Scenes From Tick Physiology: Proteins of Sialome Talk About Their Biological Processes

Ticks are blood-sucking parasites with different strategies of feeding depending on the tick family. The major families are Ixodidae or Argasidae, being slow or fast feeders, respectively. In the recent years, the advances in molecular sequencing techniques have enabled to gain knowledge about the proteome of the tick''s salivary glands. But an holistic view of the biological processes underlying the expression of the sialome has been neglected. In this study we propose the use of standard biological processes as a tool to draw the physiology of the tick''s salivary glands. We used published data on the sialome of Rhipicephalus sanguineus s.l. (Ixodidae) and Ornithodoros rostratus (Argasidae). A partial set of proteins obtained by these studies were used to define the biological process(es) in which proteins are involved. We used a directed network construction in which the nodes are proteins (source) and biological processes (target), separately for the low-level processes ("children") and the top-level ones ("parents"). We applied the method to feeding R. sanguineus at different time slices, and to different organs of O. rostratus. The network connects the proteins and the processes with a strength directly proportional to the transcript per millions of each protein. We used PageRank as a measure of the importance of each biological process. As suggested in previous studies, the sialome of unfed R. sanguineus express about 30% less biological processes than feeding ticks. Another decrease (25%) is noticed at the middle of the feeding and before detachment. However, top-level processes are deeply affected only at the onset of feeding, demonstrating a redundancy in the feeding. When ixodid-argasid are compared, large differences were observed: they do not share 91% of proteins, but share 90% of the biological processes. However, caution must be observed when examining these results. The hypothesis of different proteins linked to similar biological process(es) in both ticks is an extreme not confirmed in this study. Considering the limitations of this study, carried out with a selected set of proteins, we propose the networks of proteins of sialome linked to their biological processes as a tool aimed to explain the biological processes behind families of proteins

Detection of seeds in citrus using MRI under motion conditions and improvement with motion correction

Magnetic resonance imaging (MRI) is studied under an online strategy. Axial FLASH images (780 ms acquisition time) have been analyzed to identify seed-containing oranges conveyed at 50 and 100 mm/s through a 4.7 Tesla spectrometer. Developed algorithms enable an automated identification of oranges with more than one seed, though axial images under motion conditions suffer from significant blurring artifacts. To overcome this hindrance, coronal FLASH images have been acquired (279 ms acquisition time), developing devoted algorithms for motion correction with encouraging results for quality improvement of dynamic image

Corrección de desfase en imágenes de Resonancia Magnética

La imagen de Resonancia Magnética (IRM) se ha estudiado para su aplicación en línea. Se han adquirido dos tipos de imágenes FLASH coronales (tiempo de adquisición 279 ms para limones y 703 para naranjas) de muestras estáticas y conducidas a 54 mm/s a través de un espectrómetro de 4.7 Teslas. Los algoritmos desarrollados para la corrección automática del movimiento has mostrado una mejora notoria en la calidad de las imágenes dinámicas. Las imágenes estáticas y dinámicas corregidas fueron comparadas mediante sus histogramas acumulados loscuales mostraron altos coeficientes de determinación (R2 = 0.96 para limones y 0.98 para naranjas). Un análisis de varianza de los parámetros extraídos de las imágenes estáticas y dinámicas corregidas mostró diferencias no significativas

Tenofovir Nephrotoxicity: 2011 Update

Tenofovir is an acyclic nucleotide analogue reverse-transcriptase inhibitor structurally similar to the nephrotoxic drugs adefovir and cidofovir. Tenofovir is widely used to treat HIV infection and approved for treatment of hepatitis B virus. Despite initial cell culture and clinical trials results supporting the renal safety of tenofovir, its clinical use is associated with a low, albeit significant, risk of kidney injury. Proximal tubular cell secretion of tenofovir explains the accumulation of the drug in these mitochondria-rich cells. Tenofovir nephrotoxicity is characterized by proximal tubular cell dysfunction that may be associated with acute kidney injury or chronic kidney disease. Withdrawal of the drug leads to improvement of analytical parameters that may be partial. Understanding the risk factors for nephrotoxicity and regular monitoring of proximal tubular dysfunction and serum creatinine in high-risk patients is required to minimize nephrotoxicity. Newer, structurally similar molecular derivatives that do not accumulate in proximal tubules are under study

Response to "Practice what you preach : Ensuring scientific spheres integrate Indigenous Peoples' and Local Communities' rights and agency too" by Lopez-Maldonado

Non peer reviewe

Toxic Habits and Well-Being Measures in Spanish Healthcare University Students during the COVID-19 Pandemic

Background: Unhealthy lifestyles are strongly entrenched in healthcare universities and have sometimes been linked to stress or lack of sleep. This study investigated the prevalence of toxic habits (smoking, patterns of harmful alcohol use, and illicit drug use), stress levels, perceived health status, and sleep duration and assessed the connections between toxic habits and said well-being measures, as well as healthcare students’ perception of the influence of the COVID-19 pandemic on these health-related behaviors. Methods: In a cross-sectional study, healthcare students from Alfonso X University (Spain) completed a health survey composed of Alcohol Use Disorders Identification Test (AUDIT-C), Perceived Stress Scale (PSS-10), self-perceived health status, and the number of hours of sleep. Results: A total of 997 healthcare students completed the survey, of which 982 were analyzed. Being a smoker (32.2%) was associated with worse health status and insufficient sleep. Risk drinkers (33.2%) were associated with being female, and the consumption of cannabinoids (6.7%), with being male. These three toxic habits were related to each other. High levels of stress (28.2%) were correlated with worse ratings in the perception of health status (29.2%) and with insufficient sleep (45.8%), and all of them were associated with the female sex. Respectively, 49.3% and 44.2% of students recognized a worsening in their perception of stress and their sleep habits during the pandemic. Conclusion: Healthcare universities must carry out health promotion programs for stress management, sleep habits, and unhealthy lifestyles

Angiocrine polyamine production regulates adiposity.

Reciprocal interactions between endothelial cells (ECs) and adipocytes are fundamental to maintain white adipose tissue (WAT) homeostasis, as illustrated by the activation of angiogenesis upon WAT expansion, a process that is impaired in obesity. However, the molecular mechanisms underlying the crosstalk between ECs and adipocytes remain poorly understood. Here, we show that local production of polyamines in ECs stimulates adipocyte lipolysis and regulates WAT homeostasis in mice. We promote enhanced cell-autonomous angiogenesis by deleting Pten in the murine endothelium. Endothelial Pten loss leads to a WAT-selective phenotype, characterized by reduced body weight and adiposity in pathophysiological conditions. This phenotype stems from enhanced fatty acid β-oxidation in ECs concomitant with a paracrine lipolytic action on adipocytes, accounting for reduced adiposity. Combined analysis of murine models, isolated ECs and human specimens reveals that WAT lipolysis is mediated by mTORC1-dependent production of polyamines by ECs. Our results indicate that angiocrine metabolic signals are important for WAT homeostasis and organismal metabolism.We thank members of the Endothelial Pathobiology and Microenvironment Group for helpful discussions. We thank the CERCA Program/Generalitat de Catalunya and the Josep Carreras Foundation for institutional support. The research leading to these results has received funding from la Fundación BBVA (Ayuda Fundacion BBVA a Equipos de Investigación Científica 2019, PR19BIOMET0061) and from SAF2017-82072-ERC from Ministerio de Ciencia, Innovación y Universidades (MCIU) (Spain). The laboratory of M.G. is also supported by the research grants SAF2017-89116R-P (FEDER/EU) co-funded by European Regional Developmental Fund (ERDF), a Way to Build Europe and PID2020-116184RB-I00 from MCEI; by the Catalan Government through the project 2017-SGR; PTEN Research Foundation (BRR-17-001); La Caixa Foundation (HR19-00120 and HR21-00046); by la Asociación Española contra el Cancer-Grupos Traslacionales (GCTRA18006CARR, also to A.C.); European Foundation for the Study of Diabetes/Lilly research grant, also to M.C.); and by the People Programme (Marie Curie Actions; grant agreement 317250) of the European Union’s Seventh Framework Programme FP7/2007-2013 and the Marie Skłodowska-Curie (grant agreement 675392) of the European Union’s Horizon 2020 research. The laboratory of A.C. is supported by the Basque Department of Industry, Tourism and Trade (Elkartek) and the department of education (IKERTALDE IT1106-16), the MCIU (PID2019-108787RB-I00 (FEDER/ EU); Severo Ochoa Excellence Accreditation SEV-2016-0644; Excellence Networks SAF2016-81975-REDT), La Caixa Foundation (ID 100010434), under the agreement LCF/PR/HR17, the Vencer el Cancer foundation and the European Research Council (ERC) (consolidator grant 819242). CIBERONC was co-funded with FEDER funds and funded by Instituto de Salud Carlos III (ISCIII). The laboratory of M.C. is supported by the ERC under the European Union’s Horizon 2020 research and innovation programme (grant agreement 725004) and CERCA Programme/Generalitat de Catalunya (M.C.). The laboratory of D.S. is supported by research grants from MINECO (SAF2017- 83813-C3-1-R, also to L.H., cofounded by the ERDF), CIBEROBN (CB06/03/0001), Government of Catalonia (2017SGR278) and Fundació La Marató de TV3 (201627- 30). The laboratory of R.N. is supported by FEDER/Ministerio de Ciencia, Innovación y Universidades-Agencia Estatal de Investigación (RTI2018-099413-B-I00 and and RED2018-102379-T), Xunta de Galicia (2016-PG057 and 2020-PG015), ERC under the European Union’s Horizon 2020 research and innovation programme (grant agreement 810331), Fundación BBVA, Fundacion Atresmedia and CIBEROBN, which is an initiative of the ISCIII of Spain, which is supported by FEDER funds. The laboratory of J.A.V. is supported by research grants from MICINN (RTI2018-099250-B100) and by La Caixa Foundation (ID 100010434, LCF/PR/HR17/52150009). P.M.G.-R. is supported by ISCIII grant PI15/00701 cofinanced by the ERDF, A Way to Build Europe. Personal support was from Marie Curie ITN Actions (E.M.), Juan de la Cierva (IJCI-2015-23455, P.V.), CONICYT fellowship from Chile (S.Z.), Vetenskapsradet (Swedish Research Council, 2018-06591, L.G.) and NCI K99/R00 Pathway to Independence Award (K99CA245122, P. Castel).S

Genetic manipulation of LKB1 elicits lethal metastatic prostate cancer

Gene dosage is a key defining factor to understand cancer pathogenesis and progression, which requires the development of experimental models that aid better deconstruction of the disease. Here, we model an aggressive form of prostate cancer and show the unconventional association of LKB1 dosage to prostate tumorigenesis. Whereas loss of Lkbl alone in the murine prostate epithelium was inconsequential for tumorigenesis, its combination with an oncogenic insult, illustrated by Pten heterozygosity, elicited lethal metastatic prostate cancer. Despite the low frequency of LKB1 deletion in patients, this event was significantly enriched in lung metastasis. Modeling the role of LKB1 in cellular systems revealed that the residual activity retained in a reported kinase-dead form, LKB1(K781), was sufficient to hamper tumor aggressiveness and metastatic dissemination. Our data suggest that prostate cells can function normally with low activity of LKB1, whereas its complete absence influences prostate cancer pathogenesis and dissemination