ASSESSING RISK INTRODUCED THROUGH A CODE CHANGE

Techniques are presented herein that shift the risk assessment focus during a software development process, away from the traditional end-of-process review (when a new feature is delivered, or an application is deployed) to earlier in the process when developers are actively at work. Such an approach allows a developer to assess the risk that a candidate software change is about to introduce prior to the developer committing that change, providing the developer with time (during the early portion of the process) to revisit the software and eliminate the identified risk. Aspects of the presented techniques leverage elements of a continuous integration (CI) and continuous deployment (CD) facility, the results that are available from existing unit and end-to-end tests, and the collection and analysis of OpenTelemetry (OTEL)-based metrics, events, logs, and traces (MELT) data to deliver security insights

IDENTIFYING ENTERPRISE RISK BASED ON BUSINESS CONTEXT WITH THREAT INTELLIGENCE

Presented herein are techniques that facilitate prioritizing risk mitigation efforts for business-critical services and transactions through the incorporation of a business context into threat intelligence scoring. Under aspects of the presented techniques, traditional threat intelligence tools may be employed to evaluate the risk that is associated with an enterprise asset; the results of such an evaluation may then be augmented with an enterprise-assigned business value for the asset to derive the asset’s business risk; and such a business risk may be leveraged to prioritize risk mitigation efforts, may be combined with other business risks, etc. The above-described process may be referred to herein as Business Risk Management (BRM)

Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy

Sensory neurons have the capacity to produce, release, and respond to acetylcholine (ACh), but the functional role of cholinergic systems in adult mammalian peripheral sensory nerves has not been established. Here, we have reported that neurite outgrowth from adult sensory neurons that were maintained under subsaturating neurotrophic factor conditions operates under cholinergic constraint that is mediated by muscarinic receptor–dependent regulation of mitochondrial function via AMPK. Sensory neurons from mice lacking the muscarinic ACh type 1 receptor (M(1)R) exhibited enhanced neurite outgrowth, confirming the role of M(1)R in tonic suppression of axonal plasticity. M(1)R-deficient mice made diabetic with streptozotocin were protected from physiological and structural indices of sensory neuropathy. Pharmacological blockade of M(1)R using specific or selective antagonists, pirenzepine, VU0255035, or muscarinic toxin 7 (MT7) activated AMPK and overcame diabetes-induced mitochondrial dysfunction in vitro and in vivo. These antimuscarinic drugs prevented or reversed indices of peripheral neuropathy, such as depletion of sensory nerve terminals, thermal hypoalgesia, and nerve conduction slowing in diverse rodent models of diabetes. Pirenzepine and MT7 also prevented peripheral neuropathy induced by the chemotherapeutic agents dichloroacetate and paclitaxel or HIV envelope protein gp120. As a variety of antimuscarinic drugs are approved for clinical use against other conditions, prompt translation of this therapeutic approach to clinical trials is feasible