bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nationwide analysis of incidence and predictors of 30-day readmissions in patients with decompensated cirrhosis
Authors: Gajendran Mahesh , Umapathy Chandraprakash , Perisetti Abhilash , Loganathan Priyadarshini , Dwivedi Alok , Alvarado Luis A , Zuckerman Marc J , Goyal Hemant , Elhanafi Sherif 
Published: July 2021

Background and objectiveCirrhosis is the number one cause of non-cancer deaths among gastrointestinal diseases and is responsible for significant morbidity and healthcare utilisation. The objectives were to measure the 30-day readmissions rate following index hospitalisation, to determine the predictors of readmission, and to estimate the cost of 30-day readmission in patients with decompensated cirrhosis.MethodsWe performed a retrospective cohort study of patients with decompensated cirrhosis using 2014 Nationwide Readmission Database from January to November. Decompensated cirrhosis was identified based on the presence of at least one of the following: ascites, hepatic encephalopathy, variceal bleeding, spontaneous bacterial peritonitis and hepatorenal syndrome. We excluded patients less than 18 years of age, pregnant patients, patients with missing length of stay data, and those who died during the index admission.ResultsAmong 57 305 unique patients with decompensated cirrhosis, the 30-day readmission rate was 23.2%. The top three predictors of 30-day readmission were leaving against medical advice (AMA), ascites and acute kidney injury, which increased the risk of readmission by 47%, 22% and 20%, respectively. Index admission for variceal bleeding was associated with a lower 30-day readmission rate by 18%. The estimated total cost associated with 30-day readmission in our study population was US$234.4 million.ConclusionIn a nationwide population study, decompensated cirrhosis is associated with a 30-day readmission rate of 23%. Leaving AMA, ascites and acute kidney injury are positively associated with readmission. Targeted interventions and quality improvement efforts should be directed toward these potential risk factors to reduce readmissions.
‘You withhold what you are feeling so you can have a family’: Latinas’ perceptions on community values and postpartum depression
Authors: Sampson McClain , Yu Miao , Mauldin Rebecca , Mayorga Angelina , Gonzalez Lorena G 
Published: July 2021

ObjectiveThe purpose of this study was to explore the postpartum depression (PPD) beliefs and experiences of mothers who access local community faith-based organisations providing family services to low-income, predominantly immigrant Latino populations.DesignUsing a qualitative research design, we conducted 18 focus groups with Latina mothers to inquire about their community values and beliefs of PPD. All groups were conducted in Spanish.SettingAn academic research team located in Houston, Texas, USA, partnered with six faith-based organisations in five cities to recruit and host focus groups at the site of the organisation.ParticipantsOne hundred and thirty-three women participated in the focus groups across all sites. Thirty-seven of them (27.8%) had given birth to a child in less than 1 year. Inclusion criteria included mothers 18 years and older and Latino ethnicity.ResultsA six-step process was used to apply thematic analysis to sort data into the themes. All mothers had heard of depression after childbirth, some had experienced it and most remarked that the personal experience and community acceptance of it vary by family. The main findings suggest that mothers take pride in parenting by instilling values to support family and the value of relying on family for emotional support. Findings reveal that many mothers suffer and sacrifice for their children, they feel judged and feel they must hide their emotions. Factors such as birth and postpartum customs from a native country, gender roles and beliefs of what a good mother shape their beliefs and messages about PPD.ConclusionOur findings indicate that programme developers should consider family and community focused education and intervention efforts to help decrease stigma and increase understanding of PPD.
Long-term open-label continuation study of the safety and efficacy of belimumab for up to 7 years in patients with systemic lupus erythematosus from Japan and South Korea
Authors: Tanaka Yoshiya , Bae Sang-Cheol , Bass Damon , Curtis Paula , Chu Myron , DeRose Kathleen , Ji Beulah , Kurrasch Regina , Lowe Jenny , Meizlik Paige , Roth David A 
Published: July 2021

ObjectivesTo evaluate the long-term safety and efficacy of belimumab in patients with systemic lupus erythematosus (SLE) from Japan and South Korea.MethodsIn this phase III, open-label continuation study (BEL114333;NCT01597622), eligible completers of BEL113750 (NCT01345253) or BEL112341 (NCT01484496) received intravenous belimumab 10 mg/kg every 28 days for ≤7 years. Primary endpoint was safety. Secondary endpoints: SLE Responder Index (SRI)4 response rate, proportion of patients meeting individual SRI4 criteria, SLE flares and prednisone use. Analyses were based on observed data from the first belimumab exposure (either in parent or current study) through to study end.ResultsOf 142 enrolled patients who received belimumab, 73.2% completed the study. The study population comprised patients with moderate SLE, mean (SD) Safety of Estrogens in Lupus Erythematosus National Assessment-SLE Disease Activity Index (SELENA-SLEDAI) baseline score of 9.3 (3.9) and 98.6% receiving corticosteroids. Most patients (97.9%) experienced adverse events (AEs); 33.8% experienced serious AEs. Increase in SRI4 (Year 1, Week 24: 47.8%; Year 6, Week 48: 68.2%) and SELENA-SLEDAI responders suggested reductions in disease activity. Proportions of patients with no worsening in Physician Global Assessment/no new organ damage remained stable throughout. Severe SLE flares occurred in 14.8% of patients. Among patients with baseline prednisone-equivalent dose >7.5 mg/day (n=81), the median (min, max) number of days anytime post-baseline that the daily dose was ≤7.5 mg/day or had been reduced by 50% from baseline was 584 (0, 2267).ConclusionsFavourable safety profile and treatment responses were maintained for ≤7 years in patients with SLE from Japan and South Korea.
Hydroxychloroquine in patients with inflammatory and erosive osteoarthritis of the hands: results of the OA-TREAT study—a randomised, double-blind, placebo-controlled, multicentre, investigator-initiated trial
Authors: Kedor Claudia , Detert Jacqueline , Rau Rolf , Wassenberg Siegfried , Listing Joachim , Klaus Pascal , Braun Tanja , Hermann Walter , Weiner Stefan Markus , Buttgereit Frank , Burmester Gerd R 
Published: July 2021

ObjectivesHand osteoarthritis (OA) is a condition characterised by cartilage degradation and frequently erosive changes. Analgesics and non-steroidal anti-inflammatory drugs are used for symptomatic relief but are often poorly tolerated or contraindicated. Previous publications suggest hydroxychloroquine (HCQ) as a possible treatment for hand OA. The OA-TREAT study aimed to investigate the efficacy and safety of HCQ in patients with inflammatory and erosive hand OA (EOA).MethodsOA-TREAT was an investigator-initiated, multicentre, randomised, double-blind, placebo (PBO)-controlled trial. Patients with inflammatory and EOA, according to the ACR criteria, with radiographically erosive disease were randomised 1:1 to HCQ 200–400 mg/day or PBO for 52 weeks (W52). Both groups received stable standard therapy. The primary endpoint was Australian Canadian Hand Osteoarthritis Index (AUSCAN) for pain and hand disability at W52.Results75 patients were randomised to HCQ and 78 to PBO. At W52, mean AUSCAN pain was 26.7 in HCQ and 26.5 in PBO patients (p=0.92). Hand disability measured by AUSCAN function (mean) was 48.1 in HCQ and 51.3 in PBO patients (p=0.36). Changes in radiographic scores did not differ significantly (p>0.05) between treatment groups. There were 7 serious adverse events in the HCQ and 15 in the PBO group.ConclusionsOA-TREAT is the first large randomised PBO controlled trial focusing on EOA. HCQ was no more effective than PBO for changes in pain, function and radiographic scores in the 52-week period. Overall safety findings were consistent with the known profile of HCQ.
Frame covariant formalism for fermionic theories
Authors: Finn Kieran , Karamitsos Sotirios , Pilaftsis Apostolos 
Published: July 2021

AbstractWe present a frame- and reparametrisation-invariant formalism for quantum field theories that include fermionic degrees of freedom. We achieve this using methods of field-space covariance and the Vilkovisky–DeWitt (VDW) effective action. We explicitly construct a field-space supermanifold on which the quantum fields act as coordinates. We show how to define field-space tensors on this supermanifold from the classical action that are covariant under field reparametrisations. We then employ these tensors to equip the field-space supermanifold with a metric, thus solving a long-standing problem concerning the proper definition of a metric for fermionic theories. With the metric thus defined, we use well-established field-space techniques to extend the VDW effective action and express any fermionic theory in a frame- and field-reparametrisation-invariant manner.
Exact $$\beta $$-functions for $$\mathcal{N}=1$$ supersymmetric theories finite in the lowest loops
Authors: Stepanyantz K. V. 
Published: July 2021

AbstractWe consider a one-loop finite $$\mathcal{N}=1$$

N
=
1

supersymmetric theory in such a renormalization scheme that the first L contributions to the gauge $$\beta $$
β
-function and the first $$(L-1)$$

(
L
-
1
)

contributions to the anomalous dimension of the matter superfields and to the Yukawa $$\beta $$
β
-function vanish. It is demonstrated that in this case the NSVZ equation and the exact equation for the Yukawa $$\beta $$
β
-function in the first nontrivial order are valid for an arbitrary renormalization prescription respecting the above assumption. This implies that under this assumption the $$(L+1)$$

(
L
+
1
)

-loop contribution to the gauge $$\beta $$
β
-function and the L-loop contribution to the Yukawa $$\beta $$
β
-function are always expressed in terms of the L-loop contribution to the anomalous dimension of the matter superfields. This statement generalizes the result of Grisaru, Milewski, and Zanon that for a theory finite in L loops the $$(L+1)$$

(
L
+
1
)

-loop contribution to the $$\beta $$
β
-function also vanishes. In particular, it gives a simple explanation why their result is valid although the NSVZ equation does not hold in an arbitrary subtraction scheme.
Notes on Solutions for Some Systems of Complex Functional Equations in

ℂ

2
Authors: Li Hong , Xu Hong Yan 
Published: July 2021

The purpose of this article is to give the details of finding the transcendental entire solutions with finite order for the systems of nonlinear partial differential-difference equations

∂

f

1

z

1

,

z

2

/
∂

z

1

+

∂

f

1

z

1

,

z

2

/
∂

z

2

n

1

+

P

1

z

f

2

z

1

+

c

1

,

z

2

+

c

2

m

1

=

Q

1

z

,

∂

f

1

z

1

,

z

2

/
∂

z

1

+

∂

f

1

z

1

,

z

2

/
∂

z

2

n

2

+

P

2

z

f

1

z

1

+

c

1

,

z

2

+

c

2

m

2

=

Q

2

z

,

where

P

1

z

,

P

2

z

,

Q

1

z

,
and

Q

2

z

are polynomials in

ℂ

2

;

n

1

,

n

2

,

m

1

,
and

m

2

are positive integers, and

c
=

c

1

,

c

2

∈

ℂ

2

. We obtain that there exist some pairs of the transcendental entire solutions of finite order for the above system, which is a very powerful supplement to the previous theorems given by Xu and Cao and Xu and Yang.
A Method for Overcoming Plasma Protein Inhibition of Tyrosine Kinase Inhibitors
Authors: Young David J. , Nguyen Bao , Li Li , Higashimoto Tomoyasu , Levis Mark J. , Liu Jun O. , Small Donald 
Published: July 2021

AbstractFMS-like tyrosine kinase 3 (FLT3) is the most frequently mutated gene in acute myeloid leukemia and a target for tyrosine kinase inhibitors (TKI). FLT3 TKIs have yielded limited improvements to clinical outcomes. One reason for this is TKI inhibition by endogenous factors. We characterized plasma protein binding of FLT3 TKI, specifically staurosporine derivatives (STS-TKI) by alpha-1-acid glycoprotein (AGP), simulating its effects upon drug efficacy. Human AGP inhibits the antiproliferative activity of STS-TKI in FLT3/ITD-dependent cells, with IC50 shifts higher than clinically achievable. This is not seen with nonhuman plasma. Mifepristone cotreatment, with its higher AGP affinity, improves TKI activity despite AGP, yielding IC50s predicted to be clinically effective. In a mouse model of AGP drug inhibition, mifepristone restores midostaurin activity. This suggests combinatorial methods for overcoming plasma protein inhibition of existing TKIs for leukemia as well as providing a platform for investigating the drug–protein interaction space for developing more potent small-molecule agents.Significance:Our data provide a mechanism for the failure of some previous TKI clinical trials. The ability of mifepristone to disinhibit TKIs suggests an approach by which the combination of TKIs with already approved and well-tolerated drugs may restore TKI activity.This article is highlighted in the In This Issue feature, p. 403
Mutation Signatures of Pediatric Acute Myeloid Leukemia and Normal Blood Progenitors Associated with Differential Patient Outcomes
Authors: Brandsma Arianne M. , Bertrums Eline J.M. , van Roosmalen Markus J. , Hofman Damon A. , Oka Rurika , Verheul Mark , Manders Freek , Ubels Joske , Belderbos Mirjam E. , van Boxtel Ruben 
Published: July 2021

Abstract

Acquisition of oncogenic mutations with age is believed to be rate limiting for carcinogenesis. However, the incidence of leukemia in children is higher than in young adults. Here we compare somatic mutations across pediatric acute myeloid leukemia (pAML) patient-matched leukemic blasts and hematopoietic stem and progenitor cells (HSPC), as well as HSPCs from age-matched healthy donors. HSPCs in the leukemic bone marrow have limited genetic relatedness and share few somatic mutations with the cell of origin of the malignant blasts, suggesting polyclonal hematopoiesis in patients with pAML. Compared with normal HSPCs, a subset of pAML cases harbored more somatic mutations and a distinct composition of mutational process signatures. We hypothesize that these cases might have arisen from a more committed progenitor. This subset had better outcomes than pAML cases with mutation burden comparable with age-matched healthy HSPCs. Our study provides insights into the etiology and patient stratification of pAML.

Significance:
Genome-wide analysis of pAML and patient-matched HSPCs provides new insights into the etiology of the disease and shows the clinical potential of these analyses for patient stratification.
This article is highlighted in the In This Issue feature, p. 403
Abstract 16: Amyloidogenic Modifications of Apolipoprotein A-I Promote a Strong Pro-inflammatory Response in Macrophages, but Formation of Amyloid Fibrils Abrogates the Pro-inflammatory Effect
Authors: Witkowski Andrzej , Chan Gary K , Li Nancy J , Lu Rui , Yokoyama Shinji , Cavigiolio Giorgio 
Published: July 2021

Inflammation is central to atherosclerosis, as inactivation of inflammation pathways strongly reduces atherosclerosis progression. Particulate matter, such as cholesterol crystals and amyloid materials, promotes release of the potent pro-inflammatory cytokine IL-1β in macrophages. Recently, it has been demonstrated that soluble substances that are precursors of particulate matter, such as free cholesterol, oxidized LDL and amyloidogenic peptides (i.e. amyloid-β, IAPP), can also induce an inflammatory response.
In this study, we investigated the interplay between oxidation of apolipoprotein A-I (apoA-I), amyloid formation, and the inflammatory response of macrophages. We previously reported that oxidation of apoA-I methionines (MetO-ApoA-I) promotes protein aggregation and formation of amyloid fibrils when MetO-ApoA-I is incubated at pH 6.0. In contrast, at physiological pH, MetO-ApoA-I remains soluble and perfectly functional, as it promotes cholesterol efflux from macrophages with the same efficiency of intact-ApoA-I. However, upon incubation of mouse bone marrow derived macrophages with soluble pre-fibrillar MetO-ApoA-I, levels of pro-IL-1β synthesis were more than 2-fold higher than those induced by intact-ApoA-I. In contrast, amyloid fibrils produced by MetO-ApoA-I did not increase the levels of pro-IL-1β synthesis compared to intact-ApoA-I. Furthermore, the pro-inflammatory effect was not observed in macrophages derived from MyD88/TRIF knock-out mice, indicating that the response is membrane TLR receptors-dependent. In contrast, the >2-fold increase (MetO-ApoA-I vs. intact-apoA-I) in pro-IL-1β synthesis was maintained in macrophages derived from CD36 knock-out mice. This observation suggests that the signaling pathway is not exclusively dependent on the TLR2/TLR6/CD36 membrane complex. Thus, in atherosclerotic lesions, oxidized apoA-I species that are amyloidogenic, but otherwise functional, may induce a pro-inflammatory response in macrophages. Amyloid fibril formation in contrast, could reduce, rather than exacerbate, the inflammatory burden produced by these pro-inflammatory apoA-I species by sequestering them in the form of inert amyloids.
Abstract P107: Differences in Cardiovascular Mortality Risk Among African Americans in the Minnesota Heart Survey, 1985-2015, versus African Americans in the Atherosclerosis Risk in Communities Study (ARIC) Cohort: 1987-2015
Authors: George Kristen M , Folsom Aaron R , Steffen Lyn M , Wagenknecht Lynne E , Mosley Thomas H 
Published: July 2021

Geographic differences in CVD mortality across the U.S. are well-established, but frequently overlooked. ARIC enrolled African Americans (AA) from Jackson, MS and Forsyth County, NC, areas of the Southeast with some of the highest CVD mortality rates, especially among AAs. The Minnesota Heart Survey enrolled AAs from Minnesota where CVD rates are among the lowest. However, it is not known whether AAs in Minnesota also have low rates. Using these two cohorts, we assessed whether CVD-related mortality risk among AAs differs by region.
Baseline measures of CVD risk factors for MHS were taken in 1985 from a population based sample of AAs, ages 45 to 65, living in the Minneapolis-St. Paul metropolitan area. These same measures were made at ARIC visit 1 (1987-89) in AA participants of the same age residing in Jackson, MS and Forsyth County, NC. CVD and total mortality were identified using ICD codes for underlying cause of death from State and National Death Index records in both cohorts. We compared MHS and ARIC on CVD death rates using Poisson regression, prevalence of risk factors, and risk factor hazard ratios using Cox regression.

After risk factor adjustment, AA men in MHS had a rate of 5.2 (95% CI: 3.2, 7.2) CVD deaths per 1000 person-years compared to 15.1 (95% CI: 13.1, 17.1) for AA men in ARIC. For AA women, MHS had 4.1 (95% CI: 2.7, 5.5) CVD deaths per 1000 person-years versus 10.2 (95% CI: 9.0, 11.4) in ARIC. CVD mortality rates were higher in Jackson than Forsyth County within ARIC. CVD death rates paralleled risk factor prevalence at baseline. Compared to MHS, ARIC had significantly higher total cholesterol (215 vs. 202 mg/dL), albeit higher HDL cholesterol (55 vs. 53 mg/dL), as well as higher anti-hypertensive medication use (41 vs. 30%), diabetes (13 vs. 11%) and BMI (30 vs. 29 kg/m
2
), while smoking did not differ. Despite risk factor differences, hazard ratios of CVD death associated with each risk factor did not differ between studies even after inclusion of a competing risk of non-CVD death.

In conclusion, the CVD death rate was lower in AAs in MHS than in AAs residing in the Southeast in ARIC largely due to lower risk factor levels, since the hazard of CVD death for each risk factor did not differ. Study differences reflect incompletely identified geographic variation that need further exploration, especially in the context of health disparities, but support maintaining low risk as a key to CVD prevention.
Abstract P152: Health Informatics: A New Hope for Familial Hypercholesterolemia
Authors: Joseph Amy P , Mullett Charles J , Armistead Matthew , Cox Jeff , Denney Michael , Neal William A , Pyles Lee A 
Published: July 2021

Introduction:
Electronic Health Records (EHRs) benefit record keeping, information collation, error prevention, and charge capture. They provide a large database of clinical information that can be used for research. Sorting vast amounts of data manually is inefficient, hence, an effectual, validated method is required to uncover information from large sets of data and generate knowledge.

The U.S., and especially West Virginia, has a tremendous burden of cardiovascular disease (CVD). Undiagnosed Familial Hypercholesterolemia (FH) is an important factor for CVD in the U.S. FH results in elevated levels of LDL from childhood and early atherosclerotic disease. We are interested in better screening processes for FH. One method is to detect adults with coronary artery disease (CAD) and determine if their lipid levels are indicative of FH. Relatives and children can then be screened for FH and treated. Efficient identification of a CAD phenotype from EHRs is an important initial step in this screening process.

Hypothesis:
We hypothesized that a CAD phenotype detection algorithm that uses discrete data elements from EHRs can be validated as a precursor to detection of FH.

Methods:
We developed an algorithm to detect a CAD phenotype, which searched through discrete data elements, such as diagnoses lists (ICD-10) and procedure (CPT) codes. Direct inspection of EHR discrete data avoided the need for artificial intelligence, such as natural language processing.

The algorithm was applied to a cohort of 1,000 patients with varying characteristics. We then determined which patients had CAD by systematically going through EHRs.
Following this, we revised the algorithm by refining the constraints under which it operated. We ran the algorithm again on the same 1,000 patients, and determined the accuracy of the modified algorithm.

Results:
Manual validation of the 1,000 patients resulted in 413 with CAD and 587 without. The original algorithm distinguished 488 CAD positive patients and 512 CAD negative patients. This was 89% accurate, 96% sensitive, and 85% specific.

After revising the algorithm and applying it to the same cohort, it determined that there were 474 CAD patients and 526 without CAD. This was 93% accurate, 99% sensitive, and 89% specific.

Conclusion:
EHR usage has created a large pool of minable clinical data. However, without an efficient method to obtain inferences from it, the information cannot be effectually utilized. We have created an algorithm that detects CAD on a large scale with high accuracy. It has proven to be useful among a varied patient population. Since the constraints that are used, such as ICD codes and CPT codes, are universal, it can be utilized across many hospital systems; although, local validation is prudent. Using this algorithm can select a population with a propensity for FH, thereby allowing us to screen and manage patients with undiagnosed FH or other familial dyslipidemias.