Future research must move beyond descriptive studies to include more advanced research methods. Few practice-guiding implications can be gained from this body of research because of the lack of intervention studies.
Background: To reduce the spread of coronavirus disease 2019 (COVID-19), many substance use disorder treatment programs have transitioned to telemedicine. Emergency regulatory changes allow buprenorphine initiation without an in-person visit. We describe the use of videoconferencing for buprenorphine initiation combined with street outreach to engage 2 patients experiencing homelessness with severe opioid use disorder (OUD). Case Presentation: Patient 1 was a 30-year-old man with severe OUD who had relapsed to injection heroin/fentanyl after incarceration. A community drop-in center outreach harm reduction specialist facilitated a videoconference with an addiction specialist at an OUD bridge clinic. The patient completed a community buprenorphine/ naloxone initiation and self-titrated to his prior dose, 8/2 mg twice daily. One week later, he reconnected with the outreach team for a follow-up videoconference visit. Patient 2, a 36-year-old man with severe OUD, connected to the addiction specialist via a syringe service program harm reduction specialist. He had been trying to connect to a community buprenorphine/naloxone provider, but access was limited due to COVID-19, so he was using diverted buprenorphine/naloxone to reduce opioid use. He was restarted on his previous dose of 12/3 mg daily which was continued via phone follow-up 16 days later. Conclusions: COVID-19-related regulatory changes allow buprenorphine initiation via telemedicine. We describe 2 cases where telemedicine was combined with street outreach to connect patients experiencing homelessness with OUD to treatment. These cases highlight an important opportunity to provide access to life-saving OUD treatment for vulnerable patients in the setting of a pandemic that mandates reduced face-to-face clinical interactions.
The nucleophilic small molecule catalyst (-)-tetramisole was found to catalyze the kinetic resolution of monofunctional secondary alcohols via enantioselective silylation. Optimization of this new methodology allows for selectivity factors up to 25 utilizing commercially available reagents and mild reaction conditions.
Objective
Patients with end-stage lung disease experience significant decrements in quality of life (QOL). Although coping strategies are related to QOL in patients with end-stage lung disease, the extent to which specific native lung disease moderates this relationship is unknown.
Methods
We investigated the relationship between coping, native lung disease, and QOL among 187 patients awaiting lung transplantation, including 139 patients with chronic obstructive pulmonary disease (COPD) and 48 patients with cystic fibrosis (CF). Participants completed a psychosocial battery assessing psychological QOL, physical QOL, and coping strategies.
Results
For both COPD and CF patients, higher levels of Active Coping (P < .0001) and lower levels of Disengagement (P < .0001) were associated with better psychological QOL. For physical QOL, we observed a native disease by coping interaction (P = .01) such that Active Coping was associated with better physical QOL in patients with COPD but not in patients with CF.
Conclusion
The relationship between coping and QOL may vary as a function of native lung disease. In order to develop effective interventions to help patients cope successfully with end stage lung disease, patients’ native disease may need to be considered.
Objective-Apolipoprotein (apo)A-I exists in 3 forms in plasma: as lipid-free apoA-I, as a component of pre--migrating discoidal high density lipoproteins (HDLs), and as a component of ␣-migrating spherical HDLs. This study investigates (1) the in vivo metabolism of apoA-I in each of these forms and (2) the effects of hepatic lipase (HL) on apoA-I metabolism. Methods and Results-Wild-type and HL transgenic rabbits were studied. When lipid-free 125 I-apoA-I and 125 I-apoA-I in pre--migrating discoidal reconstituted HDLs (rHDLs) were injected into wild-type rabbits, the label rapidly appeared in ␣-migrating particles and decayed with the same fractional catabolic rate (FCR) as when they were injected as a component of spherical rHDLs. Spherical rHDLs did not change in size when they were injected into wild-type rabbits but were reduced in size in HL transgenic rabbits. The FCR of apoA-I in HL transgenic rabbits was double that in wild-type rabbits. Conclusions-In vivo, (1) lipid-free apoA-I rapidly incorporates into preexisting ␣-migrating particles, (2) pre--migrating discoidal HDLs are rapidly converted into ␣-migrating HDLs, (3) the FCR of apoA-I is independent of the form in which it is introduced into plasma, and (4) Key Words: apolipoprotein A-I Ⅲ hepatic lipase Ⅲ high density lipoproteins Ⅲ metabolism Ⅲ rabbits T he discovery that HDLs protect against the development of atherosclerosis 1,2 has stimulated a major interest in the factors that regulate these lipoproteins. This interest has applied particularly to the regulation of apoA-I, the main protein constituent of HDL.Most of the HDLs in normal plasma are spherical particles that exhibit ␣-migration when subjected to agarose gel electrophoresis. They consist of a surface monolayer of apolipoproteins, phospholipids, and unesterified cholesterol (UC) surrounding a core of cholesteryl esters (CEs) and triglycerides. However, there is the potential for apoA-I also to circulate in a lipid-free (or lipid-poor) form and as a component of pre--migrating discoidal complexes containing apoA-I, phospholipid, and UC. 3 In vitro studies have shown that apoA-I cycles between the lipid-free and lipid-associated forms in processes mediated by lecithin:cholesterol acyltransferase (LCAT), CE transfer protein (CETP), phospholipid transfer protein, and hepatic lipase (HL). 4 It has also been shown in vitro that pre--migrating discoidal HDLs are converted into ␣-migrating spherical particles by the action of LCAT. 5,6 In vitro studies have also shown that ␣-migrating HDLs are increased in size by LCAT and that they decrease in size when they interact with CETP, HL, and triglyceride-rich lipoproteins. 4 The reduction in size is accompanied by a dissociation of lipid-free apoA-I from the HDL. [7][8][9] Despite the abundant evidence that HDL remodeling occurs in vitro, its contribution to HDL metabolism in vivo remains unclear. Indeed, the fact that apoA-I exists predominantly in ␣-migrating spherical HDLs in the plasma of most species, including humans, raises questions a...
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