Lithovius-pappissuvun palkkaus ja pappilat Limingan pitäjässä 1575-1730

Markku Kuorilehto Lithovius-pappissuvun palkkaus ja pappilat Limingan pitäjässä 1575 1730 Pohjois-Pohjanmaan Limingan keskiaikainen pitäjä syntyi maankohoamisen seurauksena muodostuneelle niittylaakiolle. Pitäjä levittäytyi pohjoisessa ja idässä Oulujokilaaksosta Oulujärven latvavesille asti. Laajat ja hyvätuottoiset niityt mahdollistivat karjatalouden lisääntymisen sekä peltoviljelyn paremmin kuin monissa muissa lähipitäjissä. Limingan pitäjä oli myös kalavesiltään runsas. Luonnonolosuhteiden ja hyvin kehittyneen elinkeinorakenteen vuoksi Limingasta kehittyi talopoikaisasutukseltaan vauras ja suurin pitäjä Pohjois- Pohjanmaalla. Talonpoikien tulokehitys heijastui myös suurempana papiston palkkauksena. Limingan kirkkoherraksi määrättiin Henrik Laurinpoika vuonna 1575. Hänestä polveutui laaja Lithovius-pappissuku. Suvun mieskantaisia jäseniä Limingan kirkkoherroina oli yhteensä seitsemän. Yhteensä sukuun kuuluvia pappeja Limingassa oli lähes kaksikymmentä. Lithovius-suvun ajan palkkauskehityksen vaikutuksesta pitäjään halusi hakeutua useita erittäin ansioituneita hakijoita, kun suvun valtakausi päättyi 1720-luvun lopulla. Tässä pro gradu -tutkielmassa on tarkasteltu papiston palkkauksen rakennetta: kymmenyksiä, muita maksuja sekä virkataloetuutena pappiloita. Kymmenykset jakaantuivat päälinjoiltaan vilja-, karja-, voi- ja kalakymmenyksiin. Kymmenyksiä on pidetty usein vuosittain vaihtelevana palkkauksena, mutta tutkimukseni osoittaa, että papistolle määrättiin välillä kiinteä palkkaus. Lisäksi papisto sai erinäisiä maksuja pitäjänsä kierroista juhlapyhien aikana. Limingan pappilaa ylläpidettiin ja rakennettiin seurakuntalaisten kanssa hyvässä yhteishengessä ja pappilan asema korostui etenkin 1670-luvulta lähtien. Palkkaus ja edut paranivat, ja niistä tuli suvulle merkittävä tulonlähde. Eri hallitsijat pyrkivät uudistamaan papiston palkkausta useampaan kertaan. Pohjalaiset papit ja pitäjäläiset eivät usein suostuneet näihin uudistuksiin, vaan pysyivät entisissä toteutustavoissa. Uudistaminen liittyi Ruotsin ja kirkon yhtenäistämispolitiikkaan, joka epäonnistui papiston palkkauksessa 1600-luvulla Pohjanmaalla. Limingassa papisto ja seurakuntalaiset noudattivat vahvaa keskinäistä yhteistyötä. Lähteiden perusteella Limingassa ei ole havaittavissa kuin vähäisiä palkkaukseen ja pappiloihin liittyviä riitoja. Tämä kuvastaa Limingan pitäjän vahvaa sopimus- ja tapaoikeudellista yhteishenkeä yli kruunun tavoitteiden. Tämä yhteishenki turvasi myös Lithoviuksien pitkäaikaisen valta-aseman Limingassa

Power Consumption Analysis of Operating Systems for Wireless Sensor Networks

In this paper four wireless sensor network operating systems are compared in terms of power consumption. The analysis takes into account the most common operating systems—TinyOS v1.0, TinyOS v2.0, Mantis and Contiki—running on Tmote Sky and MICAz devices. With the objective of ensuring a fair evaluation, a benchmark composed of four applications has been developed, covering the most typical tasks that a Wireless Sensor Network performs. The results show the instant and average current consumption of the devices during the execution of these applications. The experimental measurements provide a good insight into the power mode in which the device components are running at every moment, and they can be used to compare the performance of different operating systems executing the same tasks

Statins, bone, and neurofibromatosis type 1

Neurofibromatosis type 1 (NF1) is a dominantly inherited multi-system disorder. Major features include pigmentary abnormalities, benign tumors of the nerve sheath (neurofibromas), malignant tumors, learning disabilities, and skeletal dysplasia. The NF1 gene functions as a tumor suppressor, but haploinsuffiency probably accounts for some aspects of the non-tumor phenotype. The protein product, neurofibromin, is a Ras GTPase-activating protein, and various Ras pathway inhibitors are being tested in preclinical models and clinical trials for effectiveness in treating NF1 complications. This month in BMC Medicine, a paper by Kolanczyk et al describes a preclinical mouse model for tibial dysplasia and provides evidence that the drug lovastatin – in use to treat cardiovascular disease – may be beneficial, opening the door to clinical trials in humans

A Solar Energy Powered Autonomous Wireless Actuator Node for Irrigation Systems

The design of a fully autonomous and wireless actuator node ("wEcoValve mote") based on the IEEE 802.15.4 standard is presented. The system allows remote control (open/close) of a 3-lead magnetic latch solenoid, commonly used in drip irrigation systems in applications such as agricultural areas, greenhouses, gardens, etc. The very low power consumption of the system in conjunction with the low power consumption of the valve, only when switching positions, allows the system to be solar powered, thus eliminating the need of wires and facilitating its deployment. By using supercapacitors recharged from a specifically designed solar power module, the need to replace batteries is also eliminated and the system is completely autonomous and maintenance free. The "wEcoValve mote" firmware is based on a synchronous protocol that allows a bidirectional communication with a latency optimized for real-time work, with a synchronization time between nodes of 4 s, thus achieving a power consumption average of 2.9 mW. © 2011 by the authors.This work was supported by the I + D + i program of the Generalitat Valenciana, R&D Project GV05/043, and the Vicerecorate of Investigation, Development and Innovation of Universidad Politecnica de Valencia PAID-06-06-002-61 and PAID-10-11.Lajara Vizcaino, JR.; Alberola, J.; Pelegrí Sebastiá, J. (2011). A Solar Energy Powered Autonomous Wireless Actuator Node for Irrigation Systems. Sensors. 11:329-340. doi:10.3390/s110100329S3293401

Calcifications in the descending thoracic aorta predict postoperative anastomotic leakages after esophagectomy for cancer

Background: Anastomotic leak is one of the most feared complications of esophagectomy. Previous studies have suggested a potential link between aortic calcifications detected on routine preoperative CT scans and increased risk of anastomotic leak after esophagectomy. This study aims to investigate whether clinicians' assessment of aortic calcifications can predict the occurrence of anastomotic leaks in patients undergoing esophagectomy for cancer. Methods: A long-term follow-up was conducted on consecutive patients with esophageal cancer who underwent elective open esophagectomy at a Finnish tertiary hospital. Aortic calcifications were evaluated based on CT scans and categorized on a 0–3 scale reflecting the number of calcifications in the affected segment of the aorta. Reviewers assessing the calcifications were blinded to clinical details and postoperative outcomes. Results: The study included 97 patients (median age: 64 years and range: 43–78; 20% female), with a median follow-up time of 1307 (2–1540) days. Among them, 22 patients (23%) had postoperative anastomotic leak. We observed a significant association between calcifications in the descending aorta and a higher risk of anastomotic leak (p = 0.007), as well as an earlier occurrence of leak postoperatively (p = 0.013). However, there was no association between aortic calcifications and increased mortality. Conclusions: Presence of calcifications in the descending aorta is independently associated with an increased risk of anastomotic leaks following esophagectomy for cancer. Identifying patients at higher risk for this complication could facilitate appropriate pre- and postoperative interventions, as well as enable earlier diagnosis and treatment to mitigate the severity of the complication.Peer reviewe

A QoS-Guaranteed Coverage Precedence Routing Algorithm for Wireless Sensor Networks

For mission-critical applications of wireless sensor networks (WSNs) involving extensive battlefield surveillance, medical healthcare, etc., it is crucial to have low-power, new protocols, methodologies and structures for transferring data and information in a network with full sensing coverage capability for an extended working period. The upmost mission is to ensure that the network is fully functional providing reliable transmission of the sensed data without the risk of data loss. WSNs have been applied to various types of mission-critical applications. Coverage preservation is one of the most essential functions to guarantee quality of service (QoS) in WSNs. However, a tradeoff exists between sensing coverage and network lifetime due to the limited energy supplies of sensor nodes. In this study, we propose a routing protocol to accommodate both energy-balance and coverage-preservation for sensor nodes in WSNs. The energy consumption for radio transmissions and the residual energy over the network are taken into account when the proposed protocol determines an energy-efficient route for a packet. The simulation results demonstrate that the proposed protocol is able to increase the duration of the on-duty network and provide up to 98.3% and 85.7% of extra service time with 100% sensing coverage ratio comparing with LEACH and the LEACH-Coverage-U protocols, respectively

Modelling neurofibromatosis type 1 tibial dysplasia and its treatment with lovastatin

<p>Abstract</p> <p>Background</p> <p>Bowing and/or pseudarthrosis of the tibia is a known severe complication of neurofibromatosis type 1 (NF1). Mice with conditionally inactivated neurofibromin (Nf1) in the developing limbs and cranium (Nf1Prx1) show bowing of the tibia caused by decreased bone mineralisation and increased bone vascularisation. However, in contrast to NF1 patients, spontaneous fractures do not occur in Nf1Prx1 mice probably due to the relatively low mechanical load. We studied bone healing in a cortical bone injury model in Nf1Prx1 mice as a model for NF1-associated bone disease. Taking advantage of this experimental model we explore effects of systemically applied lovastatin, a cholesterol-lowering drug, on the Nf1 deficient bone repair.</p> <p>Methods</p> <p>Cortical injury was induced bilaterally in the <it>tuberositas tibiae </it>in Nf1Prx1 mutant mice and littermate controls according to a method described previously. Paraffin as well as methacrylate sections were analysed from each animal. We divided 24 sex-matched mutant mice into a lovastatin-treated and an untreated group. The lovastatin-treated mice received 0.15 mg activated lovastatin by daily gavage. The bone repair process was analysed at three consecutive time points post injury, using histological methods, micro computed tomography measurements and <it>in situ </it>hybridisation. At each experimental time point, three lovastatin-treated mutant mice, three untreated mutant mice and three untreated control mice were analysed. The animal group humanely killed on day 14 post injury was expanded to six treated and six untreated mutant mice as well as six control mice.</p> <p>Results</p> <p>Bone injury repair is a complex process, which requires the concerted effort of numerous cell types. It is initiated by an inflammatory response, which stimulates fibroblasts from the surrounding connective tissue to proliferate and fill in the injury site with a provisional extracellular matrix. In parallel, mesenchymal progenitor cells from the periost are recruited into the injury site to become osteoblasts. In Nf1Prx1 mice bone repair is delayed and characterised by the excessive formation and the persistence of fibro-cartilaginous tissue and impaired extracellular matrix mineralisation. Correspondingly, expression of Runx2 is downregulated. High-dose systemic lovastatin treatment restores Runx2 expression and accelerates new bone formation, thus improving cortical bone repair in Nf1Prx1 tibia. The bone anabolic effects correlate with a reduction of the mitogen activated protein kinase pathway hyper-activation in Nf1-deficient cells.</p> <p>Conclusion</p> <p>Our data suggest the potential usefulness of lovastatin, a drug approved by the US Food and Drug Administration in 1987 for the treatment of hypercholesteraemia, in the treatment of Nf1-related fracture healing abnormalities. The experimental model presented here constitutes a valuable tool for the pre-clinical stage testing of candidate drugs, targeting Nf1-associated bone dysplasia.</p

The Coverage Problem in Video-Based Wireless Sensor Networks: A Survey

Wireless sensor networks typically consist of a great number of tiny low-cost electronic devices with limited sensing and computing capabilities which cooperatively communicate to collect some kind of information from an area of interest. When wireless nodes of such networks are equipped with a low-power camera, visual data can be retrieved, facilitating a new set of novel applications. The nature of video-based wireless sensor networks demands new algorithms and solutions, since traditional wireless sensor networks approaches are not feasible or even efficient for that specialized communication scenario. The coverage problem is a crucial issue of wireless sensor networks, requiring specific solutions when video-based sensors are employed. In this paper, it is surveyed the state of the art of this particular issue, regarding strategies, algorithms and general computational solutions. Open research areas are also discussed, envisaging promising investigation considering coverage in video-based wireless sensor networks

The Haploinsufficient Hematopoietic Microenvironment Is Critical to the Pathological Fracture Repair in Murine Models of Neurofibromatosis Type 1

Germline mutations in the NF1 tumor suppressor gene cause neurofibromatosis type 1 (NF1), a complex genetic disorder with a high predisposition of numerous skeletal dysplasias including short stature, osteoporosis, kyphoscoliosis, and fracture non-union (pseudoarthrosis). We have developed murine models that phenocopy many of the skeletal dysplasias observed in NF1 patients, including reduced bone mass and fracture non-union. We also show that the development of these skeletal manifestations requires an Nf1 haploinsufficient background in addition to nullizygous loss of Nf1 in mesenchymal stem/progenitor cells (MSCs) and/or their progenies. This is replicated in two animal models of NF1, PeriCre+;Nf1flox/− and Col2.3Cre+;Nf1flox/−mice. Adoptive transfer experiments demonstrate a critical role of the Nf1+/− marrow microenvironment in the impaired fracture healing in both models and adoptive transfer of WT bone marrow cells improves fracture healing in these mice. To our knowledge, this is the first demonstration of a non-cell autonomous mechanism in non-malignant NF1 manifestations. Collectively, these data provide evidence of a combinatory effect between nullizygous loss of Nf1 in osteoblast progenitors and haploinsufficiency in hematopoietic cells in the development of non-malignant NF1 manifestations