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Background and aims Dwell time is a critical component of automated peritoneal dialysis (APD) prescription, the stage at which transmembrane mass and fluid transfer occur. Loss of prescribed dwell time (LDT) can negatively influence the efficiency of APD. We investigated the incidence of LDT and related causes using APD in the acute care setting at a tertiary care center.Methods Retrospective analysis was conducted of all inpatients receiving APD treatments from 1 December 2021 to 1 June 2023. Patient demographics, comorbidities, laboratory, and treatment data were extracted from electronic medical records and a propriety database.Results N = 235 cycler treatments completed by 32 patients were included for analysis. The total LDT per treatment exceeding 30 minutes and 60 minutes occurred in 27% and 20% of all treatments. LDT of more than 10 minutes per each cycle exchange occurred in 26%. Session disruptions were caused by slow out-flow (55%), inadequate drain volumes (32%), patient line occlusions (20%), and priming errors (23%). The slow flow alarm requiring user intervention was reported to occur in about one-third of all treatments (31%).Conclusion There was significant LDT and inadequate drain volume seen in about one-quarter and one-third of all inpatient APD treatments respectively. This can impact solute clearance and ultrafiltration. Slow flow alarms were the most prevalent and the leading cause of LDT followed by inadequate drain volume. Future studies are required to investigate measures to reduce slow drain and improve drain volume in the hospital setting.

Shee Wen Chua,1,2 Mushawiahti Mustapha,1 Kon Ken Wong,3 Malisa Ami,4 Aida Zairani Mohd Zahidin,5 Rona Asnida Nasaruddin1 1Department of Ophthalmology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia; 2Ophthalmology Department, Faculty of Medicine and Health Science, Universiti Malaysia Sabah, Kota Kinabalu, Sabah, Malaysia; 3Department of Medical Microbiology and Immunology, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia; 4Sunway Specialist Center Damansara, Petaling Jaya, Selangor, Malaysia; 5Gleneagles Hospital, Kuala Lumpur, Kuala Lumpur, MalaysiaCorrespondence: Mushawiahti MustaphaDepartment of Ophthalmology, Faculty of Medicine, Universiti Kebangsaan Malaysia Medical Center, Kuala Lumpur, 56000, MalaysiaTel +60391455981Email drmusha@gmail.comPurpose: The objectives of this study were to determine the prevalence of microbial contamination of multi-user preserved ophthalmic drops (POD) in Ophthalmology Outpatient Clinic (OOC), to compare the rate of contamination between the dropper tip and the residual contents in the bottle, and to identify the contaminating organisms.Methods: This was an observational cross-sectional study using a convenience sampling method conducted in the OOC of Universiti Kebangsaan Malaysia Medical Center, Malaysia. The samples of POD bottles were divided into groups obtained after 14 days (T14) and after 30 days (T30) of use. The contamination rate at the dropper tip and in the residual contents was determined and the contaminating organisms were identified.Results: A total of 140 of 149 extended-use POD bottles were included. The prevalence of contamination was 30%. There was a statistically significant difference in the rate of contamination between samples T14 and T30 (19% and 11%, respectively; p=0.046). Proparacaine and tropicamide showed higher contamination rates in the T14 samples (p=0.027 and p=0.497, respectively) than in the T30 samples. The site of contamination was higher at the dropper tip than in the residual contents (p> 0.05). Coagulase-negative Staphylococcus species were the most frequently identified contaminants (89%).Conclusion: The dropper tip was more contaminated than the residual contents, and coagulase-negative Staphylococcus species, which are common commensal flora of the ocular conjunctiva and skin, were the most frequently identified organisms.Keywords: contamination rate, extended period, preserved ophthalmic drops, multi-user

Angioleiomyoma is a benign soft tissue tumor originating from vascular smooth muscle. We report a case of a 20-year-old student who presented with pain in the right shoulder of 4 years duration. Shoulder movements were pain-free throughout the range of motion except resisted external rotation. Magnetic resonance imaging visualized a well-circumscribed lesion over the infraspinatus tendon. The lesion was surgically removed and sent for histopathological analysis. Morphology and immunohistochemistry results were suggestive of angioleiomyoma. The most common location for such a lesion is the lower limb, with less than 1% being reported in the upper arm, of which an angioleiomyoma of the shoulder is extremely rare.

Abstract Objective Adult polyglucosan body disease (APBD) is an adult‐onset neurological variant of glycogen storage disease type IV. APBD is caused by recessive mutations in the glycogen branching enzyme gene, and the consequent accumulation of poorly branched glycogen aggregates called polyglucosan bodies in the nervous system. There are presently no treatments for APBD. Here, we test whether downregulation of glycogen synthesis is therapeutic in a mouse model of the disease. Methods We characterized the effects of knocking out two pro‐glycogenic proteins in an APBD mouse model. APBD mice were crossed with mice deficient in glycogen synthase (GYS1), or mice deficient in protein phosphatase 1 regulatory subunit 3C (PPP1R3C), a protein involved in the activation of GYS1. Phenotypic and histological parameters were analyzed and glycogen was quantified. Results APBD mice deficient in GYS1 or PPP1R3C demonstrated improvements in life span, morphology, and behavioral assays of neuromuscular function. Histological analysis revealed a reduction in polyglucosan body accumulation and of astro‐ and micro‐gliosis in the brains of GYS1‐ and PPP1R3C‐deficient APBD mice. Brain glycogen quantification confirmed the reduction in abnormal glycogen accumulation. Analysis of skeletal muscle, heart, and liver found that GYS1 deficiency reduced polyglucosan body accumulation in all three tissues and PPP1R3C knockout reduced skeletal muscle polyglucosan bodies. Interpretation GYS1 and PPP1R3C are effective therapeutic targets in the APBD mouse model. These findings represent a critical step toward the development of a treatment for APBD and potentially other glycogen storage disease type IV patients.

Abstract Background The use of psychotropic medications is not uncommon among patients with newly diagnosed cancer. However, the impact of psychotropic polypharmacy on healthcare utilization during the initial phase of cancer care is largely unknown. Methods We used a claims database to identify adults with incident breast, prostate, lung, and colorectal cancers diagnosed during 2011–12. Psychotropic polypharmacy was defined as concurrent use of two or more psychotropic medication classes for at least 90 days. A multivariable logistic regression was performed to identify significant predictors of psychotropic polypharmacy. Multivariable Poisson and negative binomial regressions were used to assess the associations between psychotropic polypharmacy and healthcare utilization. Results Among 5604 patients included in the study, 52.6% had breast cancer, 30.6% had prostate cancer, 11.4% had colorectal cancer, and 5.5% had lung cancer. During the year following incident cancer diagnosis, psychotropic polypharmacy was reported in 7.4% of patients, with the highest prevalence among patients with lung cancer (14.4%). Compared with patients without psychotropic polypharmacy during the initial phase of care, patients with newly diagnosed cancer with psychotropic polypharmacy had a 30% higher rate of physician office visits, an 18% higher rate of hospitalization, and a 30% higher rate of outpatient visits. The rate of emergency room visits was similar between the two groups. Conclusion Psychotropic polypharmacy during the initial phase of cancer care was associated with significantly increased healthcare resource utilization, and the proportion of patients receiving psychotropic polypharmacy differed by type of cancer. Impact Findings emphasize the importance of evidence-based psychotropic prescribing and close surveillance of events causing increased healthcare utilization among patients with cancer receiving psychotropic polypharmacy.

In this study, we reported the prevalence and mechanism associated with the extended-spectrum beta-lactamase (ESBL)-positive phenotype in Laribacter hongkongensis isolated from patients and fish. Using the inhibition zone enhancement test, 20 (95.2%) of the 21 patient strains and 8 (57.1%) of the 14 fish strains were tested ESBL-positive. However, ESBL genes, including SHV, TEM, CTX-M, GES, and PER, were not detected in all of these 28 L. hongkongensis isolates. No ESBL gene could be detected in either the complete genome of L. hongkongensis HLHK9 or the draft genome of PW3643. PCR and DNA sequencing revealed that all the 35 L. hongkongensis isolates (showing both ESBL-positive and ESBL-negative phenotypes) were positive for the ampC gene. When the AmpC deletion mutant, HLHK9ΔampC, was subject to the zone enhancement test, the difference of zone size between ceftazidime/clavulanate and ceftazidime was less than 5 mm. When boronic acid was added to the antibiotic disks, none of the 28 “ESBL-positive” isolates showed a ≥ 5 mm enhancement of inhibition zone size diameter between ceftazidime/clavulanate and ceftazidime and between cefotaxime/clavulanate and cefotaxime. A high prevalence (80%) of ESBL-positive phenotype is present in L. hongkongensis. Overall, our results suggested that the ESBL-positive phenotype in L. hongkongensis results from the expression of the intrinsic AmpC beta-lactamase. Confirmatory tests should be performed before issuing laboratory reports for L. hongkongensis isolates that are tested ESBL-positive by disk diffusion clavulanate inhibition test.

Abstract Background Human adenoviruses are common causes of community-acquired respiratory tract and enteric infections. Severe disseminated infections with high mortality rates may be seen in immunocompromised individuals. An accurate and cost-effective quantitative assay is essential not only for laboratory diagnosis of adenoviral infections, but also for monitoring of response to antiviral treatment. The diagnostic performance of an in-house quantitative polymerase chain reaction assay was compared to a commercial system. Methods The analytical sensitivity, specificity, linearity, precision and accuracy of an in-house adenovirus quantitative polymerase chain reaction assay were evaluated against the RealStar® Adenovirus PCR Kit (Altona Diagnostics GmbH, Hamburg, Germany), using 122 clinical specimens and 18 proficiency testing samples. Results Linear regression analysis of the quantitative results by the in-house assay showed the dynamic range from 2.60 to 9 log10 (plasma) and 2.94 to 9 log10 (viral transport medium) copies/mL, with the coefficient of determination (R2) of 0.996 and 0.998, respectively. A dilution series demonstrated the limits of detection and lower limits of quantification for plasma were 2.06 log10 and 2.60 log10 copies/mL and those for viral transport medium were 2.31 log10 and 2.94 log10 copies/mL respectively. The precision of the in-house assay was highly reproducible among runs with coefficients of variance ranging from 0.07 to 3.21% for plasma and 0.17% to 2.11% for viral transport medium. A comparison of 52 matched samples showed an excellent correlation between the quantitative viral loads measured by the in-house assay and the RealStar® Adenovirus PCR Kit (R2 = 0.984), with an average bias of − 0.16 log10 copies/mL. Conclusions The in-house adenovirus assay is a sensitive and reliable assay with lower cost for the detection and quantification of adenoviral DNA when compared to the RealStar® Adenovirus PCR Kit.

Illinois is home to the sixth largest Asian American and Pacific Islander (AAPI) population nationwide. AAPIs suffer higher incidence, morbidity, and mortality rates from certain cancers, infectious, and chronic diseases. Despite the exponential growth of the AAPI population, few state-level data sources exist that provide detailed and accurate information regarding AAPI health disparities and needs. Efforts to improve health care for this population will require improved data collection and funding for research on AAPI ethnic groups.

Abstract Lafora disease (LD) is a fatal progressive epilepsy essentially caused by loss‐of‐function mutations in the glycogen phosphatase laforin or the ubiquitin E3 ligase malin. Glycogen in LD is hyperphosphorylated and poorly hydrosoluble. It precipitates and accumulates into neurotoxic Lafora bodies (LBs). The leading LD hypothesis that hyperphosphorylation causes the insolubility was recently challenged by the observation that phosphatase‐inactive laforin rescues the laforin‐deficient LD mouse model, apparently through correction of a general autophagy impairment. We were for the first time able to quantify brain glycogen phosphate. We also measured glycogen content and chain lengths, LBs, and autophagy markers in several laforin‐ or malin‐deficient mouse lines expressing phosphatase‐inactive laforin. We find that: (i) in laforin‐deficient mice, phosphatase‐inactive laforin corrects glycogen chain lengths, and not hyperphosphorylation, which leads to correction of glycogen amounts and prevention of LBs; (ii) in malin‐deficient mice, phosphatase‐inactive laforin confers no correction; (iii) general impairment of autophagy is not necessary in LD. We conclude that laforin's principle function is to control glycogen chain lengths, in a malin‐dependent fashion, and that loss of this control underlies LD.

Summary: Lafora disease (LD) and adult polyglucosan body disease (APBD) are glycogen storage diseases characterized by a pathogenic buildup of insoluble glycogen. Mechanisms causing glycogen insolubility are poorly understood. Here, in two mouse models of LD (Epm2a−/− and Epm2b−/−) and one of APBD (Gbe1ys/ys), the separation of soluble and insoluble muscle glycogen is described, enabling separate analysis of each fraction. Total glycogen is increased in LD and APBD mice, which, together with abnormal chain length and molecule size distributions, is largely if not fully attributed to insoluble glycogen. Soluble glycogen consists of molecules with distinct chain length distributions and differential corresponding solubility, providing a mechanistic link between soluble and insoluble glycogen in vivo. Phosphorylation states differ across glycogen fractions and mouse models, demonstrating that hyperphosphorylation is not a basic feature of insoluble glycogen. Lastly, model-specific variances in protein and activity levels of key glycogen synthesis enzymes suggest uninvestigated regulatory mechanisms. : EPM2A, EPM2B, or GBE1 deficiency causes insoluble glycogen accumulation and neurodegenerative diseases. Sullivan et al. show that these defects do not impair the construction of WT-like soluble glycogen. Demonstrating varying chain length distributions and correlating precipitation propensity among WT-glycogen molecules, a mechanistic explanation emerges for the structural characteristics of insoluble glycogen. Keywords: Lafora disease, laforin, malin, APBD, glycogen branching enzyme, glycogen synthase, glycogen storage disease, polyglucosan bodies, phosphorylation, glycogen chain length distribution

Thromboembolism continues to be a major concern in patients with mechanical heart valves, especially in those with unsatisfactory anticoagulation levels. The new On-X valve (On-X Life Technologies, Austin, TX, USA) has been reported as having unique structural characteristics that offer lower thrombogenicity to the valve. We report a case where the patient received no or minimal systemic anticoagulation after placement of On-X mitral and aortic valves due to development of severe mucosal arterio-venous malformations yet did not show any evidence of thromboembolism. This case report reinforces the findings of recent studies that lower anticoagulation levels may be acceptable in patients with On-X valves and suggests this valve may be particularly useful in those in whom therapeutic levels of anticoagulation cannot be achieved due to increased risk of bleeding.