Researchers developed a transgenic mouse model of the rare neurodegenerative disorder HDL2 to study its pathogenesis. The study found overlapping polyQ-mediated mechanisms with Huntington's disease and identified a novel expanded polyQ protein driving disease progression in HDL2 mice.
A new study reveals that rapamycin can reverse cardiac muscle damage in a mouse model of LEOPARD syndrome, a rare congenital heart disease. The research demonstrates the importance of targeted therapies in managing congenital diseases and offers a potential new treatment option for patients with LEOPARD syndrome.
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Researchers at University of South Florida found that spirulina supplementation delayed motor symptoms and disease progression in a mouse model of ALS. The study suggests a dual antioxidant and anti-inflammatory effect on motor neurons, offering potential clinical benefits for ALS patients.
Overexpression of PGC-1α significantly improves neurological function in HD-model transgenic mice by reducing htt protein aggregation and oxidative stress. This discovery may lead to therapies targeting PGC-1α function for treating Huntington's disease and related disorders.
Researchers at Joslin Diabetes Center discovered that diabetes can reduce brain cholesterol synthesis, which could impact brain function and increase the risk of Alzheimer's disease. This finding has broad implications for people with diabetes and may also play a role in diabetic neuropathy.
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Joslin researchers found that brain cholesterol synthesis decreases in mouse models of diabetes, affecting nerve function and potentially leading to increased appetite and weight gain. The study suggests a link between diabetes and altered brain function, including changes in Alzheimer's disease risk and diabetic neuropathy.
A new mouse model created by Japanese scientists confirms the link between mutated beta-synuclein protein and neurodegeneration in diseases like Parkinson's and Alzheimer's. The discovery establishes B-synuclein as a potential target for developing new therapies.
Researchers identify hyperactive c-Met protein as key player in ADPKD cyst growth, leading to potential therapeutic target. Pharmacological inhibition of c-Met decreases mTOR activity and blocks cyst formation in mouse model.
A single stimulatory molecule has been found to sustain human insulin-producing cell replication in a mouse model of diabetes, indicating potential treatment options for the condition.
Researchers at Biogen Idec Inc. have found that targeting the TIM-1 protein may be effective in treating asthma. The study used a humanized mouse model to show that an antibody binding to a specific region of TIM-1 reduced inflammation and airway hyperresponsiveness.
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Researchers at Columbia University Medical Center found a genetic variant causing disrupted communication between brain regions, leading to working memory deficits and increasing the risk of schizophrenia. The study used a mouse model with a 22q11 deletion mutation, which showed impaired neural activity and behavior in cognitive tasks.
Researchers have identified CD99 as a potential new drug target for Ewing sarcoma. A novel type of cellular senescence has also been found to suppress prostate tumorigenesis. Additionally, the protein USAG-1 has been linked to the development of Alport syndrome, suggesting a promising therapeutic approach.
Researchers have identified a potential new set of targets to improve the efficiency of pancreatic islet transplantation. The study found that treatment with an antibody targeting HMGB1 prevented early pancreatic islet loss and inhibited IFN-gamma production by NKT cells and Gr-1+CD11b+ cells.
Researchers found that taking nonsteroidal anti-inflammatory drugs (NSAIDs) like ibuprofen or naproxen can prevent the early sign of Alzheimer's disease in mice. However, these same drugs do not reverse existing neuronal cell cycle events in affected animals.
Researchers at Caltech have shown that a highly specific intrabody can stall the development of Huntington's disease in various mouse models. The treatment successfully attenuated symptoms and increased life span by targeting an amino-acid sequence unique to the mutant huntingtin protein.
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Researchers have developed a new mouse model of amyotrophic lateral sclerosis (ALS) that closely replicates human symptoms, including progressive paralysis and muscle loss. The genetically engineered mice also exhibit damage to motor neurons and protein clumps, similar to human ALS pathology.
A team of researchers led by Dr. Alon Monsonego has created a humanized mouse model that responds specifically to an A-beta-peptide vaccine, reducing plaque and inflammation in the brain. The study provides a basis for developing individualized immunotherapeutic approaches to Alzheimer's disease.
Scientists have developed a new mouse model of X-linked nephrogenic diabetes insipidus, a severe kidney disease. The model shows that selective EP4 receptor agonists alleviate the symptoms of the disease, suggesting these compounds as potential therapeutics.
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Researchers have identified a new mechanism underlying sex-specific gene expression in mice, with PPAR-alpha repressing genes involved in immunity and steroid production. The study also found that this repression is mediated by sumoylation, a process only occurring in female mice, and suggests potential new approaches to prevent estrog...
Researchers created a mouse model with low kalirin levels that developed schizophrenia symptoms as an adolescent, mimicking human delayed onset. The study suggests stimulating kalirin activity could help alleviate cognitive symptoms, offering new treatment direction.
Research reveals that blood-derived macrophages with interleukin-10 expression have an anti-inflammatory effect on spinal cord injuries. This finding suggests that these cells may contribute to the recovery process after injury.
Researchers have identified protein Nox4 as crucial for hemangioma growth and found a potent inhibitor fulvene-5 to substantially inhibit its growth. This discovery suggests targeting Nox4 using fulvene derivatives may attenuate hemangioma growth.
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A team of scientists at Children's Hospital of Pittsburgh UPMC has discovered an enzyme crucial for maintaining a robust immune system into old age. The study found that the novel mouse model has a thymus that remains intact throughout its life.
A new mouse model has been developed to understand the cause of progressive hearing loss, opening up avenues for treatment. The study found that a genetic mutation in microRNA seed region influences sensory hair cell production, leading to impaired hearing.
Scientists have created a mouse model of Wolf-Hirschorn Syndrome, a genetic disorder characterized by physical abnormalities and developmental delays. The model, which mimics the disease's effects on cardiac valves and facial structures, offers a valuable tool for researchers studying human development and disease.
A humanized mouse infected with HIV has enabled researchers to test antiviral protection against AIDS. The study shows that pre-exposure treatment and post-exposure treatment can prevent both vaginal and rectal transmission of the virus.
A team of Columbia University researchers has identified a new investigational therapy for bladder cancer, inhibiting the mTOR signaling pathway with rapamycin. The discovery demonstrates that p53 and PTEN tumor suppressor genes are inactivated in invasive bladder cancer.
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Recent research reveals that migraine mice have an imbalance in excitation and inhibition, leading to increased neuronal activity. Glutamate release is found to be elevated, facilitating the propagation of cortical spreading depression (CSD), a phenomenon linked to migraine aura.
Researchers found that CD4+ T cells play a significant role in Parkinson's disease progression. Infiltration of these immune cells in the brain contributes to neurodegeneration. Targeting the immune system might offer a new therapeutic approach.
Researchers developed a transgenic mouse model expressing mutant prion protein, resulting in a fatal neurological disorder. The discovery may help unravel the mystery of this progressive disease affecting humans and animals.
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Researchers found that two statins can block the molecular pathway causing pregnancy loss in mice with antiphospholipid syndrome. The study suggests statins could be a treatment option for women experiencing similar complications.
Jackson Laboratory scientists have developed a simple and cost-effective method to freeze mouse sperm, achieving high fertilization rates with mouse eggs. This breakthrough will significantly reduce the cost of developing new mouse models for human diseases.
Researchers found that 22% of essential human genes are nonessential in mice, and this discrepancy affects waste management. The study's results suggest that efficient waste management became increasingly important as life span increased in humans, making certain genes more essential.
Researchers at Gladstone Institutes have found that modulating enkephalin peptides in the brain may reduce cognitive deficits seen in Alzheimer's disease. Increased levels of preproenkephalin mRNA and enkephalins in brain regions affected by AD were observed, suggesting a potential new therapy target.
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A new study found that bosentan prevents experimentally induced vaso-occlusive crises in a mouse model of SCD, reducing blood vessel resistance and preventing organ damage. Bosentan may provide a new way to limit VOCs and thereby reduce mortality and morbidity in individuals with Sickle Cell Disease.
A study by Genhong Cheng and colleagues has identified the mechanism by which IFN-beta reduces disease in multiple sclerosis. Administration of IL-27 alleviates symptoms in mice with MS, suggesting a key role for this molecule in the treatment's benefits.
A new drug, ABS-75, has been shown to protect nerve cells from damage in mice with multiple sclerosis. The treatment markedly reduced disease progression and was associated with decreased nerve cell degradation.
Scientists have established a mouse model for human malignant mesothelioma, an aggressive cancer originating from the mesothelial lining of the pleural cavity. The model closely resembles human MM, allowing researchers to study disease onset, progression, and test new therapeutic strategies.
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Researchers have created a highly accurate mouse model of inflammatory bowel disease (IBD), which closely resembles the most serious form of human ulcerative colitis. Treating the mice with broad-spectrum antibiotics reduced gut inflammation and increased survival, providing hope for new treatments.
Researchers found an association between leptin resistance and high blood pressure in people with Bardet-Biedl syndrome, a rare genetic disorder. Leptin resistance disrupts brain signals that regulate appetite and metabolism.
A study found that neutralizing IL-22 prevents psoriasis-like disease in mice by reducing skin thickening and inflammatory responses. Administering IL-22 into normal mice induced psoriasis-like skin lesions, supporting the role of IL-22 in the disease.
Researchers found that delivering the IL-22 gene to the intestines of mice with ulcerative colitis reduced inflammation and enhanced mucus production. Local delivery of the IL-22 gene also neutralized chemical-induced intestinal inflammation in normal mice, suggesting a potential therapeutic approach for UC.
Researchers at Massachusetts General Hospital have identified a compound, C2-8, that may delay the loss of motor control and reduce neurological damage in a mouse model of Huntington's Disease. The study found that C2-8 slows the progress of HD and shows promise as a potential treatment.
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Researchers created a genetically engineered mouse that models both anatomical and behavioral defects of schizophrenia, a complex brain disorder. The new mouse is based on a genetic change in the DISC1 gene, which affects nerve cell function, and shows characteristic defects in brain structure and behavior.
Researchers have developed a groundbreaking new mouse model for lung transplantation, which could lead to breakthroughs in preventing transplant rejection. The study aims to understand the molecular mechanisms controlling lung graft survival and develop therapies to counteract chronic rejection.
Researchers have identified a gene, GLIS2, that protects against a serious kidney disease called nephronopthisis. Mutations in this gene cause the disease, which leads to kidney degeneration and failure.
Scientists have developed a mouse model for synovial sarcoma, revealing that the tumor arises from skeletal muscle precursor cells called myoblasts. The study also showed that expression of a chimeric fusion protein called SYT-SSX in these cells is sufficient to induce synovial sarcoma with 100% penetrance.
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New research in mice suggests that reversing CaMKII inhibition alleviates Angelman syndrome neurological problems. The study identifies potential therapeutic targets for treating symptoms, and the findings may apply to other unexplained mental retardation syndromes.
Researchers found that losartan improves muscle regeneration and repair in a mouse model of Duchenne muscular dystrophy, a devastating disease characterized by rapid progression of muscle degeneration. The study also showed that losartan can attenuate the entire disease when treated over time.
U of MN researchers developed a mouse model for centronuclear myopathy, a poorly understood muscle disease. They found that knocking out the gamma actin gene impaired muscle cell function, leading to muscle cell death, and identified this protein as a key player in muscle structure.
Researchers identified a connection between pregnane X receptor (PXR) and neuroprotection in a mouse model of Niemann-Pick type C disease. Activating PXR with known activators, such as dilantin and St. John's Wort, may help clear toxic cholesterol byproducts.
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Researchers have discovered that neurons can produce a key protein linked to Alzheimer's disease under certain conditions. The study uses a unique mouse model to show that apoE production is regulated by the brain's response to injury, shedding light on the mechanisms underlying this complex disorder.
Researchers have identified NRL as the earliest marker of rod precursors, allowing them to pinpoint the exact time at which rods are formed. This discovery provides a new vantage point for understanding healthy visual system development and raises the possibility of re-directing cell production to stave off eye disease.
Researchers at Howard Hughes Medical Institute have created a mouse model of medulloblastoma, a common childhood brain cancer. The study found that mice lacking the XRCC4 gene or both XRCC4 and p53 died early from tumors, which displayed genetic abnormalities characteristic of human medulloblastomas. This new model will help understand...
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Researchers discovered a mechanism by which misfolded SOD1 proteins form aggregates that kill motor neurons in ALS. The normal form of SOD1 is recruited to participate in disease formation through intermolecular disulfide bonds, providing potential sites for therapeutic intervention.
Karen Duff, a young British scientist, received the Potamkin Prize for her innovative work on developing transgenic mouse models of age-related human brain diseases. Her research has led to significant advancements in understanding Alzheimer's disease and identifying potential treatments.
Researchers have discovered that Alzheimer's disease is caused by abnormal cell division in neurons, which starts months before amyloid plaques form. The study suggests that another cellular problem triggers the disease process after abnormal cell cycling begins.
Researchers at UCSD develop mice models expressing high amounts of alpha-synuclein to study its effects on the nervous system. The models aid in understanding the causes of multiple system atrophy and developing treatments to slow disease progression, potentially benefiting patients with Parkinson's disease as well.
Researchers at EMBL and universities in Heidelberg and Ulm found that blocking a specific signal within brain cells may help prevent cell death after a stroke. The study suggests new therapies could be developed by controlling a molecule involved in passing the signal.
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A new therapeutic target has been identified in the inherited brain tumor disorder neurofibromatosis 1 (NF1). Fumagillin, an established drug, has been found to suppress the activity of MetAP2, which is abnormally high in NF1-associated brain tumors. This discovery may lead to new treatments for patients with NF1.