Disparity in female and Asian representation amongst cardiology journal editorial boards members: a call for empowerment.

BACKGROUND: While progress is evident in gender and ethnic representation in the workplace, this disparity remains prevalent in academic positions. OBJECTIVES: We examined gender and Asian ethnic representation in editorial boards of cardiology journals. METHODS: A cross-sectional analysis was conducted using publicly available data on Cardiology and Cardiovascular medicine journals in the first quartile of the 2020 Scimago Journal & Country Rank indicator. The proportions of female and Asian editorial board members, associate editors and editors-in-chief were assessed. Subgroup analyses were conducted based on the journal's geographical origin, subspecialty and demographic of the editor-in-chief. RESULTS: Seventy-six cardiology journals, involving 8915 editorial board members, were included. Only 19.6% of editorial board members were female, 20.8% Asians and 4.0% Asian females. There were less female representation amongst editors-in-chief (9.9%) compared to associate editors (22.3%). European (18.1%) and North American-based journals (21.1%) had higher female representation compared to Asian-based journals (8.7%). There was lower Asian representation in European (18.1%) and North American-based journals (19.9%) compared to Asian-based journals (72.3%). Females were underrepresented in interventional (14.5%) journals, while Asians were underrepresented in general cardiology (18.3%) and heart failure (18.3%) journals. Journals led by female editors-in-chief had significantly higher female representation compared to male-led ones, while journals with Asian editors-in-chief had greater Asian representation compared to non-Asian led ones. CONCLUSION: This study highlights the female and Asian ethnic underrepresentation in academic roles in cardiology journal editorial boards. Further analysis is needed for other ethnicities, while the community pushes towards gender-balanced and ethnic diversity across editorial boards.

Attitudes toward and Barriers to Acetaminophen Use in the Chronic Pain Population: A Cross-Sectional Study.

The use of acetaminophen is recommended in pain management, particularly acute pain management, to reduce opioid utilization and opioid related adverse drug events. Acetaminophen's role in chronic pain conditions is understudied. This cross-sectional study was performed in a pain management office to explore how chronic pain patients use acetaminophen. The final study sample included 100 patients. Current users of acetaminophen were most likely to report that a doctor had recommended acetaminophen to them (86.4%) compared to ever (66.7%) and never (55.6%) users (p < .001). Patients who were recommended taking acetaminophen by a physician were 3.60 times as likely (95% CI 1.58, 8.25) to be a current or ever user of acetaminophen as compared to those who did not receive such a recommendation from their physician. There were no significant differences between current, ever, and never users on their knowledge of the maximum daily dose of acetaminophen of 4 g (p = .925). The study suggests that patients are often unaware of acetaminophen's role in the treatment of their chronic pain.

Radiofrequency Ablation of the Stellate Ganglion for Management of Acute Digital Ischemia: A Case Report.

The authors present a report of a pulsed radiofrequency ablation of the stellate ganglion performed on a patient with microemboli to the hand from a thrombosed abandoned arteriovenous fistula. The patient was initially managed using vasodilators and anticoagulation. However, the patient's skin mottling, pain, and decreased strength persisted. Ablation of the stellate ganglia increased perfusion to his hand and likely prevented amputation that has lasted for approximately 1 year. While radiofrequency ablation is more commonly used for pain syndromes, this is an example of its use in the treatment and potential treatment of acute ischemia.

Experimental heart failure modelled by the cardiomyocyte-specific loss of an epigenome modifier, DNMT3B.

Differential DNA methylation exists in the epigenome of end-stage failing human hearts but whether it contributes to disease progression is presently unknown. Here, we report that cardiac specific deletion of Dnmt3b, the predominant DNA methyltransferase in adult mouse hearts, leads to an accelerated progression to severe systolic insufficiency and myocardial thinning without a preceding hypertrophic response. This was accompanied by widespread myocardial interstitial fibrosis and myo-sarcomeric disarray. By targeted candidate gene quantitative RT-PCR, we discovered an over-activity of cryptic splice sites in the sarcomeric gene Myh7, resulting in a transcript with 8 exons missing. Moreover, a region of differential methylation overlies the splice site locus in the hearts of the cardiac-specific conditional knockout (CKO) mice. Although abundant and complex forms of alternative splice variants have been reported in diseased hearts and the contribution of each remains to be understood in further detail, our results demonstrate for the first time that a link may exist between alternative splicing and the cardiac epigenome. In particular, this gives the novel evidence whereby the loss of an epigenome modifier promotes the development and progression of heart disease.

Present-day investigations cannot adequately determine the risk of acute coronary syndromes.

It is an important irony that present-day clinical stress testing methods including exercise electrocardiogram, stress echocardiography and even coronary angiography are not able to demonstrate vulnerable coronary plaques at risk of rupture. A vulnerable plaque may in fact be invisible on clinical stress test and perhaps only visualized directly through less available techniques such as coronary angioscopy. Landmark pathological studies have deepened our understanding of the mechanisms behind acute coronary syndromes over the last decade. Thrombosis plays a key role and is a unifying feature in the pathogenesis. Platelet-rich thrombus superimposed over the disrupted atherosclerotic plaque or eroded plaque endothelium, with or without fibrin-thrombus extension, is evident in post-mortem necropsy and angioscopic studies. However features which contribute to the risk of acute events lie in the atherosclerotic plaque itself. Plaque content and not plaque size is the important factor. Clinical stress testing demonstrates plaque size but not plaque content. A plaque will be prone to rupture if it has only a thin cap and a proportionally larger lipid core. In such a plaque there is preponderance of activated macrophages and T-lymphocytes, and high activity of matrix metalloproteinases. Smooth muscle cell proliferation and collagen synthesis are downregulated. These features may serve as possible targets for devising clinical methods to detect plaques at risk or for reversing the risk in vulnerable plaques.

Complications in tunneled CVL versus PICC lines in very low birth weight infants.

OBJECTIVE: Comparison of complications associated with tunneled central venous lines (TCVLs) versus peripherally inserted central catheters (PICCs) in infants <1500 g. STUDY DESIGN: A retrospective cohort study at a university medical center. A total of 96 catheters were placed in 60 infants between 4/94 and 3/99. A retrospective review of these infants' medical record was done to review associated complications of catheter placement. RESULTS: Both groups had similar weights and gestational ages. The duration of catheterization was 28 days in TCVLs and 11 days in PICCs (p<0.05). Total, infectious, and mechanical complications between the two groups were similar. Survival function estimates showed no difference between the two groups up to the 15th day of catheterization. CONCLUSION: There is no difference in efficacy or associated complications between the two groups. If one could anticipate needing a catheter longer than 15 days, then a TCVL might be the better choice.

Detection of pneumococcal capsular antigen in saliva of children with pneumonia.

The concentration of pneumococcal capsular antigen (PCA) in saliva was examined in 44 Thai children aged between 2 months and 2 years admitted with community-acquired pneumonia and in 52 healthy controls. None of the children with pneumonia had a positive blood culture. PCA was detected by latex agglutination in the saliva of 12/44 (27%) children with pneumonia compared with 9/52 (17%) of the controls. More cases than controls had a PCA titre > or = 10 (9/44 (20%) vs 1/52 (2%), p < 0.01). Three of the five cases with a saliva PCA titre > or = 1000 were urine PCA antigen-positive. The salivary PCA titres were higher, but not significantly, in children with heavier pneumococcal carriage. Quantitative measurement of PCA in the saliva may be valuable in helping to make an aetiological diagnosis in children with pneumonia.

Inhibition of platelet thrombosis using an activated protein C-loaded stent: in vitro and in vivo results.

In high-risk and complicated coronary intervention, the risk of acute closure is unpredictable. Thrombus and platelet deposition at the intervention site may also have further effects on subsequent restenosis. In vivo infusion of activated protein C has previously been shown to achieve potent anticoagulation without any haemostatic side effects. We now evaluated the in vitro and in vivo efficacy of polymer-coated coronary stents loaded with purified rabbit Activated Protein C (APC). By measuring 125I-fibrinogen/fibrin deposition APC-loaded stent-wires were antithrombotic compared to albumin-loaded, inhibited-APC-loaded, plain polymer-coated and stainless steel stent-wires. In a balloon injury rabbit iliac artery model, APC-loaded stents did not occlude (0/14) compared to plain stents (9/15) and BSA-loaded stents (2/4). Relative 111In-labelled platelet deposition showed a similarly significant degree of inhibition. In conclusion, APC-loading could render stents significantly less thrombotic. Whether an effective antithrombogenic stent like this effectively reduces restenosis rates warrants further evaluation.

Concepts in acute coronary syndromes.

Landmark pathological studies have deepened our understanding of the mechanisms behind acute coronary syndromes over the last decade. Thrombosis plays a key role and is a unifying feature in the pathogenesis. Platelet-rich thrombus superimposed over the disrupted atherosclerotic plaque or eroded plaque endothelium, with or without fibrin-thrombus extension, is evident in postmortem necropsy, angiographic and angioscopic studies. However features which contribute to the risk of acute events lie in the atherosclerotic plaque itself. Plaque content and not plaque size is the important factor. A vulnerable plaque may be invisible on clinical stress testing and even coronary angiography; but it is prone to rupture if it has only a thin cap and a proportionally larger lipid core. There is a cellular preponderance of activated macrophages and T-lymphocytes; and high activity of matrix metalloproteinases in vulnerable plaques. Smooth muscle cell proliferation and collagen synthesis are downregulated. These features may serve as possible targets for detecting plaques at risk or for reversing the risk of vulnerable plaques.

[Antibiotic resistance and plasmid profiles of Vibrio isolates from cultured Sparus sarba].

A total of 51 potential pathogenic vibrios were isolated from moribund silver seabream Sparus sarba, which were collected from local fish farms of Hong Kong. All the isolates were classified and identified as 7 species by the API 20 E system and the scheme of Alsina & Blanch. These species were Vibrio alginolyticus (24 strains), Vibrio vulnificus (12 strains), Vibrio parahaemolyticus(7 strains), Vibrio logei(4 strains), Vibrio pelagius II(2 strains), Vibrio fluvialis (1 strains) and Vibrio meditterranei (1 strains). Among these isolates, the three predominant species (V. alginolyticus, V. vulnificus and V. parahaemolyticus) were confirmed to be virulent to sea bream by experimental challenge. All isolates were also screened for plasmid DNA by agarose gel electrophoresis and tested for susceptibility to 16 antimicrobial agents by the agar dilution method. Of the 51 isolates examined, all strains were sensitive to ceftriaxone, streptomycin, nalidixic acid and rifampicin, and almost all were sensitive to ceftazidime, netilimicin, chloramphenicol and sulfamethoxazole except one or two strains. Most isolates were resistant to ampicillin (60. 8%), cefuroxime (66.7%), amikacin(55%), kanamycin(58.8%) and trimethoprinm (76.5%). Fifteen of the 51 isolates harboured 1-4 plasmids, with sizes ranging from 9 to 123 kb. Both the plasmids and the associated antimicrobial resistance (ampicillin, cefuroxime and trimethoprim) of 9 isolates could be transferred to recipient by single-step conjugation, however, the frequencies were very low, ranging from 10(-11) to 10(-9). The present results indicate that resistance to these antibiotics is chromosomal.

Fetal outcome in mothers with impaired glucose tolerance in pregnancy.

A 75 g oral glucose tolerance test was carried out on 953 pregnant women who were identified on the basis of clinical risk factors. The tests were analysed by the WHO criteria: 826 were normal, 120 showed impaired glucose tolerance, and 7 identified diabetes. A number of obstetric and perinatal outcome measures were compared between the groups with normal and impaired glucose tolerance, and also with 135 women who had pre-existing Type 1 diabetes and delivered during the study period. There was no significant difference in the incidence of antenatal complications between mothers with normal and impaired glucose tolerance. There was a higher rate of induced labour (p < 0.05) and caesarean section (p < 0.01) in the impaired glucose tolerance group compared to the normal group, but no difference in fetal outcome or neonatal morbidity. All of these outcome measures were increased in the Type 1 diabetic pregnancies.