With its discovery in 1920, the molecule vitamin D achieved prominence as a nutritionally essential vitamin important for calcium homeostasis, particularly in the intestine and bone. Then in 1932, the elucidation of vitamin D's chemical structure revealed that this vitamin was in fact a steroid. But it was not until the late 1960s that it was appreciated that the steroid vitamin D was a precursor of a new steroid hormone, 1alpha,25(OH)2-vitamin D3 [1alpha,25(OH)2D3], that is produced by the kidney acting as an endocrine gland. The discovery in 1969 of the nuclear vitamin D receptor (VDR) for 1alpha,25(OH)2D3 initiated a two-decade-long proliferation of reports that collectively described the broad sphere of influence of the vitamin D endocrine system that is defined by the presence of the VDR in over 30 tissue/organs of man. The new genomic frontiers defined by the cellular presence of the VDR include the immune system's B and T lymphocytes, hair follicle, muscle, adipose tissue, bone marrow, and cancer cells. Unexpectedly in the mid 1980s, a new world of 1alpha,25(OH)2D3-mediated rapid responses (RR) was discovered. These were responses that occurred too rapidly (minutes to an hour) to be explained as the simple consequence of the nuclear VDR regulating gene transcription. Some RR examples include the rapid intestinal absorption of calcium (transcaltachia), secretion of insulin by pancreatic beta-cells, opening of voltage-gated Ca2+ and Cl- channels in osteoblasts, and the rapid migration of endothelial cells. The question then arose as to whether there was a second receptor, apart from the nuclear VDR, which responded to the presence of 1alpha,25(OH)2D3 to generate RR? After some false starts, it now appears that the classic VDR, long known to reside in the cell nucleus, in some cells is also associated with caveolae present in the plasma membrane. Furthermore, the chemical properties of the conformationally flexible 1alpha,25(OH)2D3 allow it to generate different shaped ligands for the VDR that are selective either for genomic or for RR. This minireview summarizes a proposed conformational ensemble model of the VDR that provides insight into how different ligand shapes of 1alpha,25(OH)2D3 acting through the VDR in different cellular locations can selectively mediate both genomic and RR.

/pdf/minireview-vitamin-d-receptor-new-assignments-for-an-already-2vt1xqrkxz.pdf

Minireview: vitamin D receptor: new assignments for an already busy receptor. - eScholarship

Maternal and fetal exposure to cadmium, lead, manganese and mercury: The MIREC study

Air pollution, environmental chemicals, and smoking may trigger vitamin D deficiency: Evidence and potential mechanisms

This study measured the effects of vitamin D (VD) supplementation on the underlying molecular pathways involved in renal and testicular damage induced by lead (Pb) toxicity. Thirty two adult male Wistar rats were divided equally into four groups that were treated individually or simultaneously, except the negative control, for four weeks with lead acetate in drinking water (1,000 mg/L) and/or intramuscular VD (1,000 IU/kg; 3 days/week). Pb toxicity markedly reduced serum VD and Ca2+, induced substantial renal and testicular injuries with concomitant significant alterations in the expression of VD metabolising enzymes, its receptor and binding protein, and the calcium sensing receptor. Pb also significantly promoted lipid peroxidation and pro-inflammatory cytokines (IL-4 and TNF-α) in the organs of interest concomitantly with declines in several anti-oxidative markers (glutathione, glutathione peroxidase and catalase) and the anti-inflammatory cytokine, IL-10. The co-administration of VD with Pb markedly mitigated renal and testicular injuries compared with positive controls. This was associated with restoration of the expression of VD related molecules, promotion of anti-oxidative and anti-inflammatory markers, but tissue Pb concentrations were unaffected. In conclusion, this report is the first to reveal potential protective effects for VD against Pb-induced renal and testicular injuries via anti-inflammatory and anti-oxidative mechanisms.

/pdf/vitamin-d-alleviates-lead-induced-renal-and-testicular-jrawh8ohgb.pdf

Vitamin D alleviates lead induced renal and testicular injuries by immunomodulatory and antioxidant mechanisms in rats.

BACKGROUND: Food intolerance mediated by food specific IgG antibodies has been implicated in a variety of disorders. OBJECTIVES: To assess the prevalence of food specific IgG antibodies among patie...

Prevalence of IgG-mediated food intolerance among patients with allergic symptoms.

Objective To evaluate the prevalence of vitamin D deficiency and insufficiency, as well as their association with Hb and elevated blood lead levels (BLL) in children in China. Design A cross-sectional and 1-year retrospective study. Setting Department of Laboratory Medicine, West China Second University Hospital, Sichuan University, China. Subjects Children aged from 6 months to 14 years living in south-west China who were taken to physical examinations (January–December 2011). Results Of 1218 children included in the study, 25-hydroxyvitamin D (25(OH)D) concentration (mean 33·18 (sd 16·48) ng/ml) was deficient in 21·6 % and insufficient in 27·4 %, which were higher than the prevalence of both anaemia at 8·5 % and elevated BLL (Pb ≥ 10 μg/dl) at 1·8 %, but lower than mildly elevated BLL prevalence (5 μg/dl ≤ Pb 0·05). After multivariable adjustment, the significant predictors of 25(OH)D deficiency and insufficiency were increasing child age especially between 8 and 14 years (OR = 18·29; 95 % CI 10·14, 32·99; P < 0·001) and BLL (OR = 1·01; 95 % CI 1·00, 1·02; P = 0·045). Conclusions The prevalence of 25(OH)D deficiency and insufficiency was much higher than that of anaemia or elevated BLL in south-west China, and associated with increasing age and BLL.

/pdf/association-of-25-hydroxyvitamin-d-with-hb-and-lead-in-j41c1k9gxa.pdf

Association of 25-hydroxyvitamin D with Hb and lead in children: a Chinese population-based study.

Abstract Background Central sensitization has been widely accepted as an underlying pathophysiological mechanism of chronic migraine (CM), activation of cannabinoid type-1 receptor (CB1R) exerts antinociceptive effects by relieving central sensitization in many pain models. However, the role of CB1R in the central sensitization of CM is still unclear. Methods A CM model was established by infusing inflammatory soup (IS) into the dura of male Wistar rats for 7 days, and hyperalgesia was assessed by the mechanical and thermal thresholds. In the periaqueductal gray (PAG), the mRNA and protein levels of CB1R and hyperpolarization-activated cyclic nucleotide-gated cation channel 2 (HCN2) were measured by qRT–PCR and western blotting. After intraventricular injection of Noladin ether (NE) (a CB1R agonist), ZD 7288 (an HCN2 blocker), and AM 251 (a CB1R antagonist), the expression of tyrosine phosphorylation of N-methyl-D-aspartate receptor subtype 2B (pNR2B), calcium-calmodulin-dependent kinase II (CaMKII), and phosphorylated cAMP-responsive element binding protein (pCREB) was detected, and central sensitization was evaluated by the expression of calcitonin gene-related peptide (CGRP), c-Fos, and substance P (SP). Synaptic-associated protein (postsynaptic density protein 95 (PSD95) and synaptophysin (Syp)) and synaptic ultrastructure were detected to explore synaptic plasticity in central sensitization. Results We observed that the mRNA and protein levels of CB1R and HCN2 were both significantly increased in the PAG of CM rats. The application of NE or ZD 7288 ameliorated IS-induced hyperalgesia; repressed the pNR2B/CaMKII/pCREB pathway; reduced CGRP, c-Fos, SP, PSD95, and Syp expression; and inhibited synaptic transmission. Strikingly, the application of ZD 7288 relieved AM 251-evoked elevation of pNR2B, CGRP, and c-Fos expression. Conclusions These data reveal that activation of CB1R alleviates central sensitization by regulating HCN2-pNR2B signaling in CM rats. The activation of CB1R might have a positive influence on the prevention of CM by mitigating central sensitization. 

/pdf/activation-of-cb1r-alleviates-central-sensitization-by-1x6jqo3t.pdf

Activation of CB1R alleviates central sensitization by regulating HCN2-pNR2B signaling in a chronic migraine rat model

Objective To investigate the epidemiological characteristics of intolerance to 14 foods in children and the relationship between food intolerance and disease of various systems. Methods Serum samples of 2434 children with diseases were collected for food intolerance testing between January 2009 and October 2012. Allergen-specific IgG antibodies to 14 foods were detected using enzyme-linked immunosorbent assay. The children's intolerance to different foods and its relationship with age, sex and disease of various systems were analyzed. Results Among these children, positive rates of intolerance to milk and eggs were as high as 74.16% and 66.47% respectively, while positive rates of intolerance to chicken and pork were relatively low (0.29% and 0.21% respectively). The overall positive rates of food intolerance were 12.579% and 12.470% in males and females respectively. For infants, the highest intolerance rate was to milk; for preschool and school-age children, the highest intolerance rates were to milk and eggs respectively; for children in adolescence, the highest intolerance rate was to eggs. Among children with food intolerance involving single system, those with developmental abnormality or immune system disease had the highest overall positive rate of food intolerance. Children with double-system diseases had an overall positive rate of food intolerance as high as 13.393%. Among the children involving various systems, the positive rate of intolerance to milk and eggs were higher than other food. Conclusions Factors influencing food intolerance in children include food categories and age. There may be a relationship between food intolerance and disease of various systems, and this is significant to the growth and development of children.

An epidemiological study of food intolerance in 2434 children

Pancreatic adenocarcinoma (PAAD) is a malignant tumor with one of the highest associated mortality rates worldwide, and a 5-year survival rate of <5%. Fibroblast growth factors (FGFs) serve important roles in numerous cellular functions, and dysregulation of FGFs contributes to various cancer types. However, there are few reports on the function of FGFs in PAAD. The Assistant for Clinical Bioinformatics database, Gene Expression Profiling Interactive Analysis, Kaplan-Meier plotter and Tumor Immune Estimation Resource were utilized to perform the protein-protein interaction network, functional enrichment, univariate Cox regression, least absolute shrinkage and selection operator (LASSO) Cox, differential expression, prognostic value and immune cell infiltration analyses of FGFs in patients with PAAD. Immunohistochemistry (IHC) was used to verify the predictive value of the model. A total of 22 FGF genes were identified. Based on the results of LASSO Cox regression analysis, a total of six genes, including FGF2, FGF8, FGF9, FGF13, FGF17 and FGF22, were selected for the establishment of the prognostic gene signature. High transcriptional levels of FGF17 and FGF22 were significantly associated with long overall survival. The expression of FGFs was associated with the infiltration of various immune cells. According to univariate and multivariate analyses, FGF2 and FGF8 may be useful independent prognostic biomarkers for the prognosis of patients with PAAD. IHC demonstrated that FGF2 and FGF8 were more highly expressed in PAAD tissues compared with that in normal tissues. The present findings offer a novel understanding for the selection of FGF prognostic biomarkers in PAAD.

/pdf/systematic-analysis-of-expression-profiles-and-prognostic-3njmuszm.pdf

Systematic analysis of expression profiles and prognostic significance of the FGF gene family in pancreatic adenocarcinoma

Since the reports of “To err is human: building a safer health system” focused on medical errors [1], the errors in and outside laboratory medicine have received worldwide attention. The International Federation of Clinical Chemistry and Laboratory Medicine (IFCC) has established the Working Group “Laboratory Errors and Patient Safety” to take charge of promoting and encouraging investigations into errors in laboratory medicine for improving patient safety [2]. An incorrect report, caused by different kinds of errors, may influence most medical decisions including diagnosis, prognosis, treatments and etc., even lead to adverse clinical reactions. Therefore, corrected reports rate, the percent of reports that are corrected, is considered as one of the important quality indicators in laboratory medicine [3]. Numerous articles studied the errors in the total test process; however, few studies are about the corrected reports in laboratory medicine. In this study, the information about corrected reports in laboratory medicine was analyzed. The data of corrected reports was collected at the Department of Laboratory Medicine in a university hospital in southwest China, providing service especially for women and children. The Department of Laboratory Medicine in this hospital is a laboratory that has been accredited both by ISO 15189 in 2006 and by CAP in 2013. The laboratory tests over 1 million specimens per year at present. In this study, corrected reports from 2010 to 2012 in the laboratory were collected. The corrected report was generated by manual corrections of patients’ test reports that had been released. In our accounting systems, one panel was counted as one test report. One panel is a single billed test report in which analytes are grouped together according to subdisciplines. The proficiency test and non-patient test are not included. The data of corrected reports were extracted from the laboratory information system (LIS). Information from corrected reports about the reports’ panel, the changed results, the reviewer, etc. can be obtained from the LIS. Corrections detected before or during analysis and the final validation were not included. Six subgroups’ corrected reports in our laboratory were collected for statistical analysis, including chemistry (not involving POCT), hematology, immunology, blood bank, urinalysis and stool microscopy, Vaginal secretions microscopy (test for scored gram stain of vaginosis). The corrected reports rate is calculated as the following formula:

Corrected reports in laboratory medicine in a Chinese university hospital for 3 years.

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