Zymomonas mobilis have characteristics that classify it as probiotic. Thus, this study aimed to evaluate the effect of regular consumption of fermented broth of this strain on the intestinal function of individuals with changes in intestinal transit. This is a randomized, descriptive and quantitative clinical trial, a sample composed of undergraduate students from a university center in Caruaru. After screening for individuals with constipation according to the inclusion and exclusion criteria, only 13 agreed to participate in the study. They were divided into groups group 1 received Zymomonas mobilis fermented broth once a day; group 2 also received the fermented broth in the same concentration cells being twice a day; group 3 received cell-free fermented broth once daily; and group 4, placebo, received saline once daily, all groups drank for fifteen days, and laboratory tests were performed to check lipid profile before and after that period. Observed an increase in evacuation days in all groups averaged in media 7.0-10.5 days. Groups 1 and 2 showed an increase in total cholesterol (0.5% and 5.0%, respectively), HDL cholesterol (4.1% and 24.1%), LDL cholesterol (4.9% and 8.4%), VLDL cholesterol (17.9% and 11.2%) and triglycerides (19.1% and 27.9%). In group 3, there was a reduction of total cholesterol (-2.4%), LDL cholesterol (-11.2%), VLDL cholesterol (-15.9%), triglycerides (-27.7%) and increase in HDL cholesterol (25.7%). Thus, the broth fermented with Zymomonas mobilis regulated the intestinal transit, but did not improve the lipid profile, while the without cells broth showed a better lipid profile.Donnai-Barrow syndrome (DBS) is an autosomal-recessive disorder characterized by multiple pathologies including malformation of forebrain and eyes, as well as resorption defects of the kidney proximal tubule. The underlying cause of DBS are mutations in LRP2, encoding the multifunctional endocytic receptor megalin. Here, we identified a unique missense mutation R3192Q of LRP2 in an affected family that may provide novel insights into the molecular causes of receptor dysfunction in the kidney proximal tubule and other tissues affected in DBS. Using patient-derived induced pluripotent stem cell lines we generated neuroepithelial and kidney cell types as models of the disease. Using these cell models, we documented the inability of megalin R3192Q to properly discharge ligand and ligand-induced receptor decay in lysosomes. Thus, mutant receptors are aberrantly targeted to lysosomes for catabolism, essentially depleting megalin in the presence of ligand in this affected family.Chronic kidney disease (CKD) is common, with hypertension and diabetes mellitus acting as major risk factors for its development. Cardiovascular disease is the leading cause of death worldwide and the most frequent end point of CKD. There is an urgent need for more precise methods to identify patients at risk of CKD and cardiovascular disease. Alterations in microvascular structure and function contribute to the development of hypertension, diabetes, CKD, and their associated cardiovascular disease. Homology between the eye and the kidney suggests that noninvasive imaging of the retinal vessels can detect these microvascular alterations to improve targeting of at-risk patients. Retinal vessel-derived metrics predict incident hypertension, diabetes, CKD, and cardiovascular disease and add to the current renal and cardiovascular risk stratification tools. The advent of optical coherence tomography (OCT) has transformed retinal imaging by capturing the chorioretinal microcirculation and its dependent tissue with near-histological resolution. In hypertension, diabetes, and CKD, OCT has revealed vessel remodeling and chorioretinal thinning. Clinical and preclinical OCT has linked retinal microvascular pathology to circulating and histological markers of injury in the kidney. The advent of OCT angiography allows contrast-free visualization of intraretinal capillary networks to potentially detect early incipient microvascular disease. Combining OCT’s deep imaging with the analytical power of deep learning represents the next frontier in defining what the eye can reveal about the kidney and broader cardiovascular health.The association between dietary sodium and potassium intake with the development of kidney disease remains unclear, particularly among younger individuals. Here, we determined whether dietary sodium and potassium intake are associated with incident chronic kidney disease (CKD) using data from 1,030 adults (age 23-35 in 1990-1991) from the Coronary Artery Risk Development In Young Adults study, based on repeated measurements of estimated glomerular filtration rate (eGFR) and urinary albumin to creatinine ratio (ACR) from 1995 through 2015. Urinary sodium and potassium excretion (mg/day), calculated from three 24-hour urine collections in 1990-1991, were averaged to measure sodium and potassium intake. Serum creatinine was used to calculate eGFR using the CKD EPI equation; spot urine albumin and creatinine were used to calculate ACR, each at five visits from 1995-1996 through 2015-2016. CKD was defined as decreased eGFR (under 60 ml/min/1.73m2) or the development of albuminuria (ACR over 30 mg/g). We used log binomial regression models adjusted for socio-demographic, behavioral, and clinical factors to determine whether sodium and potassium intake were associated with incident CKD (decreased eGFR or developed albuminuria) among those free of CKD in 1995. Dietary sodium intake was not significantly associated with incident CKD. However, every 1,000 mg/day increment of potassium intake in 1990 was significantly associated with a 29% lower risk of incident albuminuria (relative risk 0.71, 95% confidence interval 0.53, 0.95), but not eGFR. Thus, higher dietary potassium intake may protect against the development of kidney damage, particularly albuminuria.Mitochondrial dysfunction plays a critical role in the pathogenesis of kidney diseases via ATP depletion and reactive oxygen species overproduction. Nonetheless, few studies have reported the renal mitochondrial status clinical settings, partly due to a paucity of methodologies. Recently, a positron emission tomography probe, 18F-BCPP-BF, was developed to non-invasively visualize and quantitate the renal mitochondrial status in vivo. Here, 18F-BCPP-BF positron emission tomography was applied to three mechanistic kidney disease models in rats kidney ischemia-reperfusion, 5/6 nephrectomy and anti-glomerular basement membrane glomerulonephritis. In rats with ischemia-reperfusion, a slight decrease in the kidney uptake of 18F-BCPP-BF was accompanied by morphological abnormality of the mitochondria in the proximal tubular cells after three hours of reperfusion, when the kidney function was slightly declined. In 5/6 nephrectomy and rats with anti-glomerular basement membrane glomerulonephritis, the kidney uptake of 18F-BCPP-BF cumulatively decreased with impairment of the kidney function, which was accompanied by a reduction of mitochondrial protein and a pathological tubulointerstitial exacerbation rather than glomerular injury. The 18F-BCPP-BF uptake in the injured kidney was suggested to represent the volume of healthy tubular epithelial cells with normally functioning mitochondria. Thus, this positron emission tomography probe can be a powerful tool for studying the pathophysiological meanings of the mitochondrial status in kidney disease.Cytomegalovirus (CMV) reactivation from latently infected donor organs post-transplantation and its dissemination cause significant comorbidities in transplant recipients. Transplant-induced inflammation combined with chronic immunosuppression has been thought to provoke CMV reactivation and dissemination, although sequential events in this process have not been studied. Here, we investigated this process in a high-risk donor CMV-positive to recipient CMV-negative allogeneic murine kidney transplantation model. Recipients were either treated with indefinite immunosuppression or tolerized in a donor-specific manner. Untreated recipients served as controls. Kidney allografts from both immunosuppressed and tolerized recipients showed minimal alloimmunity-mediated graft inflammation and normal function for up to day 60 post-transplantation. However, despite the absence of such inflammation in the immunosuppressed and tolerized groups, CMV reactivation in the donor positive kidney allograft was readily observed. Interestingly, subsequent CMV replication and dissemination to distant organs only occurred in immunosuppressed recipients in which CMV-specific CD8 T cells were functionally impaired; whereas in tolerized recipients, host anti-viral immunity was well-preserved and CMV dissemination was effectively prevented. Thus, our studies uncoupled CMV reactivation from its dissemination, and underscore the potential role of robust transplantation tolerance in preventing CMV diseases following allogeneic kidney transplantation.Introduction Gender and/or sex have a major impact on staying healthy, becoming ill, or care dependent. Differences between men and women have been described for socioeconomic positions, health behaviors, courses and severities of diseases and mortality rates. Consequently, sex and/or gender need to be adequately taken into account while developing and implementing evidence-based healthcare. Evidence regarding differences between men and women in pressure ulcer care is limited. Our research aim was to measure possible differences between male and female hospital patients and nursing home residents in prevention and treatment of institutional-acquired pressure ulcers. Methods A secondary data analysis was conducted including data sets collected in nursing homes and hospitals in Germany annually from 2001 to 2016. Relevant variables were compared according to biological sex (men/woman). Results The study included 38,655 nursing home residents (mean age 85.4 years women, 77.3 years men) and 58,760 hospital patients (mean age 66.7 years women, 63.4 years men). More women were underweight and at pressure ulcer risk in both settings. The proportion of institutional-acquired pressure ulcers was higher for men in hospitals. Slightly more men had a PU category 2 to 4 (OR 0.87, 95% CI 0.76 to 0.99) in nursing homes or developed an institutional-acquired pressure ulcers category 2 to 4 in both settings (OR 0.85, 95% CI 0.76 to 0.95). Special mattresses were more often used by women at PU risk. More men with an institutional-acquired pressure ulcer in hospitals received counseling of relatives (OR 0.53, 95% CI 0.39 to 0.72). Conclusion Although slightly more men had institutional-acquired pressure ulcers than women, overall differences regarding pressure ulcer occurrence were minor. Gender and/or sex can rather not be considered as an independent risk factor for pressure ulcer development and differences regarding pressure ulcer prevention interventions seem to be minor.Objective To evaluate the effects of constant rate infusions (CRIs) of dexmedetomidine and remifentanil alone and their combination on minimum alveolar concentration (MAC) of sevoflurane in dogs. Study design Randomized crossover experimental study. Animals A total of six (three males, three females) healthy, adult neutered Beagle dogs weighing 12.6 ± 1.4 kg. Methods Anesthesia was induced with sevoflurane in oxygen until endotracheal intubation was possible and anesthesia maintained with sevoflurane using positive-pressure ventilation. Each dog was anesthetized five times and was administered each of the following treatments saline (1 mL kg-1 hour-1) or dexmedetomidine at 0.1, 0.5, 1.0 or 5.0 μg kg-1 loading dose intravenously over 10 minutes followed by CRI at 0.1, 0.5, 1.0 or 5.0 μg kg-1 hour-1, respectively. Following 60 minutes of CRI, sevoflurane MAC was determined in duplicate using an electrical stimulus (50 V, 50 Hz, 10 ms). Then, CRI of successively increasing doses of remifentanil (0.15, 0.60 and 2.