JAK2V617F was present in 10 subjects and CALR mutation in one. No other somatic mutations were identified in next generation sequencing. After a median follow-up of 101 months (IQR, 40-160 months), no subject had disease progression or blast transformation. Incidence of post-diagnosis or recurrent thrombosis was 3.9 events (95% confidence interval, 3.5-4.0) and 5.0 events (4.6-5.6) per 100 person-years. Features of subjects with atypical myeloproliferative disorder differed markedly from those of 546 subjects with prefibrotic myelofibrosis.
 
  Our data indicate that these 15 persons have a distinct myeloproliferative neoplasm. We propose naming this new disorder clonal megakaryocyte dysplasia with normal blood values.
 Our data indicate that these 15 persons have a distinct myeloproliferative neoplasm. We propose naming this new disorder clonal megakaryocyte dysplasia with normal blood values.
  Patients with CKD frequently have anemia that results from iron-restricted erythropoiesis and inflammation. Anemia of CKD is currently managed with iron supplements and erythropoiesis-stimulating agents (ESAs) to promote erythropoiesis and with RBC transfusion in severe cases. Hyporesponse to ESAs, or the need for larger than usual doses to attain a given hemoglobin (Hb) level, is associated with increased morbidity and mortality and presents a pressing clinical challenge, particularly for patients on dialysis. This paper reviews ESA hyporesponse and potential new therapeutic options in the management of anemia of CKD.
 
  The most common causes of ESA hyporesponse include iron deficiency and inflammation, and to a lesser degree, secondary hyperparathyroidism, inadequate dialysis, malnutrition, and concomitant medications. Management of ESA hyporesponse is multipronged and involves treating low level infections, ensuring adequate nutrition, and optimizing iron status and dialysis modality, although some patieal oral HIF-PH inhibitors have been evaluated in patients with anemia of CKD and have been shown to increase Hb and reduce hepcidin regardless of inflammation, iron status, or dialysis modality. These sustained effects are achieved through more modest increases in endogenous EPO compared with ESAs. Key Messages Treatments that address ESA hyporesponse remain a significant unmet clinical need in patients with anemia of CKD. New therapies such as HIF-PH inhibitors have the potential to address fundamental aspects of ESA hyporesponse and provide a new therapeutic option in these patients.The prescription of carboplatin is commonly based on the Calvert formula, and low serum creatinine values can lead to an overestimation of the glomerular filtration rate and of the carboplatin dose. Limited data recommend to cap carboplatin dose at 800 mg, but the risk of suboptimal carboplatin dose is concerning. This study compared hematologic toxicity occurrence and survival outcomes in lung cancer patients receiving carboplatin > or 800 mg, but no significant difference appears for the both survival criteria. This study aims to improve the determination of carboplatin dosage to know the real impact of carboplatin capping and to find the optimum balance between excessive toxicity and substandard therapeutics outcomes.
  Acute kidney injury (AKI) in patients with COVID-19 can be caused by multiple mechanisms. Renal resistive index (RRI) is a noninvasive instrument to evaluate kidney hemodynamics, and it is obtained by analysis of intrarenal arterial waves using Doppler ultrasound. This study aimed to determine the role of RRI in predicting AKI and adverse outcomes in critically ill patients with COVID-19.
 
  This cross-sectional study included 65 patients with confirmed SARS-CoV-2 pneumonia admitted to the critical care unit from April 1, 2020, to June 20, 2020. Informed consent was obtained from all individual participants included in the study. Cardiac, pulmonary, and kidney ultrasonographic evaluations were performed in a protocolized way.
 
  In this cohort, 65 patients were included, mean age was 53.4 years, 79% were male, and 35% were diabetic. Thirty-four percent of patients developed AKI, 12% required RRT, and 35% died. Of the patients who developed AKI, 68% had RRI ≥ 0.7. Also, 75% of the patients who required RRT had RRI ≥ 0.7. In the adjusted Cox model, the RRI ≥ 0.7 was associated with higher mortality (HR 2.86, 95% CI 1.19-6.82, p = 0.01).
 
  Critical care ultrasonography is a noninvasive, reproducible, and accurate bedside method that has proven its usefulness. An elevated RRI may have a role in predicting AKI, RRT initiation, and mortality in patients with severe SARS-CoV-2 pneumonia.
 Critical care ultrasonography is a noninvasive, reproducible, and accurate bedside method that has proven its usefulness. An elevated RRI may have a role in predicting AKI, RRT initiation, and mortality in patients with severe SARS-CoV-2 pneumonia.
  Although several candidate-gene association studies have been conducted to investigate noise-induced hearing loss (NIHL) in humans, most are underpowered, unreplicated, and account for only a fraction of the genetic risk. Mouse genome-wide association studies (GWASs) have revolutionized the field of genetics and have led to the discovery of hundreds of genes involved in complex traits. The hybrid mouse diversity panel (HMDP) is a collection of classic inbred and recombinant inbred strains whose genomes have been either genotyped at high resolution or sequenced. To further investigate the genetics of NIHL, we report the first GWAS based on distortion product otoacoustic emission (DPOAE) measurements and the HMDP.
 
  A total of 102 strains (n = 635) from the HMDP were evaluated based on DPOAE suprathreshold amplitudes before and after noise exposure. DPOAE amplitude variation was set at 60 and 70 dB SPL of the primary tones for each frequency separately (8, 11.3, 16, 22.6, and 32 kHz).  https://www.selleckchem.com/  These values provided anplitudes before and after noise exposure. Our results identified a number of novel loci and candidate genes for susceptibility to NIHL, especially the Eya1 and Efr3a genes. Our findings validate the power of the HMDP for detecting NIHL susceptibility genes.
 For the first time, an association analysis with correction for population structure was used to map several loci for hearing traits in inbred strains of mice based on DPOAE suprathreshold amplitudes before and after noise exposure. Our results identified a number of novel loci and candidate genes for susceptibility to NIHL, especially the Eya1 and Efr3a genes. Our findings validate the power of the HMDP for detecting NIHL susceptibility genes.