190 research outputs found

    The Internationalization of Oil&Gas Family Businesses

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    The internalization of family businesses– i.e. of the companies that implement it - can be stimulated by numerous reasons: one of these is linked to the target markets, not in terms of market development, but of resource to be used / exploited. What makes the oil companies distinguishing is that: they follow the territory and the exploitation of the underground resources, wherever they are in the world. In the Italian context, this characteristic of oilfield companies is very noticeable due to the scarcity of underground resources, which characterize our territory. We propose an empirical approach. It has been considered the case of a specific Italian Oil&Gas family firm. The study consists of: a first part, in which an analysis of the main economic and managerial literature, both national and international, was made (on internationalization, SMEs and family businesses, industrial districts, oilfield environment); a second part, in which an empirical analysis was developed: interviews have been conducted with the owners and top management of the company, in order to study and analyze the firm development strategies

    The Management, Sharing and Transfer of Knowledge in the Oil Districts - The Case Study of An Italian District

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    Knowledge management is one of the most innovative and effective tools available to companies to manage an economic and organizational ever-changing environment. The chapter is based on an empirical study starting from the classification of oil district and aims to understand how firms’ position affect knowledge transfer process within the district. We support the idea that knowledge transfer is deeply affected by firms’ contractual power as well as by their position within the district. The companies of the industrial districts have the advantage of exploiting and sharing knowledge with each other. The literature generally holds that knowledge transfer requires a sense of equality and fairness among the firms, to create conditions in which firms will share their own knowledge for joint competitive advantage. However, empirical evidence shows that the value chains are often characterized by hierarchical relations and asymmetry between the parties: this feature is particularly evident in the oil districts. For companies attempting to acquire new information, the typologies of their intercompany collaboration and their cultural relationships are crucial

    Understanding pain perception through genetic painlessness diseases: The role of NGF and proNGF.

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    Nerve growth factor (NGF), by binding to TrkA and p75(NTR) receptors, regulates the survival and differentiation of sensory neurons during development and mediates pain transmission and perception during adulthood, by acting at different levels of the nervous system. Key to understanding the role of NGF as a pain mediator is the finding that mutations (namely, R121W, V232fs and R221W) in the NGF gene cause painlessness disease Hereditary Sensory and Autonomic Neuropathy type V (HSAN V). Here we shall review the consequences of these NGF mutations, each of which results in specific clinical signs: R221W determines congenital pain insensitivity with no overt cognitive disabilities, whereas V232fs and R121W also result in intellectual disability, thus showing similarities to HSAN IV, which is caused by mutations in TrkA, rather than to HSAN V. Comparing the cellular, biochemical and clinical findings of these mutations could help in better understanding not only the possible mechanisms underlying HSAN V, but also mechanisms of NGF signalling and roles. These mutations alter the balance between NGF and proNGF in favour of an accumulation of the latter, suggesting a possible role of proNGF as a molecule with an analgesic role. Furthermore, the neurotrophic and pronociceptive functions of NGF are split by the R221W mutation, making NGF variants based on this mutation interesting for designing therapeutic applications for many diseases. This review emphasizes the possibility of using the mutations involved in "painlessness" clinical disorders as an innovative approach to identify new proteins and pathways involved in pain transmission and perception.Outstanding questions: Why do homozygous HSAN V die postnatally? What is the cause of this early postnatal lethality?Is the development of a mouse or a human feeling less pain affecting higher cognitive and perceptual functions?What is the consequence of the HSAN V mutation on the development of joints and bones? Are the multiple fractures observed in HSAN V patients due exclusively to the carelessness consequent to not feeling pain, or also to an intrinsic frailty of their bones?Are heterodimers of NGF(WT) and NGF(R221W) in the heterozygote state formed? And if so, what are the properties of these heterodimeric proteins?How is the processing of proNGF(R221W) to NGF(R221W) affected by the mutation

    Acceptability, Waste and Nutritional Adequacy of Primary School Canteen Menus: An Observational Study in Pavia, Northern Italy

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    The aim of the study was to determine the acceptability, waste and nutritional adequacy of lunches served in all public primary school canteens in Pavia, Northern Italy. School canteens of all public primary schools were investigated to determine the acceptability, waste and nutritional adequacy of their menus. In addiction, the environment of the canteens (brightness, noisiness, size, crowding, cleanliness, attractiveness) was observed. The observations were conducted from April to June 2012. In each school canteen, lunch was supervised for three consecutive days by 5 trained dietitians. In total, 13 schools, 22 classes and 448 schoolchildren aged 7-8.5 years were investigated. The school canteens were found to be hygienically appropriate and homely. The menus offered appeared nutritionally adequate but portion sizes were often too big for the children's age. Consequently a lot of waste was encountered, especially fruit and vegetables (70% of children refused vegetables), but first and main courses were also wasted (50% of children consumed a first course and the same proportion consumed a main course). The meals offered by the school canteens appeared nutritionally appropriate although portion-sizes were often too large for 7-8.5 aged schoolchildren. The quality and variety of the menus were good and the raw materials were usually D.O.P. (Protected Denomination of Origin) as a guarantee of high quality. This study has drawn attention to the need to adapt the menus to the children's age in order to reduce waste

    A triheptanoin-supplemented diet rescues hippocampal hyperexcitability and seizure susceptibility in FoxG1+/- mice

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    The Forkhead Box G1 (FOXG1) gene encodes a transcription factor with an essential role in the mammalian telencephalon development. FOXG1-related disorders, caused by deletions, intragenic mutations or duplications, are usually associated with severe intellectual disability, autistic features, and, in 87% of subjects, epileptiform manifestations. In at least a subset of the patients with FoxG1 mutations, seizures remain intractable, prompting the need for novel therapeutic options. To address this issue, we took advantage of a haploinsufficient animal model, the FoxG1+/- mouse. In vivo electrophysiological analyses of FoxG1+/- mice detected hippocampal hyperexcitability, which turned into overt seizures upon delivery of the proconvulsant kainic acid, as confirmed by behavioral observations. These alterations were associated with decreased expression of the chloride transporter KCC2. Next, we tested whether a triheptanoin-based anaplerotic diet could have an impact on the pathological phenotype of FoxG1+/- mice. This manipulation abated altered neural activity and normalized the enhanced susceptibility to proconvulsant-induced seizures, in addition to rescuing the altered expression of KCC2 and increasing the levels of the GABA transporter vGAT. In conclusion, our data show that FoxG1 haploinsufficiency causes dysfunction of hippocampal circuits and increases the susceptibility to a proconvulsant insult, and that these alterations are rescued by triheptanoin dietary treatment

    Speech outcome in tongue cancer surgery: objective evaluation by acoustic analysis software

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    BACKGROUND. Cancer of the oral cavity is one of the most common malignancies of which 60% affect the tongue. Carcinoma of the tongue causes significant alterations of the articulatory and swallowing functions. The gold standard of care remains primary surgical resection with or without postoperative adjuvant therapy. Whereas T1 and T2 tongue tumors can be treated with more conservative surgeries, as partial glossectomies, the larger tumors require total and aggressive glossectomies which increase survival, but, on the other hand, they might often make speech, chewing and swallowing impossible. MATERIAL AND METHODS. Our study was performed on a total of 21 patients with Squamous Cell Carcinoma of the tongue who underwent either partial resection or hemiglossectomy. Each subject (either surgical patients or controls) was asked to pronounce the vowels /a/, /e/, /i/, /u/, and all signals were evaluated separately by two operators. Acoustic (F0, jitter, shimmer, NHR) and vowel metric (the ratio F2i/F2u, tVSA, qVSA, FCR) features have been extracted. In order to define the speech intelligibility, all patients were evaluated by two doctors and one speech therapist and all patients received the Speech Handicap Index (SHI) translated into Italian language before recording. RESULTS. No statistically significant variations were observed, regardless of the gender, between controls and surgically resected patients when tumor staging was T1-T2. On the contrary, when patients had to undergo more extensive surgical resection due to the presence of a T3-T4 tumor, a dramatic increase of F2u could be observed. This change, together with a decrease of F2i, led to a highly significant reduction in the F2i/F2u parameter in surgically resected patients as compared to controls. The other parameters which were reduced in a statistically significant manner in T3-T4 surgically resected patients were tVSA and qVSA. Instead, two parameters increased in a statistically significant manner in T3-T4 surgically resected patients: FCR and SHI. Again, none of the above-mentioned parameters was altered in a statistically significant manner in early tumor stage resected patients, regar dless of the gender. CONCLUSION. For the first time, we used a series of newly developed formant parameters, introduced by various authors for the study of the articulatory undershoot of the tongue in various neurodegenerative diseases. The statistical analysis of our results highlighted in an incontrovertible way a strong correlation and significance of each of our parameters F2 / i / / F2 / u /, FCR, tVSA, qVSA, with the entity of the TNM, and therefore of the surgical extension of the resection, and in parallel with the loss of the intelligibility of the speech that proportionally reaches higher values in the advanced stages of the disease as can be deduced from the SHI trend

    Atrial natriuretic peptide stimulates autophagy/mitophagy and improves mitochondrial function in chronic heart failure

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    Mitochondrial dysfunction, causing increased reactive oxygen species (ROS) production, is a molecular feature of heart failure (HF). A defective antioxidant response and mitophagic flux were reported in circulating leucocytes of patients with chronic HF and reduced ejection fraction (HFrEF). Atrial natriuretic peptide (ANP) exerts many cardiac beneficial effects, including the ability to protect cardiomyocytes by promoting autophagy. We tested the impact of ANP on autophagy/mitophagy, altered mitochondrial structure and function and increased oxidative stress in HFrEF patients by both ex vivo and in vivo approaches. The ex vivo study included thirteen HFrEF patients whose peripheral blood mononuclear cells (PBMCs) were isolated and treated with αANP (10-11 M) for 4 h. The in vivo study included six HFrEF patients who received sacubitril/valsartan for two months. PBMCs were characterized before and after treatment. Both approaches analyzed mitochondrial structure and functionality. We found that levels of αANP increased upon sacubitril/valsartan, whereas levels of NT-proBNP decreased. Both the ex vivo direct exposure to αANP and the higher αANP level upon in vivo treatment with sacubitril/valsartan caused: (i) improvement of mitochondrial membrane potential; (ii) stimulation of the autophagic process; (iii) significant reduction of mitochondrial mass-index of mitophagy stimulation-and upregulation of mitophagy-related genes; (iv) reduction of mitochondrial damage with increased inner mitochondrial membrane (IMM)/outer mitochondrial membrane (OMM) index and reduced ROS generation. Herein we demonstrate that αANP stimulates both autophagy and mitophagy responses, counteracts mitochondrial dysfunction, and damages ultimately reducing mitochondrial oxidative stress generation in PBMCs from chronic HF patients. These properties were confirmed upon sacubitril/valsartan administration, a pivotal drug in HFrEF treatment
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