Canine Crackdown: Unreliable Drug Sniffs Threaten Civil Liberties and Equal Law Enforcement

This paper explores the history of drug detection dogs in law enforcement, critically examines their ability to successfully detect illicit substances, and investigates the legal repercussions of dog alerts in the field. While drug dog programs have experienced substantial success in the U.S. with annual drug seizures valued between $2 and$3 billion, experiments on police-trained dogs have shown that though canines have incredible sensitivity in controlled settings, other factors including the breed of the dog, handler bias, and even the race of the suspect have been shown to significantly reduce a dog’s detection accuracy. These reports raise serious questions about the efficacy of drug detecting dogs, and if a dog alert should generate probable cause for a search or seizure of property that is otherwise protected under the Fourth Amendment. In particular, the threat of racial discriminatory practices raises the concern that dogs can be used to inappropriately extend law enforcement authority against ethnic minorities. Though these canines must complete a rigorous training course in order to search for narcotics, police are not required to keep careful records of their dogs’ performances on drug detection. As exemplified by a successful investigation and the subsequent removal of the ineffective drug detection dog program in New South Wales, this article calls the U.S. to similarly investigate the accuracy of its drug sniffs in order to protect its citizens from seemingly unreliable dog alerts and the warantless searches and seizures that follow

Canine Crackdown: Unreliable Drug Sniffs Threaten Civil Liberties and Equal Law Enforcement

This paper explores the history of drug detection dogs in law enforcement, critically examines their ability to successfully detect illicit substances, and investigates the legal repercussions of dog alerts in the field. While drug dog programs have experienced substantial success in the U.S. with annual drug seizures valued between $2 and$3 billion, experiments on police-trained dogs have shown that though canines have incredible sensitivity in controlled settings, other factors including the breed of the dog, handler bias, and even the race of the suspect have been shown to significantly reduce a dog’s detection accuracy. These reports raise serious questions about the efficacy of drug detecting dogs, and if a dog alert should generate probable cause for a search or seizure of property that is otherwise protected under the Fourth Amendment. In particular, the threat of racial discriminatory practices raises the concern that dogs can be used to inappropriately extend law enforcement authority against ethnic minorities. Though these canines must complete a rigorous training course in order to search for narcotics, police are not required to keep careful records of their dogs’ performances on drug detection. As exemplified by a successful investigation and the subsequent removal of the ineffective drug detection dog program in New South Wales, this article calls the U.S. to similarly investigate the accuracy of its drug sniffs in order to protect its citizens from seemingly unreliable dog alerts and the warantless searches and seizures that follow

Beyond the Cell Surface: Targeting Intracellular Negative Regulators to Enhance T cell Anti-Tumor Activity

It is well established that extracellular proteins that negatively regulate T cell function, such as Cytotoxic T-Lymphocyte-Associated protein 4 (CTLA-4) and Programmed Cell Death protein 1 (PD-1), can be effectively targeted to enhance cancer immunotherapies and Chimeric Antigen Receptor T cells (CAR-T cells). Intracellular proteins that inhibit T cell receptor (TCR) signal transduction, though less well studied, are also potentially useful therapeutic targets to enhance T cell activity against tumor. Four major classes of enzymes that attenuate TCR signaling include E3 ubiquitin kinases such as the Casitas B-lineage lymphoma proteins (Cbl-b and c-Cbl), and Itchy (Itch), inhibitory tyrosine phosphatases, such as Src homology region 2 domain-containing phosphatases (SHP-1 and SHP-2), inhibitory protein kinases, such as C-terminal Src kinase (Csk), and inhibitory lipid kinases such as Src homology 2 (SH2) domain-containing inositol polyphosphate 5-phosphatase (SHIP) and Diacylglycerol kinases (DGKs). This review describes the mechanism of action of eighteen intracellular inhibitory regulatory proteins in T cells within these four classes, and assesses their potential value as clinical targets to enhance the anti-tumor activity of endogenous T cells and CAR-T cells

EGFR Signaling Stimulates Autophagy to Regulate Stem Cell Maintenance and Lipid Homeostasis in the Drosophila Testis.

Although typically upregulated upon cellular stress, autophagy can also be utilized under homeostatic conditions as a quality control mechanism or in response to developmental cues. Here, we report that autophagy is required for the maintenance of somatic cyst stem cells (CySCs) in the Drosophila testis. Disruption of autophagy in CySCs and early cyst cells (CCs) by the depletion of autophagy-related (Atg) genes reduced early CC numbers and affected CC function, resembling decreased epidermal growth factor receptor (EGFR) signaling. Indeed, our data indicate that EGFR acts to stimulate autophagy to preserve early CC function, whereas target of rapamycin (TOR) negatively regulates autophagy in the differentiating CCs. Finally, we show that the EGFR-mediated stimulation of autophagy regulates lipid levels in CySCs and CCs. These results demonstrate a key role for autophagy in regulating somatic stem cell behavior and tissue homeostasis by integrating cues from both the EGFR and TOR signaling pathways to control lipid metabolism

EGFR Signaling Stimulates Autophagy to Regulate Stem Cell Maintenance and Lipid Homeostasis in the Drosophila Testis.

Although typically upregulated upon cellular stress, autophagy can also be utilized under homeostatic conditions as a quality control mechanism or in response to developmental cues. Here, we report that autophagy is required for the maintenance of somatic cyst stem cells (CySCs) in the Drosophila testis. Disruption of autophagy in CySCs and early cyst cells (CCs) by the depletion of autophagy-related (Atg) genes reduced early CC numbers and affected CC function, resembling decreased epidermal growth factor receptor (EGFR) signaling. Indeed, our data indicate that EGFR acts to stimulate autophagy to preserve early CC function, whereas target of rapamycin (TOR) negatively regulates autophagy in the differentiating CCs. Finally, we show that the EGFR-mediated stimulation of autophagy regulates lipid levels in CySCs and CCs. These results demonstrate a key role for autophagy in regulating somatic stem cell behavior and tissue homeostasis by integrating cues from both the EGFR and TOR signaling pathways to control lipid metabolism