Resistance and functional training reduces knee extensor position fluctuations in functionally limited older adults

The purpose of this study was to determine the effect of task-specificity on knee extensor steadiness adaptations in functionally limited older adults. Twenty-four functionally limited older adults (74.6±7.6 years: 22 women, 2 men) completed a 10-week control period followed by 10 weeks (2 days/week) of resistance (RT), functional (FT) (practicing everyday tasks, i.e., chair rises) or functional + resistance (FRT) training, which featured both shortening and lengthening movements. During testing, subjects performed a steady isometric [10, 25, 50% of maximal voluntary contraction (MVC)] and shortening/lengthening (5, 30, 65% of MVC) knee extensor contractions. There were no steadiness (isometric, shortening or lengthening contractions) changes in the control period and no adaptations in isometric steadiness due to training. RT induced a 37% reduction in shortening fluctuations at 5% of MVC and 35% reduction in lengthening fluctuations at both 30% and 65% of MVC. FRT induced a 60% reduction in shortening fluctuations at 30% of MVC. No adaptations in dynamic steadiness were observed in the FT group. Further analysis indicated that those who were the least steady at baseline showed the greatest training effects during isometric (RT: R ²=0.25, FRT: R ²=0.49, FT: R ²=0.38), shortening (RT: R ²=0.36, FRT: R ²=0.36, FT: R ²=0.35) and lengthening (RT: r ²=0.29, FRT: r ²=0.44) contractions. In conclusion, steadiness improvements in groups performing resistance exercise, without a concomitant improvement in the FT group, supports a role for task-specificity in explaining steadiness adaptations, particularly for unsteady older adults.     

A Brief Educational Intervention to Increase ED Initiation of Buprenorphine for Opioid Use Disorder (OUD)

BackgroundDespite the evidence in support of the use of buprenorphine in the treatment of OUD and increasing ability of emergency medicine (EM) clinicians to prescribe it, emergency department (ED)-initiated buprenorphine is uncommon. Many EM clinicians lack training on how to manage acute opioid withdrawal or initiate treatment with buprenorphine. We developed a brief buprenorphine training program and assessed the impact of the training on subsequent buprenorphine initiation and knowledge retention.MethodsWe conducted a pilot randomized control trial enrolling EM clinicians to receive either a 30-min didactic intervention about buprenorphine (standard arm) or the didactic plus weekly messaging and a monetary inducement to administer and report buprenorphine use (enhanced arm). All participants were incentivized to complete baseline, immediate post-didactic, and 90-day knowledge and attitude assessment surveys. Our objective was to achieve first time ED buprenorphine prescribing events in clinicians who had not previously prescribed buprenorphine in the ED and to improve EM-clinician knowledge and perceptions about ED-initiated buprenorphine. We also assessed whether the incentives and reminder messaging in the enhanced arm led to more clinicians administering buprenorphine than those in the standard arm following the training; we measured changes in knowledge of and attitudes toward ED-initiated buprenorphine.ResultsOf 104 EM clinicians enrolled, 51 were randomized to the standard arm and 53 to the enhanced arm. Clinical knowledge about buprenorphine improved for all clinicians immediately after the didactic intervention (difference 19.4%, 95% CI 14.4% to 24.5%). In the 90 days following the intervention, one-third (33%) of all participants reported administering buprenorphine for the first time. Clinicians administered buprenorphine more frequently in the enhanced arm compared to the standard arm (40% vs. 26.3%, p = 0.319), but the difference was not statistically significant. The post-session knowledge improvement was not sustained at 90 days in the enhanced (difference 9.6%, 95% CI − 0.37% to 19.5%) or in the standard arm (difference 3.7%, 95% CI − 5.8% to 13.2%). All the participants reported an increased ability to recognize patients with opioid withdrawal at 90 days (enhanced arm difference .55, 95% CI .01–1.09, standard arm difference .85 95% CI .34–1.37).ConclusionsA brief educational intervention targeting EM clinicians can be utilized to achieve first-time prescribing and improve knowledge around buprenorphine and opioid withdrawal. The use of weekly messaging and gain-framed incentivization conferred no additional benefit to the educational intervention alone. In order to further expand evidence-based ED treatment of OUD, focused initiatives that improve clinician competence with buprenorphine should be explored.Trial RegistrationClinicalTrials.gov Identifier: {"type":"clinical-trial","attrs":{"text":"NCT03821103","term_id":"NCT03821103"}}NCT03821103.Supplementary InformationThe online version contains supplementary material available at 10.1007/s13181-022-00890-7.     

Implementing automated surveillance for tracking Clostridium difficile infection at multiple healthcare facilities

Automated surveillance using electronically available data has been found to be accurate and save time. An automated Clostridium difficile infection (CDI) surveillance algorithm was validated at 4 Centers for Disease Control and Prevention Epicenter hospitals. Electronic surveillance was highly sensitive, specific, and showed good to excellent agreement for hospital-onset; community-onset, study facility-associated; indeterminate; and recurrent CDI.     

2,3,7,8-tetrachlorodibenzo-p-dioxin inhibits zebrafish caudal fin regeneration.

Adult zebrafish completely regenerate their caudal fins following partial amputation. Fin regrowth can easily be monitored in vivo and regenerating tissues can be used to study this dynamic developmental process. In this study we determined that fin regeneration is significantly affected by exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Zebrafish caudal fins were partially amputated, and the fish received intraperitoneal (ip) injection of 2.8, 14, or 70 ng/g weight TCDD or vehicle control. By 7 days postamputation, fish exposed to the highest concentration of TCDD regenerated 15% of their fin compared to 65% regrowth in control fish. To determine if this effect was stage specific, zebrafish were exposed to 70 ng/g TCDD on 1, 2, 3, or 4 days postamputation. Fin regeneration was significantly inhibited at all time points following TCDD exposure. TCDD exposure also induced hyperpigmentation in de novo tissue. Zebrafish were dosed with BrdU, following fin amputation and TCDD exposure, to study changes in cell proliferation. By 4 days postamputation, cell proliferation rates were significantly lower in TCDD-exposed fish. TCDD toxicity is mediated through the aryl hydrocarbon receptor (AHR), and RT-PCR experiments confirmed AHR2, ARNT2b, and TCDD-dependent CYP1A expression in the regenerating tissue. These results demonstrate that zebrafish caudal fin regeneration is a unique model to investigate molecular mechanism(s) of TCDD toxicity.     

Randomized, Double-blind, Placebo-controlled Trial of Diazepam, Nitroglycerin, or Both for Treatment of Patients with Potential Cocaine-associated Acute Coronary Syndromes

INTRODUCTION: To the authors' knowledge, treatment of patients with cocaine-associated acute coronary syndromes has not been rigorously investigated in symptomatic patients. OBJECTIVE: To perform a randomized double-blind trial of diazepam, nitroglycerin, or both for treatment of patients with potential cocaine-associated acute coronary syndromes. METHODS: Patients with potential cocaine-associated acute coronary syndromes were randomized to treatment with either diazepam, nitroglycerin, or both every 5 minutes or until symptom resolution. Outcomes were chest pain resolution (measured by visual analog scale), and changes in blood pressure, pulse rate, cardiac output (L/min), cardiac index (L/min/m2), stroke volume (mL/beat), and stroke index (mL/beat/m2) over the 15-minute treatment period. To adjust for seven outcomes using the Bonferroni correction, alpha was set at 0.007. RESULTS: Forty patients were enrolled (diazepam, 12; nitroglycerin, 13; both, 15). Patients had a mean age (+/-SD) of 35.4 (+/-7.5) years; 75% were male. They presented a mean of 5 hours and 37 minutes after cocaine use. Baseline demographics, cocaine use patterns, chest pain characteristics, and initial electrocardiograms were similar for all groups. Chest pain severity improved similarly in the three groups [-33.3 mm (+/-8.0); -30.7 mm (+/-7.1); -33.0 mm (+/-7.9); p = 0.6]. The stroke index decreased during the 15-minute treatment period for all groups (diazepam, -8.7 (+/-3.3); nitroglycerin, -3.1 +/- 2.8; both, -1.8 (+/-3.1) mL/beat/m2; p = 0.03). After adjustment for differences between baseline hemodynamic and cardiac profiles and multiple comparisons, there was no difference in any response to therapy over time for the different treatments. CONCLUSIONS: For treatment of patients with potential cocaine-associated acute coronary syndromes, chest pain resolutions and changes in cardiac performance are not different in patients treated with diazepam or nitroglycerin. In this study, the use of both agents did not offer any advantage over either agent alone.     

The Potato virus X TGBp3 protein associates with the ER network for virus cell-to-cell movement

Potato virus X (PVX) TGBp3 is required for virus cell-to-cell movement. Cell-to-cell movement of TGBp3 was studied using biolistic bombardment of plasmids expressing GFP:TGBp3. TGBp3 moves between cells in Nicotiana benthamiana, but requires TGBp1 to move in N. tabacum leaves. In tobacco leaves GFP:TGBp3 accumulated in a pattern resembling the endoplasmic reticulum (ER). To determine if the ER network is important for GFP:TGBp3 and for PVX cell-to-cell movement, a single mutation inhibiting membrane binding of TGBp3 was introduced into GFP:TGBp3 and into PVX. This mutation disrupted movement of GFP:TGBp3 and PVX. Brefeldin A, which disrupts the ER network, also inhibited GFP:TGBp3 movement in both Nicotiana species. Two deletion mutations, that do not affect membrane binding, hindered GFP:TGBp3 and PVX cell-to-cell movement. Plasmids expressing GFP:TGBp2 and GFP:TGBp3 were bombarded to several other PVX hosts and neither protein moved between adjacent cells. In most hosts, TGBp2 or TGBp3 cannot move cell-to-cell.     

Toxicity from the use of niacin to beat urine drug screening

Niacin (vitamin B3) is promoted for rapidly clearing the body of drugs of abuse, such as cocaine and cannabis, and is alleged to interfere with urine drug screening. We present 4 cases of such novel use associated with significant adverse effects. Two cases had isolated skin manifestations, whereas the other 2 presented with life-threatening manifestations, including nausea, vomiting, dizziness, hepatotoxicity, metabolic acidosis, and hypoglycemia evolving into hyperglycemia. One patient also had profound neutrophilia and QT(C)-interval prolongation. All patients improved after cessation of the drug use and supportive treatment. Health care providers should be aware of these potential adverse effects of niacin and of the misguided use of this vitamin by patients seeking to interfere with urine drug screening.