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Human embryonic stem (ES) cell culture has developed over the years allowing the subtle procedures that are easy to manipulate. Feeder-free ES cell culture is an important milestone for human pluripotent stem cell research which eliminates the feeder cells. Various matrices and medium formulations have been generated for feeder-independent culture. Here we described an mTeSR™1 based feeder-independent human ES cell culture on Matrigel® matrix. Culture, freeze/thaw, passaging and initiation of differentiation in suspension culture were described.Healthy vocal fold mucosa is composed of two major cell types, non-keratinized stratified squamous epithelium and vocal fold fibroblasts. Although dysfunction of the epithelium may play a significant pathogenic role in vocal fold diseases, studies at the genetic and molecular level using primary epithelial cells or models of human vocal fold mucosa have been significantly limited by the availability of relevant tissue types, poor growth, and heterogeneity of primary vocal fold epithelial cells. Here, we describe in vitro developmental differentiation of human induced pluripotent stem cells into vocal fold basal epithelial progenitors that were reseeded on collagen-fibroblast constructs to induce stratification and generate a three-dimensional model of human vocal fold mucosa. The engineered vocal fold mucosa represents physiologically relevant and clinically useful model that can be used as a tool for disease modeling and testing of therapeutic approaches for the treatment of laryngeal and VF inflammation.
To identify the evidence that supports the effect of interventions made by hospital pharmacists, individually or in collaboration with a multidisciplinary team, in terms of healthcare outcomes,a more effective utilization of resources and lower costs in older polymedicated inpatients.
We searched the following databases MEDLINE, EMBASE and the Cochrane Library. We also conducted a hand search by checking the references cited in the primary studies and studies included in reviews identified during the process of research. Four review authors working by pairs searched for studies, extracted data, and drew up the results tables.
Twenty-six studies were included in the review. In 13 of them pharmacists carried out their intervention exclusively while the patients were in hospital, whereas in 13 interventions were delivered during admission and after hospital discharge. Outcomes identified were mortality, length of stay, visits to the emergency department, readmissions and reported quality of life, among othtions in older polymedicated patients. Mortality does not show as a relevant outcome. Other health care outcomes, such as hospital readmissions, visits to the emergency department and healthcare costs, seem to be more relevant and amenable to change. Interventions that include pharmacists in multidisciplinary geriatric teams seem to be more promising that isolated pharmacist interventions. Interventions prolonged after hospital discharge seem to be more appropriate that interventions delivered only during hospital admission. Better-designed studies should be conducted in the future to provide further insight into the effect of hospital pharmacist interventions.Dioctophyme renale, the giant kidney worm, is a renal nematode from domestic and wild mammals that has zoonotic potential. In humans, dioctophimosis has been reported in several countries, mainly on the Asian continent, totaling more than 40 cases, which describe the parasite mainly infecting the kidneys, bladder, urethra and skin. Infection in animals and humans is related to the ingestion of the infective larva (L3) present in the aquatic oligochaete annelid (mandatory intermediate host) or fish and anurans (facultative paratenic hosts). Thus, the infection is related to the habit of drinking water contaminated with the mandatory intermediate host, as well as raw or undercooked meat from the facultative paratenic hosts. Dioctophimosis destroys the renal parenchyma and, in some cases, can cause the death of its hosts. In this chapter, we discuss the main topics regarding dioctophimosis in humans, domestic and wild animals, highlighting its importance in public health.Analysis of fluoride in body fluids (urine and serum) is essential for fluorosis diagnosis. Although 24-h urine collection is adopted to assess community defluoridation/fluoride supplementation program/research studies, but not feasible for Clinical/Pathological laboratories. Patients are reluctant to bring 24-h urine samples. Hence, spot urine samples are collected in clean, dry polypropylene bottles (not glass) without any preservative and analyzed on the same day by the Ion analyzer (ISE method). Equal volumes of Total Ionic Strength Adjustment Buffer (TISAB) solution are then added with body fluids before analysis and mixed well to eliminate interference from other ions besides pH adjustment and to provide a constant ionic strength. Results are reported as mg of Fluoride/l (ppm). High fluoride level in body fluids is an indication of confirmed cases of fluorosis. Two interventions, e.g. withdrawal of fluoride intake and intake of nutritive diet was introduced for prevention and control of fluorosis. The present study is to provide useful guidelines for monitoring of fluorosis disease in human beings, those who are at the risk of fluoride exposure.Our general goal was to non-invasively evaluate kidney tubular dysfunction. We developed a strategy based on cysteine (Cys) disulfide stress mechanism that underlies kidney dysfunction. There is scarce information regarding the fate of Cys-disulfides (CysSSX), but evidence shows they might be detoxified in proximal tubular cells by the action of N-acetyltransferase 8 (NAT8). This enzyme promotes the addition of an N-acetyl moiety to cysteine-S-conjugates, forming mercapturates that are eliminated in urine. Therefore, we developed a strategy to quantify mercapturates of CysSSX in urine as surrogate of disulfide stress and NAT8 activity in kidney tubular cells. We use a reduction agent for the selective reduction of disulfide bonds. The obtained N-acetylcysteine moiety of the mercapturates from cysteine disulfides was monitored by fluorescence detection. The method was applied to urine from mice and rat as well as individuals with healthy kidney and kidney disease.From the theory of homeostasis, it can be deduced that urine is the source of sensitive disease markers reflecting early changes of the body. The study of urinary biomarkers using animal models is essential to prove this theory and encourage people to continue exploring the potential of urine. In clinical research, when disease-related changes are greater than individual variances, disease-related biomarkers with potential clinical application can be obtained by directly dividing samples into disease groups and control groups. To discover small early changes in disease, pre-and-post control of the same person can minimize most interfering factors. In this way, changes in urinary proteins before, during and after disease and/or treatment can be found, which can provide useful information for early detection and evaluation of the disease condition and treatment effect. In the study of clinical urinary biomarkers, regional and ethnic factors cannot be completely ignored. Diseases such as autism, which have only social behavior changes, may also be reflected in the urine proteome. Current research on urinary biomarkers is not sufficient to earn the recognition it deserves in the field of biomarkers. The recognition of urinary biomarkers will require the cooperation of more doctors and scientists and the participation of more foundations and companies.Chronic glomerulonephritis (CGN) is a disease with a steady progressive course that involves the development of nephrosclerosis, which is especially evident in clinical courses with incidences of high proteinuria (PU). Currently, proteinuria is considered the main laboratory feature (sign) of CGN activity and progression because proteinuria is closely related to the process of tubulointerstitial fibrosis, which is correlated with the grade of renal insufficiency. The injury to podocytes, which are key components of the filtration barrier, plays a central role in proteinuria development. The detachment of podocytes from the glomerular basement membrane leading to podocytopenia is suggested to induce glomerulosclerosis and hyalinosis with obliteration of capillary loops and the progression of chronic kidney disease. Urinary markers of podocyte dysfunction could serve as useful tools while monitoring the activity and prognosis of CGN. In this chapter, the most important mechanisms of podocyte loss and urinary markers of this process are discussed.Bladder cancer (BC) is one of the most common tumor with high incidence. Relative to other cancers, BC has a high rate of recurrence, which results in increased mortality. As a result, early diagnosis and life-long monitoring are clinically significant for improving the long-term survival rate of BC patients. At present, the main methods of BC detection are cystoscopy and biopsy; however, these procedures can be invasive and expensive. This can lead to patient refusal and reluctance for monitoring. There are several BC biomarkers that have been approved by the FDA, but their sensitivity, specificity, and diagnostic accuracy are not ideal. click here More research is needed to identify suitable biomarkers that can be used for early detection, evaluation, and observation. There has been heavy research in the proteomics and genomics of BC and many potential biomarkers have been found. Although the advent of metabonomics came late, with the recent development of advanced analytical technology and bioinformatics, metabonomics has become a widely used diagnostic tool in clinical and biomedical research. It should be emphasized that despite progress in new biomarkers for BC diagnosis, there remains challenges and limitations in metabonomics research that affects its translation into clinical practice. In this chapter, the latest literature on BC biomarkers was reviewed.Cardiac troponin T (cTnT) is a sensitive and specific biomarker for detecting cardiac muscle injury. Its concentration in blood can be significantly elevated outside the normal reference range under several pathophysiological conditions. The classical analytical method in routine clinical analysis to detect cTnT in serum or plasma is a single commercial immunoassay, which is designed to quantify the intact cTnT molecule. The targeted epitopes are located in the central region of the cTnT molecule. However, in blood cTnT exists in different biomolecular complexes and proteoforms bound (to cardiac troponin subunits or to immunoglobulins) or unbound (as intact protein or as proteolytic proteoforms). While proteolysis is a principal posttranslational modification (PTM), other confirmed PTMs of the proteoforms include N-terminal initiator methionine removal, N-acetylation, O-phosphorylation, O-(N-acetyl)-glucosaminylation, N(ɛ)-(carboxymethyl)lysine modification and citrullination. The immunoassay probably detects several of those cTnT biomolecular complexes and proteoforms, as long as they have the centrally targeted epitopes in common. While analytical cTnT immunoreactivity has been studied predominantly in blood, it can also be detected in urine, although it is unclear in which proteoform cTnT immunoreactivity is present in urine. This review presents an overview of the current knowledge on the pathophysiological lifecycle of cTnT. It provides insight into the impact of PTMs, not only on the analytical immunoreactivity, but also on the excretion of cTnT in urine as one of the waste routes in that lifecycle. Accordingly, and after isolating the proteoforms from urine of patients suffering from proteinuria and acute myocardial infarction, the structures of some possible cTnT proteoforms are reconstructed using mass spectrometry and presented.
Homepage: https://www.selleckchem.com/products/Sunitinib-Malate-(Sutent).html
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