Dodecahedral ‘silicages’ could carry drugs or diagnostic agents

In mice, surgery-free technique inhibits region implicated in memory formation

Study suggests activating PPAR receptor leads to increased cellular connections in hippocampus

Modified toxin targets and silences nerves that transmit pain, offering a potential nonaddictive alternative to opioids

Bacterial products such as lipopolysaccharides (or endotoxin) cause systemic inflammation, resulting in a substantial global health burden. The onset, progression, and resolution of the inflammatory response to endotoxin are usually tightly controlled to avoid chronic inflammation. Members of the NF-κB family of transcription factors are key drivers of inflammation that activate sets of genes in response to inflammatory signals. Such responses are typically short-lived and can be suppressed by proteins that act post-translationally, such as the SOCS (suppressor of cytokine signaling) family. Less is known about direct transcriptional regulation of these responses, however. Here, using a combination of in vitro approaches and in vivo animal models, we show that endotoxin treatment induced expression of the well-characterized transcriptional repressor Krüppel-like factor 3 (KLF3), which, in turn, directly repressed the expression of the NF-κB family member RELA/p65. We also observed that KLF3-deficient mice were hypersensitive to endotoxin and exhibited elevated levels of circulating Ly6C+ monocytes and macrophage-derived inflammatory cytokines. These findings reveal that KLF3 is a fundamental suppressor that operates as a feedback inhibitor of RELA/p65 and may be important in facilitating the resolution of inflammation.

GameStop might just help you put the finishing touches on your computer setup. It’s running a PC gaming sale between now and May 16th that promises deals on a slew of hardware. To start, it’s offering a $100 gift coupon if you buy any MSI laptop with...

An experimental vaccine provided 100 percent protection against the mosquito-borne chikungunya virus in primates and mice, offering hope it will work for humans too, according to a study.

The Natural History Museum's Wildlife Photographer of the Year competition just named the winner of this year's LUMIX People's Choice Award, and the perfectly-timed photo by wildlife filmmaker and photographer Sam Rowley is just too good to keep to ourselves.Selected from over 48,000 submitted images and 25 impressive finalists, Rowley's winning photo is called "Station Squabble," and it features two mice getting into a tussle over some leftover crumbs in the London Underground.

Bone crystallite chemistry and structure change during bone maturation. However, these properties of bone can also be affected by limited uptake of the chemical constituents of the mineral by the animal. This makes probing the effect of bone-mineralization-related diseases a complicated task. Here it is shown that the combination of vibrational spectroscopy with two-dimensional X-ray diffraction can provide unparalleled information on the changes in bone chemistry and structure associated with different bone pathologies (phosphate deficiency) and/or health conditions (pregnancy, lactation). Using a synergistic analytical approach, it was possible to trace the effect that changes in the remodelling regime have on the bone mineral chemistry and structure in normal and mineral-deficient (hypophosphatemic) mice. The results indicate that hypophosphatemic mice have increased bone remodelling, increased carbonate content and decreased crystallinity of the bone mineral, as well as increased misalignment of crystallites within the bone tissue. Pregnant and lactating mice that are normal and hypophosphatemic showed changes in the chemistry and misalignment of the apatite crystals that can be related to changes in remodelling rates associated with different calcium demand during pregnancy and lactation.

Finding a mouse in your morning coffee might give you an unwelcome jolt, but there’s a strong connection between small mammals, birds and the plantations […]

The post Of mice and macchiato: Bird Friendly coffee gives a paw-up to small mammals as well appeared first on Smithsonian Insider.

A newly discovered mechanism in the throats of mice works like a supersonic jet engine.

A team of researchers restored "lost memories" in the brains of mice.

Researchers in Costa Rica are studying the vocalizations of Alston's singing mice to learn more about human speech.

Looking out for the safety of kids and pets, the EPA decides to ban some toxic rodent poisons. Here are a few pest remediation alternatives that rely on repelli

Rather than opting for the costly and complex process of using stem cells to cure age-related macular degeneration, scientists used skin cells.

The post Irreversible No Longer: Blind Mice See Again Thanks To New Method of Synthesizing Lost Cells appeared first on Good News Network.

Kyoto University researchers said the vaccine for Alzheimer’s was effective and was also shown to have zero side effects observed in the mice.

The post New Alzheimer’s Nasal Spray Shown to Reduce Proteins Which Cause the Disease in Mice appeared first on Good News Network.

This new research has outlined yet another benefit to intermittent fasting—that may arise from the time you eat, rather than what you eat.

The post New Intermittent Fasting Program Shown to Suppress Cancer and Metabolic Disease in Mice and Humans appeared first on Good News Network.

A method for engineering and utilizing large DNA vectors to target, via homologous recombination, and modify, in any desirable fashion, endogenous genes and chromosomal loci in eukaryotic cells. These large DNA targeting vectors for eukaryotic cells, termed LTVECs, are derived from fragments of cloned genomic DNA larger than those typically used by other approaches intended to perform homologous targeting in eukaryotic cells. Also provided is a rapid and convenient method of detecting eukaryotic cells in which the LTVEC has correctly targeted and modified the desired endogenous gene(s) or chromosomal locus (loci) as well as the use of these cells to generate organisms bearing the genetic modification.

The invention discloses novel morphology shifting micelles and amphiphilic coated metal nanofibers. Methods of using and making the same are also disclosed.

A green-light device for driving mice away includes a casing and a control circuit in the casing, wherein the control circuit comprises a power conversion circuit, a voltage regulating integrated circuit (IC), an amplifying circuit, a control knob, an ultrasonic frequency oscillator circuit, a logical-determination circuit and multiple green-light emitting diodes (LED) coupled to and controlled by the logical-determination circuit. The control knob is configured to be switched to lead the control circuit to create an ultrasonic wave or a special light wave such that mice can be cheated or driven away.

Method for production of cellulose and hemicellulose fibers from lignocellulose biomass obtained from sugarcane leaves and buds by applying a process comprising the stages of: a) Diminishing the particle size of the lignocellulose biomass to a range between 3 and 15 mm, b) Subjecting the product obtained to treatment with one or more solvents and/or a mixture of specific catalysts, c) Carry out sudden decompression to an atmospheric pressure, d) Collecting the pretreated material in a cyclone, e) Optionally separating the liquid and solid fractions through washing and filterung f) Optionally, treating the solid fraction in a reactor with a mixture of ethanol and chlorine dioxide, d) Wash the product obtained to achieve cellulose efficiency above 50% and of lignin of 5 to 7%, fiber lengtht in a range to 1,5 to 2,7 mm, breaking length (km) of 7,0 -8,9, Burst index (kPam2/g) of 4,5-7,2 and Tear index (mNm2/g) of 8,2-8, The obtained high-resistance cellulose and hemicellulose is especially suitable for the paper production and polymer-type plastics.

A soy protein product having a protein content of at least 60 wt % (N×6.25) d.b., preferably an isolate having a protein content of at least about 90 wt % (N×6.25) d.b., is formed from the supernatant from the precipitation of a soy protein micellar mass. A calcium salt or other divalent salt is added to the supernatant, before concentration, after initial concentration or after final concentration, to provide a conductivity of about 2 to about 30 mS. Precipitate is removed from the resulting solution and the pH of the clear soy protein solution is optionally adjusted to about 1.5 to about 4.4. The optionally pH-adjusted clear solution is concentrated to a concentration of about 50 to about 400 g/L and the clear concentrated protein solution is optionally diafiltered prior to drying. The soy protein product is soluble in acidic media and produces transparent, heat stable solutions at low pH values and, therefore, may be used for protein fortification of soft drinks and sports drinks.

A group of genetically engineered super-strong mice from Connecticut are headed to space. Their mission? Study a new therapy to prevent muscle loss.

An island of floating rock known as a pumice raft is gradually heading for Australian shores across the Coral Sea and is so expansive it can be tracked via satellite.

The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide. Although gene-environment interactions have been implicated in the etiology of several disorders, the impact of paternal and/or maternal metabolic syndrome on the clinical phenotypes of offspring and the underlying genetic and epigenetic contributors of NAFLD have not been fully explored. To this end, we used the liver-specific insulin receptor knockout (LIRKO) mouse, a unique nondietary model manifesting 3 hallmarks that confer high risk for the development of NAFLD: hyperglycemia, insulin resistance, and dyslipidemia. We report that parental metabolic syndrome epigenetically reprograms members of the TGF-β family, including neuronal regeneration–related protein (NREP) and growth differentiation factor 15 (GDF15). NREP and GDF15 modulate the expression of several genes involved in the regulation of hepatic lipid metabolism. In particular, NREP downregulation increases the protein abundance of 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) and ATP-citrate lyase (ACLY) in a TGF-β receptor/PI3K/protein kinase B–dependent manner, to regulate hepatic acetyl-CoA and cholesterol synthesis. Reduced hepatic expression of NREP in patients with NAFLD and substantial correlations between low serum NREP levels and the presence of steatosis and nonalcoholic steatohepatitis highlight the clinical translational relevance of our findings in the context of recent preclinical trials implicating ACLY in NAFLD progression.

Facioscapulohumeral muscular dystrophy (FSHD) is caused by loss of repression of the DUX4 gene; however, the DUX4 protein is rare and difficult to detect in human muscle biopsies, and pathological mechanisms are obscure. FSHD is also a chronic disease that progresses slowly over decades. We used the sporadic, low-level, muscle-specific expression of DUX4 enabled by the iDUX4pA-HSA mouse to develop a chronic long-term muscle disease model. After 6 months of extremely low sporadic DUX4 expression, dystrophic muscle presented hallmarks of FSHD histopathology, including muscle degeneration, capillary loss, fibrosis, and atrophy. We investigated the transcriptional profile of whole muscle as well as endothelial cells and fibroadiopogenic progenitors (FAPs). Strikingly, differential gene expression profiles of both whole muscle and, to a lesser extent, FAPs, showed significant overlap with transcriptional profiles of MRI-guided human FSHD muscle biopsies. These results demonstrate a pathophysiological similarity between disease in muscles of iDUX4pA-HSA mice and humans with FSHD, solidifying the value of chronic rare DUX4 expression in mice for modeling pathological mechanisms in FSHD and highlighting the importance FAPs in this disease.

Bankovní rada České národní banky ve čtvrtek snížila základní úrokovou sazbu o 0,75 procentního bodu na 0,25 procenta. Cílem snižování sazeb je zmírnit dopady šíření koronaviru na ekonomiku. Centrální banka to uvedla v tiskovém prohlášení.

A bacterial “probiotic” may enhance athletic performance. But it’s a long way from being ready for use in humans.

Mutations in retinaldehyde-binding protein 1 (RLBP1), encoding the visual cycle protein cellular retinaldehyde-binding protein (CRALBP), cause an autosomal recessive form of retinal degeneration. By binding to 11-cis-retinoid, CRALBP augments the isomerase activity of retinoid isomerohydrolase RPE65 (RPE65) and facilitates 11-cis-retinol oxidation to 11-cis-retinal. CRALBP also maintains the 11-cis configuration and protects against unwanted retinaldehyde activity. Studying a sibling pair that is compound heterozygous for mutations in RLBP1/CRALBP, here we expand the phenotype of affected individuals, elucidate a previously unreported phenotype in RLBP1/CRALBP carriers, and demonstrate consistencies between the affected individuals and Rlbp1/Cralbp−/− mice. In the RLBP1/CRALBP-affected individuals, nonrecordable rod-specific electroretinogram traces were recovered after prolonged dark adaptation. In ultrawide-field fundus images, we observed radially arranged puncta typical of RLBP1/CRALBP-associated disease. Spectral domain-optical coherence tomography (SD-OCT) revealed hyperreflective aberrations within photoreceptor-associated bands. In short-wavelength fundus autofluorescence (SW-AF) images, speckled hyperautofluorescence and mottling indicated macular involvement. In both the affected individuals and their asymptomatic carrier parents, reduced SW-AF intensities, measured as quantitative fundus autofluorescence (qAF), indicated chronic impairment in 11-cis-retinal availability and provided information on mutation severity. Hypertransmission of the SD-OCT signal into the choroid together with decreased near-infrared autofluorescence (NIR-AF) provided evidence for retinal pigment epithelial cell (RPE) involvement. In Rlbp1/Cralbp−/− mice, reduced 11-cis-retinal levels, qAF and NIR-AF intensities, and photoreceptor loss were consistent with the clinical presentation of the affected siblings. These findings indicate that RLBP1 mutations are associated with progressive disease involving RPE atrophy and photoreceptor cell degeneration. In asymptomatic carriers, qAF disclosed previously undetected visual cycle deficiency.

Haploinsufficiency of Meis homeobox 2 (MEIS2), encoding a transcriptional regulator, is associated with human cleft palate, and Meis2 inactivation leads to abnormal palate development in mice, implicating MEIS2 functions in palate development. However, its functional mechanisms remain unknown. Here we observed widespread MEIS2 expression in the developing palate in mice. Wnt1Cre-mediated Meis2 inactivation in cranial neural crest cells led to a secondary palate cleft. Importantly, about half of the Wnt1Cre;Meis2f/f mice exhibited a submucous cleft, providing a model for studying palatal bone formation and patterning. Consistent with complete absence of palatal bones, the results from integrative analyses of MEIS2 by ChIP sequencing, RNA-Seq, and an assay for transposase-accessible chromatin sequencing identified key osteogenic genes regulated directly by MEIS2, indicating that it plays a fundamental role in palatal osteogenesis. De novo motif analysis uncovered that the MEIS2-bound regions are highly enriched in binding motifs for several key osteogenic transcription factors, particularly short stature homeobox 2 (SHOX2). Comparative ChIP sequencing analyses revealed genome-wide co-occupancy of MEIS2 and SHOX2 in addition to their colocalization in the developing palate and physical interaction, suggesting that SHOX2 and MEIS2 functionally interact. However, although SHOX2 was required for proper palatal bone formation and was a direct downstream target of MEIS2, Shox2 overexpression failed to rescue the palatal bone defects in a Meis2-mutant background. These results, together with the fact that Meis2 expression is associated with high osteogenic potential and required for chromatin accessibility of osteogenic genes, support a vital function of MEIS2 in setting up a ground state for palatal osteogenesis.

Bacterial products such as lipopolysaccharides (or endotoxin) cause systemic inflammation, resulting in a substantial global health burden. The onset, progression, and resolution of the inflammatory response to endotoxin are usually tightly controlled to avoid chronic inflammation. Members of the NF-κB family of transcription factors are key drivers of inflammation that activate sets of genes in response to inflammatory signals. Such responses are typically short-lived and can be suppressed by proteins that act post-translationally, such as the SOCS (suppressor of cytokine signaling) family. Less is known about direct transcriptional regulation of these responses, however. Here, using a combination of in vitro approaches and in vivo animal models, we show that endotoxin treatment induced expression of the well-characterized transcriptional repressor Krüppel-like factor 3 (KLF3), which, in turn, directly repressed the expression of the NF-κB family member RELA/p65. We also observed that KLF3-deficient mice were hypersensitive to endotoxin and exhibited elevated levels of circulating Ly6C+ monocytes and macrophage-derived inflammatory cytokines. These findings reveal that KLF3 is a fundamental suppressor that operates as a feedback inhibitor of RELA/p65 and may be important in facilitating the resolution of inflammation.