Post-COVID-19 conditions encompass a wide range of health problems, including enteritis, but their association with parasitic infections has not yet been investigated. This study analyzed gastrointestinal symptoms, medical histories, fecal Cryptosporidium oocysts, and the history of COVID-19 infection in patients who attended the Faculty of Medicine, Cairo University, from January to July 2021. Fecal biomarkers, including H. pylori, occult blood, fecal calprotectin (FCAL), and TNF-a, were measured, and Cryptosporidium spp. genotypes were molecularly characterized among post-COVID-19 patients using RFLP. Preliminary results from 210 post-COVID-19 patients revealed that group 1 (Cryptosporidiumpositive) (n = 49) and group 2 (Cryptosporidium-negative) (n = 161) showed no significant difference in the prevalence rate of diabetes mellitus (DM). While group 2 was linked to diarrhea, only infections with Cryptosporidium post-COVID-19 were related to chronic diarrhea, vomiting, and weight loss. A total of 220 healthy subjects served as negative controls. Administering azithromycin, hydroxychloroquine, and ivermectin was significantly related to an increased risk of Cryptosporidium infection in group 1, whereas only azithromycin was more frequently recorded in group 2. Antioxidant supplementation insignificantly affected the incidence of cryptosporidiosis. Cryptosporidiosis with a history of COVID-19 was linked to H. pylori infections, increased inflammatory biomarkers (FCAL and TNF-a), and occult blood when compared with group 2. Cryptosporidium genotype 1 was the most commonly occurring subset in individuals with post-COVID-19. The findings demonstrated that aggravating gastrointestinal manifestations, increased fecal biomarkers and anti-COVID-19 therapeutic interventions are significantly related to the existence of Cryptosporidium oocysts in patients with post-COVID-19, indicating the predominance of.

Vancomycin, an antibiotic used occasionally as a last line of treatment for methicillin-resistant Staphylococcus aureus, is reportedly associated with nephrotoxicity. This study aimed at evaluating the protective effects of lutein against vancomycin-induced acute renal injury. Peroxisome proliferator-activated receptor gamma (PPARγ) and its associated role in renoprotection by lutein was also examined. Male BALB/c mice were divided into six treatment groups: control with normal saline, lutein (200 mg/kg), vancomycin (250 mg/kg), vancomycin (500 mg/kg), vancomycin (250 mg/kg) with lutein, and vancomycin (500 mg/kg) with lutein groups; they were euthanized after 7 days of treatment. Thereafter, samples of blood, urine, and kidney tissue of the mice were analyzed, followed by the determination of levels of N-acetyl-β-D-glucosaminidase (NAG) in the urine, renal creatine kinase; protein carbonyl, malondialdehyde, and caspase-3 in the kidney; and the expression of PPARγ, nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappaB (NF-κB) in renal tissue. Results showed that the levels of protein carbonyl and malondialdehyde, and the activity of NAG, creatine kinase and caspase-3, were significantly increased in the vancomycin-treatment groups. Moreover, the levels of Nrf2 significantly decreased, while NF-κB expression increased. Lutein ameliorated these effects, and significantly increased PPARγ expression. Furthermore, it attenuated vancomycin-induced histological alterations such as, tissue necrosis and hypertrophy. Therefore, we conclude that lutein protects against vancomycin-induced renal injury by potentially upregulating PPARγ/Nrf2 expression in the renal tissues, and consequently downregulating the pathways: inflammation by NF-κB and apoptosis by caspase-3.

Vancomycin, an antibiotic used occasionally as a last line of treatment for methicillin-resistant Staphylococcus aureus, is reportedly associated with nephrotoxicity. This study aimed at evaluating the protective effects of lutein against vancomycin-induced acute renal injury. Peroxisome proliferator-activated receptor gamma (PPARγ) and its associated role in renoprotection by lutein was also examined. Male BALB/c mice were divided into six treatment groups: control with normal saline, lutein (200 mg/kg), vancomycin (250 mg/kg), vancomycin (500 mg/kg), vancomycin (250 mg/kg) with lutein, and vancomycin (500 mg/kg) with lutein groups; they were euthanized after 7 days of treatment. Thereafter, samples of blood, urine, and kidney tissue of the mice were analyzed, followed by the determination of levels of N-acetyl-β-D-glucosaminidase (NAG) in the urine, renal creatine kinase; protein carbonyl, malondialdehyde, and caspase-3 in the kidney; and the expression of PPARγ, nuclear factor erythroid 2-related factor 2 (Nrf2), and nuclear factor-kappaB (NF-κB) in renal tissue. Results showed that the levels of protein carbonyl and malondialdehyde, and the activity of NAG, creatine kinase and caspase-3, were significantly increased in the vancomycin-treatment groups. Moreover, the levels of Nrf2 significantly decreased, while NF-κB expression increased. Lutein ameliorated these effects, and significantly increased PPARγ expression. Furthermore, it attenuated vancomycin-induced histological alterations such as, tissue necrosis and hypertrophy. Therefore, we conclude that lutein protects against vancomycin-induced renal injury by potentially upregulating PPARγ/Nrf2 expression in the renal tissues, and consequently downregulating the pathways: inflammation by NF-κB and apoptosis by caspase-3.

BACKGROUND AND OBJECTIVES: Bone marrow-derived mesenchymal stem cells (BM-MSCs) are adult multipotent non-haematopoietic stem cells that have regeneration potential. The current study aimed to detect the ability of BM-MSCs to improve kidney and cardiac functions in adult rats with established chronic kidney disease. METHODS: Rats were divided into sham-operated control, untreated sub totally nephrectomised and treated sub totally nephrectomised groups. Body weight, kidney and cardiac tissue weights, plasma creatinine and urea levels and arterial blood pressure were measured. ECG was recorded, and an in vitro isolated heart study was performed. Results: Stem cell treatment decreased the elevated plasma creatinine and urea levels and decreased systolic, diastolic and mean arterial blood pressure values. These changes were accompanied by a decrease in glomerular hypertrophy with apparent normal renal parenchyma. Additionally, BM-MSCs shortened Q-To and Q-Tc intervals, all time to peak tension values, the half relaxation value at 30 min of reperfusion and the contraction time at 15 and 30 min of reperfusion. Moreover, stem cell treatment significantly increased the heart rate, QRS voltage, the peak tension at the 15- and 30-min reperfusion time points and the peak tension per left ventricle at the 30-min reperfusion time point compared to the pre-ischaemia baseline. BM-MSCs resolve inter muscular oedema and lead to the re-appearance of normal cardiomyocytes. This improvement occurs with the observations of BM-MSCs in renal and heart tissues. CONCLUSIONS: BM-MSCs can attenuate chronic kidney disease progression and the associated cardiac electrophysiological and inotropic dysfunction.
Adult ; Animals ; Arterial Pressure ; Body Weight ; Creatinine ; Electrocardiography ; Heart Rate ; Heart Ventricles ; Heart ; Humans ; Hypertrophy ; In Vitro Techniques ; Kidney ; Mesenchymal Stromal Cells ; Myocytes, Cardiac ; Nephrectomy ; Plasma ; Rats ; Regeneration ; Relaxation ; Renal Insufficiency, Chronic ; Reperfusion ; Stem Cells ; Urea ; Weights and Measures