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New Method for Generation of Human Pacemaker Cardiomyocytes

The heart consists of a multitude of diverse cardiomyocyte cell types, including atrial, ventricular and pacemaker cells, which cooperate to ensure proper cardiac function and circulation throughout the body. The rhythm of the heart beat is regulated by the sinoatrial node (SAN), functionally known as the cardiac pacemaker. Loss or dysfunction of these pacemaker cardiomyocytes leads to severe cardiac arrhythmias, syncope and/or even death. Although artificial pacemakers exist to help overcome these issues, several serious limitations and problems have emerged with this approach over the past several decades including electrode fracture or damage to insulation, infection, re-operations for battery exchange, and venous thrombosis. Moreover, size mismatch and the fact that pacemaker leads do not grow with children are a concerning problem. Thus, replacing artificial pacemakers with biological pacemakers potentially overcomes these artificial pacemaker issues including the expense and complications associated with device replacement, device or lead failure, and infection. To achieve these goals, understanding how pacemaker cardiomyocytes are generated is necessary to develop a human biological pacemaker for cardiac cellular therapies.

A Novel Method For The Treatment Of Social Dysfunction Associated With Autism Spectrum Disorder (ASD) By Activating Dopamine Receptor 3 (Drd3) Signal

Children exposed to early life stress (ELS) such as physical abuse and emotional neglect during a critical period in their development are more likely to display social dysfunction later in life. Symptoms of disrupted social behaviors include decreased social motivation and a lack of interest in attending to social stimuli or seeking and enjoying reciprocal social interactions. Given that high levels of early adversity are also associated with the asocial behaviors of psychiatric patients, identifying the neural mechanisms underlying ELS-induced social dysfunction is essential for the development of treatment strategies for mental illnesses associated with social impairments, such as autism spectrum disorder (ASD), schizophrenia, and major depressive disorder (MDD).

Methods of Modifying T Cells Using Runx Family Transcription Factors

Cytotoxic T lymphocytes (CTL) mediate immunity to intracellular infections and tumors by directly killing infected or aberrant cells by delivering pro-apoptotic granzyme proteases into the cytoplasm of target cells via the pore-forming protein Perforin. During an immune response, stimulation of T cell antigen receptors (TCR) on antigen-specific naive CD8+ T cells initiates their exponential accumulation and differentiation into cells that upregulate Perforin and granzymes. Near the peak response, most responding cells in the circulation comprise terminal effector (TE) CTL, but these cells have short half-lives after the acute immune challenge is resolved. A smaller fraction comprises memory precursor (MP) effector CTL that efficiently give rise to long-lived memory CTL, which reside in lymphoid tissue as TCN and that provide a stem cell-like memory reservoir that regenerates immune responses upon re-challenge.. In addition, a fraction of CTL differentiate into cells that depart the general circulation and lodge in non-lymphoid tissues where they persist long-term as TRM (tissue-resident memory) and provide immediate protection in situ at the surfaces where infections and solid tumors originate. Until now, the molecules and mechanisms that remodel chromatin structure and transcriptional programs that drive activated CD8+ T cells to differentiate into TCM (central memory) and TRM (tissue-resident memory ) CTL, and ensure they do not "skew" into TE CTL which do not persist, were virtually unknown.

Methods To Suppress Viral Infection Of Mammalian Cells

To meet the ever-growing demand for effective, safe, and affordable protein therapeutics, decades of intense efforts have aimed to maximize the quantity and quality of recombinant proteins produced in Chinese hamster ovary (CHO) cells. CHO cells are extensively used to produce biopharmaceuticals and one advantage is their reduced susceptibility to many human virus families. However, there have been a few episodes of animal viral contamination of biopharmaceutical production runs, mostly from trace levels of viruses in raw materials. These infections more often caused by RNA viruses have led to expensive decontamination efforts and threatened the supply of critical drugs. Viral contamination in biopharmaceutical manufacturing can lead to shortages in the supply of critical therapeutics. Therefore there is a need to understand the mechanisms by which CHO cells are infected and how the cells can be universally engineered to enhance their viral resistance.

Targeting Hyaluronan as an Immunomodulator for Treatment of Inflammatory Diseases

Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract and has been associated with poor quality of life and frequent complications requiring hospitalization and surgical procedures. Current therapies for IBD typically target neutralization of inflammatory cytokines, blockade of receptors, or inhibition of inflammatory cell functions. Despite current approaches, it is still difficult to control disease severity and maintain quality of life. One important phenotype of IBD that may offer an opportunity for gaining increased understanding of the disease is that up to 40% of individuals with inflammatory diseases of the colon have extra intestinal manifestations. Foremost in these extra intestinal symptoms are skin or oral disorders such as erythema nodosum, pyoderma gangreneosum and aphthous stomatitis. The presence of diseases associated with IBD at sites far from the gut support several hypotheses that IBD is a systemic disorder of circulating bone marrow derived immunocytes, a consequence of dysbiosis of the microbiome or a generalized disorder of epithelial function. Furthermore, appropriate function of the epithelial barrier is necessary to regulate the interactions between microbes and the host and maintain health.

A Wearable Device To Monitor Sunlight Exposure

Exposure to UV radiation and sun damage can cause skin cancer. While people have increased use of sunscreen, it can be difficult to determine what length of exposure is permitted while wearing sunscreen. Active monitors have been developed, including apps for smart phones. These active monitors can predict a safe level of exposure based upon skin type, a type of sunscreen worn and a UV forecast for your location. Such smartphone apps,of course, rely upon correct input of information and correct UV forecast data. Active sensors that are separate from smartphones tend to be bulky and require external power sources. The personal ultraviolet (UV) dosimeter is a useful measurement tool to prevent UV induced dermal damages; however, conventional digital dosimeters are either bulky or require external power sources. Wearable dosimeters can address this issue by measuring an individual’s UV dose. Polysulphone films are wearable dosimeters that increase the absorbance at 330 nm upon receiving cumulative UV radiation. However, this wavelength requires spectroscopic instruments to read the results, which can be cumbersome for the end user. Colorimetric dosimeters are simpler—here, the UV  dose is indicated by a color transition in the UV sensing material. A simpler yet easily interpretable solution would be a wristband-based colorimetric dosimeter.

Methods for Inhibiting the Expression of MDM2 to Block Progression of Leukemia

RNA-editing proteins are an important class of proteins that regulate key steps in post-transcriptional RNA processing. One of the most common and best characterized is the Adenosine-to-Inosine editing (A-to-I editing) process. The cell translating machinery recognizes inosine as guanosine and A-to-I editing is accomplished by adenosine deaminase acting on RNA (ADAR) enzyme family that includes ADAR1, ADAR2, and ADAR3. While ADAR3 appears to inhibit ADAR2 editing within coding regions, ADAR1 edits primarily within double stranded RNA (dsRNA) loops formed by inverted primate-specific Alu repetitive elements. Atypical RNA editing can result in the alteration of non-coding RNAs such as miRNAs which can be present in different cancers and play a role in their development.  

A Novel Method to use tRNA Manipulation to Treat Tumors and Viral Infections

DNA damaging agents (DDA) have been successfully used therapeutically to treat an extensive range of solid tumors and blood cancers including lymphomas and leukemias. Despite its broad use, many tumors become resistant to DDA therapies over the course of the treatment. One strategy to overcome this shortcoming is the ability to reverse the resistance to DDAs. The Schlafen (SLFN) gene family members encode a diverse group of proteins, which play important roles in regulating biological functions including cellular proliferation, immune responses and suppression of viral replication. Some SLFN family members have been reported to inhibit growth in cancer cells and promote cancer cell sensitivity to chemotherapeutics. Human SLFN11 (Schlafen 11) is one such member whose expression deficiency has been observed to cause chemotherapeutics resistance in a vast collection of tumor cells. SLFN11 sensitizes tumor cells to DNA damaging agents (DDA) by preferentially inhibiting protein syntheses of multiple components of the DNA damage response and repair pathways (e.g. ATR and ATM). Alternatively, tumor cells might not only acquire drug resistance from loss of Slfn11 during treatment, but might already be drug-resistant and Slfn11-deficient a priori. Unlike those highly expressed housekeeping genes, the proteins syntheses of most genes involved in DNA damage response and repair heavily rely on tRNA-Leu-TAA (for leucine), which is cleaved by SLFN11 upon DNA damages. The inventors also have shown previously that SLFN11 inhibits HIV replication by inhibiting syntheses of viral proteins through a similar mechanism. As such, the destruction of tRNA-Leu-TAA (e.g. by antisense oligonucleotides Gapmer) or their inactivation (e.g. via leucine tRNA synthase inhibition) inhibits DNA damage repair and restores the sensitivity of DDA-resistant tumor cells to these chemotherapeutic agents, and can also be used as a novel approach to target viruses that rely on tRNA-Leu-TAA for their replication.