| 341. |
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| 342. |
- Leone, M. I., et al.
(författare)
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Fuel on the Invention Funnel : Technology Licensing-in, antecedents and invention performance
- 2009
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- Technology management has so far largely overlooked that licensing-in may represent learning opportunitiesfor the recipient firm. Attention has primarily been directed towards a more tactic explanation for the decisionof firms to in-license external technologies. However, increasing empirical evidence witnesses an inducingeffect of licensing-in on the inventive behavior of the single firm which, in turn, feeds its development andgrowth. The aim of this paper is to explore whether licensing-in in fact acts as a catalyst for inventive activitiespursued by licensee firms. We employ a two-part model to investigate the inventiveness of 133 licenseescompared to an equally sized matched sample of non-licensees. The study reveals that licensees exhibit elevatedinvention performances compared to non-licensee counterparts. This holds both when considering inventionin general and invention in licensed technological class.. In addition, the paper reveals that familiarity with thelicensed technology and technological specialization instigates the licensee to pursue a narrow invention strategyas defined by the technological classes of the licensed patent.
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| 343. |
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| 344. |
- Leone, Marica, et al.
(författare)
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Melatonin use and the risk of self-harm and unintentional injuries in youths with and without psychiatric disorders
- 2023
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Ingår i: Journal of Child Psychology and Psychiatry. - : John Wiley & Sons. - 0021-9630 .- 1469-7610. ; 64:7, s. 1027-1036
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Sleep disorders in youth have been associated with increased risks of injury, including suicidal behavior. This study investigated whether melatonin, which is the most common medication for sleep disturbances in youth in Sweden, is associated with a decreased risk of injury.METHODS: This population-based cohort study included 25,575 youths who initiated melatonin treatment between ages 6 and 18. Poisson regression was used to estimate rate of injuries in the year prior to and following melatonin treatment initiation. A within-individual design was used to estimate relative risks by comparing injury risk in the last unmedicated month with injury risks in the 12 months after medication initiation. Analyses were stratified by sex, injury type, psychiatric comorbidities and age at melatonin-treatment initiation.RESULTS: While body injuries, falls and transport accident rates were comparable in the year before and after melatonin-treatment initiation, the risk of self-harm was highest in the months immediately prior to medication, and decreased thereafter. This was particularly prominent among adolescents with depression and/or anxiety, with females displaying greater absolute risks than males. Compared to the last unmedicated month, the 12 months post medication initiation had decreased relative risks for self-harm, with an IRR [95% CI] in the month following melatonin-treatment initiation of 0.46 [0.27-0.76] among adolescent females with psychiatric disorders, after excluding antidepressant users.CONCLUSIONS: Decreased risk of intentional self-harm was observed following melatonin-treatment initiation among females with depression and anxiety, suggesting that sleep interventions could be considered in an effort to reduce risk of self-harm in this population.
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| 345. |
- Leone, Nicola, et al.
(författare)
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Systematic review and meta-analysis of cerebrospinal fluid drain-related mortality and morbidity after fenestrated-branched endovascular aortic repair
- 2024
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Ingår i: Journal of Vascular Surgery. - : Elsevier. - 0741-5214 .- 1097-6809. ; 80:2, s. 586-594
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Tidskriftsartikel (refereegranskat)abstract
- Objective: This study aimed to investigate the incidence of cerebrospinal fl uid drainage (CSFD)-related complications specifically fi cally in patients who underwent fenestrated and branched endovascular aortic repair (F/B-EVAR). This objective was chosen considering the limitations and uncertainties surrounding its efficacy i cacy in preventing spinal cord injury.Methods: A systematic review following Cochrane Handbook and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was conducted (PROSPERO; #CRD42022359223). Literature searches of MEDLINE, Embase, and Scopus were performed until May 1, 2023, focusing on studies published after January 1, 2000. The inclusion criteria encompassed studies reporting on F/B-EVAR, CSFD, and drain-related complications. Data extraction and quality assessment using the Newcastle-Ottawa Scale were performed by multiple reviewers to ensure accuracy and reliability. A proportion meta-analysis was conducted to calculate the pooled rate and 95% confidence fi dence interval (CI). The primary and secondary outcomes were CSFD-related mortality and morbidity, respectively.Results: Six retrospective, observational, single-center studies were included, totaling 1079 patients and 730 CSFD placements (all prophylactic except for one). The Newcastle-Ottawa Scale showed a high to moderate risk of bias. The analysis revealed a CSFD-related mortality rate of 1.4% (95% CI: 0.0-4.8; I2 = 67.7%) and an overall morbidity rate of 25.6% (95% CI: 13.6-39.7; I2 = 83.2%). The overall major, moderate, and minor estimated complication rates were 6.1% (95% CI: 4.18.5; I2 = 0%), 4.6% (95% CI: 2.4-7.3; I2 = 33.5%), and 26.4% (95% CI: 16.5-37.7; I2 = 84.9%), respectively. Severe complications included intracranial hemorrhage (2.8%), spinal hematoma (1.4%), subarachnoid hemorrhage (1.4%), and CSFD-related neurological deficits fi cits (1.1%). A pooled estimate of 11.4% for nonfunctioning drainage was found.Conclusions: F/B-EVAR patients showed a notable incidence of CSFD-related death and substantial morbidity. This study highlights the limitations of the available data, the high prevalence of complications associated with CSFD, and the need for further research to better understand the risks and benefits of CSFD in F/B-EVAR. This calls for careful consideration regarding the routine use of prophylactic drainage due to the accumulating evidence of the risks associated with CSFD without proven benefit in this specific context.
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| 346. |
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| 347. |
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| 348. |
- Liu, S. X., et al.
(författare)
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Association and Familial Coaggregation of Childhood-Onset Type 1 Diabetes With Depression, Anxiety, and Stress-Related Disorders: A Population-Based Cohort Study
- 2022
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Ingår i: Diabetes Care. - : American Diabetes Association. - 0149-5992 .- 1935-5548. ; 45:9, s. 1987-1993
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE To estimate the association and familial coaggregation of childhood-onset type 1 diabetes with depression, anxiety, and stress-related disorders. RESEARCH DESIGN AND METHODS This was a population-based cohort study with use of data from Swedish nationwide registers. A total of similar to 3.5 million individuals born in Sweden 1973-2007 were linked to their biological parents, full siblings and half-siblings, and cousins. Cox models were used to estimate the association and familial coaggregation of type 1 diabetes with depression, anxiety, and stress-related disorders. RESULTS Individuals diagnosed with childhood-onset type 1 diabetes (n = 20,005) were found to be at greater risks of all outcomes: any psychiatric diagnosis (adjusted hazard ratio [aHR] 1.66 [95% CI 1.59-1.72]) or specific diagnoses of depression (1.85 [1.76-1.94]), anxiety (1.41[1.33-1.50]), and stress-related disorders (1.75 [1.62-1.89]), as well as use of antidepressants or anxiolytics (1.30 [1.26-1.34]), compared with individuals without type 1 diabetes. Overall, relatives of individuals with type 1 diabetes were at elevated risks of developing these outcomes, with the highest risks seen in parents (aHRs 1.18-1.25), followed by full siblings (aHRs 1.05-1.20), and the magnitudes of risk estimates appear proportional to familial relatedness. CONCLUSIONS These results support existing evidence that children and adolescents with type 1 diabetes are at greater risks of developing depression, anxiety, and stress-related disorders and indicate that shared familial factors might contribute to these elevated risks. Our findings highlight the need for psychological consulting for children and their families in diabetes care. Quantitative and molecular genetic studies are warranted to further understand the etiology of these psychiatric disorders in type 1 diabetes.
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| 349. |
- Malan, Leoné, et al.
(författare)
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A stress syndrome prototype reflects type 3 diabetes and ischemic stroke risk : The SABPA study
- 2021
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Ingår i: Biology. - : MDPI AG. - 2079-7737. ; 10:2
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Tidskriftsartikel (refereegranskat)abstract
- Type 3 diabetes (T3D) accurately reflects that dementia, e.g., Alzheimer’s disease, represents insulin resistance and neurodegeneration in the brain. Similar retinal microvascular changes were observed in Alzheimer’s and chronic stressed individuals. Hence, we aimed to show that chronic stress relates to T3D dementia signs and retinopathy, ultimately comprising a Stress syndrome prototype reflecting risk for T3D and stroke. A chronic stress and stroke risk phenotype (Stressed) score, independent of age, race or gender, was applied to stratify participants (N = 264; aged 44 - 9 years) into high stress risk (Stressed, N = 159) and low stress risk (non-Stressed, N = 105) groups. We determined insulin resistance using the homeostatic model assessment (HOMA-IR), which is interchangeable with T3D, and dementia risk markers (cognitive executive functioning (cognitiveexe-func); telomere length; waist circumference (WC), neuronal glia injury; neuron-specific enolase/NSE, S100B). Retinopathy was determined in the mydriatic eye. The Stressed group had greater incidence of HOMA-IR in the upper quartile (≥5), larger WC, poorer cognitiveexe-func control, shorter telomeres, consistently raised neuronal glia injury, fewer retinal arteries, narrower arteries, wider veins and a larger optic cup/disc ratio (C/D) compared to the non-Stressed group. Furthermore, of the stroke risk markers, arterial narrowing was related to glaucoma risk with a greater C/D, whilst retinal vein widening was related to HOMA-IR, poor cognitiveexe-func control and neuronal glia injury (Adjusted R2 0.30; p ≤ 0.05). These associations were not evident in the non-Stressed group. Logistic regression associations between the Stressed phenotype and four dementia risk markers (cognitiveexe-func, telomere length, NSE and WC) comprised a Stress syndrome prototype (area under the curve 0.80; sensitivity/specificity 85%/58%; p ≤ 0.001). The Stress syndrome prototype reflected risk for HOMA-IR (odds ratio (OR) 7.72) and retinal glia ischemia (OR 1.27) and vein widening (OR 1.03). The Stressed phenotype was associated with neuronal glia injury and retinal ischemia, potentiating glaucoma risk. The detrimental effect of chronic stress exemplified a Stress syndrome prototype reflecting risk for type 3 diabetes, neurodegeneration and ischemic stroke.
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| 350. |
- Malan, Leoné, et al.
(författare)
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The chronic stress risk phenotype mirrored in the human retina as a neurodegenerative condition
- 2023
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Ingår i: Stress. - 1607-8888. ; 26:1
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Tidskriftsartikel (refereegranskat)abstract
- The brain is the key organ that orchestrates the stress response which translates to the retina. The retina is an extension of the brain and retinal symptoms in subjects with neurodegenerative diseases substantiated the eye as a window to the brain. The retina is used in this study to determine whether chronic stress reflects neurodegenerative signs indicative of neurodegenerative conditions. A 3-year prospective cohort (n = 333; aged 46 ± 9 years) was stratified into stress-phenotype cases (n = 212) and controls (n = 121) by applying the Malan stress-phenotype index. Neurodegenerative risk markers included ischemia (astrocytic S100 calcium-binding protein B/S100B); 24h blood pressure, proteomics; inflammation (tumor-necrosis-factor-α/TNF-α); neuronal damage (neuron-specific-enolase); anti-apoptosis of retinal-ganglion-cells (beta-nerve-growth-factor), astrocytic activity (glial-fibrillary-acidic-protein); hematocrit (viscosity) and retinal follow-up data [vessels; stress-optic-neuropathy]. Stress-optic-neuropathy risk was calculated from two indices: a newly derived diastolic-ocular-perfusion-pressure cut-point ≥68 mmHg relating to the stress-phenotype; combined with an established cup-to-disc ratio cut-point ≥0.3. Higher stress-optic-neuropathy (39% vs. 17%) and hypertension (73% vs. 16%) prevalence was observed in the stress-phenotype cases vs. controls. Elevated diastolic-ocular-perfusion-pressure, indicating hypoperfusion, was related to arterial narrowing and trend for ischemia increases in the stress-phenotype. Ischemia in the stress-phenotype at baseline, follow-up and 3-yr changes was related to consistent inflammation (TNF-α and cytokine-interleukin-17-receptor-A), neuron-specific-enolase increases, consistent apoptosis (chitinase 3-like-1, low beta-nerve-growth-factor), glial-fibrillary-acidic-protein decreases, elevated viscosity, vein widening as risk marker of endothelial dysfunction in the blood-retinal-barrier, lower vein count, and elevated stress-optic-neuropathy. The stress-phenotype and related neurodegenerative signs of ongoing brain ischemia, apoptosis and endothelial dysfunction compromised blood-retinal-barrier permeability and optic nerve integrity. In fact, the stress-phenotype could identify persons at high risk of neurodegeneration to indicate a neurodegenerative condition.
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