Poultry is one of the fastest growing segments of the agricultural economy, particularly in developing countries. By using different econometric models, this study estimated the production efficiency and effectiveness of poultry farming. The objective was to examine the socio-economic status, estimate the costs and returns and production efficiency in production of egg. A stratified random sampling technique was applied. Feed conversion ratio, egg-feed price ratio and benefit-cost ratio were analyzed statistically to estimate the production efficiency. Various social factors like age of farmers, family size and number of laying birds were found significantly affecting the poultry business. Various investment patterns in farms their respective values and worked out the level of significance was analyzed. The analysis of net return was differed significantly with farm size with higher net return in large farm. This study concluded that large farm has higher mass of egg production and lower feed conversion rate indicating higher profit margin with enlarge in farm size.

Kidney transplantation is the preferred treatment for end-stage kidney disease (ESKD). However, there is a shortage of transplantable kidneys, and donor organs can be damaged by necessary cold storage (CS). Although CS improves the viability of kidneys from deceased donors, prolonged CS negatively affects transplantation outcomes. Previously, we reported that renal proteasome function decreased after rat kidneys underwent CS followed by transplantation (CS + Tx). Here, we investigated the mechanism underlying proteasome dysfunction and the role of the proteasome in kidney graft outcome using a rat model of CS + Tx. We found that the key proteasome subunits β5, α3, and Rpt6 are modified, and proteasome assembly is impaired. Specifically, we detected the modification and aggregation of Rpt6 after CS + Tx, and Rpt6 modification was reversed when renal extracts were treated with protein phosphatases. CS + Tx kidneys also displayed increased levels of nitrotyrosine, an indicator of peroxynitrite (a reactive oxygen species, ROS), compared to sham. Because the Rpt6 subunit appeared to aggregate, we investigated the effect of CS + Tx-mediated ROS (peroxynitrite) generation on renal proteasome assembly and function. We treated NRK cells with exogenous peroxynitrite and evaluated PAC1 (proteasome assembly chaperone), Rpt6, and β5. Peroxynitrite induced a dose-dependent decrease in PAC1 and β5, but Rpt6 was not affected (protein level or modification). Finally, serum creatinine increased when we inhibited the proteasome in transplanted donor rat kidneys (without CS), recapitulating the effects of CS + Tx. These findings underscore the effects of CS + Tx on renal proteasome subunit dysregulation and also highlight the significance of proteasome activity in maintaining graft function following CS + Tx.

Background: Hypothermic machine perfusion (HMP) has been associated with reduced delayed graft function compared with static cold storage (SCS). However, the molecular mechanisms underlying these differences during cold preservation remain incompletely understood. This study compared cold-storage-related biochemical and histological changes in kidneys preserved by HMP versus SCS using a Lewis rat model prior to transplantation. Methods: Following isolation, rat kidneys were flushed with cold saline (4 °C). Left kidneys were preserved by HMP at constant flow using Belzer’s machine perfusion solution (MPS) at 4 °C, while right kidneys were stored using SCS in University of Wisconsin solution at 4 °C. After four hours of preservation, kidneys were processed for biochemical and histological analysis. Fresh biopsies were evaluated for mitochondrial complex respiration. Western blotting was performed to assess expression of NDUFS3, a complex I subunit. Histological staining for nitrotyrosine and kidney injury markers was compared across groups. Results: Mitochondrial complex respiration did not differ significantly between the SCS and HMP groups. Western blot analysis demonstrated significantly increased NDUFS3 expression in HMP-preserved kidneys compared with SCS and control kidneys. Histological evaluation revealed elevated tubular staining of nitrotyrosine and kidney injury markers in SCS kidneys relative to controls, whereas HMP preservation markedly attenuated these increases. Conclusions: HMP mitigates cold-storage-induced oxidative stress and reduces expression of kidney injury markers after four hours of preservation. These molecular findings suggest a protective effect of HMP during cold preservation. Future studies with longer preservation times and transplantation models are needed to determine whether these improvements translate into enhanced post-transplant kidney function.

Ischemia–reperfusion injury (IRI) is a major driver of acute kidney injury and development of chronic kidney disease. Although complement activation worsens IRI, the roles of upstream (C3) versus downstream (C5) components remain unclear. Renal IRI was surgically induced in C3 knockout (C3 ⁻ / ⁻ ) and C5 knockout (C5 ⁻ / ⁻ ) Lewis rats, and the renal function as well as histopathology were systematically assessed. Further, quantitative proteomics coupled with pathway enrichment analysis was performed to define complement‐dependent mechanisms. C3 and C5 deficiency conferred strong protection against renal IRI with improved renal function, reduced tubular necrosis, and lower expression of injury markers (KIM‐1, NGAL). Post‐IRI, C3 ^−/− enhanced mitochondrial, metabolic, and purine pathways while suppressing immune and extra‐cellular matrix programs. C5 ^−/− affected extracellular matrix remodeling and structural pathways with modest immune suppression. We demonstrate for the first time that upstream C3 ^−/− impacts a diverse range of renal injury and repair mechanisms compared to C5 ^−/− alone, although both interventions successfully reduced IRI‐mediated injury. Together, these findings highlight strategies for future complement‐based therapies targeting the upstream or downstream cascade.

Chronic Kidney Disease (CKD) affects approximately 14% of adults globally and is a progressive, multifactorial disorder of the kidney characterized by structural or functional nephron impairment. CKD has been linked with several other comorbidities, including diabetes, hypertension, obesity, and aging, which increase the complexity of the disease. Because early-stage CKD is frequently asymptomatic, diagnosis is frequently delayed, resulting in increased risk of progression to End-Stage Kidney Disease (ESKD). Diagnostic tools such as estimated glomerular filtration rate (eGFR) and albuminuria remain limited for early diagnosis, making the condition more threatening. Recent molecular biology research has identified chronic inflammation, oxidative stress, mitochondrial dysfunction, fibrosis, and regulated cell death as central mechanisms driving CKD progression. Novel biomarkers, including kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and cystatin C, along with multi-omics technologies, have created opportunities for earlier diagnosis, risk stratification, and precision-based therapies, although most remain investigational rather than established for routine clinical use. Current treatment approaches, such as renin–angiotensin–aldosterone system inhibitors and sodium-glucose cotransporter-2 inhibitors, can slow but not halt disease progression. This review describes CKD epidemiology, molecular mechanisms, current and experimental diagnostics, advances in therapeutic strategies, and future directions. It emphasizes the role of molecular biomarkers and precision medicine in optimizing patient care and outcomes.