An extended tissue fixation method is provided including at least one soak in a cold aldehyde-based fixative solution followed by a soak in a warm aldehyde-based fixative solution over a period greater than 2 days. Using the processes disclosed herein, improved tissue morphology and IHC staining as well as superior preservation of post-translation modification signals, e.g. biomarkers, have been accomplished relative to standard room temperature fixation protocols. Moreover, the tissue can be left in the fixative solution up to at least 14 days using these methods, which provides improved flexibility relative to other protocols, enabling fixation to be conducted during transportation, shipping, and over weekends or vacations, while still achieving acceptable staining results.

The present relates to methods for detecting DNA damage in subjects treated with an ATR inhibitor. More specifically, this invention relates to a method for measuring changes in levels of γH2AX and/or pChk1.sup.Ser345 in, e.g., surrogate tissue cells, following ex vivo stimulation with a DNA damaging agent.

In cancers such as prostate cancer, the combination of PTEN loss and activation of Myc activates an adaptive stress response that enables tumor cells to escape the stress of massively upregulated protein synthesis. This pro-survival response is mediated by the PERK-phosphorylated eIF2α axis of the UPR adaptive response. Agents that disrupt PERK-eIF2α pathways disrupt the adaptive response and lead to cancer cell death from uncontrolled growth. For example, ISRIB and derivatives may be employed as therapeutic agents to disrupt PERK-mediated adaptive mechanisms. Additionally PTEN loss and activation of Myc provides a diagnostic marker that enables better prognosis and the selection of amenable treatments.

The present disclosure relates to a system for monitoring post-translational modification of protein using a biosensor with a gap, which performs with high reliability a diagnosis of a disease associated with a target protein for which impedance is measured, by measuring an impedance of a sample introduced into a sensor and calculating a change rate of the measured impedance, and to a method of manufacturing the biosensor used for the system.

Disclosed herein are a method and a kit using a novel marker associated with depression. The marker for depression includes one or more selected from a noradrenaline transporter and a dopamine transporter. The method for determining depression includes a step of examining an expression level of the marker for depression in a blood sample collected from a subject.

Presented is a method for treating inflammation and autoimmune diseases through the use of a phosphatase rheumatoid arthritis (PT-PRA) antagonist.

The presently disclosed subject matter relates to a method for predicting increased risk of obesity on a non-obese subject. More particularly, the presently disclosed subject matter relates to a method of predicting increased risk of obesity in a non-obese subject by determining a level of neurotensin expression in a biological sample from the subject and comparing the level of neurotensin expression in the sample with a control level. The presently disclosed subject matter further relates to a method of preventing and/or treating obesity in a subject in need thereof by administering to the subject an effective amount of an agent that inhibits neurotensin.

Provided are methods and compositions which are useful for separating, isolating, detecting, and quantifying compounds of interest which have been modified chemically, enzymatically or catalytically from other compounds which have not been so modified. The modifications may take the form of functional groups which are gained, lost or retained by the compounds of interest.

A method of reducing blood glucose in a subject has been developed. In preferred embodiments, the method involves administering to the subject a specific activator of endogenous mitogen-activated protein kinase kinase 6 (MKK3), mitogen-activated protein kinase kinase 6 (MKK4), mitogen-activated protein kinase kinase 6 (MKK6), p38 mitogen-activated protein kinase (p38MAPK), mitogen-activated kinase-activated protein kinase 2 (MK2), or a combination thereof, in an effective amount to reduce blood glucose in a subject. In other embodiments, the method involves administering to the subject a specific activator to increase X-box binding protein 1 (XBP1) phosphorylation on Thr48 and Ser61 in an effective amount to reduce blood glucose in the subject. Methods of identifying agents for reducing blood glucose in a subject are also provided.

The present invention relates to a composition for repressing the sternness of stem cells, which comprises a material for regulating OCT4 modification. The material for regulating OCT4 modification according to the present invention may regulate the phosphorylation or methylation of OCT4 and inhibit Wnt signaling, thereby effectively reducing the sternness of various stem cells. Therefore, since it can be effectively used in inhibition of proliferation, recurrence and metastasis of cancer, and inhibition of resistance to an anticancer agent, and can reduce sternness even in normal stem cells, it is expected that the time for differentiation of embryonic stem cells into specific cells is shortened, and efficiency is increased.