Coordinating brain-distributed network activities in memory resistant to extinction.

Certain memories resist extinction to continue invigorating maladaptive actions. The robustness of these memories could depend on their widely distributed implementation across populations of neurons in multiple brain regions. However, how dispersed neuronal activities are collectively organized to underpin a persistent memory-guided behavior remains unknown. To investigate this, we simultaneously monitored the prefrontal cortex, nucleus accumbens, amygdala, hippocampus, and ventral tegmental area (VTA) of the mouse brain from initial recall to post-extinction renewal of a memory involving cocaine experience. We uncover a higher-order pattern of short-lived beta-frequency (15-25 Hz) activities that are transiently coordinated across these networks during memory retrieval. The output of a divergent pathway from upstream VTA glutamatergic neurons, paced by a slower (4-Hz) oscillation, actuates this multi-network beta-band coactivation; its closed-loop phase-informed suppression prevents renewal of cocaine-biased behavior. Binding brain-distributed neural activities in this temporally structured manner may constitute an organizational principle of robust memory expression.

TCR activation directly stimulates PYGB-dependent glycogenolysis to fuel the early recall response in CD8+ memory T cells.

Glycolysis facilitates the rapid recall response of CD8+ memory T (Tm) cells. However, it remains unclear whether Tm cells uptake exogenous glucose or mobilize endogenous sugar to fuel glycolysis. Here, we show that intracellular glycogen rather than extracellular glucose acts as the major carbon source for the early recall response. Following antigenic stimulation, Tm cells exhibit high glycogen phosphorylase (brain form, PYGB) activity, leading to glycogenolysis and release of glucose-6-phosphate (G6P). Elevated G6P mainly flows to glycolysis but is also partially channeled to the pentose phosphate pathway, which maintains the antioxidant capacity necessary for later recall stages. Mechanistically, TCR signaling directly induces phosphorylation of PYGB by LCK-ZAP70. Functionally, the glycogenolysis-fueled early recall response of CD8+ Tm cells accelerates the clearance of OVA-Listeria monocytogenes in an infected mouse model. Thus, we uncover a specific dependency on glycogen for the initial activation of memory T cells, which may have therapeutic implications for adaptive immunity.

T Cells in Nonlymphoid Tissues Give Rise to Lymph-Node-Resident Memory T Cells.

Immunosurveillance of secondary lymphoid organs (SLO) is performed by central memory T cells that recirculate through blood. Resident memory T (Trm) cells remain parked in nonlymphoid tissues and often stably express CD69. We recently identified Trm cells within SLO, but the origin and phenotype of these cells remains unclear. Using parabiosis of "dirty" mice, we found that CD69 expression is insufficient to infer stable residence of SLO Trm cells. Restimulation of nonlymphoid memory CD8+ T cells within the skin or mucosa resulted in a substantial increase in bona fide Trm cells specifically within draining lymph nodes. SLO Trm cells derived from emigrants from nonlymphoid tissues and shared some transcriptional and phenotypic signatures associated with nonlymphoid Trm cells. These data indicate that nonlymphoid cells can give rise to SLO Trm cells and suggest vaccination strategies by which memory CD8+ T cell immunosurveillance can be regionalized to specific lymph nodes.

Hippocampal activity predicts contextual misattribution of false memories.

Failure of contextual retrieval can lead to false recall, wherein people retrieve an item or experience that occurred in a different context or did not occur at all. Whereas the hippocampus is thought to play a crucial role in memory retrieval, we lack understanding of how the hippocampus supports retrieval of items related to a target context while disregarding related but irrelevant information. Using direct electrical recordings from the human hippocampus, we investigate the neural process underlying contextual misattribution of false memories. In two large datasets, we characterize key physiological differences between correct and false recalls that emerge immediately prior to vocalization. By differentiating between false recalls that share high or low contextual similarity with the target context, we show that low-frequency activity (6 to 18 Hz) in the hippocampus tracks similarity between the current and retrieved context. Applying multivariate decoding methods, we were able to reliably predict the contextual source of the to-be-recalled item. Our findings elucidate one of the hallmark features of episodic memory: our ability to distinguish between memories that were formed on different occasions.

Antigen exposure reshapes chromatin architecture in central memory CD8+ T cells and imprints enhanced recall capacity.

CD62L+ central memory CD8+ T (TCM) cells provide enhanced protection than naive cells; however, the underlying mechanism, especially the contribution of higher-order genomic organization, remains unclear. Systematic Hi-C analyses reveal that antigen-experienced CD8+ T cells undergo extensive rewiring of chromatin interactions (ChrInt), with TCM cells harboring specific interaction hubs compared with naive CD8+ T cells, as observed at cytotoxic effector genes such as Ifng and Tbx21. TCM cells also acquire de novo CTCF (CCCTC-binding factor) binding sites, which are not only strongly associated with TCM-specific hubs but also linked to increased activities of local gene promoters and enhancers. Specific ablation of CTCF in TCM cells impairs rapid induction of genes in cytotoxic program, energy supplies, transcription, and translation by recall stimulation. Therefore, acquisition of CTCF binding and ChrInt hubs by TCM cells serves as a chromatin architectural basis for their transcriptomic dynamics in primary response and for imprinting the code of "recall readiness" against secondary challenge.

ClusTrast: a short read de novo transcript isoform assembler guided by clustered contigs.

BACKGROUND: Transcriptome assembly from RNA-sequencing data in species without a reliable reference genome has to be performed de novo, but studies have shown that de novo methods often have inadequate ability to reconstruct transcript isoforms. We address this issue by constructing an assembly pipeline whose main purpose is to produce a comprehensive set of transcript isoforms. RESULTS: We present the de novo transcript isoform assembler ClusTrast, which takes short read RNA-seq data as input, assembles a primary assembly, clusters a set of guiding contigs, aligns the short reads to the guiding contigs, assembles each clustered set of short reads individually, and merges the primary and clusterwise assemblies into the final assembly. We tested ClusTrast on real datasets from six eukaryotic species, and showed that ClusTrast reconstructed more expressed known isoforms than any of the other tested de novo assemblers, at a moderate reduction in precision. For recall, ClusTrast was on top in the lower end of expression levels (<15% percentile) for all tested datasets, and over the entire range for almost all datasets. Reference transcripts were often (35-69% for the six datasets) reconstructed to at least 95% of their length by ClusTrast, and more than half of reference transcripts (58-81%) were reconstructed with contigs that exhibited polymorphism, measuring on a subset of reliably predicted contigs. ClusTrast recall increased when using a union of assembled transcripts from more than one assembly tool as primary assembly. CONCLUSION: We suggest that ClusTrast can be a useful tool for studying isoforms in species without a reliable reference genome, in particular when the goal is to produce a comprehensive transcriptome set with polymorphic variants.

Agreement of medical record abstraction and self-report of breast cancer treatment with an extended recall window.

BACKGROUND: Medical record abstraction (MRA) and self-report questionnaires are two methods frequently used to ascertain cancer treatment information. Prior studies have shown excellent agreement between MRA and self-report, but it is unknown how a recall window longer than 3 years may affect this agreement. METHODS: The Women's Environmental Cancer and Radiation Epidemiology (WECARE) Study is a multicenter, population-based case-control study of controls with unilateral breast cancer individually matched to cases with contralateral breast cancer. Participants who were diagnosed with a first primary breast cancer from 1985 to 2008 before the age of 55 years completed a questionnaire that included questions on treatment. First primary breast cancer treatment information was abstracted from the medical record from radiation oncology clinic notes for radiation treatment and from systemic adjuvant treatment reports for hormone therapy and chemotherapy. Agreement between MRA and self-reported treatment was assessed with the kappa statistic and corresponding 95% confidence intervals (CIs). RESULTS: A total of 2808 participants with MRA and self-reported chemotherapy treatment information, 2733 participants with MRA and self-reported hormone therapy information, and 2905 participants with MRA and self-reported radiation treatment information were identified. The median recall window was 12.5 years (range, 2.8-22.2 years). MRA and self-reported treatment agreement was excellent across treatment modalities (kappachemo, 98.5; 95% CI, 97.9-99.2; kappahorm, 87.7; 95% CI, 85.9-89.5; kapparad, 97.9; 95% CI, 97.0-98.7). There was no heterogeneity across recall windows (pchemo = .46; phorm = .40; prad = .61). CONCLUSIONS: Agreement between self-reported and MRA primary breast cancer treatment modality information was excellent for young women diagnosed with breast cancer and was maintained even among women whose recall window was more than 20 years after diagnosis.

Genetic risk accentuates dietary effects on hepatic steatosis, inflammation and fibrosis in a population-based cohort.

BACKGROUND & AIMS: Steatotic liver disease (SLD), characterized by elevated liver fat content (LFC), is influenced by genetics and diet. However, whether diet has a differential effect based on genetic risk is not well-characterized. We aimed to determine how genetic factors interact with diet to affect SLD in a large national biobank. METHODS: We included UK Biobank participants with dietary intake measured by 24-hour recall and genotyping. The primary predictors were dietary pattern, PNPLA3-rs738409-G, TM6SF2-rs58542926-T, a 16-variant hepatic steatosis polygenic risk score (PRS), and gene-environment interactions. The primary outcome was LFC, and secondary outcomes were iron-controlled T1 time (cT1, a measure of liver inflammation and fibrosis) and liver-related events/mortality. RESULTS: A total of 21,619 participants met inclusion criteria. In non-interaction models, Mediterranean diet and intake of fruit/vegetables/legumes and fish associated with lower LFC, while higher red/processed meat intake and all genetic predictors associated with higher LFC. In interaction models, all genetic predictors interacted with Mediterranean diet and fruit/vegetable/legume intake, while the steatosis PRS interacted with fish intake and the TM6SF2 genotype interacted with red/processed meat intake, to affect LFC. Dietary effects on LFC were up to 3.8-fold higher in PNPLA3-rs738409-GG vs. -CC individuals, and 1.4-3.0-fold higher in the top vs. bottom quartile of the steatosis PRS. Gene-diet interactions were stronger in participants with vs. without overweight. The steatosis PRS interacted with Mediterranean diet and fruit/vegetable/legume intake to affect cT1 and most dietary and genetic predictors associated with risk of liver-related events or mortality by age 70. CONCLUSIONS: Effects of diet on LFC and cT1 were markedly accentuated in patients at increased genetic risk for SLD, implying dietary interventions may be more impactful in these populations. IMPACT AND IMPLICATIONS: Genetic variants and diet both influence risk of hepatic steatosis, inflammation/fibrosis, and hepatic decompensation; however, how gene-diet interactions influence these outcomes has previously not been comprehensively characterized. We investigated this topic in the community-based UK Biobank and found that genetic risk and dietary quality interacted to influence hepatic steatosis and inflammation/fibrosis on liver MRI, so that the effects of diet were greater in people at elevated genetic risk. These results are relevant for patients and medical providers because they show that genetic risk is not fixed (i.e. modifiable factors can mitigate or exacerbate this risk) and realistic dietary changes may result in meaningful improvement in liver steatosis and inflammation/fibrosis. As genotyping becomes more routinely used in clinical practice, patients identified to be at high baseline genetic risk may benefit even more from intensive dietary counseling than those at lower risk, though future prospective studies are required.

Evaluation of measurement errors in the Patient-Oriented Eczema Measure (POEM) outcome.

BACKGROUND: The Patient-Oriented Eczema Measure (POEM) is the recommended core outcome instrument for atopic dermatitis (AD) symptoms. POEM is reported by recalling the presence/absence of seven symptoms in the last 7 days. OBJECTIVE: To evaluate measurement errors in POEM recordings due to imperfect recall. METHODS: Using data from a clinical trial of 247 AD patients aged 12-65 years, we analysed the reported POEM score (r-POEM) and the POEM derived from the corresponding daily scores for the same seven symptoms without weekly recall (d-POEM). We quantified recall error by comparing the r-POEM and d-POEM for 777 patient-weeks collected from 207 patients, and estimated two components of recall error: (1) recall bias due to systematic errors in measurements and (2) recall noise due to random errors in measurements, using a bespoke statistical model. RESULTS: POEM scores have a relatively low recall bias, but a high recall noise. Recall bias was estimated at 1.2 points lower for the r-POEM on average than the d-POEM, with a recall noise of 5.7 points. For example, a patient with a recall-free POEM of 11 (moderate) could report their POEM score anywhere from 5 to 14 (with 95% probability) because of recall error. Model estimates suggested that patients tend to recall itch and dryness more often than experienced (positive bias of less than 1 day), but less often for the other symptoms (bleeding, cracking, flaking, oozing/weeping and sleep disturbance; negative bias ranging 1-4 days). CONCLUSIONS: In this clinical trial data set, we found that patients tended to slightly underestimate their symptoms when reporting POEM, with significant variation in how well they were able to recall the frequency of their symptoms every time they reported POEM. A large recall noise should be taken into consideration when interpreting POEM scores.

Impaired free recall of neutral but not negative material tested 105 min after cortisol administration.

Pharmacological studies have consistently shown memory retrieval impairment after administration of cortisol, particularly pronounced for emotional laboratory material (i.e. list of emotional words). However, it is unclear how pharmacological elevation of cortisol affects memory retrieval of ecologically-relevant emotional material (i.e. similar to a newspaper article about an emotional event). In the present study, we aimed to explore whether cortisol administration affects the recall of ecologically-relevant emotional and neutral material, and when memory retrieval occurs after a longer delay (105 min). In this double-blind, pseudo-randomized, placebo-control study, 79 participants learned a negative text and a neutral text. Twenty-four hours later, they were administrated either 10 mg of hydrocortisone or placebo. After 105 min, participants engaged in free recall of both texts. The group with cortisol administration showed significantly reduced free recall compared to the placebo group. Interestingly, this memory retrieval impairment was driven by significantly lower recall after cortisol vs. placebo administration for neutral texts, but not negative texts. The current finding suggests that cortisol administration impairs neutral ecologically-relevant material while leaving emotional material unaffected. These divergent findings, compared to existing literature, emphasize the necessity of employing more ecologically validated material to gain a more comprehensive understanding of the intricate interplay between cortisol administration and memory for ecological material.

Improving Memory Search Through Model-Based Cue Selection.

We often use cues from our environment when we get stuck searching our memories, but prior research has failed to show benefits of cuing with other, randomly selected list items during memory search. What accounts for this discrepancy? We proposed that cues' content critically determines their effectiveness and sought to select the right cues by building a computational model of how cues affect memory search. Participants (N = 195 young adults from the United States) recalled significantly more items when receiving our model's best (vs. worst) cue. Our model provides an account of why some cues better aid recall: Effective cues activate contexts most similar to the remaining items' contexts, facilitating recall in an unsearched area of memory. We discuss our contributions in relation to prominent theories about the effect of external cues.

Inhibition of Estradiol Signaling in the Basolateral Amygdala Impairs Extinction Memory Recall for Heroin-Conditioned Cues in a Sex-Specific Manner.

INTRODUCTION: Relapse is a major treatment barrier for opioid use disorder. Environmental cues become associated with the rewarding effects of opioids and can precipitate relapse, even after numerous unreinforced cue presentations, due to deficits in extinction memory recall (EMR). Estradiol (E2) modulates EMR of fear-related cues, but it is unknown whether E2 impacts EMR of reward cues and what brain region(s) are responsible for E2s effects. Here, we hypothesize that inhibition of E2 signaling in the basolateral amygdala (BLA) will impair EMR of a heroin-associated cue in both male and female rats. METHODS: We pharmacologically manipulated E2 signaling to characterize the role of E2 in the BLA on heroin-cue EMR. Following heroin self-administration, during which a light/tone cue was co-presented with each heroin infusion, rats underwent cued extinction to extinguish the conditioned association between the light/tone and heroin. During extinction, E2 signaling in the BLA was blocked by an aromatase inhibitor or specific estrogen receptor (ER) antagonists. The next day, subjects underwent a cued test to assess heroin-cue EMR. RESULTS: In both experiments, females took more heroin than males (mg/kg) and had higher operant responding during cued extinction. Inhibition of E2 synthesis in the BLA impaired heroin-cue EMR in both sexes. Notably, E2s actions are mediated by different ER mechanisms, ERα in males but ERß in females. CONCLUSIONS: This study is the first to demonstrate a behavioral role for centrally-produced E2 in the BLA and that E2 also impacts EMR of reward-associated stimuli in both sexes.

Differential recall bias in estimating treatment effects in observational studies.

Observational studies are frequently used to estimate the effect of an exposure or treatment on an outcome. To obtain an unbiased estimate of the treatment effect, it is crucial to measure the exposure accurately. A common type of exposure misclassification is recall bias, which occurs in retrospective cohort studies when study subjects may inaccurately recall their past exposure. Particularly challenging is differential recall bias in the context of self-reported binary exposures, where the bias may be directional rather than random and its extent varies according to the outcomes experienced. This paper makes several contributions: (1) it establishes bounds for the average treatment effect even when a validation study is not available; (2) it proposes multiple estimation methods across various strategies predicated on different assumptions; and (3) it suggests a sensitivity analysis technique to assess the robustness of the causal conclusion, incorporating insights from prior research. The effectiveness of these methods is demonstrated through simulation studies that explore various model misspecification scenarios. These approaches are then applied to investigate the effect of childhood physical abuse on mental health in adulthood.

Association analysis of self-reported outcomes with a validated subset.

In health-science research, outcomes ascertained through surveys and interviews are subject to potential bias with respect to the true outcome status, which is only ascertainable with clinical and laboratory assessment. This measurement error may lead to biased inference when evaluating associations between exposures and outcomes of interest. Here, we consider a cohort study in which the outcome of interest is ascertained via questionnaire, subject to imperfect ascertainment, but where a subset of participants also have a clinically assessed, validated outcome available. This presents a methodological opportunity to address potential bias. Specifically, we constructed the likelihood in two parts, one using the validated subset and the other using a subset without validation. This work expands on that proposed by Pepe and enables inference with standard statistical software. Weighted generalized linear model estimates for our method and maximum likelihood estimates (MLE) for Pepe's method were computed, and the statistical inference was based on the standard large-sample likelihood theory. We compare the finite sample performance of two approaches through Monte Carlo simulations. This methodological work was motivated by a large cohort study of long-term childhood cancer survivors, allowing us to provide a relevant application example where we examined the association between clinical factors and chronic health conditions.

Impedance cardiogram based exploration of cardiac mechanisms in post-traumatic stress disorder during trauma recall.

Post-traumatic stress disorder (PTSD) is an independent risk factor for developing heart failure; however, the underlying cardiac mechanisms are still elusive. This study aims to evaluate the real-time effects of experimentally induced PTSD symptom activation on various cardiac contractility and autonomic measures. We recorded synchronized electrocardiogram and impedance cardiogram from 137 male veterans (17 PTSD, 120 non-PTSD; 48 twin pairs, 41 unpaired singles) during a laboratory-based traumatic reminder stressor. To identify the parameters describing the cardiac mechanisms by which trauma reminders can create stress on the heart, we utilized a feature selection mechanism along with a random forest classifier distinguishing PTSD and non-PTSD. We extracted 99 parameters, including 76 biosignal-based and 23 sociodemographic, medical history, and psychiatric diagnosis features. A subject/twin-wise stratified nested cross-validation procedure was used for parameter tuning and model assessment to identify the important parameters. The identified parameters included biomarkers such as pre-ejection period, acceleration index, velocity index, Heather index, and several physiology-agnostic features. These identified parameters during trauma recall suggested a combination of increased sympathetic nervous system (SNS) activity and deteriorated cardiac contractility that may increase the heart failure risk for PTSD. This indicates that the PTSD symptom activation associates with real-time reductions in several cardiac contractility measures despite SNS activation. This finding may be useful in future cardiac prevention efforts.

Evaluating Recall Periods for Patient-Reported Outcome Measures: A Systematic Review of Quantitative Methods.

OBJECTIVES: The current guidance for selection of recall periods recommends considering the design of the study, nature of the condition, patient's burden and ability to recall, and intent of the outcome measure. Empirical study of the accuracy of recall periods is recommended; however, there is not consensus on how to quantitatively evaluate the consistency of results from patient-reported outcome measures (PROMs) with different recall periods. We conducted a systematic review to describe quantitative methods for evaluating results obtained from PROMs with differing recall periods to lay the groundwork for establishing consensus. METHODS: We searched MEDLINE, Embase, Scopus, and American Psychological Association PsycINFO for studies where participants are given the same health-related measure (eg, quality of life, well-being, functioning, and pain) with differing recall periods. RESULTS: A total of 7174 abstracts were screened. The 30 included studies reflected a wide range of domains, including pain, fatigue, and sexual behavior and function. The recall periods ranged from momentary to 6 months. The analytic approaches varied, including different methods for assessing relative agreement, absolute agreement, and for assessing combined relative and absolute agreement. CONCLUSIONS: We found variability in how PROM recall periods were evaluated, suggesting an opportunity for greater consensus on methodological approach. As a starting point, we provide recommendations for which methods are preferred for which contexts.

Achieving high diet quality at eating occasions: findings from a nationally representative study of Australian adults.

This study examined differences in food groups consumed at eating occasions by the level of adherence to dietary guidelines in Australian adults (≤19 years) and whether consumption differed with respect to age, sex and education levels. Secondary analysis of the 2011-2012 National Nutrition and Physical Activity Survey (n 9054) was performed, using one 24-h dietary recall with self-reported eating occasions. Dietary Guideline Index scores were used to assess adherence to the 2013 Australian Dietary Guidelines. Mean differences (95 % CI) in servings of the five food groups and discretionary foods at eating occasions were estimated for adults with higher and lower diet quality, stratified by sex, age group and education. Using survey-based t-tests, differences of at least half a serving with P values < 0·05 were considered meaningful. Compared with adults with lower diet quality, women and men aged 19-50 years with higher diet quality consumed more serves of vegetables at dinner (mean difference (95 % CI), women; 1·0; 95 % CI (0·7, 1·2); men: 0·9; 95 % CI (0·6, 1·3)) and fewer serves of discretionary foods at snacks (women: -0·7; 95 % CI (-0·9, -0·5); men: -1·0; 95 % CI (-1·4, -0·7). Other food groups, such as grains, dairy products and alternatives, meats and alternatives, were not significantly different between adults with lower and higher diet quality, across any eating occasions and age groups. Discretionary food intake at lunch, dinner and snacks was consistently greater among adults with lower diet quality, regardless of education level. Our findings identify dinner and snacks as opportunities to increase vegetable intake and reduce discretionary food intake, respectively.

Two biases in incubation time estimation related to exposure.

BACKGROUND: Estimation of the SARS-CoV-2 incubation time distribution is hampered by incomplete data about infection. We discuss two biases that may result from incorrect handling of such data. Notified cases may recall recent exposures more precisely (differential recall). This creates bias if the analysis is restricted to observations with well-defined exposures, as longer incubation times are more likely to be excluded. Another bias occurred in the initial estimates based on data concerning travellers from Wuhan. Only individuals who developed symptoms after their departure were included, leading to under-representation of cases with shorter incubation times (left truncation). This issue was not addressed in the analyses performed in the literature. METHODS: We performed simulations and provide a literature review to investigate the amount of bias in estimated percentiles of the SARS-CoV-2 incubation time distribution. RESULTS: Depending on the rate of differential recall, restricting the analysis to a subset of narrow exposure windows resulted in underestimation in the median and even more in the 95th percentile. Failing to account for left truncation led to an overestimation of multiple days in both the median and the 95th percentile. CONCLUSION: We examined two overlooked sources of bias concerning exposure information that the researcher engaged in incubation time estimation needs to be aware of.

Improving regional medical laboratory center report quality through a report recall management system.

OBJECTIVES: Currently, most medical laboratories do not have a dedicated software for managing report recalls, and relying on traditional manual methods or laboratory information system (LIS) to record recall data is no longer sufficient to meet the quality management requirements in the large regional laboratory center. The purpose of this article was to describe the research process and preliminary evaluation results of integrating the Medical Laboratory Electronic Record System (electronic record system) laboratory report recall function into the iLab intelligent management system for quality indicators (iLab system), and to introduce the workflow and methods of laboratory report recall management in our laboratory. METHODS: This study employed cluster analysis to extract commonly used recall reasons from laboratory report recall records in the electronic record system. The identified recall reasons were validated for their applicability through a survey questionnaire and then incorporated into the LIS for selecting recall reasons during report recall. The statistical functionality of the iLab system was utilized to investigate the proportion of reports using the selected recall reasons among the total number of reports, and to perform visual analysis of the recall data. Additionally, we employed P-Chart to establish quality targets and developed a "continuous improvement process" electronic flow form. RESULTS: The reasons for the recall of laboratory reports recorded in the electronic recording system were analyzed. After considering the opinions of medical laboratory personnel, a total of 12 recall reasons were identified, covering 73.05 % (1854/2538) of the recalled laboratory reports. After removing data of mass spectra lab with significant anomalies, the coverage rate increased to 82.66 % (1849/2237). The iLab system can generate six types of statistical graphs based on user needs, including statistical time, specialty labs (or divisions), test items, reviewers, reasons for report recalls, and distribution of the recall frequency of 0-24 h reports. The control upper limit of the recall rate of P-Chart based on laboratory reports can provide quality targets suitable for each professional group at the current stage. Setting the five stages of continuous process improvement reasonably and rigorously can effectively achieve the goal of quality enhancement. CONCLUSIONS: The enhanced iLab system enhances the intelligence and sustainable improvement capability of the recall management of laboratory reports, thus improving the efficiency of the recall management process and reducing the workload of laboratory personnel.

Effects of the valsartan recall on heart failure patients: A nationwide analysis.

BACKGROUND: Valsartan is commonly used for cardiac conditions. In 2018, the Food and Drug Administration recalled generic valsartan due to the detection of impurities. Our objective was to determine if heart failure patients receiving valsartan at the recall date had a greater likelihood of unfavorable outcomes than patients using comparable antihypertensives. METHODS: We conducted a cohort study of Optum's de-identified Clinformatics® Datamart (July 2017-January 2019). Heart failure patients with commercial or Medicare Advantage insurance who received valsartan were compared to persons who received non-recalled angiotensin receptor blockers (ARBs) and angiotensin converting enzyme-inhibitors (ACE-Is) for 1 year prior and including the recall date. Outcomes included a composite for all-cause hospitalization, emergency department (ED), and urgent care (UC) use and a measure of cardiac events which included hospitalizations for acute myocardial infarction and hospitalizations/ED/UC visits for stroke/transient ischemic attack, heart failure or hypertension at 6-months post-recall. Cox proportional hazard models with propensity score weighting compared the risk of outcomes between groups. RESULTS: Of the 87 130 adherent patients, 15% were valsartan users and 85% were users of non-recalled ARBs/ACE-Is. Valsartan use was not associated with an increased risk of all-cause hospitalization/ED/UC use six-months post-recall (HR 1.00; 95% CI 0.96-1.03), compared with individuals taking non-recalled ARBs/ACE-Is. Similarly, cardiac events 6-months post-recall did not differ between individuals on valsartan and non-recalled ARBs/ACE-Is (HR 1.04; 95% CI 0.97-1.12). CONCLUSIONS: The valsartan recall did not affect short-term outcomes of heart failure patients. However, the recall potentially disrupted the medication regimens of patients, possibly straining the healthcare system.