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The emergence and efficacy of chimeric antigen receptor (CAR) T cell therapy in previously incurable malignancies represents a promising paradigm shift in cancer care. However, it is not without significant clinical, operational, and financial considerations. Pharmacists should be prepared to fulfill the various roles in CAR T cell therapy provision including policy development; electronic medical record build; patient and staff education; patient selection; procurement, storage, and handling; medication administration and supportive care; management of adverse reactions; and quality tracking. Our commentary provides an overview of the opportunities for pharmacy involvement in the implementation and maintenance of a CAR T cell therapy program with an emphasis on the importance of pharmacy involvement as part of a multidisciplinary approach to care. Although some institutions have dedicated a CAR T cell pharmacist to meet the demands of emerging CAR T cell therapy, we believe that clinical pharmacists practicing in hematopoietic stem cell transplant and hematology/oncology have the skills and training to fulfill the pharmacist's role in CAR T cell therapy.<br /><br /> The incidence of neuropathy with checkpoint inhibitors is 0.3-1%, typically occurring 2-12 weeks after treatment initiation. Common neuropathy phenotypes include inflammatory myopathies, myasthenia gravis, acute and chronic demyelinating polyradiculopathies, vasculitic neuropathies, isolated cranial neuropathies, aseptic meningitis, autoimmune encephalitis, multiple sclerosis and hypophysitis. Carpal tunnel syndrome is the most common entrapment neuropathy in the general population; however, the association of carpal tunnel syndrome with checkpoint inhibitors is exceedingly rare.<br /><br /> We report two cases of patients with no prior history of carpal tunnel syndrome treated with checkpoint inhibitors that developed de novo bilateral carpal tunnel syndrome.<br /><br /> For both patients, the neurologic symptoms improved with cessation of the checkpoint inhibitor and initiation of corticosteroids.<br /><br /> Given the prevalence of carpal tunnel syndrome in the general population, a high index of suspicion for carpal tunnel in patients receiving checkpoint inhibitors and prompt treatment with corticosteroids is essential.<br /><br />Given the prevalence of carpal tunnel syndrome in the general population, a high index of suspicion for carpal tunnel in patients receiving checkpoint inhibitors and prompt treatment with corticosteroids is essential.<br /><br /> Follow-up calls in the oncology setting are frequently used to augment care and encourage oral antineoplastic adherence. However, limited data are available on patient populations that would benefit from this intervention versus populations that may require alternative interventions. The purpose of this study was to identify characteristics among patients on oral antineoplastic agents that influence their likelihood to respond to follow-up calls.<br /><br /> Patients receiving care from one of the eight community oncology clinics within the same branch were analyzed. Patients were included if they were ≥18 years, received a new oral antineoplastic agent that was electronically prescribed between August 2018-October 2018, and picked up their first fill from their pharmacy of choice. Patients received up to six follow-up calls after picking up their first prescription. Calls were categorized as adherent (≥3 monthly interactions) or non-adherent (&lt;3 monthly interactions). Logistic regression models were used to evalu<br /><br /> Crystalline arthritis (CA), characterized by acute joint pain and erythema secondary to calcium pyrophosphate deposition (CPPD, or pseudogout) or monosodium urate crystals (gout), is a potentially underreported complication following allogeneic hematopoietic cell transplant (alloHCT). Graft-versus-host disease prophylaxis with calcineurin inhibitors (CNIs) causes hypomagnesemia and hyperuricemia, resulting in CA. CA related to tacrolimus has yet to be characterized following alloHCT.<br /><br /> We retrospectively reviewed records of 450 consecutive patients undergoing alloHCT and identified 15 (3.3% incidence) who developed CA on tacrolimus. Large joints were involved in 10 (66.7%) patients, all patients had recent hypomagnesemia, and no patient had hyperuricemia, suggesting CPPD was the most likely etiology.<br /><br /> Eleven (73.3%) patients received systemic corticosteroids; 6 as initial therapy and 5 added to or substituted for colchicine in the setting of slow or inadequate response. The median duration of corticosteroidary to CNIs is likely the precipitating factor for CPPD in this population. Patients can effectively be managed with systemic corticosteroids and/or colchicine, however prolonged duration of treatment and even maintenance may be necessary. Based on the Naranjo Algorithm, CPPD secondary to tacrolimus induced hypomagnesemia is a possible adverse drug event, with a score of 3-4.<br /><br /> Increased expression of α-Syn (α-Synuclein) is known to mediate secondary brain damage after stroke. We presently studied if α-Syn knockdown can protect ischemic brain irrespective of sex and age.<br /><br /> Adult and aged male and female mice were subjected to transient middle cerebral artery occlusion. α-Syn small interfering RNA (siRNA) was administered intravenous at 30 minutes or 3 hour reperfusion. Poststroke motor deficits were evaluated between day 1 and 7 and infarct volume was measured at day 7 of reperfusion.<br /><br /> α-Syn knockdown significantly decreased poststroke brain damage and improved poststroke motor function recovery in adult and aged mice of both sexes. However, the window of therapeutic opportunity for α-Syn siRNA is very limited.<br /><br /> α-Syn plays a critical role in ischemic brain damage and preventing α-Syn protein expression early after stroke minimizes poststroke brain damage leading to better functional outcomes irrespective of age and sex.<br /><br />α-Syn plays a critical role in ischemic brain damage and preventing α-Syn protein expression early after stroke minimizes poststroke brain damage leading to better functional outcomes irrespective of age and sex.<br /><br /> There is an urgent need to develop adjunct therapies that can be added onto reperfusion for acute ischemic stroke. Recently, mitochondrial transplantation has emerged as a promising therapeutic approach for boosting brain tissue protection. In this proof-of-concept study, we investigate the feasibility of using placenta as a source for mitochondrial transplantation in a mouse model of transient focal cerebral ischemia-reperfusion.<br /><br /> Mitochondria-enriched fractions were isolated from cryopreserved mouse placenta. [https://www.selleckchem.com/products/mk-8353-sch900353.html SCH900353 order] Mitochondrial purity and JC1 membrane potentials were assessed by flow cytometry. Adenosine triphosphate and mitochondrial proteins were measured by luminescence intensity and western blot, respectively. Therapeutic efficacy of mitochondrial fractions was assessed in a mouse model of transient focal cerebral ischemia-reperfusion.<br /><br /> Flow cytometry analysis demonstrated that about 87% of placental mitochondria were viable and maintained JC1 membrane potentials after isolation. Placental mitochondrial fractions contained adenosine triphosphate equivalent to mitochondrial fractions isolated from skeletal muscle and brown fat tissue.