DataSheet1_Safety of midodrine in patients with heart failure with reduced ejection fraction: a retrospective cohort study.PDF

Background: Heart failure with reduced ejection fraction (HFrEF) poses significant health risks. Midodrine for maintaining blood pressure in HFrEF, requires further safety investigation. This study explores midodrine’s safety in HFrEF through extensive matched analysis.Methods: Patients with HFrEF (LVEF Results: After 1:1 PSM, 5813 cases were included in each group. The midodrine group had higher risks of respiratory failure (HR: 1.16, 95% CI: 1.08–1.25), ICU admissions (HR: 1.14, 95% CI: 1.06–1.23), hospitalizations (HR: 1.21, 95% CI: 1.12–1.31), and mortality (HR: 1.090, 95% CI: 1.01–1.17). Interestingly, midodrine use reduced ER visits (HR: 0.77, 95% CI: 0.71–0.83). Similar patterns of lower ER visit risk and higher risks for ICU admissions, respiratory failure, and overall hospitalizations were observed in most subgroups.Conclusion: In this large-scale study, midodrine use was associated with reduced ER visits but increased risks of respiratory failure, prolonged ICU stays, higher hospitalizations, and elevated mortality in HFrEF patients. Further research is needed to clarify midodrine’s role in hemodynamic support and strengthen existing evidence.</p

Treatment effects of different immunosuppressive regimens in paraquat-poisoned patients with hemoperfusion treatment.

<p>Cox regression analysis of mortality rates among different treatment groups, adjusted for age and sex, was used to calculate the hazard ratio. Abbreviations: No IST: No immunosuppressive treatment (Hemoperfusion alone); IST: Immunosuppressive treatment; MP: Methylprednisolone; CP: Cyclophosphamide; DEX: Dexamethasone.</p

Hazard ratio and adjusted (age and sex) hazard ratio in patients with paraquat poisoning with different comorbidities.

<p>Abbreviations: HR: Hazard ratio; RF: Respiratory failure; AKI: Acute kidney injury; HD: Hemodialysis; DM: Diabetes mellitus; HTN: Hypertension; CVA: Cerebral vascular accident; CHF: Congestive heart failure; CAD: Coronary artery disease; COPD: Chronic obstructive pulmonary disease.</p>*<p>Cox regression analysis among different treatment groups adjusted for age and sex or not adjusted were used for analysis.</p

Kaplan-Meier survival plot of the MP+CP+DEX subgroup (n = 100) versus the non-IST group (n = 1046, log rank test, P<0.001).

<p>Abbreviations: MP: Methylprednisolone; CP: Cyclophosphamide; DEX: Dexamethasone; IST: Immunosuppressive treatment.</p

Hazard ratios of individual comorbidity of the CHADS2 score for mortality in incident hemodialysis patients.

<p>Hazard ratios of individual comorbidity of the CHADS2 score for mortality in incident hemodialysis patients.</p

Hydronephrotic Urine in the Obstructed Kidney Promotes Urothelial Carcinoma Cell Proliferation, Migration, Invasion through the Activation of mTORC2-AKT and ERK Signaling Pathways

<div><p>Obstructive nephropathy is the most common presentation of urothelial carcinoma. The role of the urine in the obstructed kidney namely “hydronephrotic urine” in urothelial carcinoma has not been extensively explored. This study aims to evaluate whether hydronephrotic urine in the obstructed kidney could promote urothelial carcinoma. The hydronephrotic urine was collected from the obstructed kidneys of Sprague-Dawley rats induced by different periods of unilateral ureteral obstruction (UUO). By the inhibition of LY294002 and PD184352, we confirm that hydronephrotic urine promotes urothelial carcinoma cell (T24) and immortalized normal urothelial cells (E6) proliferation, migration and invasion in a dose-dependent manner through the activation of the mTORC2-AKT and ERK signaling pathways. Hydronephrotic urine also increases the expression of cyclin-D2, cyclin-B and CDK2. It also decreases the expression of p27 and p21 in both urothelial carcinoma cells and normal urothelial cells. By the protein array study, we demonstrate that many growth factors which promote tumor cell survival and metastasis are over-expressed in a time-dependent manner in the hydronephrotic urine, including beta-FGF, IFN-γ, PDGF-BB, PIGF, TGF-β, VEGF-A, VEGF-D and EGF. These results suggest that hydronephrotic urine promotes normal and malignant urothelial cells proliferation, migration and invasion, through the activation of the mTORC2-AKT and ERK signaling pathways. Further investigation using live animal models of tumor growth may be needed to clarify aspects of these statements.</p> </div

Characteristics of study subjects with or without immunosuppressive treatment.

<p>Abbreviations: IST: Immunosuppressive treatment; HP: Hemoperfusion; ESRD: End stage renal disease; DM: Diabetes mellitus; HTN: Hypertension; CVA: Cerebral vascular accident; CHF: Congestive heart failure; CAD: Coronary artery disease; COPD: Chronic obstructive pulmonary disease.</p>*<p>Independent t-test, Chi-square test and Cox regression analysis were used for analysis.</p>#<p>Cox regression analysis among different treatment groups, adjusted for age and sex.</p

Correction: Hydronephrotic Urine in the Obstructed Kidney Promotes Urothelial Carcinoma Cell Proliferation, Migration, Invasion through the Activation of mTORC2-AKT and ERK Signaling Pathways

<p>Correction: Hydronephrotic Urine in the Obstructed Kidney Promotes Urothelial Carcinoma Cell Proliferation, Migration, Invasion through the Activation of mTORC2-AKT and ERK Signaling Pathways</p

Selection and grouping of the patients with paraquat poisoning.

<p>Abbreviations: IST: Immunosuppressive treatment.</p