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Pediatric Hematology Oncology Building Education and Training Success (PHO BEATS): A Conference to Raise Awareness and Interest for Residents and Medical Students
No full textNovel Use of the Right Atrial Appendage as a Neopulmonary Valve in a Child With Infective Endocarditis
No full textInfective endocarditis (IE) is a serious complication following any cardiac surgery. Pseudomonas as the causative organism is very rare. The authors report a case of IE post cardiac surgery for ventricular septal defect closure which was found to be caused by Pseudomonas involving the pulmonary valve. It was successfully managed by resection of a considerable amount of vegetation that had damaged the pulmonary valve. A previously placed patch was removed and pulmonary valve reconstruction using the right atrial appendage was accomplished
Kir4.1/Kir5.1 of Distal Convoluted Tubule Is Required for Short-Term Angiotensin-II-Induced Stimulation of Na-Cl Cotransporter
No full textAngiotensin-II (Ang-II) perfusion stimulates inwardly-rectifying potassium channels 4.1 and 5.1 (Kir4.1/Kir5.1) in distal convoluted tubule (DCT) and thiazide-sensitive Na-Cl cotransporter (NCC). The aim of the present study is to explore the role of Kir4.1/ Kir5.1 in mediating the effect of Ang-II on NCC. We used immunoblotting and patch-clamp experiments to examine the effect of 1- or 7-day Ang-II perfusion on basolateral Kir4.1/Kir5.1 in the DCT and NCC using kidney-tubule-specific (Ks) angiotensin II type 1a receptor (AT1Ar)-knockout (KO), Ks-Kir4.1-knockout and the corresponding wild-type mice. Ang-II perfusion for 1 and 7 days increased phospho-NCC (pNCC) and total-NCC (tNCC) expression and the effect of Ang-II perfusion on pNCC and tNCC was abolished in Ks-AT1aR-KO. Ang-II perfusion for 1 day robustly stimulates Kir4.1/Kir5.1 in the late DCT (DCT2) and to a lesser degree in the early DCT (DCT1), an effect was absent in Ks-AT1aR-KO mice. However, Ang-II perfusion for 7 days did not further stimulate Kir4.1/Kir5.1 in the DCT2 and only modestly increased Kir4.1/Kir5.1-mediated K+ currents in DCT1. Deletion of Kir4.1 not only significantly decreased the expression of pNCC and tNCC, but also abolished the effect of 1-day Ang-II perfusion on the expression of phospho-with-no-lysine kinase-4 (pWNK4), phospho-ste-20-proline-alanine-rich kinase (pSPAK), Pncc, and tNCC. However, 7-day Ang-II perfusion was still able to significantly stimulate the expression of pSPAK, pWNK4, pNCC, and tNCC, and increased thiazide-induced natriuresis in Ks-Kir4.1-KO mice without obvious changes in K+ channel activity in the DCT. We conclude that short-term Ang-II-induced stimulation of pWNK4, pSPAK, and pNCC depends on Kir4.1/Kir5.1 activity. However, long-term Ang-II is able to directly stimulate pWNK4, pSPAK, and pNCC by a Kir4.1/Kir5.1 independent mechanism
The Risk Analysis Index as a Predictor of 30-Day Mortality for Elderly Obese Patients Undergoing Elective Total Joint Arthroplasty
No full textIntroduction: The older population of the United States of America is continuing to increase, leading to rising rates of degenerative joint disease. Combined with the high prevalence of obesity in the US, orthopaedic surgeons are performing record numbers of elective total joint arthroplasty (TJA) procedures in higher risk patients. As age and obesity are risk factors for mortality following TJA, preoperative risk stratification tools such as frailty may be used to optimize surgical candidate selection to mitigate adverse outcomes. Methods: The American College of Surgeons National Surgical Quality Improvement Program database was queried for patients ≥65 years of age with a BMI of ≥30 kg/m2 who underwent elective primary total knee or total hip arthroplasty for degenerative joint disease. Frailty was measured using the 5-item Modified Frailty Index (mFI-5) and the Risk Analysis Index (RAI). Multivariate regression was performed to evaluate predictive value of frailty and discriminatory accuracy was quantified using receiver operating characteristic (ROC) analysis. Results: There were 169,065 patients who met the inclusion criteria from 2015 to 2019. The median age was 71 years, 60.8 % were women and 72.6 % were White. Increasing frailty predicted greater mortality as measured by the RAI and mFI-5. Further, the RAI had superior discrimination compared to the mFI-5 when quantified using ROC analysis. Discussion: Frailty as measured by the RAI has superior clinical applicability, predictive value and discrimination for identifying patients at risk of mortality following TJA in an older obese population. Given this, orthopaedic surgeons may use the RAI as a tool for optimizing candidate selection and identifying high risk patients preoperatively
Amyloidosis of the Heart: Pathophysiology, Diagnosis, and Treatment
No full textIntroduction: Cardiac amyloidosis is characterized by amyloid fibril aggregation due to misfolded circulating proteins and their deposition in the heart, leading to cardiac damage and dysfunction. Given cardiac amyloidosis is associated with a poor prognosis without treatment, early diagnosis and management are critical to increase survival from the disease. Areas covered: This article provides an overview of the disease process, diagnostic modalities, and therapies for cardiac amyloidosis. Expert opinion: Recent technological advances have led to the development of reliable and accurate diagnostic modalities for identifying cardiac amyloidosis. Recent introduction of novel disease-modifying therapies for cardiac amyloidosis has resulted in improvements in the management and prognosis of the disease
Exploring the Relationship Between Frailty and Nonunion Fractures in Upper Extremity Injuries: Insights From the National Inpatient Sample
No full textIntroduction: Frailty, a physiological decline in functional capacity, may influence nonunion risk. This study aimed to investigate the association between frailty, as measured by the modified Frailty Index-5 (mFI-5), and the likelihood of nonunion fractures of the upper extremity. Methods: This retrospective cohort study utilized the national inpatient sample (NIS) from 2015 to 2019. Patients aged 18 and older with upper extremity fractures, identified by ICD-10-CM codes, were included. Patients were categorized into routine healing and nonunion groups. Frailty was assessed using the mFI-5, classifying patients as robust, prefrail, frail, or severely frail. Multivariate logistic regression, controlling for age, sex, and Injury Severity Score (ISS), was performed to determine the association between frailty and nonunion. Results: The study included 21,618 patients, with 3782 presenting with nonunion fractures. The median age was 69 years, and 60.5% were female. The most common fracture types in the routine healing group were forearm (40.1%), clavicle (18.4%), and humerus (16.9%), while in the nonunion group, humerus (30.4%) and scapula (32.1%) were most common. Multivariate logistic regression showed that frail and severely frail patients had a decreased risk of nonunion (OR 0.751 and 0.705, respectively, p \u3c 0.001). Each unit increase in mFI-5 score was associated with a decreased risk of nonunion (OR 0.868, p \u3c 0.001). Sub-analysis revealed a decreased risk of nonunion with increasing frailty for humerus, clavicle, scapula, and phalanx fractures, but no significant association for wrist, forearm, or metacarpal fractures. Conclusion: Contrary to expectations, increasing frailty, as measured by the mFI-5, was associated with a decreased risk of nonunion fractures in the upper extremity. This paradoxical finding may be due to closer medical supervision and improved treatment compliance in frail patients. Further prospective studies are needed to explore the complex interplay between frailty, treatment adherence, and fracture healing
Cognitive Impairment in IBS: A Narrative Overview
No full textIrritable Bowel Syndrome (IBS) is a prevalent functional gastrointestinal disorder that significantly impacts the quality of life and the healthcare system. Beyond well-established symptoms such as recurrent abdominal pain and altered bowel habits, emerging evidence highlights a crucial yet underexplored aspect of cognitive dysfunction in patients suffering from IBS. This review aims to investigate the potential mechanisms linking IBS to cognitive dysfunction, emphasizing the role of the gut-brain axis and its biological and psychosocial determinants. A literature review was conducted using major medical databases, including Pubmed and Scopus, to identify relevant studies published in the last decade, focusing on clinical and experimental research assessing cognitive impairment in IBS patients. The review underscores the need for increased clinical recognition of cognitive dysfunction in IBS by highlighting the cognitive dysfunction in IBS patients with a focus on pathogenesis from disturbances in gut microbiota, inflammation, altered neurotransmitter levels, and psychological stress with various treatment modalities targeting these pathways, including probiotics, cognitive-behavioural therapy, and pharmacological interventions, showing promising results in mitigating cognitive symptoms
Compounded Topical Cidofovir as Salvage Therapy for Acyclovir-Resistant Genital HSV-2 in an Immunocompromised Pregnant Patient
No full textAlpha-Synuclein Null Mutation Exacerbates the Phenotype of a Model of Menkes Disease in Female Mice
No full textHuman SNCA, which encodes a-synuclein protein (SNCA), was the first gene linked to familial Parkinson\u27s disease (PD). Since the discovery of the genetic link of SNCA to Parkinson\u27s nearly three decades ago, many studies have investigated the normal function of SNCA protein. However, understanding of the normal function of SNCA is complicated by the lack of a reliable mammalian model of PD; indeed, mice with homozygous null mutations in the Snca gene live a normal lifespan and have only subtle synaptic deficits. Here, we report the first genetic modifier (a sensitized mutation) of a murine Snca null mutation, namely the ATPase copper transporting alpha (Atp7a), an X-linked gene that escapes inactivation in both mice and humans. In humans, mutations in Atp7a are linked to Menkes disease, a disease with pleiotropic and severe neurological phenotypes. Atp7aencodes a copper transporter that supplies the copper co-factor to enzymes that pass through the ER-Golgi network; under some conditions, Atp7a protein may also act to increase copper flux across the cell membrane. Male mice that carry a mutation in Atp7a die within 3 weeks of age regardless of Snca genotype. In contrast, female mice that carry the Atp7a mutation, on an Snca null background, die earlier (prior to 35 days) at a significantly higher rate than those that carry the Atp7a mutation on a wildtype Snca background. Thus, Snca null mutations sensitize female mice to mutations in Atp7a,suggesting that Snca protein may have a protective effect in females, perhaps in neurons, given the co-expression patterns. This study adds to the growing literature suggesting that alterations in a-synuclein structure and/or quantity may manifest in neurological differences in males and females including phenotypes of developmental delays, seizures, muscle weakness and cognitive function