Logistik: Hur påverkar Just-In-Time på lönsamheten av ett företag?

Ett företag har som grunduppgift att hållas verksamt genom att ekonomiskt prestera bättre för varje år. Logistik är det verksamhetsområde som står för majoriteten av ett företags kostnader. Kostnader i sig är en dålig sak för företag, men det är även en möjlighet för logistiken att sänka dessa kostnader, vilket i sin tur är bra för företagets lön-samhet. Just-In-Time (JIT) är en produktions- och styrfilosofi inom logistiken, där det huvudsakliga målet är att minska lagernivåerna och att eliminera allt onödigt. Syftet med denna studie är att finna ett samband mellan JIT och lönsamhet ur ett logistiskt perspektiv. Vid studien används DuPont-modellen som definition av lönsamhet samt som ett jämförelseverktyg där sex olika finansiella faktorer mäts. Metoden för studien är kvalitativ i form av en litteraturstudie. Materialet som analyseras hämtas endast från Arcadas databaser och analysen av materialet sker i form av innehållsanalys. Resultaten av materialet som analyserades är väldigt blandat. Många studier påpekar att det råder brist på forskning inom detta ämnesområdet, vilket även kan vara orsaken till dessa blandade resultat. Det går dock att urskilja tre finansiella mått från DuPont-modellen som påver-kas positivt av JIT. Dessa är: intäkter, kostnader och lager. Ingen studie visade att JIT skulle ha negativ inverkan på ett företags lönsamhet. Andra intressanta faktorer som JIT hade en positiv inverkan på är operativa prestanda, t.ex. minskade ledtider

Postnatal dexamethasone, respiratory and neurodevelopmental outcomes at two years in babies born extremely preterm.

IMPORTANCE: Postnatal dexamethasone is associated with reduction in bronchopulmonary dysplasia. There remains, however, concern that its short-term benefits are accompanied by long-term adverse effects e.g. poorer neurodevelopmental outcomes. OBJECTIVE: Our aim was to determine the effects of administration of postnatal dexamethasone on respiratory and neurodevelopmental outcome at two years of age after adjusting for neonatal and infant risk factors. MATERIALS AND METHODS: The study included 412 infants born at 23-28 weeks of gestation, 29% had received postnatal dexamethasone. Two outcomes were examined, respiratory hospital admissions in the past 12 months and neurodevelopmental impairment. Logistic regression, adjusted for sex, birthweight z-score, gestation, maternal smoking, oxygen dependency at 36 weeks, airleak, patent ductus arteriosus, pulmonary haemorrhage, major ultrasound abnormality, mode of ventilation and age at assessment, was undertaken. RESULTS: After adjustment, postnatal dexamethasone was associated with significantly increased proportions of both respiratory hospital readmission: (0.35 vs 0.15, difference = 0.20; 95% CI: 0.08, 0.31) and neurodevelopmental impairment (0.59 vs 0.45, difference = 0.14; 95% CI: 0.02, 0.26). CONCLUSIONS: Postnatal dexamethasone use in extremely preterm infants is associated with increased risks of respiratory hospital admissions and neurodevelopmental impairment. These associations were not explained by excess neonatal morbidities

The therapeutic response in Gorham’s syndrome to the beta-blocking agent propranolol is correlated to VEGF-A, but not to VEGF-C or FLT1 expression

International audienceBACKGROUND:Gorham's syndrome is a rare illness of unknown etiology. It is characterized by a local proliferation of blood or lymphatic vessels that in bones leads to progressive resorption and destruction. The cause of the disease is not elucidated, and therapeutic options remain limited.CASE PRESENTATION:We report herein the case of a young female Caucasian patient aged 18 years with diffuse Gorham syndrome. In tissue specimens angiogenesis and massive lymphangiogenesis as well as the expression of vascular endothelial growth factor-A (VEGF-A) and neuropilins was observed. Lymphangiogenesis is a prominent feature of the disease and a number of lymphatic markers were found to be expressed, however only VEGF-A, but not vascular endothelial growth factor-C (VEGF-C) was found to be elevated in the circulation. Circulating levels of soluble VEGF receptor-1 were also not elevated. Furthermore, the patient responded favorably and the disease was stabilized following treatment with the beta-blocking agent Propranolol alone which acts on VEGF-A alone, but not on soluble VEGF receptor-1 levels.CONCLUSION:This suggests that the disease is dependent on VEGF-A, but on neither VEGF-C, the major driver of lymphangiogenesis, nor FLT1. Furthermore, Propranolol acts on VEGF-A but not FLT1 expression

Mesoscopic Rigid Body Modelling of the Extracellular Matrix Self-Assembly

The extracellular matrix (ECM) plays an important role in supporting tissues and organs. It even has a functional role in morphogenesis and differentiation by acting as a source of active molecules (matrikines). Many diseases are linked to dysfunction of ECM components and fragments or changes in their structures. As such it is a prime target for drugs. Because of technological limitations for observations at mesoscopic scales, the precise structural organisation of the ECM is not well-known, with sparse or fuzzy experimental observables. Based on the Unity3D game and physics engines, along with rigid body dynamics, we propose a virtual sandbox to model large biological molecules as dynamic chains of rigid bodies interacting together to gain insight into ECM components behaviour in the mesoscopic range. We have preliminary results showing how parameters such as fibre flexibility or the nature and number of interactions between molecules can induce different structures in the basement membrane. Using the Unity3D game engine and virtual reality headset coupled with haptic controllers, we immerse the user inside the corresponding simulation. Untrained users are able to navigate a complex virtual sandbox crowded with large biomolecules models in a matter of seconds

Mesoscopic Rigid Body Modelling of the Extracellular Matrix Self-Assembly

International audienc

Additional file 1: of The therapeutic response in Gorham’s syndrome to the beta-blocking agent propranolol is correlated to VEGF-A, but not to VEGF-C or FLT1 expression

CARE Checklist (2013) of information to include when writing a case report

Umbrella Visualization: a method of analysis dedicated to glycan flexibility with UnityMol.

International audienc

New visualization of dynamical flexibility of N-Glycans: Umbrella Visualization in UnityMol.

International audienc

Helicobacter pylori interferes with an embryonic stem cell micro RNA cluster to block cell cycle progression

Background MicroRNAs, post-transcriptional regulators of eukaryotic gene expression, are implicated in host defense against pathogens. Viruses and bacteria have evolved strategies that suppress microRNA functions, resulting in a sustainable infection. In this work we report that Helicobacter pylori, a human stomach-colonizing bacterium responsible for severe gastric inflammatory diseases and gastric cancers, downregulates an embryonic stem cell microRNA cluster in proliferating gastric epithelial cells to achieve cell cycle arrest. Results Using a deep sequencing approach in the AGS cell line, a widely used cell culture model to recapitulate early events of H. pylori infection of gastric mucosa, we reveal that hsa-miR-372 is the most abundant microRNA expressed in this cell line, where, together with hsa-miR-373, it promotes cell proliferation by silencing large tumor suppressor homolog 2 (LATS2) gene expression. Shortly after H. pylori infection, miR-372 and miR-373 synthesis is highly inhibited, leading to the post-transcriptional release of LATS2 expression and thus, to a cell cycle arrest at the G1/S transition. This downregulation of a specific cell-cycle-regulating microRNA is dependent on the translocation of the bacterial effector CagA into the host cells, a mechanism highly associated with the development of severe atrophic gastritis and intestinal-type gastric carcinoma. Conclusions These data constitute a novel example of host-pathogen interplay involving microRNAs, and unveil the couple LATS2/miR-372 and miR-373 as an unexpected mechanism in infection-induced cell cycle arrest in proliferating gastric cells, which may be relevant in inhibition of gastric epithelium renewal, a major host defense mechanism against bacterial infections

Maternal Voice and Tactile Stimulation Modulate Oxytocin in Mothers of Hospitalized Preterm Infants: A Randomized Crossover Trial

Prematurity is a major risk factor for perinatal stress and neonatal complications leading to systemic inflammation and abnormal mother–infant interactions. Oxytocin (OT) is a neuropeptide regulating the inflammatory response and promoting mother–infant bonding. The release of this hormone might be influenced by either vocal or tactile stimulation. The main objective of the current randomized, crossover, clinical trial was to assess the salivary OT/cortisol balance in mothers following the exposure of their baby born preterm to two types of sensorial interventions: maternal voice without or with contingent tactile stimulation provided by the mother to her infant. Among the 26 mothers enrolled, maternal voice intervention alone had no effect on OT and cortisol levels in the mothers, but when associated with tactile stimulation, it induced a significant increase in maternal saliva oxytocin (38.26 ± 30.26 pg/mL before vs 53.91 ± 48.84 pg/mL after, p = 0.02), particularly in the mothers who delivered a female neonate. Maternal voice intervention induced a significant reduction in cortisol and an increase in OT levels in mothers when the maternal voice with a tactile stimulation intervention was performed first. In conclusion, exposure to the maternal voice with a contingent tactile stimulation was associated with subtle changes in the maternal hormonal balance between OT and cortisol. These findings need to be confirmed in a larger sample size and may ultimately guide caregivers in providing the best intervention to reduce parental stress following preterm delivery