Collective property rights lead to secondary forest growth in the Brazilian Amazon.

Forests serve a crucial role in our fight against climate change. Secondary forests provide important potential for conservation of biodiversity and climate change mitigation. In this paper, we explore whether collective property rights in the form of indigenous territories (ITs) lead to higher rates of secondary forest growth in previously deforested areas. We exploit the timing of granting of property rights, the geographic boundaries of ITs and two different methods, regression discontinuity design and difference-in-difference, to recover causal estimates. We find strong evidence that indigenous territories with secure tenure not only reduce deforestation inside their lands but also lead to higher secondary forest growth on previously deforested areas. After receiving full property rights, land inside ITs displayed higher secondary forest growth than land outside ITs, with an estimated effect of 5% using our main RDD specification, and 2.21% using our difference-in-difference research design. Furthermore, we estimate that the average age of secondary forests was 2.2 y older inside ITs with secure tenure using our main RDD specification, and 2.8 y older when using our difference-in-difference research design. Together, these findings provide evidence for the role that collective property rights can play in the push to restore forest ecosystems.

Anti-factor H Autoantibody-Associated Hemolytic Uremic Syndrome: A Rare Entity in a Pediatric Patient.

An 11-year-old patient presented with the primary complaint of hematuria and vomiting. On further investigation and a series of diagnostic tests, including a biopsy and thrombotic microangiopathy (TMA) profile, the patient was diagnosed with thrombotic microangiopathy. TMA is a pathological process involving endothelial cell injury, leading to thrombocytopenia and microangiopathic hemolytic anemia. This case highlights the importance of considering TMA in pediatric patients presenting with nonspecific symptoms, such as loss of appetite. Further research is needed to understand the pathophysiology and optimal management strategies for pediatric TMA. This case adds to the growing body of literature on pediatric TMA and underscores the need for a high index of suspicion in similar clinical scenarios.

Lupus Nephritis Disguised: The Diagnostic Challenge of Eosinophilic Enteritis - A Case Report.

Systemic lupus erythematosus (SLE) is a multi-systemic disorder affecting almost all systems of the body. Involvement of the kidney in this condition is known as lupus nephritis (LN). LN is one of the important disease manifestations of SLE with considerable influence on patient outcomes in terms of morbidity and mortality. A 33-year-old female came to the OPD with complaints of abdominal pain, infrequent loose stools since 4 months. The patient also had joint pain, predominantly small joints, since 2 months. Patient was admitted and all routine investigations were done. Patient underwent an oesophagogastroduodenoscopy (OGD) and colonoscopy for her abdominal pain and loose stools which did not respond to routine medication. Grossly there was edema present in the oesophagus and colon which on microscopy showed eosinophilic infiltration. Urine routine of the patient showed protein 1+and 24-hour urine protein quantification of 1427 mg/24 h. On further evaluation patient was found to have a positive ANA blot (dsDNA, AMAM2, Ro52 and Sm). The patient was planned for a renal biopsy in view of the proteinuria and positive ANA blot. The patient underwent a renal biopsy under USG guidance and was found to have Lupus nephritis Class 3 (ISN RPS staging). SLE is a multi-organ involving disease which if not diagnosed at the earliest can have serious complications and lead to end stage organ failure and even death. Atypical presentations often pose a diagnostic dilemma and may delay diagnosis and treatment. Early diagnosis and treatment can give patients of SLE a long and normal life. Diagnostic guidelines have helped in the diagnosis of such atypical presentations.

Study of the Urinary TGF-ß1 Profile in Diabetic Nephropathy: A Single-Center Experience From India.

Background Diabetic nephropathy is one of the important causes of end-stage kidney disease (ESKD). Of the various cytokines playing a role in the pathogenesis of diabetic nephropathy, transforming growth factor beta-1 (TGF-ß1) is an important one. Its major role is to mediate extracellular matrix deposition. Increased renal expression of TGF-ß1 is found in diabetic nephropathy and its urinary excretion can serve as a useful marker of outcomes. Material and methods A prospective observational study was conducted, which included 10 cases of diabetic nephropathy in group A with age ≥ 18 years and a urinary protein creatinine ratio (UPCR) value of > 0.5 mg/mg and 10 healthy controls in group B. Patients with active urinary tract infection, chronic kidney disease (CKD) stage Vd patients on maintenance hemodialysis, and renal transplant recipients were excluded from the study. Urinary TGF-ß1 level estimation in a 24-hour urine sample, 24-hour urine protein, and other baseline laboratory investigations were done. Results In diabetic nephropathy cases (group A), the mean value of urinary TGF-ß1 levels was 88.33± 12.44 ng/24 hours. In the control group (group B), the mean value of urinary TGF-ß1 was 29.03 ± 3.23 ng/24 hours. Urinary TGF-ß1 levels were significantly elevated in group A as compared to group B (p<0.001). There was no significant correlation between urinary TGF-ß1 levels and estimated glomerular filtration rate (eGFR) (r=0.376, p= 0.285) as well as the urinary TGF-ß1 levels and 24-hour urine protein levels (p = 0.334, r = 0.341) in diabetic nephropathy cases. Glycosylated hemoglobin (HbA1c) levels didn't correlate with the urinary TGF-ß1 levels (r = -0.265, p = 0.46). Conclusion The urinary TGF-ß1 levels were significantly elevated in diabetic nephropathy patients as compared to healthy controls. There was no significant correlation between urinary TGF-ß1 levels and proteinuria, eGFR, or HbA1c levels in diabetic nephropathy patients.

Measured Glomerular Filtration Rate in Live Related Kidney Donors Three Months Post-Kidney Donation: A Single-Center Experience From Western India.

Background Glomerular filtration rate (GFR) estimation is pivotal in the evaluation of kidney donors. There are various methods available for assessing GFR, but there has been a lack of consensus on the measurement of GFR and the frequency of renal evaluation after kidney donation. Our study aims to analyze the measured GFR (m-GFR) before and three months after kidney donation and note the compensatory abilities of the remnant kidney in live related kidney donors. Methods This prospective observational study was conducted at the Department of Nephrology, Dr. D. Y. Patil Medical College, Hospital & Research Centre, Pune, from April 2021 to December 2022. The study included 30 donors from both genders aged between 23 and 73 years. The measured GFR was calculated using a technetium-99m diethylene triamine pentaacetic acid (Tc-99m DTPA) scan. We analyzed donor characteristics and various parameters that included demography, anthropometry, blood pressure, and serum creatinine and measured GFR (m-GFR) using a Tc-99m DTPA scan, which was compared before and three months after donor nephrectomy. Results Of the 30 donors, 25 (83.3%) were females and five (16.7%) were males. The mean age of donors was 49.23 ± 12.29 years. The mean body mass index (BMI) was noted to be 24.73 ± 5.58 kg/m2, whereas the mean body surface area (BSA) was 1.59 ± 0.12 m2. In terms of the measured GFR by DTPA scan, pre-donation and post-donation, the average GFR for our population was 103.83 ± 10.07 mL/minute/1.73 m2 and 60.47±6.57 mL/minute/1.73 m2, respectively. The mean measured GFR of remnant kidney increased by 9.21 ± 4.39 mL/minute/1.73 m2 in 28 donors, while two donors had a fall in the mean measured GFR by 6.8 ± 1.69 mL/minute/1.73 m2. Conclusions To safeguard donor health, accurate measurement of GFR at various timelines after kidney donation should be considered as there are various limitations associated with the use of serum creatinine-based GFR estimating equations for solitary kidneys. However, long-term studies are required to analyze the changes in GFR after nephrectomy and determine the adequacy of compensatory changes in the remnant kidney post-kidney donation.

A MoSe2/N-doped hollow carbon sphere host for rechargeable Na-Se batteries.

Sodium-selenium (Na-Se) batteries are promising alternatives to lithium-ion batteries for energy storage systems owing to their high energy density and natural abundance of Na resources. However, their drawbacks of low Se loading, dissolution of intermediate sodium polyselenides in the electrolyte and volumetric expansion of Se impede their real applications. To address these issues, herein, we report a multifunctional Se host with MoSe2 nanosheets coupled with nitrogen-doped porous carbon hollow spheres for the first time. The N-doped hollow carbon sphere structure could provide a large space for Se loading (Se content up to 72 wt%) and accommodate the volume expansion of Se species upon cycling. MoSe2 was chosen as a polar coupling component for the carbon matrix, owing to its low conversion reaction voltage. Based on density functional theory (DFT) calculations, the MoSe2 nanosheets coupled with hollow spheres could enhance the adsorption energy of the host to polyselenides chemically, which benefits the immobilization of polyselenides. Therefore, as a cathode for Na-Se batteries, the as-prepared composite exhibits excellent energy storage performance with long cycling life and superior rate performance. Our study of introducing transition metal selenides into Na-Se batteries may stimulate the designing of diverse Se-based cathodes.

Role of T-lymphocytes in Kidney Disease.

Background The role of T-regulatory cells (Tregs) in inflammatory renal disease is not yet established. We attempted to study peripherally circulating T-cells expressing RORγt+Foxp3+ dynamics in acute kidney injury (AKI) and chronic kidney disease (CKD). Aim To determine the role of T-regulatory cells in AKI and CKD. Research methodology  This is a cross-sectional study conducted between January 2019 to January 2021 at a single tertiary care centre in Pune, India. Candidates enrolled in the study were either patients with CKD not on maintenance hemodialysis or newly diagnosed cases of AKI. Kidney transplant recipients, patients with autoimmune diseases like systemic lupus erythematosus (SLE), IgA nephropathy, or those receiving immuno-suppressants were excluded. T-lymphocytes were analyzed using a flow cytometer.  Results We studied 80 patients with kidney injury, 40 each belonging to the AKI and CKD study groups and 10 healthy volunteers as controls. The rationale behind having a small control group was to merely get an idea of T helper 17 (Th17):Treg ratio and different immune cell-phenotype profiles in healthy volunteers without kidney injury, diabetes, hypertension or any other risk factors. The ratio of RORγt:Foxp3 was ≤ 1 in these individuals (control group) while this ratio was significantly altered (MFI RORγt:Foxp3 ≥1) in the AKI/CKD study arm. We examined peripherally circulating T-lymphocytes in acute kidney injury and chronic kidney disease, comparing their activity to healthy volunteers. Biopsy-proven kidney injury patients (29/80) were also included in this study. We found that the ratio of RORγt:Foxp3 was altered in patients with kidney injury (acute and chronic) and was statistically significant compared to controls, indicating that injury may be attributed to T-cell dysfunction.  Conclusion Our study provides some evidence of T-cell dysfunction in the pathology of kidney injury in acute and chronic kidney disease via activity of Foxp3 and RORγt. We found that there is evidence of altered Th17/Treg activity in kidney injury, more prevalent in acute than chronic, when compared to healthy volunteers.