Journal articles on the topic 'Serum 25D'
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Chun, Rene F., Ivan Hernandez, Renata Pereira, Leon Swinkles, Tonnie Huijs, Rui Zhou, Nancy Q. Liu, et al. "Differential Responses to Vitamin D2 and Vitamin D3 Are Associated With Variations in Free 25-Hydroxyvitamin D." Endocrinology 157, no. 9 (July 13, 2016): 3420–30. http://dx.doi.org/10.1210/en.2016-1139.
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25-Hydroxyvitamin D (25D) circulates bound primarily to serum vitamin D binding protein (DBP), with DBP showing higher binding affinity for 25D3 than 25D2. We therefore hypothesized that vitamin D2 (D2) promotes higher serum levels of unbound 25D (free 25D), with different functional responses, relative to vitamin D3 (D3). Week 3 C56BL/6 mice were placed on diets containing either D2 or D3 alone (both 1000 IU/kg). At week 8 and week 16, D2 mice had only 25D2 in circulation (26.6 ± 1.9 and 33.3 ± 4.4 ng/mL), and D3 mice had only 25D3 (28.3 ± 2.0 and 31.7 ± 2.1 ng/mL). At week 8 (44.5 ± 6.4 vs 62.4 ± 11.6 pg/mL, P < .05) and week 16 (78.4 ± 12.6 vs 95.5 ± 11.6), D2 mice had lower serum 1,25-dihydroxyvitamin D relative to D3 mice. By contrast, measured free 25D was significantly higher in D2 mice at week 8 (16.8 ± 0.65 vs 8.4 ± 0.63 pg/mL, P < .001) and week 16 (17.4 ± 0.43 vs 8.4 ± 0.44, P < .001). A two-way ANOVA of bone histomorphometry showed that week 8 D2 mice had significantly higher osteoclast surface/bone surface, eroded surface/bone surface, and mineral apposition rate compared with D3 mice. Osteoblast surface/bone surface was higher in week 8 D2 females but not week 8 D2 males. At week 16, D2 mice had significantly higher bone volume/total volume and trabecular number compared with D3 mice. Differences in bone phenotype were observed despite D2 mice reaching similar serum 25D levels and lower 1,25D levels compared with D3 mice. These data indicate that 25D2 binds less well to DBP than 25D3, with resulting higher levels of free 25D promoting differential effects on bone in mice exposed to D2 alone.
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Berg, Anders H., Camille E. Powe, Michele K. Evans, Julia Wenger, Guillermo Ortiz, Alan B. Zonderman, Pirianthini Suntharalingam, et al. "24,25-Dihydroxyvitamin D3 and Vitamin D Status of Community-Dwelling Black and White Americans." Clinical Chemistry 61, no. 6 (June 1, 2015): 877–84. http://dx.doi.org/10.1373/clinchem.2015.240051.
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Abstract BACKGROUND 24,25-Dihydroxyvitamin D [24,25(OH)2D] is a metabolite of 25-hydroxyvitamin D (25D). Blacks frequently have low total 25D without manifestations of vitamin D deficiency, suggesting that total serum 25D may incorrectly reflect vitamin D status in different racial groups. The ratio of serum 24,25(OH)2D to 25D [vitamin D metabolite ratio (VMR)] represents a new candidate biomarker for vitamin D status. METHODS We measured 24,25(OH)2D3 and 25D3 by mass spectrometry in a random community cohort of black (n = 212) and white (n = 164) Americans to evaluate VMR as a marker for vitamin D status. We measured parathyroid hormone concentrations by immunoassay to compare VMR and 25D3 against a physiological indicator of vitamin D deficiency. RESULTS Serum 24,25(OH)2D3 strongly correlated with 25D3 in both black and white study participants (r = 0.90, P < 0.001 and r = 0.86, P < 0.001 respectively). Blacks had lower mean 25D3 than whites [17.0 (7.8) vs 27.5 (11.3) ng/mL; 42.4 (19.5) vs 68.6 (28.2) nmol/L, P < 0.001] and lower mean 24,25(OH)2D3 [2.1 (1.3) vs 3.6 (2.0) ng/mL; 5.1 (3.1) vs 8.7 (4.8) nmol/L, P < 0.001]. In contrast to total 25D3 concentrations, mean VMR values were similar in blacks and whites [11.9 (4.0) vs 12.5 (3.4), P = 0.16, respectively] and were negatively correlated with parathyroid hormone concentrations in both races (rs = −0.26, P < 0.001, and rs = −0.25, P < 0.001, respectively). CONCLUSIONS Our results provide further evidence that measurement of total 25D for assessment of vitamin D status in patients of African descent deserves reevaluation and suggest that alternative measures such as VMR should be considered.
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Strugnell, Stephen A., Akhtar Ashfaq, and Charles W. Bishop. "LBSAT229 Extended-release Calcifediol Effectively Raised 25-hydroxyvitamin D In CKD Despite Obesity." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A153. http://dx.doi.org/10.1210/jendso/bvac150.312.
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Abstract Inadequate levels of serum total 25-hydroxyvitamin D (25D) in chronic kidney disease (CKD) are associated with an increased risk of secondary hyperparathyroidism (SHPT). Serum 25D can be difficult to raise sufficiently with vitamin D supplements (cholecalciferol or ergocalciferol) to effectively lower elevated parathyroid hormone (PTH) levels especially in overweight patients. Obesity is common in CKD and requires attention when vitamin D repletion is considered. Vitamin D supplements are fat-soluble molecules which accumulate in adipose tissue. They have low affinity for serum vitamin D binding protein and are poorly mobilized from adipose tissue into circulation for hepatic activation. Recent studies suggest that serum 25D levels of ≥50 ng/mL are necessary to produce significant PTH reductions in nondialysis patients. Data were analyzed from two identical randomized clinical trials investigating the efficacy and safety of treating adult nondialysis patients with extended-release calcifediol (ERC; n=285) or placebo (n=144) to see if ERC raised 25D to at least 50 ng/mL in all body weight categories, with subgroup analyses by race, gender and age. On enrollment, subjects had eGFR of ≥15 and <60 mL/min/1.73 m2, PTH ≥85 and <500 pg/mL, serum 25D ≥10 and <30 ng/mL, corrected serum calcium ≥8.4 and <9.8, serum phosphorus ≥2. 0 and <5. 0, absence of nephrotic range proteinuria (>3 mg/mg creatinine) and no history of parathyroidectomy or renal transplantation. These subjects had mean (SD) age of 65.4 (10.9) years, serum 25D at baseline of 19.6 (5.4) ng/mL, body weight of 97.8 (24.3) kg and BMI of 34.7 (7.9) kg/m2. Fifty percent were male, 64. 0% White, 32.9% African-American or Black, and 3.1% Other, and 20% were Hispanic. A total of 356 subjects completed a 20- to 26-week treatment period per-protocol and were included in the analysis. Enrolled subjects ingested a 30 mcg capsule of ERC (OPKO Pharmaceuticals, Miami) daily for 12 weeks followed by one or two capsules (30 or 60 mcg) daily for a 14 more weeks. Control subjects received matching placebo. Mean (SD) serum 25D remained unchanged with placebo treatment but rose progressively with ERC treatment to 67.1 (21.6) ng/mL (mean of weeks 20-26). The observed increases in serum 25D were inversely related to body weight but exceeded 50 ng/mL in all body weight categories, irrespective of race (White vs. African-American or black), gender or age (<70 vs. ≥70 years). Side effects observed at these levels were similar to placebo. These data showed that ERC successfully raised mean serum 25D to at least 50 ng/mL irrespective of body weight, race, gender or age. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
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Ashfaq, Akhtar, Stephen Strugnell, Samir Tabash, Laura Johnson, and Charles W. Bishop. "LBSAT131 Extended-release Calcifediol Reduced Ipth And Normalized 1,25-dihydroxyvitamin D In Esrd." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A149. http://dx.doi.org/10.1210/jendso/bvac150.304.
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Abstract Background Extended-release calcifediol (ERC) has been shown in randomized clinical trials to effectively and safely treat secondary hyperparathyroidism (SHPT) in adults with stage 3-4 chronic kidney disease (CKD) and vitamin D insufficiency when administered at 210 or 420 mcg per week (30 or 60 mcg/day), doses which gradually raise serum total 25-hydroxyvitamin D (25D) to mean steady-state levels of 50-56 ng/mL. Clinical Case A 41-year-old male Caucasian with end-stage renal disease (ESRD) requiring regular hemodialysis (HD) experienced an overdose during participation in a phase 2 study of ERC for treating SHPT. Medical history included hypertension, type II diabetes, glomerulonephritis, bilateral lower extremity edema, muscle cramps, pruritus, shortness of breath, sporadic hypercalcemia and hyperphosphatemia, and iron deficiency anemia. Treatment with ERC began at an incorrect dosage of 2,700 mcg per week (900 mcg per HD) for 10 weeks as the study coordinator misunderstood the protocol-specified dose of 900 mcg per week. A 2.5% calcium dialysate was used during the study. Serum 25D gradually increased from 19 to 339 ng/mL (32-100), serum total 1,25-dihydroxyvitamin D (1,25D) increased from 6.3 to 137 pg/mL (24-86), plasma iPTH decreased from 440 to 146 pg/mL (15-65), and corrected serum calcium (Ca) decreased from 9.3 to 9.1 mg/dL (8.6-10.4). The subject remained asymptomatic throughout. Discovery of the overdose was delayed due to limited monitoring access during the pandemic and occurred when the ERC supply was prematurely exhausted. A physical exam and retrospective review of study records were promptly undertaken with no abnormalities noted. ERC administration, after a 1-dose hiatus, resumed at the correct dose (900 mcg per week). Serum 25D decreased over the next 4 weeks to 251 ng/mL, 1,25D decreased to 46. 0 pg/mL, iPTH increased to 186 pg/mL, and Ca remained stable (9. 0 mg/dL). The subject completed the full 6-month treatment period without adverse events. Clinical Lessons Gradual elevation of serum 25D and 1,25D with ERC to high levels had no impact on serum Ca or adverse events in the described subject suggesting that hypercalcemia observed with other vitamin D therapies used during HD results from abrupt increases in these metabolites. Serum 1,25D normalized with 25D elevation despite the lack of functional kidneys, indicating that extra-renal 1,25D production can become sufficient to control increased iPTH in ESRD when serum 25D is elevated well above the current clinical practice target of 30 ng/mL. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
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Yamamoto, Koichiro, Manami Fujita, Hiroyuki Honda, Yoshihisa Hanayama, Kazuki Tokumasu, Yasuhiro Nakano, Kou Hasegawa, Mikako Obika, and Fumio Otsuka. "Characteristics of Serum Ratios of 1,25-Dihydroxyvitamin D to 25-Hydroxyvitamin D for Assessment of Bone Metabolism." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A272—A273. http://dx.doi.org/10.1210/jendso/bvab048.553.
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Abstract Vitamin D is obtained in the body by food intake or by production from 7-dehydrocholesterol by exposure of the skin to ultraviolet B radiation. It is first metabolized in the liver to 25-hydroxyvitamin D (25D), which is a major circulating metabolite. In the kidney, 25D is subsequently metabolized to the hormonally active form, 1,25-dihydroxyvitamin D (1,25D), via 1α-hydroxylase encoded by the CYP27B1 gene. 1,25D has a cellular effect through the vitamin D receptor, which leads to calcium absorption in the gut, bone metabolism, and parathyroid function. A recent study showed that a low vitamin D status is common worldwide and is associated with various diseases including kidney, heart, and liver failure, secondary hyperparathyroidism, osteomalacia, inflammatory bowel disease, granuloma-forming disorders (sarcoidosis and tuberculosis), and cancer. Vitamin D deficiency also increases the risks of falls, fractures, bone loss, sarcopenia, leading to worse outcomes of illness severity, morbidity, and mortality. The 1,25D/25D ratio is considered to be a useful tool for diagnosis of ocular sarcoidosis; however, its clinical utility and relevance to pathophysiology of evaluation of the ratio 1,25D/25D which indicates vitamin D activation have remained unknown. To clarify the clinical usefulness of markers for vitamin D activation, 87 patients in whom serum 25D and 1,25D level was measured were retrospectively reviewed in the present study. Data for 79 patients (33 males and 46 females) were analyzed after exclusion of 8 patients taking vitamin D. The median serum 1,25D/25D ratio was significantly lower in males than in females: 4.1 (IQR: 2.3–5.8) x 10−3 versus 6.8 (3.0–9.8) x 10−3. However, individual levels of 25D and 1,25D were not different in males and females. The major categories of main disorders were endocrine (30.6 %), inflammatory (18.5 %), and bone-related (16.7 %) disorders. The ratios of serum 1,25D/25D had significant negative correlations with femoral dual energy X-ray absorptiometry % young adult mean (DEXA %YAM) (R=-0.35) and lumbar DEXA %YAM (R=-0.32). Significant correlations were found between 1,25D/25D ratio and serum levels of inorganic phosphate (R=-0.34), intact parathyroid hormone (R=0.64) and alkaline phosphatase (R=0.46) in all patients. Of interest, the 1,25D/25D ratio had gender-specific characteristics: the ratio had a significant correlation with age in males (R=0.49), while it had a significant correlation with body mass index (BMI) in females (R=0.34). Collectively, the results revealed that the ratio of serum 1,25D/25D as a marker for activation of vitamin D had relevance to clinical parameters, especially bone turnover, with gender-specific features. It is suggested that the existence of a gender-specific difference of aging males and obese females regarding the activation of vitamin D that is functionally linked to bone metabolism.
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Vieth, R. "Simple method for determining specific binding capacity of vitamin D-binding protein and its use to calculate the concentration of "free" 1,25-dihydroxyvitamin D." Clinical Chemistry 40, no. 3 (March 1, 1994): 435–41. http://dx.doi.org/10.1093/clinchem/40.3.435.
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Abstract A quantitative method to measure the specific binding capacity for 25-hydroxyvitamin D (25D-binding capacity) is described that resembles the qualitative "T3-uptake" assay. Patient's serum or standard (10 microL) is mixed with 0.5 mL of reagent containing 0.5 mumol/L 25-hydroxyvitamin D [25(OH)D3] plus 3000 counts/min [3H]25(OH)D3. After 0.5 h at 37 degrees C, the samples are treated with dextran/charcoal on ice for 1 h and centrifuged. The radioactivity of the bound tracer in the supernate is counted. Calibration is linear to approximately 10 mumol/L. 25D-binding capacity in reference-group serum samples was 4.33 (0.58 SD) mumol/L. The relationship between the inverse of 25D-binding capacity and the free fraction of [3H]1,25-dihydroxyvitamin D3 [1,25(OH)2D3] measured by ultrafiltration isodialysis was essentially linear (r = 0.934, P < 0.0001). Given this relationship, the calculated free fraction of 1,25(OH)2D3 equals 4.88 x 10(-3)/25D-binding capacity. The 25D-binding capacity was significantly lower in newborn babies and in adults with liver disease, and was increased during pregnancy (P < 0.01 for each). This method is applicable to situations where the biologically available concentration of 1,25(OH)2D is of interest.
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Pehlivantürk Kızılkan, Melis, Sinem Akgül, Filiz Akbıyık, Orhan Derman, and Nuray Kanbur. "Evaluation of Serum Vitamin D Levels in Adolescents with Pubertal Gynecomastia." Breast Care 11, no. 5 (2016): 333–37. http://dx.doi.org/10.1159/000451074.
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Background: Since vitamin D has an inhibitory function on ductal morphogenesis of the pubertal mammary gland, it may have a role in the development of gynecomastia. The aim of this study was to determine the effect of vitamin D deficiency on the development of pubertal gynecomastia. Methods: Serum 25-hydroxyvitamin D (25D) levels in 50 adolescents with pubertal gynecomastia and 54 healthy controls between the ages of 11 and 17 years were compared. Results: Mean 25D level was 14.03 ± 6.38 (5.0-32.5) ng/ml in the pubertal gynecomastia group and 15.19 ± 6.49 (5.0-33.2) ng/ml in the control group (p = 0.361). According to the vitamin D status classification of the American Academy of Pediatrics, 66% of the pubertal gynecomastia group was found to be deficient and 14% were insufficient. In the control group these values were 53.7% and 29.6%, respectively (p = 0.158). Conclusion: From our results we hypothesize that, rather than low serum levels of 25D, a dysregulation of the vitamin D signal pathway, vitamin D metabolism or vitamin D storage within the mammary tissue might be the contributing factors to the development of gynecomastia.
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Fadda, George, Michael J. Germain, Varshasb Broumand, Andy Nguyen, November McGarvey, Matthew Gitlin, Charles W. Bishop, and Akhtar Ashfaq. "Real-World Assessment: Clinical Effectiveness and Safety of Extended-Release Calcifediol." American Journal of Nephrology 52, no. 10-11 (2021): 798–807. http://dx.doi.org/10.1159/000518545.
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<b><i>Introduction:</i></b> The safety and efficacy of extended-release calcifediol (ERC) as a treatment for secondary hyperparathyroidism (SHPT) in adults with stage 3 or 4 chronic kidney disease (CKD) and vitamin D insufficiency (VDI) has been demonstrated in prospective randomized clinical trials (RCTs). ERC (Rayaldee<sup>®</sup>) was approved by the Food and Drug Administration in 2016 on the basis of these prospective RCTs. The current retrospective study assessed the postlaunch data available with respect to ERC’s efficacy and safety in increasing serum 25-hydroxyvitamin D (25D) and reducing parathyroid hormone (PTH) in the indicated population. <b><i>Materials and Methods:</i></b> Medical records of 174 patients who met study criteria from 15 geographically representative United States nephrology clinics were reviewed for 1 year before and after initiation of ERC treatment. Enrolled subjects had ages ≥18 years, stage 3 or 4 CKD, and a history of SHPT and VDI. Key study variables included patient demographics, medication usage, and laboratory results, including serial 25D and PTH determinations. <b><i>Results:</i></b> The enrolled subjects had a mean age of 69.0 years, gender and racial distributions representative of the indicated population, and were balanced for CKD stage. Most (98%) received 30 mcg of ERC/day during the course of treatment (mean follow-up: 24 weeks). Baseline 25D and PTH levels averaged 20.3 ± 0.7 (standard error) ng/mL and 181 ± 7.4 pg/mL, respectively. ERC treatment raised 25D by 23.7 ± 1.6 ng/mL (<i>p</i> < 0.001) and decreased PTH by 34.1 ± 6.6 pg/mL (<i>p</i> < 0.001) with nominal changes of 0.1 mg/dL (<i>p</i> > 0.05) in serum calcium (Ca) and phosphorus (P) levels. <b><i>Discussion/Conclusion:</i></b> Analysis of postlaunch data confirmed ERC’s effectiveness in increasing serum 25D and reducing PTH levels without statistically significant or notable impact on serum Ca and P levels. A significant percentage of these subjects achieved 25D levels ≥30 mg/mL and PTH levels which decreased by at least 30% from baseline. Dose titration to 60 mcgs was rarely prescribed. Closer patient monitoring and appropriate dose titration may have led to a higher percentage of subjects achieving an increase in 25D levels to at least 50 ng/mL and a reduction in PTH levels of at least 30%.
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Reyes, Rachel, Brandon Rafison, Andy Hur, Peter Joyce, Robert Modlin, Philip Liu, and John Adams. "Racial disparities in the vitamin D-mediated innate immune response following supplementation (P3379)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 202.12. http://dx.doi.org/10.4049/jimmunol.190.supp.202.12.
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Abstract We have previously demonstrated that innate (Toll-like receptor 2/1) and adaptive (IFN-γ) immune signals converge on a common vitamin D-dependent antimicrobial pathway in the human macrophage against Mycobacterium tuberculosis, including activation of CYP27B1 which converts 25D into the active 1,25D hormone as well as expression of antimicrobial peptides cathelicidin and human beta defensin 4. This antimicrobial activity is dependent on the level of extracellular 25D in culture. Therefore, we asked if this antimicrobial response could be recapitulated using sera from 25D deficient subjects before and after vitamin D repletion of the host in vivo. Serum has been collected prospectively from 67 Hispanic/Latino, 12 black and 21 non-Hispanic white, vitamin D-insufficient/deficient (8-29 ng/ml) before and after treatment with 500,000 IU vitamin D3. The mean total serum 25D in all three ethnic groups was 20ng/ml before and rose significantly (p<0.001) after vitamin D3 repletion, with a mean fold-change of 2.0, 2.9 and 3.0 in white, Hispanic and blacks, respectively. Despite the most substantial rise in total 25D in the minority populations, the ability of the sera from white donors to increase IFN-γ-stimulated macrophage cathelicidin was 3-fold (p<0.01) and 2-fold greater (p<0.05) than in cells conditioned in African and Hispanic/Latino American sera, respectively. These data suggest an ethnic/racial disparity in response to vitamin D supplementation.
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Norris, Keith, Opeyemi Olabisi, M. Barnett, Yuan-Xiang Meng, David Martins, Chamberlain Obialo, Jae Lee, and Susanne Nicholas. "The Role of Vitamin D and Oxidative Stress in Chronic Kidney Disease." International Journal of Environmental Research and Public Health 15, no. 12 (November 30, 2018): 2701. http://dx.doi.org/10.3390/ijerph15122701.
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Chronic kidney disease (CKD) is a major non-communicable disease associated with high rates of premature morbidity and mortality. The prevalence of hypovitaminosis D (deficiency of 25(OH)D or 25D) is greater in racial/ethnic minorities and in patients with CKD than the general population. Low 25D is associated with bone and mineral disorders as well as immune, cardiometabolic and cardiovascular (CV) diseases. Thus, it has been suggested that low 25D contributes to the poor outcomes in patients with CKD. The prevalence of hypovitaminosis D rises progressively with advancing severity of kidney disease with over 30% of patients with CKD stage 3 and 70% patients with CKD stage 5 estimated to have low levels of 25D. This report describes several of the abnormal physiologic and counter-regulatory actions related to low 25D in CKD such as those in oxidative stress and inflammatory systems, and some of the preclinical and clinical evidence, or lack thereof, of normalizing serum 25D levels to improve outcomes in patients with CKD, and especially for the high risk subset of racial/ethnic minorities who suffer from higher rates of advanced CKD and hypovitaminosis D.
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Kogawa, Masakazu, David M. Findlay, Paul H. Anderson, Renee Ormsby, Cristina Vincent, Howard A. Morris, and Gerald J. Atkins. "Osteoclastic Metabolism of 25(OH)-Vitamin D3: A Potential Mechanism for Optimization of Bone Resorption." Endocrinology 151, no. 10 (August 25, 2010): 4613–25. http://dx.doi.org/10.1210/en.2010-0334.
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The extrarenal synthesis of 1α,25 dihydroxyvitamin D3 (1,25D) has been demonstrated in a number of cell types including osteoblasts and cells of the monocyte/macrophage lineage. The skeleton appears responsive to serum levels of the 1,25D precursor, 25 hydroxyvitamin D3 (25D), in terms of bone mineralization parameters. The effect of metabolism of 25D into active 1,25D by osteoclast lineage cells is unknown. We found that CYP27B1 mRNA expression increased with exposure of human peripheral blood mononuclear cells (PBMCs) to macrophage colony-stimulating factor in the presence or absence of receptor activator of nuclear factor-κB ligand. Consistent with this, human osteoclast cultures incubated with 25D produced measurable quantities of 1,25D. Osteoclast formation from either mouse RAW264.7 cells or human PBMCs in the presence of physiological concentrations of 25D resulted in significant up-regulation of the key osteoclast transcription factor, nuclear factor of activated T cells-c1 in PBMCs and a number of key osteoclast marker genes in both models. The expression of the osteoblast coupling factor, ephrin-b2, was also increased in the presence of 25D. Levels of CYP27B1 and nuclear factor of activated T cells-1 mRNA correlated during osteoclastogenesis and also in a cohort of human bone samples. CYP27B1 short-hairpin RNA knockdown in RAW264.7 cells decreased their osteoclastogenic potential. 25D dose dependently reduced the resorptive capacity of PBMC-derived osteoclasts without compromising cell viability. 25D also reduced resorption by RAW264.7- and giant cell tumor-derived osteoclasts. Conversely, osteoclasts formed from vitamin D receptor-null mouse splenocytes had increased resorptive activity compared with wild-type cells. We conclude that 25D metabolism is an important intrinsic mechanism for optimizing osteoclast differentiation, ameliorating osteoclast activity, and potentially promoting the coupling of bone resorption to formation.
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Xu, Hongjian, Quanyu Zhang, Lihua Wang, Chengrui Zhang, Yang Li, and Yonggen Zhang. "Effects of 25-Hydroxyvitamin D3 and Oral Calcium Bolus on Lactation Performance, Ca Homeostasis, and Health of Multiparous Dairy Cows." Animals 11, no. 6 (May 28, 2021): 1576. http://dx.doi.org/10.3390/ani11061576.
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Little information is available regarding the effect of supplementing 25-hydroxyvitamin D3 during the transition period combined with a postpartum oral calcium bolus on Ca homeostasis. The objectives of the current study were to evaluate the effects of 25-hydroxyvitamin D3 combined with postpartum oral calcium bolus on lactation performance, serum minerals and vitamin D3 metabolites, blood biochemistry, and antioxidant and immune function in multiparous dairy cows. To evaluate the effects of 25-hydroxyvitamin D3 combined with oral calcium, 48 multiparous Holstein cows were randomly assigned to one of four treatments: (1) supplementing 240 mg/day vitamin D3 without a postpartum oral Ca bolus (control), (2) supplementing 240 mg/day vitamin D3 with an oral Ca bolus containing 90 g of Ca immediately post-calving (Ca + VitD), (3) supplementing 6 g/day 25-hydroxyvitamin D3 without an oral Ca bolus (25D), and (4) supplementing 6 g/day 25-hydroxyvitamin D3 with an oral Ca bolus containing 90 g of Ca immediately post-calving (Ca + 25D). Lactation performance during the first 21 days was measured. Blood was collected at the initiation of calving and then 1, 2, 7, 14, and 21 days relative to the calving date. The yield of milk (0.05 < p < 0.10), energy-corrected milk (p < 0.05), 3.5% fat-corrected milk (p < 0.05), and milk protein (p < 0.05) were significantly higher in 25-hydroxyvitamin D3-treated groups within 3 weeks of lactation than in vitamin D3-treated cows. The iCa (p < 0.05) and tCa (p < 0.05) were higher in both Ca and 25D + Ca cows than in the control and 25D groups within 48 h. The concentrations of serum tCa (p < 0.05), tP (p < 0.05), and 25-hydroxyvitamin D3 (p < 0.05) in 25D and 25D + Ca cows were higher than those in control and Ca cows within 21 days postpartum. Feeding 25-hydroxyvitamin D3 also showed a lower concentration of malondialdehyde (p < 0.05), interleukin 6 (p < 0.05), and tumor necrosis factor-alpha (TNF-α) (p < 0.05), as well as a higher concentration of alkaline phosphatase (p < 0.05), total antioxidant capacity (p < 0.05), and immunoglobulin G (p < 0.05) than vitamin D3. Supplementing Ca bolus also showed lower concentrations of alanine transaminase (p < 0.05) and TNF-α (p < 0.05). In conclusion, supplementing 25-hydroxyvitamin D3 during the transition period combined with a postpartum oral calcium bolus improved lactation performance, Ca homeostasis, and antioxidant and immune function of medium-production dairy cows within 21 days postpartum.
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Lu, Chien-Lin, Dong-Feng Yeih, Yi-Chou Hou, Guey-Mei Jow, Zong-Yu Li, Wen-Chih Liu, Cai-Mei Zheng, et al. "The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD." Nutrients 10, no. 12 (December 3, 2018): 1890. http://dx.doi.org/10.3390/nu10121890.
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In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.
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Gili-Kovács, Judit, Robert Hoepner, Anke Salmen, Maud Bagnoud, Ralf Gold, Andrew Chan, and Myriam Briner. "An algorithm using clinical data to predict the optimal individual glucocorticoid dosage to treat multiple sclerosis relapses." Therapeutic Advances in Neurological Disorders 14 (January 2021): 175628642110200. http://dx.doi.org/10.1177/17562864211020074.
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Background: Glucocorticoid (GC) pulse therapy is used for multiple sclerosis (MS) relapse treatment; however, GC resistance is a common problem. Considering that GC dosing is individual with several response-influencing factors, establishing a predictive model, which supports clinicians to estimate the maximum GC dose above which no additional therapeutic value can be expected presents a huge clinical need. Method: We established two, independent retrospective cohorts of MS patients. The first was an explorative cohort for model generation, while the second was established for its validation. Using the explorative cohort, a multivariate regression analysis with the GC dose used as the dependent variable and serum vitamin D (25D) concentration, sex, age, EDSS, contrast enhancement on cranial magnetic resonance imaging (MRI), immune therapy, and the involvement of the optic nerve as independent variables was established. Results: In the explorative cohort, 113 MS patients were included. 25-hydroxyvitamin D (25D) serum concentration and the presence of optic neuritis were independent predictors of the GC dose needed to treat MS relapses [(25D): −25.95 (95% confidence interval (CI)): −47.40 to −4.49; p = 0.018; optic neuritis: 2040.51 (95% CI: 584.64–3496.36), p = 0.006]. Validation of the multivariate linear regression model was performed within a second cohort. Here, the predicted GC dose did not differ significantly from the dose administered in clinical routine (mean difference: −843.54; 95% CI: −2078.08–391.00; n = 30, p = 0.173). Conclusion: Our model could predict the GC dose given in clinical, routine MS relapse care, above which clinicians estimate no further benefit. Further studies should validate and improve our algorithm to help the implementation of predictive models in GC dosing.
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Anderson, R. L., S. B. Ternes, K. A. Strand, and M. J. Rowling. "Vitamin D homeostasis is compromised due to increased urinary excretion of the 25-hydroxycholecalciferol-vitamin D-binding protein complex in the Zucker diabetic fatty rat." American Journal of Physiology-Endocrinology and Metabolism 299, no. 6 (December 2010): E959—E967. http://dx.doi.org/10.1152/ajpendo.00218.2010.
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Altered serum concentrations of the major circulating form of vitamin D [25-hydroxycholecalciferol (25D3)] and its active hormone derivative [1,25-dihydroxycholecalciferol (1,25D3)] have been linked to non-insulin-dependent diabetes mellitus (NIDDM). However, a mechanistic basis for this occurrence has not been fully elucidated. Normally, renal reabsorption of vitamin D-binding protein-bound 25D3 absolutely requires receptor-mediated endocytosis via a receptor complex containing megalin, cubilin, and disabled-2 (Dab2), whereas an absence of megalin or its endocytic partners can lead to a marked urinary loss of 25D and severe vitamin D deficiency. Therefore, we hypothesized that reduced serum vitamin D status in NIDDM may be due to reduced expression of megalin and/or its endocytic partners and increased urinary excretion of protein-complexed 25D3. In the present study, we utilized Zucker diabetic fatty Rats (ZDF) to demonstrate that renal reuptake of the 25D3-DBP complex was compromised in ZDF animals, which was reflected by a reduction in expression of megalin and Dab2. Moreover, serum levels of both 25D3 and 1,25D3 were reduced, and urinary 25D3, 1,25D3, and DBP excretion were elevated in the ZDF animals compared with their lean controls regardless of vitamin D levels in the diet. Taken together, these are the first reports to our knowledge that associate compromised renal reabsorption of the 25D3-DBP complex with expression of megalin and its endocytic partners in NIDDM, which in turn can lead to compromised vitamin D status.
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Stavenuiter, Andrea W. D., Maria Vittoria Arcidiacono, Evelina Ferrantelli, Eelco D. Keuning, Marc Vila Cuenca, Piet M. ter Wee, Robert H. J. Beelen, Marc G. Vervloet, and Adriana S. Dusso. "A Novel Rat Model of Vitamin D Deficiency: Safe and Rapid Induction of Vitamin D and Calcitriol Deficiency without Hyperparathyroidism." BioMed Research International 2015 (2015): 1–5. http://dx.doi.org/10.1155/2015/604275.
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Vitamin D deficiency is associated with a range of clinical disorders. To study the mechanisms involved and improve treatments, animal models are tremendously useful. Current vitamin D deficient rat models have important practical limitations, including time requirements when using, exclusively, a vitamin D deficient diet. More importantly, induction of hypovitaminosis D causes significant fluctuations in parathyroid hormone (PTH) and mineral levels, complicating the interpretation of study results. To overcome these shortcomings, we report the successful induction of vitamin D deficiency within three weeks, with stable serum PTH and minerals levels, in Wistar rats. We incorporated two additional manoeuvres compared to a conventional diet. Firstly, the vitamin D depleted diet is calcium (Ca) enriched, to attenuate the development of secondary hyperparathyroidism. Secondly, six intraperitoneal injections of paricalcitol during the first two weeks are given to induce the rapid degradation of circulating vitamin D metabolites. After three weeks, serum 25-hydroxyvitamin D3(25D) and 1,25-dihydroxyvitamin D3(1,25D) levels had dropped below detection limits, with unchanged serum PTH, Ca, and phosphate (P) levels. Therefore, this model provides a useful tool to examine the sole effect of hypovitaminosis D, in a wide range of research settings, without confounding changes in PTH, Ca, and P.
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Teoh, Chin May, Karisa Renteria, Analynn Cooper, Jie Zhu, Michelle Lane, and Gar Yee Koh. "Supplementation of a High-Fat High-Sucrose Diet With Methyl-Donor Nutrients During Pregnancy and Lactation Modulates the Colonic Vitamin D Signaling Pathway in Weaned Rats." Current Developments in Nutrition 6, Supplement_1 (June 2022): 1195. http://dx.doi.org/10.1093/cdn/nzac074.024.
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Abstract Objectives Suboptimal vitamin D status is highly prevalent in obese individuals, predisposing them to higher risks for gastrointestinal and immunological dysfunctions. Evidence has shown that maternal methyl-donor nutrient supplementation (MS) can modify DNA methylation status and improve metabolic health in their offspring. Here, we investigated if MS supplementation in an obesogenic diet during pregnancy and lactation can modulate the vitamin D signaling pathway and gut immunity in offspring at weaning. Methods After mating, 12-week-old female Sprague-Dawley rats were randomly assigned (n = 10/group) to receive control diet (CON), CON supplemented with methyl-donor nutrients (CON-MS), high-fat high-sucrose diet (HFS), or HFS supplemented with methyl-donor nutrients (HFS-MS). Diets were given during gestation and lactation periods. At weaning (21 days), the offspring (n = 6/group/sex) were euthanized. Serum, colonic mucosa, and cecal content were collected for analysis. Results Serum levels of 25-hydroxycholecalciferol (25D) in weaned pups from CON-MS and HFS-MS dams were 50% greater (P < 0.001) than pups born to CON dams but did not differ from pups born to HFS dams. Diets did not affect serum 25D levels in dams. Gene expressions of colonic vitamin D receptor (VDR), and its downstream target, cathelicidin, in pups from HFS-MS dams was 3-fold (P < 0.008) and 2.5-fold (P < 0.062) lower, respectively, than pups of HFS dams, and did not differ from pups of CON or CON-MS dams. A positive correlation was demonstrated between colonic VDR and the mRNA expressions of colonic pro-inflammatory modulators, TLR4, IL-1β, and IL-6, and the tight junction protein, ZO-1, respectively. Conclusions Our results support a role for MS in regulating colonic vitamin D signaling in offspring born to HFS dams, independent of maternal vitamin D status. The upregulation of VDR and the production of antimicrobial peptide, cathelicidin, in pups born to HFS dams could be a compensatory mechanism to suppress colonic low-grade inflammation induced by maternal high-fat diet. Further investigation is warranted to delineate the role of MS in vitamin D-mediated immune regulation, and whether an early establishment of vitamin D status is essential for health outcomes in adulthood. Funding Sources This study is supported by Texas State University startup and indirect cost return funds.
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Milovanova, Ludmila Yu, Lidia V. Lysenko (Kozlovskaya), Svetlana Yu Milovanova, Marina V. Taranova, Vasiliy V. Kozlov, Vladimir A. Reshetnikov, Marina V. Lebedeva, Tatyana V. Androsova, Daria O. Zubacheva, and Natalia V. Chebotareva. "Low serum Klotho level as a predictor of calcification of the heart and blood vessels in patients with CKD stages 2–5D." Terapevticheskii arkhiv 92, no. 6 (July 9, 2020): 37–45. http://dx.doi.org/10.26442/00403660.2020.06.000670.
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Cardiovascular calcification (CVC) makes a significant contribution to the manifestation of cardiovascular complications in patients with chronic kidney disease. Early CVC markers are currently being actively studied to optimize cardio-renoprotective strategies. We performed a prospective comparative analysis of the following factors: FGF-23, a-Klotho, sclecrostin, phosphate, parathyroid hormone, the estimated glomerular filtration rate (eGFR), central systolic pressure as an independent determinant of CVC.
Materials and methods. The study included 131 patients with chronic kidney disease 25D st. Serum levels of FGF-23, Klotho, and sclerostin were evaluated using the ELISA method. Vascular augmentation (stiffness) indices, central arterial pressure (using the SphygmoCor device), calcification of heart valves and the degree of aortic calcification (aortic radiography) were also investigated. The observation period was 2 years.
Results. According to the Spearman correlation analysis, the percent of calcification increase and the change in Klotho level are most related. According to ROC analysis, a decrease in serum levels of Klotho by 50 units or more is a significant predictor of an increase in aortic calcification of 50% or more with a sensitivity of 86% and a specificity of 77%. Using logistic regression analysis, it was found that a serum Klotho level 632 pg/L predicts an eGFR below a median level of 48 ml/min/1.73 m2 with a sensitivity of 85.5% and a specificity of 78.5%. Wherein OR 17.477 (CI 95% 8.04637.962; p0.001).
Conclusion. The factor most associated with CVC is Klotho. Decreased serum level of Klotho is a predictor of aortic calcification. In addition, the initial serum level of Klotho is a predictor of eGFR after 2 years.
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Marra, A., M. A. Horwitz, and H. A. Shuman. "The HL-60 model for the interaction of human macrophages with the Legionnaires' disease bacterium." Journal of Immunology 144, no. 7 (April 1, 1990): 2738–44. http://dx.doi.org/10.4049/jimmunol.144.7.2738.
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Abstract The facultative intracellular pathogen, Legionella pneumophila, multiplies within and kills human monocytes and alveolar macrophages. We show that L. pneumophila strain Philadelphia-1 infects, multiplies within and kills the promyelocyte HL-60 cell line after its differentiation into macrophage-like cells. The characteristics of the interaction between L. pneumophila and differentiated HL-60 cells closely resemble those between L. pneumophila and human peripheral blood monocytes. With both cell types, C receptors and serum C mediate attachment of L. pneumophila, which are taken up by coiling phagocytosis. The replicative phagosome is lined with ribosomes; intracellular multiplication is iron-dependent; and replicating bacteria ultimately destroy the host cell. As in human monocytes, an avirulent mutant derivative of L. pneumophila Philadelphia-1, 25D, does not replicate in and is not cytopathic for differentiated HL-60 cells. Differentiated HL-60 cells therefore provide a convenient and faithful model for the study of L. pneumophila-mononuclear phagocyte interaction.
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Mougiakakos, Dimitrios, Heiko Bruns, Martin Böttcher, Mirjeta Qorraj, Mario Fabri, Jochen Dindorf, Leonhard Busch, Regina Jitschin, and Andreas Mackensen. "Vitamin D Blocks CLL Cell-Mediated MDSC Induction." Blood 128, no. 22 (December 2, 2016): 4355. http://dx.doi.org/10.1182/blood.v128.22.4355.4355.
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Abstract Chronic lymphocytic leukemia (CLL) is the leukemia with the highest incidence amongst adults. CLL-associated immune defects promote tumor immune escape and antagonize immune-based therapies. We and others have reported the accumulation of so-called myeloid-derived suppressor cells (MDSCs) in CLL. Accumulation of immunosuppressive CD14+HLA-DRlow monocytic MDSCs is associated with advanced disease and poor prognosis. The mechanisms re-polarizing CLL-monocytes remain unknown. Here, we describe that CLL-cell-derived exosomes elicit a phenotypical and functional skewing of regular monocytes towards MDSCs. However, pre-treating CLL-cells with vitamin D led to a loss of the exosomes' MDSC-promoting capability. In fact, higher vitamin 25D serum concentrations were linked to lower levels of circulating MDSCs in CLL. A plethora of bioactive molecules including microRNAs (miRs) is shuttled in exosomes. MiR-155 is found abundantly in CLL-exosomes and using antagomir against miR-155 prevented exosomal MDSC-induction. Furthermore, exosomes from patients with lower vitamin D levels contained more miR-155 copies. Accordingly, vitamin D application reduced miR-155 production in CLL-cells Overall, we identified that exosomal miR-155 transfer promotes MDSCs in CLL. Vitamin D interferes with this interplay and could thereby represent a mean for enhancing immune responses in CLL. Disclosures No relevant conflicts of interest to declare.
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Gastelum, Alheli Arce, Jimmy J. Mao, and Gina N. Woods. "PSAT223 A Delayed Diagnosis of Oncogenic Osteomalacia Presenting with Bone Pain, Muscle Weakness and Elevated Alkaline Phosphatase." Journal of the Endocrine Society 6, Supplement_1 (November 1, 2022): A219. http://dx.doi.org/10.1210/jendso/bvac150.450.
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Abstract Background Tumor-induced osteomalacia (TIO) is a rare bone disease caused by excess production of FGF23 by a phosphaturic mesenchymal tumor, resulting in severe hypophosphatemia, bone demineralization, insufficiency fractures, bone pain and muscle weakness. The Fibroblast Growth Factor-23 (FGF23) is a phosphaturic hormone produced by osteocytes, whose primary effect is to decrease serum phosphate by suppressing proximal tubular phosphate reabsorption and intestinal phosphate absorption (via diminished 1,25D production). Clinical case A 65-year-old male was referred to endocrinology clinic for a second opinion due to severe rib pain and elevated alkaline phosphatase levels. His first endocrinologist diagnosed Paget's disease of the bone based on symptoms of rib pain, an elevated alkaline phosphatase level, and abnormal Tc99 bone scintigraphy demonstrating uptake in multiple areas, including bilateral humeri, ribs, knees, ankles, and L4 vertebral body. He received 5 mg IV zoledronate for treatment of Paget's disease, and immediately post-infusion reported worsening of severe rib pain. Upon presentation to our institution, he reported ongoing severe rib pain and bilateral knee pain. On exam, he had extreme difficulty rising from a seated position. Laboratories revealed calcium 9.0 mg/dL, albumin 5.0 g/dL, alkaline phosphatase 116 U/L, 25D 43 ng/dL, PTH 66 pg/mL and serum phosphorous 1.5 mg/dL. Tubular Reabsorption of Phosphate (TRP) was 59%, based on a spot second morning void with corresponding fasting morning blood draw. 1,25D was 13 pg/mL (19-79 pg/mL). Intact FGF23 was 346 pg/mL (<59 pg/nL). CT revealed bilateral tibial plateau insufficiency fractures. When asked if he noticed any "lumps or bumps", the patient reported a lump under his left second toe. MRI showed a 1.8 cm soft tissue mass. A GA68-DOTA-TATE PET CT revealed a 2.3 cm soft tissue mass plantar to the 2nd left proximal phalanx with intense activity mass (SUVmax 39.8). This mass was surgically excised. Post-operative FGF23 levels were as follows: 38 pg/mL → 15 pg/mL → <14 pg/mL. Within 14 days, the patient's ability to rise from a seated position was markedly improved. His severe rib pain persisted for three weeks but was significantly improved by six weeks post-op. Despite treatment with 1 mcg calcitriol daily and 5000 IU vitamin D daily, he developed evidence of post-operative hungry bone syndrome with calcium 8.3 mg/dL, PTH 64 pg/mL, and alk phos 157 U/L. Conclusion Tumor-induced osteomalacia is a rare but treatable condition, presenting with severe hypophosphatemia, bone pain, bone demineralization, insufficiency fractures, and muscle weakness. Due to the nonspecific nature of the presenting symptoms, delays in diagnosis are common. Serum phosphorous should be obtained in all patients presenting with unexplained elevations in alkaline phosphatase. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
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Jowett, Nigel I. "Milky Serum:." Practical Diabetes International 19, no. 3 (2002): 90. http://dx.doi.org/10.1002/pdi.252.
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Donnelly, James G., Steven J. Soldin, Daniel A. Nealon, and Jocelyn M. Hicks. "Stability of Twenty-Five Analytes in Human Serum at 22d`C, 4d`C, and -20d`C." Pediatric Pathology & Laboratory Medicine 15, no. 6 (January 1995): 869–74. http://dx.doi.org/10.3109/15513819509027023.
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Matveeva, L. V., L. M. Mosina, and M. A. Stenina. "Changes in Serum Levels of Growth Factors in Chronic Gastritis." RUDN Journal of Medicine 23, no. 3 (December 15, 2019): 250–56. http://dx.doi.org/10.22363/2313-0245-2019-23-3-250-256.
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Chronic inflammation, contributing to atrophy of the gastric epithelium, can develop in the induction of Helicobacter pylori and other microorganisms secretion of cytokines by cells of the gastric mucosa, including growth factors. Violation of the processes of repair of the gastric mucosa in terms of immune and microbiotic imbalance is the basis of ulcer and carcinogenesis. The aim of the study was to determine the serum level and diagnostic value of growth factors in exacerbation of chronic gastritis. Materials and methods . With informed consent in 122 patients with exacerbation of chronic gastritis and 40 healthy volunteers, sampling of gastrobioptates with esophagogastroduodenoscopy (for histological and microbiological examination), 5 ml of venous blood with serum separation (for enzyme immunoassay of serum levels of growth factors) was performed. Results . The amount of granulocyte-macrophage colony stimulating factor, erythropoietin, vascular endothelial growth factor (VEGF) in the serum of patients with atrophic gastritis exceeded the values of healthy individuals, were directly related to the degree and stage of gastritis, Helicobacter pylori infection, and among themselves. The greatest diagnostic value in atrophy gastric epithelial was determined in VEGF (sensitivity - 95,9%, specificity - 48,98%, criterion more 225 pg/ml, AUC 0,654, p = 0,0072). Conclusion. Determination of serum growth factors, especially VEGF, with exacerbation of chronic gastritis is diagnostically valuable, should be used for early diagnosis of atrophy of the gastric epithelium.
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Rakhmatullin, Shamil Gafiullovich, Baer Serekpaevich Nurzhanov, Ksenia Sergeevna Inchagova, and Galimzhan Kalikhanovich Duskaev. "The use of lactone in diets changes the biochemical composition of blood serum and muscle tissue of broilers." Proceedings of the Kuban State Agrarian University, no. 92 (2021): 251–58. http://dx.doi.org/10.21515/1999-1703-92-251-258.
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Hoonpongsimanont, W., C. L. Anderson, L. Danishgar, O. Mobayed, and S. Loftipour. "256 Validating AUDIT Using Serum Phosphatidylethanol." Annals of Emergency Medicine 70, no. 4 (October 2017): S101—S102. http://dx.doi.org/10.1016/j.annemergmed.2017.07.234.
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Seguy, David, Majd Ben Rejeb, Valerie Coiteux, Caroline Dendoncker, Helene Baudelle, Francis Bauters, Jean-Pierre Jouet, and Ibrahim Yakoub-Agha. "Five-Year Experience of Early Enteral Feeding in Patients Undergoing Allogeneic Stem Cell Transplantation Following Myeloablative Conditioning." Blood 110, no. 11 (November 16, 2007): 3004. http://dx.doi.org/10.1182/blood.v110.11.3004.3004.
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Abstract Since the early 2003 with the encouraging preliminary results of our pivotal study (Seguy, transplantation), all pts refereed to our unit for myeloablative Allogenic Stem Cell Transplantation (allo-CST) were offered right away enteral feeding via a naso-gastric tube (NGT). The aim of this work was to investigate the evolution of our practices regarding nutritional support and its impact on early outcomes over the last five years. During a systematic individual pre-transplantation interview, all pts were provided with comprehensive information regarding NGT feeding. They received advice on an ongoing basis from a multidisciplinary team. Between Jan 01 and Dec 05, 121 pts who underwent myeloablative allo-SCT were offered EN. Among them, 94 (78%) agreed to receive EN (EN group) and 27 (22%) refused the NGT (without EN group: WEN group) and received either parenteral nutrition (PN) (n=22) or oral feeding only (n=5). The NGT was inserted shortly after transplantation. Bacteriological high-controlled oral diet intake was encouraged for as long as the patient was able to sustain it. The daily oral intake was scheduled to provide 100% of estimated requirements for energy (30–35 kcal/kg/day). Overnight NGT feeding, was gradually increased depending on the patient’s tolerance in order to reach 50–70% of energy requirement within 5 days. In case of intolerance toward EN, additional or total PN was given. In the WEN group, pts received PN when total oral intake was less than two-thirds of the average energy requirement over 5 days. Except for the pts’ age (EN-group, 38y vs WEN 28y, p=.038), the two groups were comparable in terms of initial pts’ characteristics and transplantation modalities. Median duration of EN was 14 days (1–59) and 61 pts received no additional PN while the median duration of the PN was 12 days (2–70). There was no significant difference between the two groups regarding duration of hospitalization, nutritional status at discharge and duration and grade of mucositis. Significant differences were observed, however: engraftment, 100% vs 93%, p=.05, duration of neutropenia, 20d (10–64) vs 25d (18–100), p=.0001 and thrombopenia 27d (6–100) vs 56d (50–100), p=.014; serum albumine level at discharge < 35g/L, 45% vs 76%, p=.005 for EN-group vs WEN-group, respectively. Pts with EN developed less often acute grade III/IV GVHD (9% vs 37%; p=0.001) and non-bacterial infections (9% vs 41%; p=.0002). In addition, pts with enteral feeding had better 100-day survival (92% vs. 67%, P=0.001) with less infection-related deaths. In multivariate analysis the absence of enteral nutrition was the only factor adversely influencing 100-day survival (CI 95%: 1.55–14.9 0.646; P=.007). In order to evaluate the practices over time regarding nutritional support in our unit, we compared the initial period (2001–02) when pts (n=41) had the choice between EN and PN with the second period (2003–05) when EN was offered systematically (n=80). In the second period, pts received less often PN (73% vs. 31%, p<.0001) and more often EN (49% vs. 93%, p<.0001) with longer duration (10d vs. 15d; p=.001). In addition, EN started earlier after transplantation (5d vs 2d, p=.004). CONCLUSION: EN has been well tolerated and dramatically reduced the proportion of pts requiring PN. This study confirms the positive impact of EN on early outcome of pts undergoing myeloablative allo-CST. When possible EN should be preferred to PN.
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Yedla, Niharika, and Xiangbing David Wang. "Appropriate Cutoff for 25OHD Levels in the Diagnosis of Normocalcemic Primary Hyperparathyroidism (NPHPT): A Systematic Review." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A254—A255. http://dx.doi.org/10.1210/jendso/bvab048.517.
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Abstract Introduction: The Fourth International Workshop in 2014 delineated guidelines for the diagnosis of NPHPT which include ruling out secondary causes of hyperparathyroidism, and recommended cutoffs for 25 vitamin D (25OHD) to be ≥20ng/mL. Keeping in mind that the exact levels to optimize 25OHD in hyperparathyroid states are unknown, we aim to review possible variation in the prevalence of NPHPT if 25OHD cutoffs were to be raised to rule out vitamin D deficiency with more specificity. Methods: A PubMed search was conducted with key words “normocalcemic primary hyperparathyroidism” to review studies about NPHPT and 25OHD status. 533 articles were found, and 127 articles were identified by title/abstract screening with year of publication between 2014 to 2020. Ten studies were identified for the systematic review based on full text review for relevance. Results: Studies have been conducted in various countries across all continents to characterize NPHPT further. 5/10 studies used 25OHD cutoff of ≥20ng/mL and 4 studies had a cutoff of ≥30ng/mL and 1 study looked into the difference in prevalence with both cutoffs. All 3 studies from Italy used the higher cutoff. Rosario et al from Brazil reported a decrease in prevalence of NPHPT from 6.8% (25OHD≥20ng/mL) to 0.74% by supplementing those subjects to 25OHD ≥30ng/mL without any increase in serum calcium or parathyroid hormone (PTH) levels.1 Wang et al found that when total 25OHD levels were kept between 30–40 ng/mL, free 25OHD levels were actually lower compared to normal subjects.2 Conclusion: The levels of 25OHD that would define deficiency in NPHPT remain undetermined and both >20 ng/mL and >30ng/mL have been studied as cutoffs. It is well known that vitamin D insufficiency (25D 20-30ng/mL) drives up PTH and supplementation to 30-40ng/mL is required to reduce such effects. Wang et al suggest that free 25OHD levels correlate better with PTH as compared to total 25OHD and maybe a more reliable marker of 25OHD status. We suggest that a diagnostic criterion of ≥30ng/mL would be more appropriate in ruling out 25OHD deficiency in this special population. The role of free 25OHD levels in PHPT needs further evaluation. References: 1. Rosário PW, Calsolari MR. Normocalcemic Primary Hyperparathyroidism in Adults Without a History of Nephrolithiasis or Fractures: A Prospective Study. Horm Metab Res. 2019 Apr;51(4):243–247. doi: 10.1055/a-0859-1020. Epub 2019 Mar 6. PMID: 30840998. 2. Wang X, Meng L, Su C, Shapses SA. LOW FREE (BUT NOT TOTAL) 25-HYDROXYVITAMIN D LEVELS IN SUBJECTS WITH NORMOCALCEMIC HYPERPARATHYROIDISM. Endocr Pract. 2020 Feb;26(2):174–178. doi: 10.4158/EP-2019-0325. Epub 2019 Sep 26. PMID: 31557077
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Cardoso, Silas Klein. "A revolta das formigas: a insurreição de Labayu e seus filhos em EA 252-256." Caminhando 23, no. 1 (June 29, 2018): 99. http://dx.doi.org/10.15603/2176-3828/caminhando.v23n1p99-113.
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A comunicação entre Labayu, rei siquemita, e seus filhos e a administração egípcia de el Amarna demonstra as tensões, fragilidades e artimanhas políticas do período da Canaã dominada pelo Egito no século XIV aEC. Além de serem fundamentais à reconstrução histórica do período, tais documentos apresentam um uso aprimorado da retórica. Nesse ínterim, este artigo oferece análise histórico-literária das cartas de EA 252-256. A partir da tradução, análise da estrutura retórica e exploração dos estudos de proveniência das tabuletas, oferecemos um comentário para tais documentos, elucidando o conteúdo e devidas implicações históricas. Ao final, apresentamos uma proposta de reconstrução histórica da revolta de Labayu.
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Ismail, Adnan M., and Eman S. Saleh. "Estimation of Serum CD200 and CD200R1 Levels in a Sample of Iraqi Women with Breast Cancer: Their Role as Diagnostic and Prognostic Markers." Iraqi Journal of Pharmaceutical Sciences ( P-ISSN: 1683 - 3597 , E-ISSN : 2521 - 3512) 29, no. 2 (December 30, 2020): 253–58. http://dx.doi.org/10.31351/vol29iss2pp253-258.
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Breast cancer is a disease in which cells in the breast grow out of control. CD200 is a cell surface glycoprotein expressed on many cells, it belongs to the immunoglobulin family (Ig) and have a great role in the regulation of inflammation in autoimmunity. CD200 is the ligand for CD200R1 receptor. To determine if serum level of CD200 and its receptor CD200R1 can be used as a diagnostic and prognostic marker in patients with breast cancer.This case control study was carried out at Oncology Teaching Hospital – Medical city in Baghdad. Six groups were enrolled, four groups were confirmed with breast cancer stage (I, II, III and IV), fifth group (benign) and sixth group was control (healthy individual). Serum is divided to measure CD200 and CD200R1 by utilizing quantitative sandwich enzyme-linked immunosorbent assay (ELISA) Kits.
Serum level of CD200 was significantly different (P=0.000088) between breast cancer patients and control only, serum level of CD200 increases with disease stage and there is a significant positive correlation. Serum level of CD200R1 was different with stage, although the differences were not significant but the level of CD200R1 is lower in stage 4 patients than other stages.
Serum CD200 level can be used as a diagnostic marker for breast cancer. Serum level of CD200R1 can be used as a prognostic marker
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Tada, K., T. Moroji, R. Sekiguchi, H. Motomura, and T. Noguchi. "Liquid-chromatographic assay of diazepam and its major metabolites in serum, and application to pharmacokinetic study of high doses of diazepam in schizophrenics." Clinical Chemistry 31, no. 10 (October 1, 1985): 1712–15. http://dx.doi.org/10.1093/clinchem/31.10.1712.
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Abstract In this rapid, sensitive method for simultaneously determining diazepam and its biologically active metabolites--nordiazepam, oxazepam, and temazepam--in serum, 250 to 1000 microL of serum is extracted with ether and the extracted compounds are quantified by "high-performance" liquid chromatography on a Shimpack FLC-C8 microparticulate column. Absorbance of the effluent is monitored at 254 nm. The limit of detection in serum is about 10 micrograms/L for each drug. Analytical recovery of each drug added to the serum varied from 91 to 102% for oxazepam and temazepam, from 82 to 99% for nordiazepam and diazepam. Within-day and between-day CVs ranged from 2 to 5% for oxazepam and temazepam, and from 2 to 7% for nordiazepam and diazepam. We also report results on using this assay in a pharmacokinetic study of high doses of diazepam used to treat chronic schizophrenic patients.
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Cuckle, H. S., I. K. Sehmi, and R. G. Jones. "Correlation between maternal serum PAPP-A and inhibin." Prenatal Diagnosis 22, no. 2 (2002): 161–62. http://dx.doi.org/10.1002/pd.253.
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Milenković, B., V. Stojćić, and O. Djurić. "257-PA10 Serum levels of ceruloplasmin in sarcoidosis." Tubercle and Lung Disease 76 (October 1995): 24–25. http://dx.doi.org/10.1016/0962-8479(95)90107-8.
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ZHANG, XiuLi, XiuLing LI, MeiQian HOU, XinMiao LIANG, and Long YU. "Glycosylation analysis of human serum alpha-1-acid glycoprotein." SCIENTIA SINICA Chimica 41, no. 3 (March 1, 2011): 544–49. http://dx.doi.org/10.1360/032010-252.
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Yalçınkaya, Esin, Mehmet Emin Tunçkaşık, İsmail Güler, Sinan Kocatürk, and Özge Gündüz. "Evaluation of the correlation of 25-hydroxyvitamin-D serum levels with allergic rhinitis." ENT Updates 5, no. 1 (April 1, 2015): 19–22. http://dx.doi.org/10.2399/jmu.2015001005.
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Öztürk, Gülfer. "The effect of serum 25(OH) vitamin D on hemogram parameters." Dicle Medical Journal / Dicle Tıp Dergisi 41, no. 2 (January 6, 2014): 332–36. http://dx.doi.org/10.5798/diclemedj.0921.2014.02.0426.
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Ou, C. N., C. L. Rognerud, L. T. Duong, and V. L. Frawley. "Liquid-chromatographic determination of amiodarone and N-desethylamiodarone in serum." Clinical Chemistry 36, no. 3 (March 1, 1990): 532–34. http://dx.doi.org/10.1093/clinchem/36.3.532.
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Abstract We have developed a stable and simple normal-phase liquid-chromatographic method for simultaneously measuring amiodarone and its metabolite, N-desethylamiodarone, within 8 min. The chromatographic system consists of a 15 cm x 3.9 mm Waters "Resolve" silica column and a mobile phase of ammonium sulfate (17 mmol/L, pH 6.8) and methanol (8/92 by vol), pumped at 1.8 mL/min and monitored at 254 nm. After 250 microL of serum is mixed with 100 microL of 0.36 mol/L NaH2PO4, 100 microL of the internal standard solution (L8040, 6 mg/L), and 200 microL of isopropyl ether, the mixture is vortex-mixed and centrifuged. Fifty microliters of the organic layer is injected onto the column. Relative recovery was 100% over the assay range of 0.1 to 20.0 mg/L for both compounds. Within-run and total (day-to-day) CVs were 3% and 7% for amiodarone and 5% and 8% for N-desethylamiodarone, respectively.
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Shenoy, Dr Radhika. "Serum electrolytes in thyroid patients." International Journal of Advanced Research in Medicine 3, no. 2 (July 1, 2021): 283–84. http://dx.doi.org/10.22271/27069567.2021.v3.i2e.257.
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Chaulin, Akeksey M. "Possible pathophysiological mechanisms of cardiac troponin level elevations in blood serum and urine in arterial hypertension." Kazan medical journal 103, no. 2 (April 12, 2022): 250–58. http://dx.doi.org/10.17816/kmj2022-250.
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The review aimed to discuss and detail the main mechanisms of myocardial cell injury and increased concentrations of cardiac specific troponin isoforms (cTnI and cTnT) in blood serum and urine in hypertension. The search and analysis of foreign and domestic literature were carried out using the MedLine, EMBASE, Scopus and eLibrary databases to achieve this goal. According to recent experimental and clinical researches using high and ultra-sensitive methods for determining cTnI and cTnT, cardiomyocytes are extremely sensitive to many damaging factors in a number of physiological and pathological conditions. The serum concentrations of cTnI and cTnT can increase at the earliest stages of cardiovascular diseases (for example, in prehypertension, latent forms of coronary heart disease, arterial hypertension) and are important for predicting subsequent complications in the form of acute and life-threatening cardiovascular diseases (myocardial infarction, stroke, heart failure, and others). Moreover, troponin molecules can be detected not only in blood serum but also in non-invasively obtained biological fluids, including urine and oral fluid, which in the future can be used as new methods for the non-invasive diagnosis of many cardiovascular diseases. Although elevated levels of cTnI and cTnT in blood serum and urine in hypertension have a fairly high diagnostic and prognostic value, the pathophysiological mechanisms of cardiac troponins level elevations in human biological fluids in this pathological condition remain unclear.
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Milenković, B., V. Stojc̆ić, and O. Djurić. "256-PA10 Elevation of serum ceruloplasmin in pulmonary tuberculosis." Tubercle and Lung Disease 76 (October 1995): 17. http://dx.doi.org/10.1016/0962-8479(95)90080-2.
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Shton, I. O., V. V. Sarnatskaya, L. V. Prokopenko, and N. F. Gamaleia. "CHLORIN e6 COMBINED WITH ALBUMIN NANOPARTICLES AS A POTENTIAL COMPOSITE PHOTOSENSITIZER FOR PHOTODYNAMIC THERAPY OF TUMORS." Experimental Oncology 37, no. 4 (December 22, 2015): 250–54. http://dx.doi.org/10.31768/2312-8852.2015.37(4):250-254.
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Aim: To synthesize and to study for photodynamic activity a composite photosensitizer consisting of chlorin e6 and human serum albumin nanoparticles (HSA NPs). Materials and Methods: Starting from sorption-purified HSA, the albumin nanoparticles with a different degree of lysine residues cross-linking (10; 20; 40, and 100%) were obtained by the coacervation method. The HSA NPs were used for synthesis of nanocomposites with chlorin e6 and fluorescein isothiocyanate (FITC)-labled preparations. Malignant lymphocytes of the MT-4 (human T-cell leukemia) line and normal lymphocytes of healthy donors served as cell targets. For photodynamic treatment, a semiconductor laser was exploited as a light source, and cell viability was assessed by MTT or trypan blue dye exclusion tests. For cell imaging and HSA NPs visualization, the fluorescence microscopy and transmission electron microscopy were applied, respectively. C57Bl/6 mice were used in animal experiments. Results: The absorption and fluorescence spectra of chlorin e6-HSA NPs composites were characterized, and by the electron microscopy investigation the size of NPs (nanospheres) was estimated: 100–120 nm. FITC-labled albumin preparations allowed to establish that HSA NPs have much higher exposition and concentration dependent affinity to malignant cell surface than initial HSA. In experiments with MT-4 cells on PDT activity of chlorin e6-HSA NPs, the nanocomposite effectiveness elevated along with increasing percentage of cross-linked aminoacid residues, and for the nanocomposite with 100% of albumin cross-linking it exceeded the activity of free chlorin e6. In contrast to malignant cells, the complexation of chlorin e6 with HSA NPs decreased its photodynamic effect on normal human lymphocytes. Intravenous introduction of the chlorin e6-HSA NPs composite to mice showed prolonged circulation of the nanocomposite in blood in comparison with free PS. Conclusion: Promising results obtained with chlorin e6-HSA NPs composites warrant conduction of full-fledged PDT studies in vivo using the nanocomposites as photosensitizers.
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Tallheden, Tommi, Josefine Van Der Lee, Camilla Brantsing, Jan-Eric Månsson, Eva Sjögren-Jansson, and Anders Lindahl. "Human Serum for Culture of Articular Chondrocytes." Cell Transplantation 14, no. 7 (August 2005): 469–79. http://dx.doi.org/10.3727/000000005783982909.
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In the field of cell and tissue engineering, culture expansion of human cells in monolayer plays an important part. Traditionally, cell cultures have been supplemented with serum to support attachment and proliferation, but serum is a potential source of foreign protein contamination and viral protein transmission. In this study, we evaluated the use of human serum for experimental human articular chondrocyte expansion and to develop a method for preparation of large volumes of high-quality human serum from healthy blood donors. Human autologous serum contained high levels of epidermal-derived growth factor and platelet-derived growth factor-AB and supported proliferation up to 7 times higher than FCS in primary chondrocyte cultures. By letting the coagulation take place in a commercially available transfusion bag overnight, up to 250 ml of growth factor-rich human serum could be obtained from one donor. The allogenic human serum supported high proliferation rate without loosing expression of cartilage-specific genes. The expanded chondrocytes were able to redifferentiate and form cartilage matrix in comparable amounts to autologous serums. In conclusion, the transfusion bags allow preparation of large volumes of growth factor-rich human serum with the capacity to support in vitro cell expansion. The data further indicate that by controlling the coagulation process there are possibilities of optimizing the release of growth factors for other emerging cell therapies.
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Cha, Hyejung, Eun Jung Lee, and Jinsil Seong. "Significance of serum interleukin-6 in patients treated with radiotherapy for hepatocellular carcinoma." Journal of Clinical Oncology 33, no. 3_suppl (January 20, 2015): 254. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.254.
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254 Background: Interleukin-6 (IL-6) is reported to contribute to aggressive tumor growth and resistance to treatment. In several cancers including esophagus, head and neck, and pancreas, high IL-6 is associated with poor treatment outcome after radiotherapy (RT). However, reports about significance of IL-6 in RT for HCC were rare. The aim of this study was to investigate the significance of serum IL-6 with treatment outcome in patients treated with RT for HCC. Methods: For patients treated with RT for HCC, blood samples were collected prospectively, before start and after completion of RT schedule. Serum IL-6 levels were measured with enzyme-linked immunosorbent assay kit. Patients’ clinical profiles were recorded. Results: Between September 2008 and October 2009, 51 patients were included in this study. Median follow-up duration was 12.3 months (range, 0.5-62.3). Baseline serum IL-6 level was 31.63 pg/ml and patients who had treatment history before RT showed higher baseline serum IL-6 levels than treatment (Tx)-naïve patients (53.09 vs. 15.35, p=0.028). Baseline IL-6 levels were higher in patients showing infield failure (59.70 vs. 14.96, p=0.022) and extrahepatic failure (40.50 vs. 17.88, p=0.072). In patients who had treatment history before RT, higher baseline IL-6 levels were associated with both infield and extrahepatic failure (p=0.014, p=0.032, respectively) in. However, this significance was not found in Tx-naïve patients. Higher baseline IL-6 levels were associated with short infield PFS (p<0.0001) in entire patients and in patients who had treatment history before RT. After RT, serum IL-6 level decreased but it was not significant (29.54 pg/ml, p=0.794). And variation of serum IL-6 level was not associated with treatment failure. Conclusions: Baseline serum IL-6 levels seem significant in predicting treatment outcome in patients treated with RT for HCC. High baseline serum IL-6 levels were associated with infield and extrahepatic failure, especially in patients who had treatment history before RT.
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Cabarkapa, Velibor, Zoran Stosic, Vera Uzurov, Vladimir Sakac, and Mirjana Djeric. "The role of holotranscobalamin in examination of vitamin B12 status." Medical review 61, no. 7-8 (2008): 389–92. http://dx.doi.org/10.2298/mpns0808389c.
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Introduction. Holotranscobalamin contains biologically available cobalamin because only holotranscobalamin promotes the uptake of the cobalamin therein by all cells, via specific receptors. Therefore holotranscobalamin has been proposed as a potentially useful alternative indicator of vitamin B12 status. The aim of the present study was to assess usefulness of holotranscobalamin in the evaluation of vitamin B12 status. Material and methods. We examined serum level of holotranscobalamin in 135 subjects divided in four groups according to the serum concentration of vitamin B12: 30 subjects with vitamin B12<154 pmol/l, 50 subjects with vitamin B12 154-250, 30 subjects with vitamin B12 251-350 pmol/l, 25 subjects with vitamin B12>350 pmol/l. Results The results show that in subjects with low vitamin B12 serum level there are those with normal holotranscobalamin concentration (60%) and that in subjects with normal vitamin B12 there are those with low holotranscobalamin concentration (22%). The obtained results also show positive significant correlation between levels of holotranscobalamin and vitamin B12 (r=0.62, p<0.001). Conclusion. We can conclude that biologically active cobalamin, holotranscobalamin, is a useful tool when examining vitamin B12 status especially in subjects with borderline and low vitamin B12 concentrations. Measurements of the serum holotranscobalamin may be superior to total serum cobalamin.
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Roy, Marlina, Asma Rahman, Hafsa Begum, Rokeya Khan, Nasrin Hasan, Perven Akter, and M. Kabir Alam. "Serum Calcium Level in Mild and Severe Preeclampsia- A study in Combined Military Hospital, Dhaka." Northern International Medical College Journal 9, no. 1 (March 12, 2018): 255–57. http://dx.doi.org/10.3329/nimcj.v9i1.35922.
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Background : Hypertensive disorders are the most common medical complications during pregnancy and are associated with high maternal and fetal mortality and morbidity.Half of the pregnant women with hypertension have preeclampsia. Association of low serum calcium level with preeclampsia(PE) is known decades together.Objectives : To assess serum calcium level in mild and severe preeclampsia(PE).Materials and Method : This was a comparative cross sectional study conducted in the department of Obstetric and Gynaecology, Combined Military Hospital (CMH),Dhaka, Bangladesh. The data were collected from 50 mild preeclampsia and 50 severe preeclampsia patients admitted in Obstetric and Gynaecology ward of CMH who fulfill the inclusion criteria. Study period was July 2015 to December 2015. Serum calcium was measured in Auto analyzer machine in the clinical pathology of Armed forced Institute of pathology (AFIP). Data were analyzed by statistical software, SPSS version 20.Results : Serum calcium level was found in severe PE was 8.12mg/dl and in mild PE was 8.85mg/dl. Study also reveals that routine calcium supplementation was consumed less in severe PE than mild PE patients.Conclusion : Serum calcium is markedly reduce in severe preeclampsia than in mild preeclampsia. Therefore routine examination of serum calcium level may be useful as diagnostic marker in high risk pregnancy.Northern International Medical College Journal Vol.9(1) July 2017: 255-257
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Yang, C. W., J. Kim, Y. H. Kim, J. H. Cha, S. Y. Mim, Y. O. Kim, Y. S. Shin, Y. S. Kim, and B. K. Bang. "Inhibition of calbindin D28K expression by cyclosporin A in rat kidney: the possible pathogenesis of cyclosporin A-induced hypercalciuria." Journal of the American Society of Nephrology 9, no. 8 (August 1998): 1416–26. http://dx.doi.org/10.1681/asn.v981416.
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A recent study by Steiner et al. (Biochem Pharmacol 51: 253-258, 1996) demonstrated a decreased calbindin D28K expression in the kidneys of cyclosporin A (CsA)-treated rats. To evaluate the association of renal calcium handling with calbindin D28K expression in CsA-treated rats, two separate experiments (vehicle [VH] versus CsA groups, 1,25-dihydroxyvitamin D3 [VitD] versus VitD + CsA groups) were done simultaneously. CsA (25 mg/kg per d, subcutaneously) and VitD (0.5 microg/kg per d, subcutaneously) were given for 7 d. The CsA group showed decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VH group. The VitD + CsA treatment decreased serum calcium, increased urine calcium excretion, and decreased calbindin D28K protein level and immunoreactivity compared with the VitD alone. CsA treatment did not affect the serum parathyroid hormone and VitD levels. This study demonstrates an association of calbindin D28K expression with the urinary calcium excretion in CsA-treated rats, and suggests that decreased calbindin D28K expression may play a role in renal calcium wasting.
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Sherry, B., R. M. Jack, A. Weber, and A. L. Smith. "Reference interval for prealbumin for children two to 36 months old." Clinical Chemistry 34, no. 9 (September 1, 1988): 1878–80. http://dx.doi.org/10.1093/clinchem/34.9.1875.
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Abstract To define a reference value for serum prealbumin (transthyretin) concentration, we used a rate immunonephelometric microassay to quantify it in 76 healthy children, ranging in age from two to 36 months. Age-specific ranges (+/- 2 SD from the mean) are: 2-5.9 months, 142-330 mg/L; 6-11.9 months, 120-274 mg/L; 12-17.9 months, 115-259 mg/L; 18-23.9 months, 143-243 mg/L; 24-36 months, 108-258 mg/L. When the data were grouped into those for subjects younger and older than 12 months of age, the mean for the 2-11.9 month age group (210 mg/L) significantly (P less than 0.01) exceeded that of the 12-36 month age group (187 mg/L). We propose that in spite of a decrease in prealbumin concentration with increasing age, it is acceptable to use the reference interval 116-281 mg/L (+/- 2 SD from the mean) for children from two to 36 months old. We also compared concentrations of prealbumin in serum and plasma of 41 individuals, finding the mean difference to be +11.7 mg/L; concentrations in plasma averaged 6.7% greater than those in serum.
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Ruggiero, Carmelinda, Marta Baroni, Vittorio Bini, Annalisa Brozzetti, Luca Parretti, Elisa Zengarini, Maria Lapenna, et al. "Effects of Weekly Supplementation of Cholecalciferol and Calcifediol Among the Oldest-Old People: Findings From a Randomized Pragmatic Clinical Trial." Nutrients 11, no. 11 (November 15, 2019): 2778. http://dx.doi.org/10.3390/nu11112778.
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Vitamin D inadequacy is pervasive in the oldest-old. Many vitamin D metabolites are available for supplementation, their effects on the recovery of adequate serum levels remain unknown. We investigate the effects of supplementation with cholecalciferol (D3) and calcifediol (25D3) on serum levels of 25(OH)D, 1-25(OH)D, bone and inflammatory markers, ultimately identifying clinical predictors of successful treatment. Sixty-seven oldest-old individuals were randomized to weekly administration of 150 mcg of 25D3 or D3, from hospital admission to 7 months after discharge. Supplementation of 25D3 and D3 were associated with increasing serum levels of 25(OH)D (p < 0.001) and 1-25(OH)D (p = 0.01). Participants on 25D3 experienced a steeper rise than those on D3 (group*time interaction p = 0.01), after adjustment for intact parathyroid hormone (iPTH) levels the differences disappeared (intervention*iPTH interaction p = 0.04). Vitamin D supplementation was associated with a decreasing trend of iPTH and C-reactive protein (CRP) (p < 0.001). Polypharmacy and low handgrip strength were predictors of failure of intervention, independent of vitamin D metabolites. In conclusion, D3 and 25D3 supplementation significantly increase vitamin D serum levels in the oldest-old individuals, with a tendency of 25D3 to show a faster recovery of acceptable iPTH levels than D3. Polypharmacy and low muscle strength weaken the recovery of adequate vitamin D serum levels.
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Sinha, Sanjeev, Kartik Gupta, Dibyakanti Mandal, B. K. Das, and R. M. Pandey. "Serum and Bronchoalveolar Lavage Fluid 25(OH)Vitamin D3 Levels in HIV-1 and Tuberculosis: A Cross-Sectional Study from a Tertiary Care Center in North India." Current HIV Research 16, no. 2 (August 15, 2018): 167–73. http://dx.doi.org/10.2174/1570162x16666180528112924.
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Background: Vitamin D is an immunomodulator, and its deficiency is associated with Tuberculosis (TB) infection. Bronchoalveolar lavage fluid (BALF) is a rich milieu of macrophages that form the first line of defense against invading TB bacilli. As there is an increased prevalence of vitamin D deficiency in TB and human immunodeficiency virus-1 (HIV-1) subjects, we intend exploring the possibility of a localized deficiency of vitamin D metabolites in BALF of these patients. Objective: The primary objective was to assess the level of 25D3 in serum and BALF of subjects and look for a significant difference among patients and controls. The secondary objective was to find a correlation between serum and BALF 25D3 levels. Methods: We performed a cross-sectional study with subjects divided into four groups: Controls (group 1), HIV positive without active TB (group 2), active TB without HIV (group 3), and HIV-TB coinfection (group 4). BALF and serum 25D3 levels were compared between the groups. Results: Among the 149 (an immunomodulator) successive subjects enrolled, there were 40 subjects in group 1 (HIV-TB-), 48 in group 2 (HIV+TB-), 37 in group 3 (HIV-TB+), and 24 in group 4 (HIV+TB+). Females constituted 31.6% of the study subjects. In groups 3 and 4, there were significantly lower serum 25D3 levels compared to group 1 (p-value group 3: 0.002; group 4: 0.012). In groups 2, 3, and 4, there were significantly lower BALF 25D3 levels compared to group 1 (p-value group 2: 0.000; group 3: 0.000; group 4: 0.001). There was a significant correlation between serum and BALF 25D3 levels (Spearman’s rank correlation coefficient 0.318, p-value = 0.0001). Conclusion: Lower levels of serum and BALF 25D3 were observed in HIV, TB, and HIV-TB coinfected patients. Localized deficiency of vitamin D metabolites might be associated with increased vulnerability to TB infection.
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Hochberg, Z., T. Amit, A. Flyvbjerg, and I. Dørup. "Growth hormone (GH) receptor and GH-binding protein deficiency in the growth failure of potassium-depleted rats." Journal of Endocrinology 147, no. 2 (November 1995): 253–58. http://dx.doi.org/10.1677/joe.0.1470253.
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Abstract Potassium (K+) deficiency is associated with growth retardation in both man and experimental animals. Growth hormone (GH) administration to such animals prevents, to some extent, weight loss and selective muscle atrophy, but does not affect tail and tibia length even with supraphysiological doses. The present study was undertaken to investigate the possible effect of K+ deficiency on the hepatic GH receptor and GH-binding protein (BP). Young female Wistar rats were maintained on K+-deficient fodder and distilled water, and compared with pair-fed and ad-libitumfed control groups. After 15 days GH-BP and electrolytes were measured in sera, GH receptors were studied in liver membranes by 125I-labeled human GH binding and muscles were weighed and saved for electrolyte measurements. K+-deficient rats showed complete growth arrest compared with an intermediate weight gain of the pair-fed group. Serum K+ was very low, at 1·5 ±0·1 mmol/l, compared with the mean value of 5·3 mmol/l of control animals. Somatogenic and lactogenic receptors in liver membranes and serum GH-BP levels were significantly (P<0·05) lower in K+ deficiency, as compared with their pair-fed controls. Liver GH receptors correlated significantly (P<0·05) with serum GH-BP levels. The growth variables correlated positively with both hepatic somatogenic and lactogenic receptors and serum GH-BP levels, with correlation coefficients that were highest against serum GH-BP and lowest against liver lactogenic receptors. Serum and muscle K+ correlated significantly (P<0·05) with both liver GH receptors and serum GH-BP, with correlation coefficients that were higher against serum GH-BP. Lactogenic receptors had a lower or no correlation. It is concluded that GH receptor deficiency may be involved in the growth retardation of K+ deficiency. Journal of Endocrinology (1995) 147, 253–258