and wild-type cytoplasmic p53, bcl-2, epidermal growth factor receptor, and c-erbB-2 oncoprotein; vascular grade; proliferation index; and extent of necrosis in non-small cell lung cancer (NSCLC). We analyzed 120 cases of early-stage NSCLCs (81 squamous cell carcinomas and 39 adenocarcinomas) treated with surgery alone (median follow-up, 63 months; range, 45-74 months). VEGF expression showed a positive association with high vascular grade (microvessel score of >75 per x250 field; P = 0.008), although about half of the LVG cases also expressed VEGF. None of the p53 antibodies examined correlated with angiogenesis. However, wt-p53 expression was inversely associated with VEGF expression, suggesting that wt-p53 is involved in the suppression of the VEGF gene. Combined analysis of VEGF, wt-p53, and microvessel counting showed that, although wt-p53 loss associates with VEGF switch-on, p53 protein may not be involved in the regulation of the angiogenic events downstream of VEGF expression. Moreover, no significant association of bcl-2 and c-erbB-2 oncoprotein expression with VEGF expression was observed. T/N stage, grade, Ki67 proliferation index, and extent of necrosis were not correlated with VEGF expression. Survival analysis showed that VEGF correlated with poor survival (P = 0.04) and was significant in node-negative cases (P = 0.03). We conclude that VEGF is an important angiogenic factor in NSCLC, its expression being dependent on wt-p53 loss.

Angiopoietin-1 is inversely related to thymidine phosphorylase expression in human breast cancer, indicating a role in vascular remodeling.

PURPOSE: Angiogenesis is essential for tumor growth and metastasis. It is a complex, dynamic process that is coordinated by several classes of angiogenic factors. One candidate family is the Tie2 tyrosine kinase, whose expression is restricted largely to endothelial cells. Tie2 has three known ligands, angiopoietin (Ang)-1, Ang-2, and Ang-4, that have different functional effects but play a requisite role in embryonic vessel remodeling. Because there are only limited data on the Tie2 pathway in human breast cancer, and our previous data have suggested that breast tumors establish a blood supply by vascular remodeling, we have investigated the expression of Ang-1, Ang-2, Ang-4, and Tie2 in a series of normal and neoplastic human breast tissues. EXPERIMENTAL DESIGN: We examined mRNA expression by reverse transcription-PCR in 6 normal and 52 malignant breast tissues and correlated expression with clinicopathological and angiogenic variables. We also examined the effect of physiological levels of estrogen on Ang expression. RESULTS: Ang-1, Ang-2, Ang-4, and Tie2 were detected in 19%, 52%, 35%, and 65%, respectively, of tumor samples. There was a significant reduction in expression of tumor Ang-1 (P = 0.04), Ang-2 (P = 0.01), Ang-4 (P = 0.004), and Tie2 (P = 0.02) compared with that in normal breast tissues. There was a significant relationship in tumors between all Angs and between each ligand and Tie2. In a multivariate analysis, there were significant positive correlations between Ang-4 and estrogen receptor (P = 0.016) and a significant inverse correlation between Ang-1 and thymidine phosphorylase expression (P = 0.01). No significant associations were observed between the other members of the Ang/Tie2 gene family and patient age, tumor size, lymph node status, tumor grade, vascular invasion, tumor vascularity, vascular maturation, thymidine phosphorylase, or vascular endothelial growth factor A expression (P > 0.05 for all). The potential regulation of Ang-4 by estrogen was further investigated in vitro. Addition of physiological concentrations of 17beta-estradiol (1 nM) to hormone-free media caused no significant change in Ang-4 mRNA abundance (P = 0.75) in the estrogen receptor-positive cell line MCF-7 after either 2 or 18 h, despite demonstrating induction for the estrogen response gene pS2. CONCLUSIONS: These findings suggest that the Ang/Tie2 pathway plays a significant role in human breast tumor angiogenesis but provide no initial evidence for direct regulation of the pathway by estrogen.

The short form of the alternatively spliced flt-4 but not its ligand vascular endothelial growth factor C is related to lymph node metastasis in human breast cancers.

Angiogenesis is essential for tumor growth and metastasis. It is regulated by numerous angiogenic factors, one of the most important being vascular endothelial growth factor (VEGF). Recently, VEGF-C, a new VEGF family member, has been identified that binds to the tyrosine kinase receptors flt-4 [VEGF receptor (VEGFR) 3] and KDR (VEGFR2). Although the importance of VEGF has been shown in many human tumor types, the contribution of VEGF-C and its primary receptor flt-4 to tumor progression is less well understood. We have therefore measured the level of VEGF-C, flt-4, and KDR mRNA by RNase protection assay and the pattern of VEGF-C expression by immunohistochemistry in 11 normal breast tissue samples and 61 invasive breast cancers. No significant difference in VEGF-C expression was observed between normal and neoplastic breast tissues (P = 0.11). There was a significant correlation between VEGF-C and both flt-4 (P = 0.02) and KDR (P = 0.0002), but no association was seen between VEGF-C and either lymph node status (P = 0.66) or number of involved nodes (P = 0.88), patient age (P = 0.83), tumor size (P = 0.20), estrogen receptor status (P = 0.67), or tumor grade (P = 0.35). No significant relationship was present between VEGF-C and vascular invasion (P = 0.30), tumor vascularity (P = 0.21), VEGF-A (P = 0.62), or thymidine phosphorylase expression (P = 1.00). VEGF-C was expressed predominantly in the cytoplasm of tumor cells, although occasional stromal components including fibroblasts were also positive. We could demonstrate no association between lymph node metastasis and either VEGF-C (P = 0.66) or flt-4 (P = 0.4). However, we did observe a significant loss of the long but not the short isoform of flt-4 in tumors compared with normal tissues (P = 0.02 and P = 0.25, respectively), and this difference was largely accounted for by the reduction of long flt-4 in node-positive tumors. These findings strongly support a role for VEGF-C/flt-4 signaling in tumor growth by enhancement of angiogenesis and/or lymphangiogenesis and suggest that differential regulation of these processes may be controlled via flt-4 isoform transcription. They further suggest that the measurement of flt-4 isoform expression may identify a patient group that is likely to have node-positive disease and therefore benefit from additional treatment and also emphasize an additional ligand interaction that could be exploited by anti-VEGFR therapy.

Susceptibility and resistance of rats to stress-induced decreases in swim-test activity: a selective breeding study.

In this study, selective breeding was used to generate two populations of rats that differed in their susceptibility to showing decreased struggling activity in a swim test after being exposed to uncontrollable electric tail-shock. After five generations of selective breeding, we obtained a population that displayed large decreases in swim-test struggling after shock (swim-test susceptible) and a population that displayed no decrease in struggling after shock (swim-test resistant). Males of this fifth generation from the two selectively-bred populations were then compared for differences in non-swim behavioral measures (home-cage 24-h spontaneous ambulatory activity and food/water intake) and several aspects of brain catecholaminergic activity, including electrophysiological activity of locus coeruleus (LC) neurons, catecholamine/metabolite concentrations in various brain regions, and in vivo tyrosine hydroxylase activity. Interestingly, swim-test resistant rats displayed larger decreases in home-cage ambulatory activity and water intake after exposure to shock than did swim-test susceptible animals. Marked differences were also seen in measures of brain noradrenergic activity. Compared to the susceptible rats, resistant rats showed higher levels of evoked activity of LC neurons, larger shock-induced depletions of norepinephrine (NE) and 3-methoxy-4-hydroxyphenylglycol (MHPG) in the LC, lower in vivo tyrosine hydroxylase (TH) activity in ventral bundle projection areas such as the hypothalamus, and larger amounts of NE in dorsal bundle projection areas. Finally, swim-test resistant rats had much higher concentrations of dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) in striatum and nucleus accumbens than susceptible rats. These results appear to be explainable on the basis that differences in swim-test struggling behavior for which the two populations were selectively bred were a consequence of differences in forebrain DA whereas stress-induced differences in other behavioral measures (i.e. spontaneous ambulation and intake) occurred because swim-test resistant animals showed greater disturbance of the LC-NE system after uncontrollable shock.

Emergency physician treatment of acute stroke with recombinant tissue plasminogen activator: a retrospective analysis.

UNLABELLED: Stroke teams are advocated for the rapid treatment of patients who have acute ischemic stroke (AIS) with recombinant tissue plasminogen activator (rt-PA). An alternate model uses existing ED resources with specialist consultation as needed. OBJECTIVES: To evaluate the treatment of AIS with rt-PA in this alternate ED model. METHODS: A retrospective observational review was performed of consecutive patients with AIS treated with rt-PA at four hospitals affiliated with an emergency medicine residency. Emergency physicians (EPs) were directly responsible for the treatment of all patients according to predefined guidelines. Records were evaluated from the implementation of the guidelines through December 15, 1997. RESULTS: 37 patients with AIS received rt-PA. Mean age+/-SD was 63+/-16 years (range 22-87), with 25 (68%) male. Patients presented 67+/-29 minutes after stroke onset. After ED arrival, they were seen by the EP in 14+/-13 minutes, had CT in 46+/-22 minutes, and were treated in 97+/-35 minutes. Neurologist consultation occurred in the department for nine patients (24.3%), and by telephone for 14 (37.8%). Symptomatic intracerebral hemorrhage (ICH) occurred in four (10.8%, 95% CI = 0.8% to 20.8%). There were two deaths, neither associated with ICH. Neurologic outcome at discharge compared with presentation in survivors was normal for four patients (11.4%), improved for 16 (45.7%), unchanged for ten (28.6%), and worse for five (14.3%). CONCLUSIONS: In this analysis, EPs, with specialty consultation as required, successfully identified patients with AIS and delivered rt-PA with satisfactory outcomes. Important elements of this model include early patient identification, preestablished protocols, and rapid access to CT scanning and interpretation.

Asymmetry of foot-floor contacts in a young athlete five years after traumatic lesion to the sciatic nerve.

This study demonstrates the need for periodic reassessments of overall function in effective rehabilitation programs. Unilateral orthotic aids to walking may correct a malfunction on the affected side and yet inadvertently contribute to malfunction of the contralateral side if attention is focused only on the impaired joint or segment. The subject of the study was an active young adult male who 5 years previously in a waterskiing accident had suffered a severely fractured pelvis, traumatized sciatic nerve, and immediate paralysis of the foot dorsiflexors. He now exhibits residual effects including a unilaterally shortened (2.6 cm) lower extremity, corrected by a heel-lift, and continued paralysis of the right foot, corrected by a drop-foot appliance. These orthotics provide appropriate contact sequences of the affected foot while walking, but unintentionally have adverse effects on foot-floor contact sequences on the unaffected side. Analysis of the ambulatory pattern by temporal sequencing kinematics reveals the extent of the problem, but not its solution.J Orthop Sports Phys Ther 1988;9(11):375-380.

Morphological characteristics of elite male field hockey players.

The main objective of this paper was to establish a data base of physical norms for elite male field hockey players. Direct measurements were made on eight parameters and a further three derived variables were calculated. With a stature of 176.3 cm and mass of 75.2 kg the hockey players were identified as ecto-mesomorphic. The lean build of the subjects was evident with a fairly low percentage body fat (11.1%) and a relatively high RPI of 41.77. Functional arm length did not appear to have any correlation with hockey playing ability. However, grip strength, in both right (54.0 kg) and left (53.1 kg) measures was above that of norms for male adults and there was no significant difference between left and right grip strength. The players appeared to have good leg strength (stand long jump mean 2.3 m) with very little variability amongst the players. On the other hand flexibility (sit and reach mean 9.7) was poor and results indicated a wide range of variability in the sample group tested.

Terrestrial and sub aquatic apneic bradycardial responses under resting and working conditions.

Morphology normalised (BSA; stature) vital capacity was used to divide a sample of 13 young adult female volunteers into two groups based on lung volume. The apneic (breath-hold) heart rate response under resting and working conditions, on land and underwater, was measured. Four conditions were imposed, during which continuous monitoring of heart-rate was undertaken: resting on land, resting underwater, swimming unconstrained underwater, carrying bricks underwater. In all conditions a significant bradycardial response was exhibited (p less than 0.05), with heart rates also significantly lower for the group with larger lung volumes. No differences were found between the groups in ratings of perceived exertion during breath-hold. We contend that the lower heart rates in the group with larger lung volumes may be caused by higher negative intrathoracic pressure which, by stimulation of baroreceptors leads to a more pronounced reflex slowing of the heart rate.

Morally autonomous practice?

The structures and contexts within which nurses work results in the moral agency and moral autonomy of the nurse being compromised. This claim results from a confusion of (1) the concept of autonomy with those of freedom and independence; and (2) a confusion of the notion of moral autonomy with that of autonomous professional practice. The drawing of appropriate distinctions allows clarification of the relevant concepts. It also underlines the responsibility of practitioners to recognize the moral dimension of their practice, and the moral implications of their actions, as they attempt to meet the health care needs of their patients and develop practice professionally.

Nurses' judgements of self-neglect: a factorial survey.

Self-neglect can be understood as the failure to engage in those activities which a given culture deems necessary to maintain a socially accepted standard of personal and household hygiene and carry out activities needed to maintain health status. Self-neglect is bound up in a discourse which equates dirt with disease and in which transgressions of self-care norms can be labelled as a medical syndrome. The notion of self-neglect as a social construction is the theoretical perspective which provides the framework for the study reported here. Judgements regarding self-neglect may be social judgements influenced by professional socialisation and cultural values. The belief that different groups of nurses may have different constructions of self-neglect will be investigated and the factors which influence these judgements will be explored in three groups of nurses. The inclusion of nursing students will allow some picture to emerge as to whether judgements develop over time or are relatively constant across the career path, albeit within the limitations of a non-longitudinal design.

Stature and seat position as factors affecting fractionated response time in motor vehicle drivers.

Motor vehicle accident fatalities are a cause for concern internationally; all drivers need to selectively attend to environmental changes, and to react swiftly and appropriately. The focus of the present paper was to investigate the effect of stature and seat positioning on fractionated response time. Eighty four young South African adults spanning a range of statures from 1.48 m to 2.00 m were tested in two extreme seat positions (near and far) using a European designed car-shell. Significant differences (p < 0.05) in knee flexion angle, but not in reaction or movement times were identified. Separation of tallest (X 1.93 m) and shortest (X 1.56 m) subjects (n = 20) revealed no significant stature-related differences in response times. However, the tall group showed significantly improved results when seated in the far position and the short group when seated in the near position. The results indicate that correct seat positioning will exert a significant effect on the overall response time of the driver, which in turn will affect the braking distance whilst driving.