Gesundheitsinformationen im Internet

Electronic Health (E-Health) increasingly strives to provide health information and services to healthcare stakeholders (e.g., insurances, physicians, hospital and patient alliances, self-help groups) via the Internet, and to actively involve patients in their care. One major chance for these participatory healthcare and patient-oriented approaches that integrate patients in healthcare are the phenomena and ideas associated with providing information and healthcare on the Internet. This paper examines the existing body of knowledge on online health information and explores the current state of research through a review of literature by classifying articles published between the last two decades in IS, BISE, and health domain-specific journals as well as a review of past and current BMBF-, DFG-, and EU-funded research projects in this field. The fundamental categories of the analysis represent the stakeholders in the healthcare sector, the connecting information flows, the information-transferring technological applications, as well as the categories of the TEMPEST model. Amongst others, the results show that most of the analyzed papers discuss conventional, transactional E-Health applications. Within the TEMPEST model the technological category has the largest share of all categories. Based on these findings, causes and future research fields are discussed.     

Do as your parents say?—Analyzing IT adoption influencing factors for full and under age applicants

The article suggests a model for examining the adoption of e-recruiting by individuals. The model is empirically evaluated using survey data from 323 full and under age applicants. The results explain substantial parts of the individual adoption decision. Interestingly, the relative importance of the adoption drivers varies with age, social environment and the level of education. While, as expected, overall Performance Expectancy is the major force behind adopting e-recruiting, the relative importance of the other factors differs a lot. Whereas Facilitating Conditions came out as an important driver for under age pupils, full age students by contrast are highly driven by the influence of their peer groups and the communication of the respective company they apply for. A major outcome is that the Subjective Norm of family and friends, teachers and professors has a weaker influence for under age pupils who mostly live with their parents than for the group of students who already left home to study at college. Consequentially we assume that the social influence of peer groups on an individual’s adoption differs with respect to age, social environment and level of education. This should be investigated more carefully in future adoption research as it might provide an answer for the varying significance of Subjective Norm in adoption research.     

Giving too much social support: social overload on social networking sites

As the number of messages and social relationships embedded in social networking sites (SNS) increases, the amount of social information demanding a reaction from individuals increases as well. We observe that, as a consequence, SNS users feel they are giving too much social support to other SNS users. Drawing on social support theory (SST), we call this negative association with SNS usage ‘social overload’ and develop a latent variable to measure it. We then identify the theoretical antecedents and consequences of social overload and evaluate the social overload model empirically using interviews with 12 and a survey of 571 Facebook users. The results show that extent of usage, number of friends, subjective social support norms, and type of relationship (online-only vs offline friends) are factors that directly contribute to social overload while age has only an indirect effect. The psychological and behavioral consequences of social overload include feelings of SNS exhaustion by users, low levels of user satisfaction, and a high intention to reduce or even stop using SNS. The resulting theoretical implications for SST and SNS acceptance research are discussed and practical implications for organizations, SNS providers, and SNS users are drawn.     

Primary aortic mural thrombus: presentation and treatment

Schizophrenic patients are extremely heavy tobacco smokers. However, a lower incidence of lung cancer in schizophrenic patients has been observed in comparison to other heavy smokers. Nicotine increases the proliferation of pulmonary neuroendocrine tissue, causing the release of a bombesin-like peptide. Thus, bombesin-like peptide levels in urine may be an indicator of precancerous, cigarette-induced lung damage. Bombesin-like peptide levels of 10 schizophrenic smokers and 11 schizophrenic nonsmokers were compared to those of nonschizophrenic subjects matched for age and pack-years of smoking. The nonschizophrenic smokers showed the expected increase in urinary bombesin-like peptide levels, as compared to nonschizophrenic nonsmokers. Schizophrenic patients had lower bombesin-like peptide levels independent of smoking effects. The mechanism of the difference in bombesin-like peptide levels between schizophrenic patients and nonschizophrenic subjects is unknown, but one possibility involves alteration in the alpha 7-nicotinic acetylcholine receptor, which mediates the growth of some neuroendocrine cell lines in vitro.     

The role of voltage-gated Ca2+ channels in anoxic injury of spinal cord white matter

Dorsal column axons of the rat spinal cord are partially protected from anoxic injury following blockade of voltage-sensitive Na+ channels and the Na+/--Ca2+ exchanger. To examine the potential contribution of voltage-gated Ca2+ channels to anoxic injury of spinal cord axons, we studied axonal conduction in rat dorsal columns in vitro following a 60-min period of anoxia. Glass microelectrodes were used to record field potentials from the dorsal columns following distal local surface stimulation. Perfusion solutions containing blockers of voltage-gated Ca2+ channels were introduced 60 min prior to onset of anoxia and continued until 10 min after reoxygenation. Pharmacological blocking agents which are relatively selective for L- (verapamil, diltiazem, nifedipine) and N- (omega-conotoxin GVIA) type calcium channels were significantly protective against anoxia-induced loss of conduction, as was non-specific block using divalent cations. Other Ca2+ channel blockers (neomycin and omega-conotoxin MVIIC) that affect multiple Ca2+ channel types were also neuroprotective. Ni2+, which preferentially blocks R-type Ca2+ channels more than T-type channels, was also protective in a dose-dependent manner. These data suggest that the influx of Ca2+, through L-, N- and possibly R-type voltage-gated Ca2+ channels, participates in the pathophysiology of the Ca2+-mediated injury of spinal cord axons that is triggered by anoxia.     

Outcome of moderate carotid artery stenosis in patients who are asymptomatic

PURPOSE: The incidence rate of disease progression and stroke after the diagnosis of a moderate (50% to 79%) carotid stenosis was determined by means of color-flow duplex scanning. METHODS: During a 4-year period, 344 male veterans with moderate internal carotid artery stenoses, on one or both sides, were examined at regular intervals for a mean period of 25 months. Carotid color-flow scans were obtained semiannually. Clinical follow-up was performed to determine the incidence rate of amaurosis fugax, transient ischemic attacks, nonhemispheric symptoms, and strokes. RESULTS: New neurologic symptoms developed in 75 patients (21.8%). Fifty-one (14.8%) had ipsilateral symptoms during follow-up: 18 amaurosis fugax (5.2%), 14 transient ischemic attacks (4%), 5 nonhemispheric symptoms (1.4%), and 14 strokes (4%). Twenty-four patients (6.9%) had contralateral symptoms: 20 strokes (5.8%) and 4 transient ischemic attacks (1.2%). Life-table analysis showed that the annual rate of ipsilateral neurologic events was 8.1%, and the annual rate of stroke was 2.1%. Seventy-five patients (22%) died in the follow-up period. Disease progression to 80% to 99% stenosis or occlusion occurred in 71 of 458 vessels (15.5%). The internal carotid arteries that showed evidence of disease progression had a significantly higher initial peak systolic velocity (251 vs 190 cm/s; P <.0001) and end diastolic velocity (74 vs 52 cm/s; P < 0.0001). Black patients and patients with ischemic heart disease were at a higher risk for disease progression. We could not identify any atherosclerotic risk factors that reliably predicted patients in whom future ipsilateral neurologic symptoms were more likely to develop. However, there was an increased risk of stroke associated with progression of disease. CONCLUSION: Patients who are asymptomatic and who have moderate carotid stenoses are at significant risk for neurologic symptoms and death, but have a relatively low incidence rate of ipsilateral events. The initial flow characteristics in the stenotic vessel are predictive of future disease progression, but they are not helpful in identifying patients in whom symptoms will develop.     

A histomorphometric evaluation of heparin-induced bone loss after discontinuation of heparin treatment in rats

Although it is well established that long-term heparin therapy causes osteoporosis, it is unknown whether heparin-induced bone loss is reversible when heparin treatment is stopped. To address this question, we randomized rats to once daily subcutaneous injections of either unfractionated heparin (1.0 U/g or 0.5 U/g) or saline for 28 days and then followed the rats for an additional 28 days off treatment. Based on histomorphometric analysis of the distal third of the right femur proximal to the epiphyseal growth plate, 1.0 U/g heparin caused a 30% loss in cancellous bone volume over the first 28 days. This was accompanied by a 137% increase in osteoclast surface and a 60% decrease in both osteoblast and osteoid surface. One month after cessation of heparin treatment, no recovery in these parameters was observed. Similarly, serum levels of alkaline phosphatase, a biochemical marker of bone formation, which continued to decrease over the course of heparin treatment, showed no signs of recovery in the subsequent 28 days off treatment. To explore the mechanism responsible for the prolonged effect of heparin on bone, we repeated the experiment giving 125I-labeled heparin in place of unlabeled heparin. 125I-labeled heparin was found to accumulate in bone during the course of its administration, and be retained in bone for at least 56 days after stopping heparin treatment. These findings suggest that heparin-induced osteoporosis is not rapidly reversible because heparin is sequestered in bone for an extended period.