text:
Q: Testing value from a list, replacing from another in Python Please, what would be "the ultimate Python" way to test whether some simple variable X is in a list (or a tuple) and if True then to return value from another list (or a tuple) at the same position? Would dictionary serve better?

A: The list.index() or tuple.index() method returns the first index of a matching value:
def mapped_value(somelist, someotherlist, value):
    try:
        index = somelist.index(value)
    except ValueError:
        return None
    return someotherlist[index]

A ValueError is raised if the value is not present, at which point None is returned instead.
This could be made a little more compact and guard against a shorter someotherlist too by catching IndexError:
def mapped_value(somelist, someotherlist, value):
    try:
        return someotherlist[somelist.index(value)]
    except (ValueError, IndexError):
        return None

However, a dictionary mapping values to other values would be much more convenient, yes. You can convert your two lists to a dictionary with:
mapping = dict(zip(somelist, someotherlist))
return mapping.get(value)

where it is assumed that the items in somelist are both unique and hashable.
Demo:
>>> somelist = ['foo', 'bar', 'baz']
>>> someotherlist = ['spam', 'ham', 'eggs']
>>> mapped_value(somelist, someotherlist, 'bar')
'ham'
>>> mapping = dict(zip(somelist, someotherlist))
>>> mapping.get('bar')
'ham'


text:
FOXN3 inhibits cell proliferation and in...
FOXN3 inhibits cell proliferation and invasion via modulating the AKT/MDM2/p53 axis in human glioma
Chaojia Wang1, , Hanjun Tu2, , Ling Yang3, , Chunming Ma4, , Juntao Hu1, , Jie Luo1, , Hui Wang1, ,
1 Department of Neurosurgery, Taihe Affiliated Hospital of Hubei University of Medicine, Shiyan 442000, China
2 First School of Clinical Medicine, Hubei University of Medicine, Shiyan 442000, China
3 Department of Pediatrics, Taihe Affiliated Hospital of Hubei University of Medicine, Shiyan 442000, China
4 Department of Rehabilitation, Taihe Affiliated Hospital of Hubei University of Medicine, Shiyan 442000, China
Received: May 9, 2021 Accepted: July 30, 2021 Published: September 12, 2021
Wang C, Tu H, Yang L, Ma C, Hu J, Luo J, Wang H, . FOXN3 inhibits cell proliferation and invasion via modulating the AKT/MDM2/p53 axis in human glioma. Aging (Albany NY). 2021; 13:21587-21598. https://doi.org/10.18632/aging.203499
Provider: TY - JOUR AU - Wang, Chaojia AU - Tu, Hanjun AU - Yang, Ling AU - Ma, Chunming AU - Hu, Juntao AU - Luo, Jie AU - Wang, Hui TI - FOXN3 inhibits cell proliferation and invasion via modulating the AKT/MDM2/p53 axis in human glioma JO - JA - Aging (Albany NY) VL - 13 IS - 17 PB - SN - UR - https://doi.org/10.18632/aging.203499 DO - 10.18632/aging.203499 SP - 21587 EP - 21598 PY - ER -
Provider: TY - JOUR AU - Wang, Chaojia AU - Tu, Hanjun AU - Yang, Ling AU - Ma, Chunming AU - Hu, Juntao AU - Luo, Jie AU - Wang, Hui TI - FOXN3 inhibits cell proliferation and invasion via modulating the AKT/MDM2/p53 axis in human glioma JO - JA - Aging (Albany NY) VL - 13 IS - 17 PB - SN - UR - https://doi.org/10.18632/aging.203499 DO - 10.18632/aging.203499 SP - 21587 EP - 21598 PY - AB - This study aimed to evaluate the biological role of forkhead box N3 (FOXN3) in human glioma and clarify the possible molecular mechanisms. FOXN3 expression patterns in clinical tissue specimens were characterized via qPCR and Western blotting. Kaplan-Meier survival curve was applied to assess the correlation between FOXN3 expression and overall survival. Effects of FOXN3 over-expression and depletion on glioma cell proliferation, apoptosis, migration and invasion were assessed by CCK8, colony formation assay, flow cytometry, scratch wound healing assay and Transwell invasion assay, respectively. Moreover, the involvement of AKT/murine double minute 2 (MDM2)/p53 pathway was evaluated. Additionally, tumor transplantation model assay was performed to determine the effects of FOXN3 over-expression on glioma cell growth in vivo. Results showed that FOXN3 was significantly down-regulated in glioma tissues compared with normal tissues. Patients with lower FOXN3 expression exhibited a shorter overall survival time. Gain- and loss-of-function analyses demonstrated that FOXN3 over-expression significantly suppressed proliferation, survival and motility of glioma cells, whereas FOXN3 knockdown remarkably promoted glioma cell proliferation, survival and motility. Furthermore, FOXN3 over-expression inhibited the activation of AKT/MDM2/p53 signaling pathway in glioma cells, while FOXN3 depletion facilitated its activation. Additionally, tumor xenograft assays revealed that FOXN3 over-expression retarded glioma cell growth in vivo. Collectively, these findings indicate that FOXN3 inhibits cell growth and invasion through inactivating the AKT/MDM2/p53 signaling pathway and that FOXN3-AKT/MDM2/p53 axis may represent a novel therapeutic target for glioma patients. ER -
Copyright: © 2021 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
This study aimed to evaluate the biological role of forkhead box N3 (FOXN3) in human glioma and clarify the possible molecular mechanisms. FOXN3 expression patterns in clinical tissue specimens were characterized via qPCR and Western blotting. Kaplan-Meier survival curve was applied to assess the correlation between FOXN3 expression and overall survival. Effects of FOXN3 over-expression and depletion on glioma cell proliferation, apoptosis, migration and invasion were assessed by CCK8, colony formation assay, flow cytometry, scratch wound healing assay and Transwell invasion assay, respectively. Moreover, the involvement of AKT/murine double minute 2 (MDM2)/p53 pathway was evaluated. Additionally, tumor transplantation model assay was performed to determine the effects of FOXN3 over-expression on glioma cell growth in vivo. Results showed that FOXN3 was significantly down-regulated in glioma tissues compared with normal tissues. Patients with lower FOXN3 expression exhibited a shorter overall survival time. Gain- and loss-of-function analyses demonstrated that FOXN3 over-expression significantly suppressed proliferation, survival and motility of glioma cells, whereas FOXN3 knockdown remarkably promoted glioma cell proliferation, survival and motility. Furthermore, FOXN3 over-expression inhibited the activation of AKT/MDM2/p53 signaling pathway in glioma cells, while FOXN3 depletion facilitated its activation. Additionally, tumor xenograft assays revealed that FOXN3 over-expression retarded glioma cell growth in vivo. Collectively, these findings indicate that FOXN3 inhibits cell growth and invasion through inactivating the AKT/MDM2/p53 signaling pathway and that FOXN3-AKT/MDM2/p53 axis may represent a novel therapeutic target for glioma patients.
Human glioma has emerged as one of the most common intracranial malignancies in recent decades, accounting for roughly 45% of all brain tumors [1–3]. It is estimated that approximately 15,000 cancer-related deaths were attributed to glioma annually in United States [4–6]. In spite of the fact that great advances regarding the standardized therapies have been made for glioma patients, the long-term prognosis of malignant glioma patients is still pretty frustrating [7–9]. Thus, there is an urgent need to better understand the exact mechanisms underlying glioma development, which could facilitate to develop effective treatment strategies and improve the prognosis for glioma patients.
It is well documented that Forkhead box N3 (FOXN3) belongs to the FOX family of transcriptional factors, which are implicated in a great variety of biological activities, including cell survival, cell proliferation and cell migration as well as cell invasion [10–12]. Recent studies have uncovered that FOXN3 functions as a key player in multiple kinds of malignant tumors, such as papillary thyroid cancer [13], tongue squamous cell carcinoma [14], melanoma [15] and breast cancer [16]. Nevertheless, potential biological functions of FOXN3 in human glioma remain largely unclear.
The current study aimed to explore potential biological functions of FOXN3 in human glioma and clarify possible molecular mechanism. Herein, it was found that FOXN3 was markedly under-expressed in glioma tissue samples and glioma cell lines. Furthermore, gain of function and loss of function researches were applied to explore effects of FOXN3 on the proliferation, colony formation and motility capabilities of glioma cells. In addition, the involvement of AKT/murine double minute 2 (MDM2)/p53 axis was also assessed. Taken together, the present study offers novel insights into elucidating biological functions of FOXN3 in glioma.
Clinical sample collection
Sixty-three glioma patients who received surgical operation were recruited in Taihe Affiliated Hospital of Hubei University of Medicine (Shiyan, China) from February 2013 to December 2018. Tumor tissue samples were obtained from patients with glioma. Normal non-tumorous brain tissue samples were collected from sixty-three volunteers who suffered from traffic accidents. Written informed consents were gathered from all the participants prior to their enrollment in this study. The fresh clinical tissue specimens were immediately placed in an ultra-low temperature freezer (–80°C) for subsequent studies. The present study gained approval from Ethics Committee of Taihe Affiliated Hospital of Hubei University of Medicine (IRB approval No. 2012090058).
Cell culture and cell transfection
Four glioma cell lines (LN229, SF126 and U87MG as well as U251MG) and HEB cells (normal human gliocytes) were obtained from Shanghai Cell Institute of Chinese Academy of Sciences. Cells were incubated in RPMI 1640 medium (Gibco, Grand Island, NY, USA) containing 10% fetal bovine serum (FBS). Cells were cultured in a 5% carbon dioxide humidified atmosphere at 37°C.
Lipofectamine 3000 (Invitrogen, Carlsbad, CA, USA) was applied to carry out cell transfection assay according to manufacturer's instructions. The pcDNA3.1 and pLKO.1 plasmids were used for over-expression and knockdown studies, respectively. FOXN3 expression vectors and short hairpin RNAs (shRNAs) specially targeting FOXN3 were constructed in Shanghai GenePharma Co. Ltd (Shanghai, China). Sequence information concerning sh-NC and shRNA#1 as well as shRNA#2 was listed as followed: sh-NC, 5′-CGCGTCCCGTGGATATTGTTCAAGAGAAATATCCACTTGGAATAGCAA-3′; shRNA#1, 5′-CACCGCC TGACATCCGATTAGAAGACGAATCTTCTAATCGGATGTCAGG-3′; shRNA#2, 5′-CACCGCCTCATAT TTATGGCCATCGCGAACGATGGCCATAAATATGAGGC-3′. Transfection efficiency was evaluated via Western blotting analysis at 48 h post-transfection.
Real-time qPCR analysis
TRIzol was used to exact total RNAs from clinical tissue samples using in line with manufacturer's protocols (Takara, Dalian, China). TaqMan High-Capacity cDNA Reverse Transcription Kit was applied to synthesize complementary DNA strand (Applied Biosystems, Carlsbad, CA, USA). Afterwards, qPCR analysis was conducted using the SYBR Green PCR Kit (Applied Biosystems) on the ABI 7500 Fast Real-time PCR System. Relative expression level of FOXN3 mRNA was calculated via the 2–ΔΔCt method. Herein, β-actin acted as an endogenous reference gene. Sequence information about specific primers was provided as followed: FOXN3, upstream 5′-CCGGACAGTGGGA ACTAACT-′3 and downstream 5′-GCTGTGGATGGC TTTTAGGG-′3; β-actin, upstream 5′-GTGGGGCGCC CCAGGCACCA-′3 and downstream 5′-CTCCTTAAT GTCACGCACGATTTC-′3. Relative FOXN3 mRNA expression was determined via triplicate experiments.
MTT assays
MTT Cell Proliferation Assay Kit (Invitrogen) was applied to evaluate cell proliferation ability. MTT assays were performed based on manufacturer's protocols. Briefly, 20 μl of MTT solution was placed into the 96-well plates and was then cultured for 4 hours at 37°C. Afterwards, 150 μl of DMSO solutions was added into the 96-well plates after discarding the supernatants. Finally, a Spectramax M5 spectrophotometer was used to detect the absorbance at 490 nm. All experiments were conducted in triplicates.
Colony formation ability analysis
Clonogenic capability of tumor cell was assessed through colony formation assays. Briefly, tumor cells were placed into the six-well plates at the concentration of 1 × 103 cells per well and were incubated for two weeks. Fifteen minutes' incubation with 10% formaldehyde was used to fix the forming colonies, followed by 0.1% crystal violet staining. In the end, the stained colonies were observed and were counted via an inverted microscope. Clonogenic ability was evaluated by triplicate experiments.
Cell apoptosis detection
Tumor cell apoptosis was analyzed using FITC-Annexin V/PI Apoptosis Detection Kit according to manufacturer's guidelines. Briefly, collected cells were resuspended in the binding buffer (0.5 ml) after being washed twice by cold PBS. The cells were maintained in the dark for 15 minutes at room temperature followed by addition of 5 Annexin V-FITC solution (5 μl) and PI solution (5 μl). Finally, flow cytometry was applied to detect the apoptotic cells. All the experiments were conducted in triplicates.
Scratch wound healing assays
The scratch wound healing assays were used to determine the Migration ability of tumor cells were determined by wound healing assays. Briefly, about 1000 cells per well were seeded into the 6-well plates. The cells were scratched using a sterile 200 μl pipette tip when reaching a confluence of 100% and were incubated in the culture medium for 24 hours. Subsequently, the wound closure was observed under a microscope. Migration abilities of tumor cells were assessed via triplicate experiments.
Transwell invasion assay
Invasive ability of tumor cells was examined by Transwell invasion method. In brief, about 2 × 104 cells were placed into the upper chamber which contained fetal bovine serum-free culture medium. Matrigel (BD Bioscience, San Jose, CA, USA) was applied to coat the upper chamber which was filled with DMEM culture with 10% fetal bovine serum. Cells were then incubated for twenty-four hours at 37°C. Subsequently, the invading cells were fixed using paraformaldehyde (4%) and were visualized using crystal violet. Finally, the stained cells were observed and were photographed. Invasion capabilities of cells were analyzed through triplicate experiments.
Tumor xenograft assay in nude mice
Animal experiment was carried out in Taihe Affiliated Hospital of Hubei University of Medicine. Animal experiment gained approval from the Animal Care and Use Committee of Taihe Affiliated Hospital of Hubei University of Medicine (IACUC approval No. 2019120746). Ten BALB/c nude mice (male) were obtained from Beijing HFK Bioscience Co. Ltd (Beijing, China) and were classified into 2 groups (n = 5). Tumor xenograft models were constructed via inoculation of empty vector or FOXN3 expression vector-treated U87MG cells (1 × 106 cells per mouse) into the flanks of nude mice. Volumes of formed tumors was determined every seven days based on the calculation formula that tumor seize (mm3) = 0.5 × width2 (mm2) × length (mm). All the mice were anesthetized via isoflurane inhalation and were sacrificed via cervical dislocation at day 28 post-transplantation. Then the tumors were peeled and weighed.
Western blotting analysis
Total proteins were extracted from tissue samples and cell samples using the lysis buffer containing protease inhibitor. The concentrations of extracted protein samples were measured via BCA Protein Assay Kit (Takara, Dalian, China), followed by 10% SDS-PAGE separation. Then protein samples were transferred onto PVDF membrane, followed by one hour's 5% non-fat milk incubation. Primary antibodies were then incubated overnight at 4°C. The primary antibodies (Abcam, Cambridge, MA, USA) were used at the following dilutions: anti-β-actin (1:2000), anti-FOXN3 (1:1000), anti-PCNA (1:1000), anti-CCND1 (1:1000), anti-cleaved caspase 3 (1:1000), anti-Bcl2 (1:1000), anti-MMP9 (1:1000), anti-Vimentin (1:1000), anti-AKT (1:1000), anti-p-AKT (1:1000), anti-MDM2 (1:1000) and anti-p53 (1:1000). Afterwards, the secondary antibody was incubated for one hour. ECL Western Blotting Detection Kit was purchased from Amersham Bioscience (Piscataway, NJ, USA) and was used to visualize protein bands.
Immunohistochemical staining was carried out as previously described. Briefly, 4 μm-thick paraffin-embedded tissue sections were subjected to deparaffinization and rehydration, followed by antigen retrieval. Subsequently, endogenous peroxide activity was quenched via incubating tissue slices with 3% H2O2. Non-specific binding was blocked through incubation of bovine serum albumin. Primary antibodies (anti-Ki67, anti-cleaved caspase 3 and anti-Vimentin) were then incubated with tissue sections at 4°C overnight, followed by one hour's incubation with horseradish peroxide (HRP)-labeled secondary antibody. The slides were visualized via diaminobenzidine (DAB) staining. The positive staining in the tissue slices was were photographed and analyzed.
SPSS v20.0 was used to conduct data analysis. Results were presented as mean ± standard deviation. The student's t-test was used to analyze the differences between two groups. One-way ANOVA and Dunnett's post-hoc comparison were performed to evaluate differences among three or more groups. Kaplan-Meier survival curve was adopted to determine the link between FOXN3 expression and overall survival time of glioma patients. A P-value of less than 0.05 indicated significantly different.
Decreased FOXN3 expression is observed in glioma tissues
In order to explore the role of FOXN3 in human glioma, qPCR analysis was performed to characterize its expression patterns in glioma tissues and healthy brain tissues. As shown in Figure 1A, FOXN3 mRNA expression were significantly decreased in the glioma tissues in comparison with normal brain tissues (P < 0.01). In consistence with the findings about FOXN3 mRNA expression, Western blotting analysis showed that FOXN3 protein was notably under-expressed in glioma tissues in comparison with normal brain tissues (Figure 1B, P < 0.01). Besides, Kaplan-Meier survival curve was adopted to analyze the link between FOXN3 mRNA expression and overall survival time of glioma patients. Kaplan-Meier survival curve manifested that glioma patients with low FOXN3 expression (n = 32) exhibited a shorter overall survival time than those with high FOXN3 expression (n = 31; Figure 1C, P < 0.05). Collectively, these results suggest that decreased FOXN3 expression correlates with glioma patients' poor prognosis.
Figure 1. Decreased FOXN3 expression is observed in glioma tissues. (A) FOXN3 mRNA expression levels in clinical tissue samples were determined via qPCR analysis. (B) FOXN3 protein expression levels in clinical tissue samples were examined using Western blotting. (C) Glioma patients were divided into high FOXN3 expression group and low FOXN3 expression group based on the median of its expression levels in cancerous tissues. Kaplan-Meier survival curve was used to analyze the correlation between FOXN3 mRNA expression level and overall survival time. **P < 0.01. Abbreviation: FOXN3: forkhead box N3.
FOXN3 represses glioma cell proliferation, survival and motility
To further characterize the possible role of FOXN3 in human glioma, we performed subsequent cell experiments. Herein, FOXN3 protein expression patterns in glioma cell lines (SF126, U87MG, LN229 and U251MG cells) and normal human gliocytes (HEB cells) were assessed via Western blotting. As exhibited in Figure 2A, FOXN3 protein expression was significantly decreased in the glioma cell lines compared with HEB cells. Afterwards, U87MG with lowest endogenous FOXN3 expression and SF126 cells with highest endogenous FOXN3 expression were selected for the following gain- and loss-of-function researches. Subsequently, Western blotting analysis was conducted to determine the transfection efficiency after treatment with FOXN3 expression vectors or specific shRNAs (shRNA#1 and shRNA#2). As shown in Figure 2B, transfection of FOXN3 expression vectors remarkably elevated FOXN3 protein expression levels in U87MG cells in comparison with the control group; whereas transfection of shRNA#1 and shRNA#2 markedly decreased the expression levels of FOXN3 in SF126 cells in comparison with sh-NC group, especially shRNA#1. Thus, shRNA#1 was chosen for further knockdown studies. As evidenced by CCK8 assay and colony forming assay, FOXN3 over-expression significantly inhibited the proliferation of U87MG cells (P < 0.01), while FOXN3 knockdown sharply accelerated the proliferation of SF126 cells (Figure 2C and 2D, P < 0.01). Moreover, flow cytometry analysis showed that FOXN3 over-expression induced a higher proportion of apoptotic cells than the control treatment (P < 0.01), whereas FOXN3 ablation triggered a lower proportion of apoptotic cells than the negative control treatment (Figure 2E, P < 0.01). Besides, scratch assay and Transwell invasion assay showed that migration and invasion abilities of U87MG cells were significantly weakened by FOXN3 over-expression treatment, while migration and invasion abilities of SF126 cells were sharply strengthened in FOXN3 depletion group in comparison with those in sh-NC group (Figure 2F and 2G, P < 0.01). To sum up, these data imply that FOXN3 could represses glioma cell proliferation, survival and motility abilities.
Figure 2. FOXN3 suppresses glioma cell proliferation, survival and invasion. (A) FOXN3 protein expression levels in normal human L02 liver cells and glioma cell lines (SF126, SK-Hep-1, Huh6 and Huh7) were determined by Western blotting. (B) Transfection efficiency was detected via Western blotting after transfection with FOXN3 expression vectors in U87MG cells or transfection with specific shRNAs in SF126 cells. (C) Cell proliferation was measured by MTT assays after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. (D) Colony formation ability was analyzed using colony formation assays after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. (E) Apoptosis was assessed via flow cytometry after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. (F) Migration capability was evaluated by scratch wound healing assays after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. (G) Invasion ability was determined via Transwell invasion assays after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. **P < 0.01. FOXN3, forkhead box N3; shRNA#1, short hairpin RNA #1 specifically targeting FOXN3; shRNA#2, short hairpin RNA #2 specifically targeting FOXN3.
FOXN3 modulates the expression of malignant phenotype-associated proteins in glioma cells
It is widely accepted that some crucial functional proteins are involved in cancer occurrence and development. In order to further analyze the impacts of FOXN3 on tumor cell proliferation, apoptosis and motility, the expression patterns of malignant phenotype-related proteins in U87MGcells and SF126 cells were also evaluated. Herein, the influences of FOXN3 over-expression and knockdown on the expression levels of proliferation-related proteins (PCNA and CCND1) were analyzed by Western blotting. As displayed in Figure 3A, reduced PCNA and CCND1 protein expression levels were found in FOXN3 over-expression group in comparison with those in control group (P < 0.01), whereas elevated PCNA and CCND1 protein expression levels were observed in FOXN3 ablation group compared with those in sh-NC group (P < 0.01). Furthermore, FOXN3 over-expression elicited a noticeable elevation in cleaved caspase-3 protein expression level and a remarkable reduction in Bcl2 protein expression level in U87MG cells in comparison with control group (P < 0.01), while FOXN3 depletion led to increased Bcl2 protein expression and decreased cleaved caspase-3 protein expression in SF126 cells (Figure 3B, P < 0.01). In addition, FOXN3 over-expression inhibited the expression of MMP9 and Vimentin proteins in U87MGcells, whereas FOXN3 depletion boosted the expression of MMP9 and Vimentin proteins in SF126 cells (Figure 3C, P < 0.01). Taken together, these observations indicate that FOXN3 repressed the expression of malignant phenotype-promoting proteins in glioma cells.
Figure 3. FOXN3 modulates the expression of malignant phenotype-associated proteins in glioma cells. (A) Protein expression levels of PCNA and CCND1 were examined by Western blotting after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. (B) Protein expression levels of cleaved caspase 3 and Bcl2 were detected via Western blotting after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. (C) Protein expression levels of Vimentin and MMP9 were determined using Western blotting after transfection with FOXN3 expression vectors in U87MG cells or transfection with shRNA#1 in SF126 cells. **P < 0.01. FOXN3, forkhead box N3; shRNA#1, short hairpin RNA #1 specifically targeting FOXN3; Abbreviations: PCNA: proliferating cell nuclear antigen; CCND1: cyclin D1; Bcl2: B cell lymphoma; MMP9: matrix metalloproteinase 9.
FOXN3 inhibits the AKT/MDM2/p53 signaling axis in glioma cells
Emerging evidence has revealed that AKT/MDM2/ p53 signaling transduction would contribute to the malignant development of diverse kinds of malignant cancers. Herein, the impacts of FOXN3 over-expression and knockdown on AKT/MDM2/p53 signaling axis were assessed in glioma cells. As exhibited in Figure 4A, reduced p-AKT and MDM2 protein expression levels as well as elevated p53 protein expression level were observed in FOXN3 over-expression group in comparison with control group (P < 0.01). Besides, increased p-AKT and MDM2 protein expression levels as well as decreased p53 protein expression level were found in FOXN3 depletion group in comparison with sh-NC group (Figure 4B, P < 0.01). These results imply that FOXN3 suppresses AKT/MDM2/p53 signaling transduction in glioma cells.
Figure 4. FOXN3 inhibits the AKT/MDM2/p53 signaling pathway in glioma cells. (A) Protein expression levels of AKT, p-AKT, MDM2 and p53 were examined by Western blotting after transfection with FOXN3 expression vectors in U87MG cells. (B) Protein expression levels of AKT, p-AKT, MDM2 and p53 were determined by Western blotting after transfection with shRNA#1 in SF126 cells. **P < 0.01. FOXN3, forkhead box N3; shRNA#1, short hairpin RNA #1 specifically targeting FOXN3; Abbreviations: p-AKT: phosphorylated AKT; MDM2: murine double minute 2.
FOXN3 over-expression retards glioma cell growth in vivo
On the basis of the observations in vitro, the tumor transplantation models were established in mice through the subcutaneous inoculation of empty vector- or FOXN3 expression vector-treated U87MGcells into the flanks of mice. As presented in Figure 5A and 5B, the tumors in FOXN3 over-expression group grew marked slower than those in control group (P < 0.01). Moreover, significantly smaller neoplasms were harvested from the FOXN3 over-expression group in comparison with control group (Figure 5A and 5C, P < 0.01). In addition, the expression patterns of Ki67, cleaved caspase-3 and Vimentin proteins in the collected tumors from nude mice were visualized by immunohistochemical staining. As displayed in Figure 5D, less Ki67-positive and Vimentin-positive cells were found in the tumors in FOXN3 over-expression group in comparison with those in control group (P < 0.01). In addition, more cleaved caspase 3-positive cells were observed in FOXN3 over-expression group in comparison with control group (Figure 5D, P < 0.01). These data demonstrate that FOXN3 over-expression retards glioma cell growth in vivo, which was in consistence with the findings in vitro.
Figure 5. FOXN3 over-expression retards glioma cell growth in vivo. (A) Representative images of tumors harvested from murine neoplasm xenograft models. (B) Tumor growth curve was plotted based on the formula that volume (mm3) = [length (mm) × width2 (mm2)]/2. (C) Neoplasms were collected and weighed at day 28 post-transplantation. (D) Protein expression patterns of Ki67, cleaved caspase 3 and Vimentin in the tumors harvested from nude mice were visualized via immunohistochemical staining. **P < 0.01. Abbreviation: FOXN3: forkhead box N3.
It is widely accepted that glioma has aroused widespread public concerns around the world due to its high morbidity and mortality in recent decades [17–19]. It is worth noting that glioma has already imposed huge economic burdens and heath pressures on the glioma patients worldwide. Even though some significant achievements concerning the diagnosis and therapy have been gained, the overall survival of most glioma patients remains very depressing. Therefore, there is an urgent need to broaden our knowledge concerning the underlying mechanisms of glioma occurrence and progression, which would facilitate to develop promising and effective treatment alternatives. Mounting reports have manifested that the aberrant expression of tumor-related crucial genes is closely linked to the malignant progression of glioma [20–22].
In the previous studies, FOXN3 has been proved as a key player during the malignant development of varied kinds of malignant tumors. Xue et al. determined the expression pattern of FOXN3 in osteosarcoma and demonstrated that decreased FOXN3 expression repressed tumor cell invasion and migration through transcriptionally regulating SIRT6 [10]. He and his research team reported a notable decrease in FOXN3 expression in adult acute myeloid leukemia and their data revealed that FOXN3 exerted tumor-suppressing roles by inhibiting cell proliferation and promoting apoptosis [11]. Zhao et al. reported that decreased FOXN3 expression was observed in papillary thyroid cancer and discovered that FOXN3 inhibited tumor cell growth and invasion via the inactivation of Wnt/ β-catenin pathway [13]. Moreover, researches by Chen et al. [14] and Sun et al. [15] manifested that FOXN3 repressed tumor cell proliferation and epithelial-to-mesenchymal transition as well as metastasis in melanoma and tongue squamous cell carcinoma. Nonetheless, the biological role of FOXN3 remains poorly understood.
In the current study, FOXN3 expression patterns in glioma tissues were characterized via qPCR analysis and Western blotting. Herein, it was found that FOXN3 was notably under-expressed in the tumorous tissues and that reduced FOXN3 expression correlated with short overall survival time of patients with glioma. Moreover, gain of function and loss of function studies showed that up-regulation of FOXN3 notably inhibited glioma cell proliferation, survival and motility, while down-regulation of FOXN3 dramatically facilitated glioma cell proliferation, survival and invasion. In addition, our findings demonstrated that FOXN3 over-expression triggered an obvious reduction in PCNA, CCND1, MMP9 and Vimentin expression levels in glioma cells, whereas FOXN3 ablation elicited a remarkable elevation in PCNA, CCND1, MMP9 and Vimentin expression levels. It is well documented that decreased PCNA and CCND1 expression is associated with retarded proliferation of tumor cells [23–25] and that reduced MMP9 and Vimentin expression is closely related to slowed invasion of cancer cells [26, 27].
With the purpose of illuminating the potential molecular mechanisms underlying the biological functions of FOXN3 in glioma, further mechanistic studies were performed. Past researches have confirmed that the abnormal activation of the AKT/MDM2/p53 signaling axis is implicated in several types of human malignant neoplasms [28–30]. In the present research, we assessed the effects of FOXN3 on AKT/MDM2/p53 signaling axis in glioma cells. Herein, it was observed that FOXN3 over-expression repressed AKT/MDM2/p53 signaling transduction in glioma cells, whereas FOXN3 ablation facilitated the activation of AKT/MDM2/p53 signaling axis. It is widely acknowledged that AKT phosphorylation could facilitate the stabilization and nuclear translocation of the transcription factor MDM2, thereby triggering subsequent ubiquitination and degradation of the tumor suppressor factor p53 [31–33]. It is worthwhile to note that the inactivation of AKT/MDM2/p53 is regarded as a promising treatment option against human malignancies [34, 35]. In addition, in vivo xenograft assays demonstrated that FOXN3 over-expression could restrain tumor growth in the nude mice models.
To sum up, our findings for the first time demonstrated that FOXN3 was markedly under-expressed in human glioma and that reduced FOXN3 expression was linked to short overall survival time of patients with glioma. Moreover, functional and mechanistic researches preliminarily revealed that FOXN3 suppressed proliferation, survival and invasion of glioma cells through inactivating the AKT/MDM2/p53 axis. Hence, the present study may offer some valuable clues for clarifying the possible molecular mechanisms underlying glioma development and progression.
Hui Wang and Chaojia Wang conceived this study and supervised this project; Chaojia Wang, Hanjun Tu and Ling Yang conducted experimental operations and data analysis; Chaojia Wang, Hanjun Tu, Ling Yang, and Chunming Ma prepared original manuscript. Juntao Hu and Jie Luo participated in project administration. All the authors have read and agreed to the final version of this manuscript.
The authors declare no conflicts of interest related to this study.
The current study was supported by Hygiene and Health Program of Hubei Province (Grant No. WJ2019F055).
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7. Takacs GP, Flores-Toro JA, Harrison JK. Modulation of the chemokine/chemokine receptor axis as a novel approach for glioma therapy. Pharmacol Ther. 2021; 222:107790. https://doi.org/10.1016/j.pharmthera.2020.107790 [PubMed]
8. Lah TT, Novak M, Breznik B. Brain malignancies: Glioblastoma and brain metastases. Semin Cancer Biol. 2020; 60:262–73. https://doi.org/10.1016/j.semcancer.2019.10.010 [PubMed]
9. Baumgarten P, Quick-Weller J, Gessler F, Wagner M, Tichy J, Forster MT, Foerch C, Seifert V, Mittelbronn M, Senft C. Pre- and early postoperative GFAP serum levels in glioma and brain metastases. J Neurooncol. 2018; 139:541–46. https://doi.org/10.1007/s11060-018-2898-1 [PubMed]
10. Xue W, Ma L, Wang Z, Zhang W, Zhang X. FOXN3 is downregulated in osteosarcoma and transcriptionally regulates SIRT6, and suppresses migration and invasion in osteosarcoma. Oncol Rep. 2019; 41:1404–14. https://doi.org/10.3892/or.2018.6878 [PubMed]
11. He H, Zhang J, Qu Y, Wang Y, Zhang Y, Yan X, Li Y, Zhang R. Novel tumor-suppressor FOXN3 is downregulated in adult acute myeloid leukemia. Oncol Lett. 2019; 18:1521–29. https://doi.org/10.3892/ol.2019.10424 [PubMed]
12. Kong X, Zhai J, Yan C, Song Y, Wang J, Bai X, Brown JAL, Fang Y. Recent Advances in Understanding FOXN3 in Breast Cancer, and Other Malignancies. Front Oncol. 2019; 9:234. https://doi.org/10.3389/fonc.2019.00234 [PubMed]
13. Zhao C, Mo L, Li C, Han S, Zhao W, Liu L. FOXN3 suppresses the growth and invasion of papillary thyroid cancer through the inactivation of Wnt/β-catenin pathway. Mol Cell Endocrinol. 2020; 515:110925. https://doi.org/10.1016/j.mce.2020.110925 [PubMed]
14. Chen S, Zhang J, Sun L, Li X, Bai J, Zhang H, Li T. miR-611 promotes the proliferation, migration and invasion of tongue squamous cell carcinoma cells by targeting FOXN3. Oral Dis. 2019; 25:1906–18. https://doi.org/10.1111/odi.13177 [PubMed]
15. Sun M, Ma X, Tu C, Wang X, Qu J, Wang S, Xiao S. MicroRNA-378 regulates epithelial-mesenchymal transition and metastasis of melanoma by inhibiting FOXN3 expression through the Wnt/β-catenin pathway. Cell Biol Int. 2019; 43:1113–24. https://doi.org/10.1002/cbin.11027 [PubMed]
16. Xu Z, Yang Y, Li B, Li Y, Xia K, Yang Y, Li X, Wang M, Li S, Wu H. Checkpoint suppressor 1 suppresses transcriptional activity of ERα and breast cancer cell proliferation via deacetylase SIRT1. Cell Death Dis. 2018; 9:559. https://doi.org/10.1038/s41419-018-0629-3 [PubMed]
17. Wu J, Lu L, Chen H, Lin Y, Zhang H, Chen E, Lin W, Li J, Chen X. Prognostic nomogram to predict the overall survival of patients with early-onset colorectal cancer: a population-based analysis. Int J Colorectal Dis. 2021; 36:1981–93. https://doi.org/10.1007/s00384-021-03992-w [PubMed]
18. Wang Y, Jiang M, Yao Y, Cai Z. WWC3 Inhibits Glioma Cell Proliferation Through Suppressing the Wnt/β-Catenin Signaling Pathway. DNA Cell Biol. 2018; 37:31–37. https://doi.org/10.1089/dna.2017.3931 [PubMed]
19. Zhang Z, Xu J, Chen Z, Wang H, Xue H, Yang C, Guo Q, Qi Y, Guo X, Qian M, Wang S, Qiu W, Gao X, et al. Transfer of MicroRNA via Macrophage-Derived Extracellular Vesicles Promotes Proneural-to-Mesenchymal Transition in Glioma Stem Cells. Cancer Immunol Res. 2020; 8:966–81. https://doi.org/10.1158/2326-6066.CIR-19-0759 [PubMed]
20. Yang AP, Liu JP, Tao WQ, Li HM. The diagnostic and predictive role of NLR, d-NLR and PLR in COVID-19 patients. Int Immunopharmacol. 2020; 84:106504. https://doi.org/10.1016/j.intimp.2020.106504 [PubMed]
21. Puigdelloses M, González-Huárriz M, García-Moure M, Martínez-Vélez N, Esparragosa Vázquez I, Bruna J, Zandio B, Agirre A, Marigil M, Petrirena G, Nuñez-Córdoba JM, Tejada-Solís S, Díez-Valle R, et al. RNU6-1 in circulating exosomes differentiates GBM from non-neoplastic brain lesions and PCNSL but not from brain metastases. Neurooncol Adv. 2020; 2:vdaa010. https://doi.org/10.1093/noajnl/vdaa010 [PubMed]
22. Cao F, Xia X, Fan Y, Liu Q, Song J, Zhang Q, Guo Y, Yao S. Knocking down of Polo-like kinase 2 inhibits cell proliferation and induced cell apoptosis in human glioma cells. Life Sci. 2021; 270:119084. https://doi.org/10.1016/j.lfs.2021.119084 [PubMed]
23. Wu J, Jiang Y, Cao W, Li X, Xie C, Geng S, Zhu M, Liang Z, Zhu J, Zhu W, Wu R, Ma X, Huang C, et al. miR-19 targeting of PTEN mediates butyl benzyl phthalate-induced proliferation in both ER(+) and ER(−) breast cancer cells. Toxicol Lett. 2018; 295:124–33. https://doi.org/10.1016/j.toxlet.2018.05.040 [PubMed]
24. Zhu M, Huang C, Ma X, Wu R, Zhu W, Li X, Liang Z, Deng F, Wu J, Geng S, Xie C, Zhong C. Phthalates promote prostate cancer cell proliferation through activation of ERK5 and p38. Environ Toxicol Pharmacol. 2018; 63:29–33. https://doi.org/10.1016/j.etap.2018.08.007 [PubMed]
25. Xie G, Yin S, Zhang Z, Qi D, Wang X, Kim D, Yagai T, Brocker CN, Wang Y, Gonzalez FJ, Wang H, Qu A. Hepatocyte Peroxisome Proliferator-Activated Receptor α Enhances Liver Regeneration after Partial Hepatectomy in Mice. Am J Pathol. 2019; 189:272–82. https://doi.org/10.1016/j.ajpath.2018.10.009 [PubMed]
26. Dai B, Yu R, Fan M, Yang T, Wang B, Zhang Y. HMQ-T-F2 suppresses migration of the human cervical cancer HeLa cells by reversing EMT via the PI3K/Akt signaling pathway. Oncol Rep. 2019; 42:1451–58. https://doi.org/10.3892/or.2019.7245 [PubMed]
27. Pei Y, Tang Z, Cai M, Yao Q, Xie B, Zhang X. The E2F3/miR-125a/DKK3 regulatory axis promotes the development and progression of gastric cancer. Cancer Cell Int. 2019; 19:212. https://doi.org/10.1186/s12935-019-0930-y [PubMed]
28. Wan W, Hou Y, Wang K, Cheng Y, Pu X, Ye X. The LXR-623-induced long non-coding RNA LINC01125 suppresses the proliferation of breast cancer cells via PTEN/AKT/p53 signaling pathway. Cell Death Dis. 2019; 10:248. https://doi.org/10.1038/s41419-019-1440-5 [PubMed]
29. Gao J, Xia R, Chen J, Gao J, Luo X, Ke C, Ren C, Li J, Mi Y. Inhibition of esophageal-carcinoma cell proliferation by genistein via suppression of JAK1/2-STAT3 and AKT/MDM2/p53 signaling pathways. Aging (Albany NY). 2020; 12:6240–59. https://doi.org/10.18632/aging.103019 [PubMed]
30. Tu Y, Kim E, Gao Y, Rankin GO, Li B, Chen YC. Theaflavin-3, 3′-digallate induces apoptosis and G2 cell cycle arrest through the Akt/MDM2/p53 pathway in cisplatin-resistant ovarian cancer A2780/CP70 cells. Int J Oncol. 2016; 48:2657–65. https://doi.org/10.3892/ijo.2016.3472 [PubMed]
31. Lin S, Yu L, Ni Y, He L, Weng X, Lu X, Zhang C. Fibroblast Growth Factor 21 Attenuates Diabetes-Induced Renal Fibrosis by Negatively Regulating TGF-β-p53-Smad2/3-Mediated Epithelial-to-Mesenchymal Transition via Activation of AKT. Diabetes Metab J. 2020; 44:158–72. https://doi.org/10.4093/dmj.2018.0235 [PubMed]
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35. Tan XL, Guo L, Wang GH. Polyporus umbellatus inhibited tumor cell proliferation and promoted tumor cell apoptosis by down-regulating AKT in breast cancer. Biomed Pharmacother. 2016; 83:526–35. https://doi.org/10.1016/j.biopha.2016.06.049 [PubMed]
Chaojia Wang
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Hui Wang
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FOXN3 cell proliferation cell migration glioma AKT/MDM2/p53 pathway

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Pregnancy is a time of great physical change. While you may notice slight changes in your skin and hair condition along with the more obvious changes to your body, should there be any changes to your feet?
Here's our guide to what to look for and how to keep your feet healthy and pain-free throughout your pregnancy.
During pregnancy the body produces approximately 50% more blood and bodily fluids than usual. This additional fluid tends to build up in the lower extremities i.e. your feet and ankles. As your growing uterus puts pressure on your veins, it also makes it more difficult for blood to flow back up to your heart. These two factors combined can make your feet grow and swell. claims that these changes are more pronounced with a person's first pregnancy than any subsequent pregnancies, and that, in most cases, the swelling reduces back to a normal state post-partum.
Due to an increase in the aptly named pregnancy hormone, Relaxin, ligaments in the body can loosen and relax, which means that your feet can widen and lengthen, and your arches can lower. This can mean that shoes that were once comfortable no longer fit, and your walking and standing posture can change.
Due to an often-rapid weight gain, many people report an overall aching foot pain as part of their pregnancy symptoms. A change in foot size and shape can often make footwear uncomfortable, and a change in posture can cause hard skin to form on your heels and toes.
With this in mind, here are some tips on how to avoid unnecessary pain and discomfort during your pregnancy.
Exercise: Gentle exercise, such as walking, will help boost your circulation, in turn reducing the swelling in your feet.
Raise them up: At the end of the day (or whenever you need to) try to put your feet up – literally! Raising your feet to an elevated position will help excess fluid to drain away.
Move: Try not to stand up for a long period of time or, if you're sat at a desk, get up and walk around every so often.
Keep cool: Hot feet will swell even more, so try to keep your feet cool by wearing comfortable open shoes or going barefoot around the house.
Wear shoes that fit: As irritating as it may be, you don't want to cause unnecessary pain, so buy new shoes that will fit your feet as they go through these changes.
If you're noticing changes to your feet during pregnancy that are causing you pain, you should visit your GP to check for any underlying causes. In many cases, they may refer you to a podiatrist to help. If your stance and posture has altered due to the changes listed above, it may be time for some orthopaedic inserts to help make your footwear more comfortable and to better support your new foot shape.
While you may not be able to see your feet anymore over the baby bump, we certainly will be able to! We will help you take care of them to reduce pain and discomfort. Contact us today to make an appointment. Our friendly team are working at clinics across London, ready and waiting to help you.


Most commercial caterers and kitchen operators have realized that no matter how good their daily cleaning is, there are some parts of the kitchen which are difficult to clean or are downright inaccessible.
The build-up carbon in ovens and the accumulation of grease deposited in ventilation system are examples, which require heavier duty cleaning than can be carried out by the kitchen staff themselves. This is the point when a specialist contractor is called in to dismantle many pieces of equipment and bring them, and the fabric of the kitchen itself, back to a sparkling, "looking like new" appearance.
Fitting in with a busy restaurant or industrial kitchen is vital and much of this type of work has to be carried out during down-time, while ensuring that the kitchen is ready for start-up the next day.
The work is hard, intensive and requires committed and fully trained personnel. Not only do technician need to be skilled in cleaning techniques and material, but also competent and trained with regard to gas installing standards if dismantling and re-installing gas equipment shall be required.
The goal for both the kitchen operator and the cleaning contractor is not only a visible and better-looking kitchen, but also confidence in visible cleanliness, which involves the removal of potentially illness-causing bacterial contamination.
Deep cleaning of kitchen has been undertaken for many, many years but until very recently the monitoring of the "invisible cleanliness" has been assumed or attempted to be checked by swabs and sampling incubation over three or so days; not that useful when the kitchen probably started operating immediately after the clean finished, while waiting for the results. Now Rentokil Hygiene Division has combined its expertise to deep cleaning kitchen with the latest rapid-result testing for showing the level of contamination on any surface, in their new service, Cater-Clean.
The programme involves the technician taking swabs of various items of equipment and surface prior to cleaning carried out. Rentokil Hygiene Division has been working in collaboration with Biotrace and is working using the Biotrace single shot swab, which is tested immediately with shot swab, which is tested immediately with the company's Uni-lite system. A print-out of the result is produced instantaneously.
What this does mean is that a " before and after" swab test can inclusively show how well the deep clean has been carried out. The results are printed out and kept by the customer in his Cater-Clean system manual, along with a dated certificate confirming the operation, the result for any particular piece of equipment or surface can also be used by the customer to monitor hot spots of activity or trends. This knowledge can also be used in preventive management techniques such as changing daily cleaning methods or even moving specific food preparation areas.
The recent changes in food hygiene legislation and recommended good practices mean that companies operating kitchens for staff or public need to show they meet the requirements. The Scottish E. coli 0157 incident and the subsequent Pinnington report highlighted the need for diligence in commercial food preparations. Combining a professional, deep-cleaning operation with tangible results of this will help those involved in running catering operation to satisfy themselves, their customers, and enforcement authorities that reach the standards set.


The following articles are available for the 'Moving or Copying Worksheets' topic. Click the article''s title (shown in bold) to see the associated article.
Need to move a worksheet from one place to another in the same workbook? Here are two easy ways to make the move.
One of the organizational tools provided by Excel is the ability to move worksheets from one workbook to another. Here's how to do it.


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Chairman of Farnworth Urban District Council: 1934-36 (Labour)
Mayor of Farnworth: 1940-41 (Labour)
Born: Farnworth 1887
Died: 7 Tulip Avenue, Farnworth 7 May 1963
He had 52 years service with Farnworth and Kearsley Co-operative Society and was also Secretary of the Farnworth branch of the National Union of Distributive and Allied Workers for 14 years.
Known as "Genial Jim Stevenson" he was a Labour supporter for 40 years and was closely associated with Harry Barnes, Alfred Jones and George Tomlinson in the ILP movement.
First Elected to Farnworth UDC in 1921 for one year and re-elected in 1926.
He served on the Council for 38 years, including 24 years as an Alderman
He was a Magistrate for 23 years, retiring aged 75.
He was made a Freeman of the Municipal Borough of Farnworth on 21 September 1961. The presentation was made by the then Mayor, Herbert Brindle. The honour was paid in connection with the 21st anniversary celebrations of the granting of the Charter of Incorporation.
He was Chairman of the most Committees and represented the Council on the Education and Higher Education Committees for 10 years. He was also a Governor of Farnworth Grammar School.
He was a former Chairman of the local Labour Party and was made a life member in 1958.
He was a delegate to the Trades Council for several years and a member of the South Lancashire Federation of NUDAW branches. His trade union service was recognised by the presentation to him of a long service certificate and gold medal.
In his earlier days he was in the choir at Dixon Green Congregational Church, at St John the Baptist Church, Little Hulton (following his marriage there) and subsequently at St Thomas's Church.
He captained Farnworth Co-op team in the Manchester Wednesday Cricket League for many years and held a championship medal. He was also a member of Ellesmere Park Bowling Club.
His son, Herbert Stevenson, worked for Worsley Town Council.
Photograph of James Stevenson as Mayor of Farnworth in Farnworth Council Chamber c. 1940.
Deputy Mayor Rev John Wilcockson and wife stand at the right of the photograph.
James Stevenson (left) and Dr Victor St Clair Lucas (right) receiving the Freedom of the Borough from Herbert Brindle, Mayor of Farnworth on 21 September 1961.


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Q: What is this disintegration-like theorem? This is cross-posted at MSE.
I'm looking for a reference for the following result. It seems like it must be known, or follow quickly from something known, but I have not been able to find it in any of the textbooks I have.
Let $(\Omega, \mathcal F, \mathbb P)$ be a probability space. Let $\mathcal G$ be a sub-$\sigma$-field. Let $\mu$ be a regular conditional probability for $\mathbb P$ given $\mathcal G$. By this I mean that $\mu: \mathcal F \times \Omega \to [0,1]$ is a probability measure (denoted $\mu_\omega$) in its first argument, $\mathcal G$ measurable in its second argument and satsifies
$$\int_G \mu_\omega(A)\mathbb P(d\omega) = \mathbb P(A \cap G)$$
for all $A \in \mathcal F$ and $G \in \mathcal G$.
Let $X: \Omega \times \Omega \to \mathbb R$ be bounded and $\mathcal G \otimes \mathcal F$ measurable. Let
$$EX(\omega) = \int X(\omega, v)\mu_\omega(dv).$$
Theorem. $EX$ is $\mathcal G$ measurable and
$$\int EX(\omega)\mathbb P(d\omega) = \int X(\omega,\omega)\mathbb P(d\omega).$$

A: The measure-theoretic formulation of conditional probability/expectation is cumbersome, so it is often easy to lose connection between intuitive facts and the formal demonstrations of them. I personally often have difficulty with arguing for seemingly obvious facts.
In this case, I think more than your theorem is true: your function $EX(\omega)$ is a regular version of the conditional expectation of $f(\omega):=X(\omega,\omega)$ given $\mathcal{G}$, i.e., $\mathbb{E}[f\,|\,\mathcal{G}]$.  By definition, this means that $EX(\omega)$ is $\mathcal{G}$-measurable and
\begin{align}
   \underbrace{\int_G EX(\omega)\,\mathrm{d}\mathbb{P}(\omega)}_{\int_G \mathbb{E}[f\,|\,\mathcal{G}]\,\mathrm{d}\mathbb{P}(\omega)} &=
   \underbrace{\int_G X(\omega,\omega)\, \mathrm{d}\mathbb{P}(\omega)}_{\int_G f(\omega) \mathrm{d}\mathbb{P}(\omega)} \;,
\end{align}
for every $G\in\mathcal{G}$.
This is almost immediate from your definition. Note that
$\quad$($\star$) for each $\omega$, we have $X(\omega,v)=X(v,v)$ for $\mu_\omega$-almost every $v$ (see @1 below).
Thus, $EX(\omega)=\int f(v)\,\mathrm{d}\mu_\omega(v)$.  That $\int f(v)\,\mathrm{d}\mu_\omega(v)$ is $\mathcal{G}$-measurable for every $f$ is standard (see @2 below).
Furthermore,
\begin{align}
   \int_G EX(\omega)\,\mathrm{d}\mathbb{P}(\omega) &=
      \int_G\int f(v)\,\mathrm{d}\mu_\omega(v)\mathrm{d}\mathbb{P}(\omega) \\
   &= \int_G f(v)\,\mathrm{d}\mathbb{P}(v) \;.
\end{align}
Further details:
@1:  I believe this can be shown using the usual measure theory trick.  Namely, first show that ($\star$) holds if $X$ is the indicator of a rectangle $G\times F$ with $G\in\mathcal{G}$ and $F\in\mathcal{F}$.  Then, show that the family of sets $A\in\mathcal{G}\otimes\mathcal{F}$ for which $X(\cdot,\cdot):=1_A$ satisfies ($\star$) is a $\sigma$-algebra.  Then, show that $(\star)$ holds if $X$ is a simple function.  Finally, show that if $X$ is the uniform limit of an increasing sequence of functions satisfying ($\star$), then $X$ itself satisfies ($\star$).
@2:  The argument for this again uses the usual trick.  We already know (by definition) that $\int f(v)\,\mathrm{d}\mu_\omega(v)$ is $\mathcal{G}$-measurable if $f$ is an indicator function.  First, show that the same holds for simple function.  Then, show that if $f$ is the uniform limit of an increasing sequence $f_1\leq f_2\leq\cdots$ such that $\int f_1(v)\,\mathrm{d}\mu_\omega(v)$ is $\mathcal{G}$-measurable, then $\int f(v)\,\mathrm{d}\mu_\omega(v)$ is also $\mathcal{G}$-measurable.

A: Let me be short in details, only giving the essential picture (though I'd be happy to clarify if asked to).
Let me also make clear: I am not suggesting that the picture below is the most economical when it comes down to writing things up.
Assume given a measurable map $f:X\to Y$ of standard Borel spaces $X, Y$,
consider the following commutative diagram
$\require{AMScd}$
\begin{CD}
        X @>id\times id>> X\times X @>p_2>> X \\
        @| @V id\times fVV @V f VV \\
        X @> id \times f>> X\times Y @>p_2>> Y @>>> \{\text{point}\}
    \end{CD}
Endowing $X$ with a probability Radon measure, we push it down the diagram and endow all spaces with the corresponding measures.
Now the diagram lives in the category of
of standard Borel spaces equipped with a Radon probability measures,
morphisms being classes of measure preserving measurable maps, defined up to a.e identification.
In fact, all spaces in this diagram but $Y$ and $\{\text{point}\}$ are isomorphic, and all morphisms but the ones around $Y$ are isomprhisms (consider the composition $X\to X\times Y \overset{p_1}{\to} X$ in order to observe that $id\times f$ is an isomorphism).
Next, we apply the functor $L^1$ from the above described category to Banach spaces and contracting maps, taking a measured space to its $L^1$-space and a morphism to the associated conditional expectation map.
The above commutative diagram gives a commutative diagram of $L^1$ spaces.
Your conditional expectation formula becomes obvious now by letting $X$ be the von-Neumann spectrum of $L^\infty(\Omega, \mathcal F, \mathbb P)$ and $Y$ be the spectrum of the subalgera of $\mathcal G$-measurable functions.

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Complete POS System with Softtouch's integrated Smart Host Reservation System. Take Reservations and assign tables to servers for walk-ins and reservations as guests arrive. Color coding allows the host/hostess to know when the table is ready or needs to be bussed.


Find the best Maine attorneys for driver's license restoration / reinstatement, traffic tickets, traffic violations, DUI offenses, and more with Driver's License Restorers!
Search the most extensive online Maine Attorney Directory for highly-rated traffic attorneys, driver's license restoration lawyers, DUI attorneys, and law firms in Maine. Compare attorney profiles to find the BEST Maine lawyer for your case.


Comprehensive style mixed with all around versatility makes it an outstanding choice! Chrysler prioritized comfort and style by including: a blind spot monitoring system, tilt steering wheel, and the power moon roof opens up the cabin to the natural environment. It features an automatic transmission, front-wheel drive, and a refined 6 cylinder engine.
View this 2019 Chrysler Pacifica Passenger Van LIMITED for sale at East Carolna Chrysler Dodge Jeep Ram in Greenville, NC.


text:
Education Week's blogs > Rick Hess Straight Up See more Opinion
Rick Hess
Education policy maven Rick Hess of the American Enterprise Institute think tank offers straight talk on matters of policy, politics, research, and reform. Follow Rick on Twitter, and also follow AEI's Education Program.
The Supreme Court Just Slashed the Odds on ESEA Reauthorization
By Rick Hess June 29, 2015 at 7:45 AM
NCLB is closer to being rewritten now than at any time since its passage. So why do I think the Supreme Court just slashed the odds of reauthorization?
NCLB/ESEA
The State of K-12 Educational Entrepreneurship
By Rick Hess June 25, 2015 at 11:24 AM
K-12 educational entrepreneurship today is marked by at least three major tensions that deserve a lot more careful attention.
Reflections on an Extraordinary Decade of New Orleans School Reform
A decade into post-Katrina education reform in New Orleans, I offer a few reflections.
This Is What 'Greenfield' Education Looks Like
Even education reform can feel bureaucratic sometimes. But recently there have been promising greenfield developments in the area of school choice.
What Kind of Workplace Would I Like to Teach in?
A question that reformers should, but rarely do, ask themselves is what kind of school and system they would like to teach in.
Teaching & Practice
5 Thoughts on Nevada's Landmark School Choice Law
Last week, Nevada governor Brian Sandoval signed into law the nation's most ambitious school choice program. I'll share five thoughts on this.
Understanding the Opt-Out Movement: A One-Woman Play (In Five Acts)
By Rick Hess June 8, 2015 at 8:00 AM
This five-act play explains the opt-out movement from the year 2000 to present.
Good Charter School Authorizing Promotes Academic Quality, Not Red Tape
Well-meaning authorizers and legislators have larded up charter school applications with requirements. If this red tape was to ensure academic success, that would be one thing. But it's not.
School Spending and the Limits of Research
A new Education Next study makes pretty massive claims about the impact of new spending. But I'm dubious, for a few reasons.
« May 2015 | Main Index | Archives | July 2015 »
The opinions expressed in Rick Hess Straight Up are strictly those of the author(s) and do not reflect the opinions or endorsement of Editorial Projects in Education, or any of its publications.
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text:
Commonwealth Scholar draws attention to global health issues
by Hannah Openshaw | May 31, 2014 | Alumni
Nicholas Neufeld is a 2007 Commonwealth Scholar who studied for his MSc in Clinical Neuroscience at University College London. He has written a research letter, 'Debates in Medicine: Global Representation in Medical Discourse', that was recently published in The Lancet.
Nicholas and his co-authors realised that research appears disproportionately geared to diseases that affect developed countries. Consequently, research and journal articles deriving from developing countries are noticeably lacking. The goal of their letter was to determine how contributions to medical research and journals are divided between developed and developing nations.
Nicholas and his colleagues decided to focus on Letters to the Editors in the medical field. This type of correspondence accurately displays the current debates and discussions within related disciplines, but does not face the obstacles that hinder articles. Structural supports and funding are just two hurdles that face developing countries' research but do not largely affect the dominance of developed countries.
Therefore, these 'Letters to the Editor' sections could offer a better reflection of the medical discourse and conversations occurring internationally. The three most influential medical journals according to Thomson Reuters' Impact Factor were chosen for this study: The Lancet, the Journal of the American Medical Association, and the New England Journal of Medicine.
A total of 773 letters – comprising 575 letters, 195 replies, 2 journal responses, and 1 retraction – were analyzed during Nicholas' research. The research material was dated between 1 July 2003 and 31 December 2013.
Corresponding authors wrote from 57 different countries. The United Kingdom and the United States were the biggest global contributors, accounting for a combined 403 letters. Nicholas and his co-authors thoroughly examined each letter to determine whether developed nations do have a monopoly over research conducted and published in the medical field.
The conclusion was that the global debate is indeed driven by members of developed nations, with possible negative outcomes. The global burden of disease casts a wider net than related research.
Ideally, countries representative of serious ailments would be the ones leading the discourse and research. The article also found a competing idea. When developed nations report on these types of diseases, stakeholders often engage in meaningful local and international debates.
The issues raised in this article relate directly to the experience Nicholas gained as a Commonwealth Scholar. He became aware of global health concerns whilst studying in London and accessing new resources. The article is a combination of Nicholas' interests that were sparked in London – connectivity, global health, and debate.
The wider aim of the article was to highlight the distribution of attention in the research arena and united efforts to draw attention to health concerns in developing nations. Nicholas and his co-authors wanted to showcase that concerted efforts to highlight health concerns in developing nations can reach global medical debates and hopefully inspire research that takes a broader, global view.
Alongside his interest in international medical studies, Nicholas focuses on clinical duties and neuroimaging research. Since his return to Canada after his Commonwealth Scholarship, Nicholas completed medical school and joined the psychiatry residency programme at the University of Toronto.
After receiving his MD Nicholas is currently in the clinician-scientist residency stream. His research now focuses on functional magnetic resonance imaging (fMRI) at the Kimel Family Translational Imaging-Genetics Laboratory at the Centre for Addiction and Mental Health. Nicholas works on imaging brain function while in the resting state. He studies the mind while it is wandering freely, rather than working on a specific task. This concept is then applied to see how brain activity varies when affected by mental disabilities. By analysing the material collected through fMRI technology, Nicholas investigates how brain activity is similar and different for patients with psychotic depression, bipolar disorder, and schizophrenia.


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The Saint Reviled by Shakespeare, Admired by Twain, and Adored by St. Therese of Liseux
The Maid of Orléans will be a focal point of artists for generations to come but most will pale in comparison to William Shakespeare, Mark Twain and the Little Flower
I'm pretty sure boasting is not an activity many saints take part in but if they did, no other saint could strut around the pearly gates asking everyone if plays and stories about them written about them by such diverse authors such as William Shakespeare, Mark Twain and St. Thérèse of Lisieux.
Few saints have captured the imagination of so many artists as Saint Joan of Arc. Pyotr Ilyich Tchaikovsky and Giuseppe Verdi both wrote operas about the saint. Voltaire and Coleridge both wrote poems of varying quality about her. But let's be honest: having Shakespeare, Twain and St. Thérèse all writing plays and books about one saint is rather unique.
I suspect Joan of Arc will continue to be the focal point of artists for generations to come but most will pale in comparison to Shakespeare, Twain, and St. Therese of Lisieux.
Lawrence Hall, HSG
BrotherBeowulf
Feast of Our Lady of Lourdes
Yes thanks. And pkease don't forget Belloc. His Joan of Arc is a gem. Like Chesterton's Dumb Ox.
Twain's uncharacteristically prolix work pales in comparison w Belloc's slender volume, btw.


Okay, tad dramatic in that title there. But for the first time I've been taking a little bit more care of my skin in the summer with my favourite summer beauty products as it is so much warmer than usual and I'm heading off to Italy in a few weeks-time.
Every skin horror you see champions the wearing of SPF and I'm getting very involved. My skin has definitely been at its worst this summer: break-outs, dryness, reacting badly to sun. Hardly ideal. I've been trialling new products and trying to find what works best for me so I thought I'd share my ultimate favourites and the ones I'll be trying to squeeze into my hand luggage for Italy.
I usually shop for my beauty products in Boots because I love the variety and affordability of the ranges they offer. Skincare is something I really begrudge spending money on and I'm also super lazy at trying new products. Practically everything in my beauty baskets are from Boots but I will be popping into Sephora in Rome, you can count on that.
Botanics are a brand I see popping up on my Instagram feed all the time and I've always been intrigued by their natural ethos. I love the pastel coloured packaging and they do a huge range of products. I picked up the All Bright Day Cream as I needed a new facial moisturiser and I went for this one as it contains SPF 15.
I'm really trying to wear SPF everyday now as I constantly see the importance of it stressed online so having a moisturiser which encompasses this makes it a lot easier. I love the light creamy texture of this moisturiser and it is infused with hibiscus which makes it smell pretty lovely too.
I first encountered a face mist with Lis on the train back from Alloa on a scorching hot day and she pulled it out her back. It was so refreshing to have a spritz on my face so when I saw the new range from The Body Shop out on display at the St Enoch Press Summer Soiree event, I knew I needed to get on board.
I struggle with the heat like the next typical Scot but that doesn't mean I don't love it and try to make the most of it anyway. I picked up the Coco Calming spray from The Body Shop and having it in my bag when I'm out and about enjoying the sun is super helpful as it always freshens up my face.
One of the biggest problems I've encountered with my skin this summer is dryness. Foundation is clinging to me in patches, some areas feel a bit red and sore and my skin just feels like it is lacking in hydration.
I've started using this Simple Hydrating Booster after applying primer and before applying foundation, just to give my skin a little extra drink. I also use it at any point in the day when my skin feels dehydrated and the handy size makes it easy to carry around.
You know when you have a perfume that you associate with a memory and every time you spray it you are taken back there? Indian Night Jasmine is that for me. It was all I wore when I went to the Bahamas in 2016 and I'm now on my third bottle in an effort to keep the memory alive. It is the perfect summery scent that instantly makes me feel fresh and at ease.
The Body Shop body mists are perfect for summer perfumes if you are on a budget. At around £8 a bottle, you get 100ml and the range of scents is varied – I have my eye on the Coconut one next.
My Glossier Balm Dot Com has been one of my favourite lip balms since I first purchased it back in 2017. It is such a hydrating formula that doesn't feel sticky or drying out on the lips and I always make sure it is in my toiletries bag when I travel.
The packaging is ~ super cute ~ (as is all of Glossier's products) and I really can't wait to purchase another Balm Dot Com at some point. I have the Rose version currently but I have my eye on the Coconut.
This post contains products that were bought with a gifted voucher. They are marked with an asterisk, read my full disclaimer here.


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Woodside Girls' Volleyball
Birdie Kwan
Girls' Varsity volleyball beats San Mateo High School in an exciting beginning-of-the-season game.
Birdie Kwan, Copy Editor
Varsity Girls' Volleyball kicked off their season on August 23, with the freshman and junior varsity teams following on September 7.
Players are excited and hopeful for the season and encourage students to cheer them on. In an exciting, recent match, the girls' varsity team defeated San Mateo High School after winning three out of the four sets. Ellery Singleton, Woodside sophomore and varsity player, looks forward to their next match against a strong opponent in a much-anticipated game.
"I'm excited to play Hillsdale because they have a lot of seniors on their team that I know of, and they're really good," Singleton said.
The three girls' volleyball teams play Hillsdale on October 14 in the New Gym, and their other games are every Tuesday and Thursday, with five remaining home games. Players are excited to bond with their teammates and compete again in the wake of COVID-19.
"I like the team aspect because you get to play with a bunch of people that you grow really close to," Singleton said.
Support Woodside girls' volleyball teams by attending games and donating to their team for new equipment, jerseys, and more.
Woodside Courses & Subjects Crossword Puzzle
Creator of the Week: Aleena Mikulin.
Spanish Class at Woodside
The SAT/ACT systematically hurts less-privileged students, so why is it still around?
Woodside in the Lunch Line
Latin Language Course: A grand Language
Looking Through the Corridor: Pictures of a Woodside Location at Different Times
Litter Around Woodside's Lush Outdoor Campus


Sand tray for burnout relief is a playful mindfulness technique that provides an option or complement to assessments and other counseling tools at Lifework Clarity Career Counseling. The opportunity to work in a sand tray with miniatures intuitively chosen on a non-verbal level engenders the state of mindfulness defined by Jon Kabat-Zinn: "the awareness that emerges through paying attention on purpose, in the present moment, and nonjudgmentally, to the unfolding of experience moment by moment."
Along with mindfulness, sand tray also draws from the fields of humanistic therapy, play therapy, Jungian psychotherapy, and sandplay. For example, sandplay brings to life a basic concept from Jungian psychotherapy. Dr. Jung developed a concept called the collective unconscious--a world of images and symbols imprinted on the human unconscious that transcends culture and history. This is the inner world we draw from when we engage in sand tray.
Sand tray uses three-dimensional figures chosen to represent aspects of universal human experience. We are drawn to and choose the figures that represent significant aspects of our unconscious inner world. They may represent long-standing obstacles blocking movement forward in our lives along with solutions to those obstacles, all of which lie below conscious thought.
We arrange these figures in a safe container (the sand tray) in the presence of a witness who is trained to be quietly supportive and nonjudgmental. We have permission to play like a child-- children instinctively engage in creating fantasy worlds to resolve existential fears. As adults we sometimes experience this process in dreams. Our first sand tray typically reveals the interplay of challenges we are facing in our current situation. Subsequent sand trays go deeper to uncover inner strengths and potential solutions.
In sand tray we reconnect with our childlike understanding. For example, when needed we can choose to use figures from the darker realms of our unconscious to help us work through long-standing fears and hurts and regain our resilience. We are then empowered to change what no longer works about job or career.
Sand tray is typically a quiet process, yet deeply playful. It reaches back into our essential nature before the many layers of roles, expectations, and obligations built up over the years (throughout our responsible adult life) and began to hide who we really are and are meant to be.
Intrigued? Give Beth a call at Lifework Clarity Career Counseling (512) 633-5474 to learn more about how using sand tray for burnout relief, a mindfulness technique, can help you get your career moving again.


From I-95 take exit 32 towards to Konterra Dr. Make a right at light to continue on Konterra then turn left onto Virginia Manor Court. We are located at the end of the court.
All buyers must check in at the Main Building on Sale Day. Buyer badges MUST be displayed while present during the auction. All Vehicles sold through IAA's auctions are sold "AS IS,WHERE IS", with NO warranty, expressed or implied, including but not limited to any warranty of fitness for a particular purpose of mechantability The Yard hours are 8:00 to 4:30. The office takes last payment at 4:30. Do not leave your vehicles on the street. Vehicles left on the street are subject to be towed and impounded at the owners expense.


The string trio has a violin, viola and cello and sounds great in an intimate setting with fewer guests!
The trio is limited in terms of the amount and variety of music available. None of the Modern quartet songs are available for trio. Listen below or contact us for a complimentary trio demo CD if you are unable to listen online.
String Trio Demo, 21 Tracks.
Read the Choosing Music article for ideas on selecting special music for a wedding ceremony.
Print the Ceremony Music Planning Worksheet to work through your special music selections.


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← Queensland anti-vaccine science teacher to teach students about immunisation?
NSW Parliament 135 – Meryl Dorey 0 →
Judy Wilyman finally comes out from under the anti-vaccine rock
Posted on May 4, 2013 by reasonable hank
Look. I have a man-cold. For all you men out there, you know how much I am suffering at the moment. But, some things cannot pass.
This morning I received a group email from Judy Wilyman, in which she has finally come clean about her anti-vaccinationist belief system. Anti-vaccinationists rarely admit that they are anti-vaccine; so, most of the time, you need to rely on the constant arguments they use to argue against vaccination. So, think of it as, "I'm not anti-vaccine, but, I rely predominantly on anti-vaccine arguments, although I'm not anti-vaccine, and I just argue against vaccines". They know anti-vaccinationism is both scientifically and ethically anathema to reason and public health, so, they deny their true selves. Sometimes I feel sorry for them. Denying your denialism cannot be good for the soul.
Wilyman starts out her email with an anti-vaccine favourite: the toxins gambit:
Re Vaccine Ingredients:
Aluminium hydroxide, Aluminium hydroxide/phosphate, Aluminium phosphate, Borax, Egg Protein, Formaldehyde, Gelatin, Gentamicin (antibiotic), Kanamycin (antibiotic), Monosodium Glutamate (MSG), Neomycin (Antibiotic), Phenol, Phenoxyethanol, Polymyxin (antibiotic), Thiomersal (mercury compound), Yeast (current up to March 2013)
If you are thinking that this list of ingredients sounds very scary, you would be right. This is always the intent of anti-vaccinationists when practising the toxins gambit. They want to scare parents. What anti-vaccinationists always fail to explain are the minute quantities contained in a vaccine, why they are there, and the fact that these toxins and poisons are not toxic or poisonous at the levels contained in a vaccine. Anti-vaccinationists know this. They just don't care. It doesn't fit their narrative to explain nuances which debunk their own arguments. Dr David Gorski's post, here, provides a thorough debunking of this argument; an argument of which Wilyman should feel ashamed to have used.
Wilyman continues:
Currently the government, doctors and the media are informing the community that if you inject the above ingredients into the tissues of developing infants you will improve the health of your children.
Bollocks. This is an inept Strawman argument. Vaccines are not provided to "improve the health of your children". Vaccines are provided as a preventative measure to give a child a higher chance of avoiding contracting a vaccine preventable disease.
Wilyman continues to make three central points to back her argument:
1. Vaccines have reduced the deaths and illness from infectious diseases.
Not True: Vaccines did not reduce the deaths and illness from infectious diseases and many vaccines have been added to the schedule without a proper debate of the risks and benefits. Therefore, it is also untrue that deaths to infectious diseases will return in developed countries if people do not vaccinate. You will notice that these diseases are still prevalent in developing countries – even though they have had vaccination programs for decades.
This is known as the vaccines didn't save us gambit. This gambit is patently false, and dishonest, as explained in this post on Respectful Insolence. Although the common tactic used by anti-vaccinationists is to use mortality rates to prove vaccines have had no effect on disease incidence (they have), it is a rare and untrustworthy anti-vaccine campaigner who will claim that vaccines have had no effect on both mortality and morbidity.
Of special note is what is happening right now, in Wales. MMR immunisation rates dropped due to Andrew Wakefield's fraudulent research, and there is now a huge outbreak, spreading beyond Wales, which is a direct consequence of the low MMR immunisation uptake a decade ago. Preliminary data is now coming in showing that the MMR vaccine has a spectacularly high success rate in preventing Measles infection:
MMR vaccine effectiveness
Data on confirmed measles cases and their immunisation history continues to be actively collected during the outbreak. The validity of the data will not be finally confirmed and published until after the outbreak is over, therefore the following statement is a preliminary and may be revised.
Current data (to 26 April 2013) from the outbreak shows very few confirmed cases have caught measles after having had the MMR vaccine. The vast majority of confirmed measles cases are individuals who have never been vaccinated with MMR.
Less than 10 laboratory confirmed cases are reported to have previously received any MMR vaccination. [out of 1039 cases]
This emerging data suggests that in the outbreak area one dose of MMR vaccine protects against measles in more than 95 out of every 100 vaccinated, and two doses protects in around 99 out of every 100 vaccinated.
Anti-vaccinationists have been noticeably quiet about the Measles outbreak. This is why.
That Wilyman invokes immunisation programs in developing countries as proof of her claims is quite startling and telling. There are many reasons, both logistical and ideological, why it is difficult to implement successful immunisation programs in developing countries. Wilyman would prefer to leave out the nuance, again, and stick the anti-vaccine line. It doesn't matter that, according to the WHO, "Measles vaccination resulted in a 71% drop in measles deaths between 2000 and 2011 worldwide." Anti-vaccinationists just don't care.
Wilyman's second point:
2. 'Vaccination' is 'immunisation'.
Not True: The government is misusing these words on its website. Vaccination is the act of getting a vaccine – not all recipients receive immunity after a vaccine therefore doctors and the government should always be referring to 'vaccination' not 'immunisation'. Immunisation implies that immunity has been achieved and this is not proven. Some vaccinated people still get the diseases they are vaccinated against so the government has a 'vaccination policy' not an 'immunisation policy' – this is being misrepresented to the public.
Apart from playing a silly semantic game, Wilyman is relying on yet another logical fallacy called the Nirvana fallacy. This is also known as the Fallacy of the Perfect World, and more recently, The Doreyan Fallacy. Anyone who uses this argument needs to feel shame: but, they don't. Basically, this immature argument states that if something is not 100% safe – even if it 99% safe – then, it is deemed to be 100% unsafe. And the same is argued with effectiveness: if it isn't 100% effective – even if it is 99% effective – then, is has zero effectiveness. I know. It's embarrassing that anyone could run those lines; but, they do, and they do it after being corrected with evidence. Vaccines induce immunity. Some do it better than others (just like the MMR, above). But, to claim that vaccines do not induce immunity is a lie. You can only forgive wilful ignorance so many times before it needs to be called a lie.
Wilyman's third point:
3. Vaccines do not cause autism
Not True: The government's schedule of vaccines has never been tested for safety against unvaccinated children (or animals and hence the policy is unethical in children) therefore it has not been proven that vaccines do not cause autism. The current scientific evidence suggests it is the most likely cause of autism.
Apart from using another logical fallacy, called the Argument from Ignorance, Wilyman is making a bold claim which has been debunked Ad nauseam (another logical fallacy), relying on another logical fallacy, the Proof by Assertion. Basically, anti-vaccinationists put forward this argument, incessantly, often unreferenced (as Wilyman has done), and using citations which do not back up their claims. We already know the citations they will use: they have been addressed here. In stark contrast to the claims of anti-vaccinationists like Wilyman, here is a list of 41 reputable studies showing that vaccines are not linked to autism. Seriously, put down the vaccine/autism zombie. Bad dog.
Wilyman continues with some health freedom verbiage. I won't bore you with it. You can read it for yourself. All I will add is that immunisation is required in some workplaces (such as health), and I wholeheartedly support this. This has nothing to do with "discrimination". Health workers who shun immunisations should be more discriminatory about which profession is right for them. Health ain't one of them.
One has to wonder how Wilyman has ever gotten as far as she has, with so little. She likes to make hay of her credentials, yet never shows us anything intellectually as to why she should hold those credentials:
She used to sign off as "PhD Researcher", which wrongly implied that she was already a successful PhD candidate. As you can see, she still signs off as "PhD Candidate", yet, attempts to distance herself from the University of Wollongong, but not really. Here is a screenshot from Wilyman's website, noting that her activism is directly linked to her academic work:
The University of Wollongong to this day defends Wilyman's work, noting that her activism is not related to her candidature. Given the topic of her thesis, and her own admission on her website, I find that hard to believe.
Maybe the University of Wollongong can offer Wilyman a place in the Physics Department. I've already made up a cover sheet, based on her work today.
This entry was posted in anti-vaccination dishonesty, australian vaccination network, meryl dorey, stop the australian vaccination network and tagged anti vaccination, australian vaccination network, AVN, Brian Martin, dishonesty, Judy Wilyman, Measles, meryl dorey, University of Wollongong. Bookmark the permalink.
0 Responses to Judy Wilyman finally comes out from under the anti-vaccine rock
Darkly Venus says:
I'm not sure about the physics department even. How about English? And a masters in creative writing?
Great job, Hank. Have you taken your echinacea? 😉
It's like people who start off sentences with "I'm not racist, but…."
Sebastian Jackson says:
"Anti-vaccinationists have been noticeably quiet about the Measles outbreak."
Oh no they haven't. Some of them have been claiming against all evidence and reality itself that the measles outbreak in the UK was made up on the fly to smear Andrew Wakefield: http://www.ageofautism.com/2013/05/trumped-up-march-uk-measles-epidemic-1-lab-confirmed-case-in-182.html
reasonablehank says:
Yes. I noticed that. A few other rabid sites have taken the conspiacy a few steps further. I noticed a post on the AVN Facebook page just after I publised this post.
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What is a myxedema coma?
Myxedema is the medical term for severe hypothyroidism. It also refers to the skin changes that can happen with this condition.
Hypothyroidism occurs when the body does not make enough of the thyroid hormones. It is estimated that 4.6 percent of the United States (U.S.) population, aged 12 years and above, has hypothyroidism.
Most cases of hypothyroidism, or underactive thyroid, are mild. However, hypothyroidism left untreated can result in myxedema.
The most life-threatening complication associated with myxedema is a myxedema coma.
When the body experiences an ongoing deficiency of thyroid hormones, there is a heightened risk of a myxedema coma.
A myxedema coma is also known as a myxedema crisis. This serious medical condition occurs when the body can no longer cope with long-term, severely low levels of thyroid hormones.
Although it is rare, a myxedema coma is a medical emergency that requires immediate attention. In some cases, it can result in death.
Despite the name, a myxedema coma does not require the presence of either myxedema (skin changes) or a coma for it to be diagnosed.
According to the American Academy of Family Physicians, the primary sign of myxedema coma is a deterioration of mental state. For example, a person may experience confusion, hallucinations, or disorientation.
Potential causes of myxedema include inflammation or removal of the thyroid gland, certain medicines, and pregnancy.
Myxedema is the result of severe hypothyroidism that is undiagnosed or not treated. It is most commonly seen in those with a history of thyroid surgery or radiotherapy.
Hashimoto's disease, an autoimmune condition and the most common cause of hypothyroidism in the U.S.
Thyroiditis, or inflammation of the thyroid gland.
Congenital hypothyroidism, a condition present from birth that is usually screened for in newborns.
Surgical removal of the thyroid due to thyroid cancer or other conditions.
Pituitary gland abnormalities caused by surgery, tumors, or medical conditions, such as Sheehan's syndrome.
Pregnancy, with some research estimating that hypothyroidism occurs in 1 out of every 1,600 to 2,000 deliveries.
In rare cases, myxedema may occur in people with normal thyroids but whose pituitary gland or hypothalamus, both of which are part of the brain, fail to send messages correctly to the thyroid gland.
Thyroid hormones regulate metabolism, or the way the body uses energy. If thyroxine levels are low, many of the body's functions slow down. Learn more about hypothyroidism.
The biggest risk factor for myxedema coma is to have hypothyroidism that is untreated.
A doctor, usually an endocrinologist, will probably be able to diagnose severe hypothyroidism or myxedema based on a person's symptoms. A diagnosis will be confirmed using blood tests.
T3 (triiodothyronine) and T4 (thyroxine). Low levels of hormones produced by the thyroid can indicate hypothyroidism.
Thyroid-stimulating hormone (TSH). Produced by the pituitary gland, a high level of TSH suggests hypothyroidism. This is because the pituitary is signaling to the thyroid that more levels of T3 and T4 are needed in the body.
Heart activity may be checked using an ECG (electrocardiogram) and the brain may be looked at with a CT scan. Lung function might also be tested.
As myxedema coma is a medical emergency and life threatening, so it requires immediate treatment, usually in an intensive care unit (ICU).
Treatment options may include thyroid hormone replacement therapy, which will be administered through an IV line.
Doctors will continually monitor the level of consciousness and vital signs of those with myxedema coma.
Thyroid hormone replacement therapy is administered through a vein, using an intravenous (IV) line.
It may take weeks for a person's thyroid hormones to return to normal levels. Once levels are restored, their symptoms will improve. However, some form of thyroid medication will be necessary for the rest of the person's life.
If doctors do not diagnose myxedema coma swiftly and treat it urgently, it can be fatal. Even with prompt diagnosis and immediate treatment, studies have suggested that between 30 and 60 percent of people die.
However, once myxedema is under control and the symptoms of myxedema coma have passed, the outlook is good, provided people follow their treatment regimen for the rest of their lives.
Article last reviewed by Fri 4 August 2017.
Leonard, Jayne. "Myxedema coma: Causes, risk factors, and outlook." Medical News Today. MediLexicon, Intl., 4 Aug. 2017. Web.


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Houston Press
HPMA Showcase: Rocks Off's Top 7 Discoveries
Houston Press | August 6, 2012 | 10:00am
Rocks Off also asked our folks covering the HPMA showcase to tell us their favorite new artist they saw Sunday - not necessary new, just new to them.
HPMA Showcase: The 12 Best Artists of 2012
SLIDESHOW: HPMA Showcase -- The Bands
SLIDESHOW: HPMA Showcase -- The Crowds
Alkari: How have I never seen these guys play before? They gave me a bit of a Bob Mould/Pixies vibe - angsty, swirly rock stuff. Their drummer was a hardass and their lyrics were complex and thoughtful. Plus, they seemed to be having a great time playing with each other. The back room at Reserve 101 was a good spot. Intimate and with decent sound. BRITTANIE SHEY
Caretta Bell: In her royal blue gown, Bell looked like a gospel singer. But flanked by a pair of voices whom it would hardly be fair to call "backup singers," she reached deep to deliver one of the best examples of the currently popular neo-soul I've seen in this city in a while.
Bell has a silky, unforgettable voice and a likable, magnetic stage presence while her band accompanies her with as much subtlety and finesse as any band we saw all day. We'll definitely be tracking her down at her regular monthly gig at Fox Hollow in Third Ward. WILLIAM MICHAEL SMITH
D.R.U.M.: The best new discovery for me was, hands down, D.R.U.M. To me, they were like reggae for people who don't normally listen to reggae. I liked how the singer basically gave the audience a mini-lesson on Bob Marley. I thought it was a great way to connect with the audience because, while not everyone listens to reggae, I think we can all agree that Marley is a music legend.
A great moment occurred when the singer encouraged people to start dancing. Though most were probably eating from the nearby food trucks, some did. CHRISTINA LYNN
Female Demand: Armed with only a drum kit, a bass guitar and a helluva lot of pedals, Female Demand shook Dirt Bar as though it were something personal, as onlookers either smiled and bobbed their heads or nervously exchanged glances, silently asking one another, "What the hell is this?"
Make no mistake; I was in the former category. And although I had never heard of them before, after a quick chat with Cory Sinclair and Justice Tirapelli-Jamail of The Manichean, I now know where I can purchase their music and keep tabs on upcoming performances. MATTHEW KEEVER
H.I.S.D.: "Houston Independent Spit District. Slang District. Soul District. Style District," announced EQuality, Savvi and Scottie Spitten, members of local rap threesome, H.IS.D., to the gatherers at House of Blues' Bronze Peacock Room.
Nominated for Best Hip-Hop Group and Best Video, H.I.S.D. talks endlessly about getting "spaced up" in their music; that is, achieving a higher level of consciousness. This Rocks Offer was at first nostalgically attracted to their performance after spending an elementary-school stint in the school district that shares the same initials, but after tonight, it's clear which district I'll be attending. School is now in session. ALTAMESE OSBOURNE
The Trimms: Appealing to both young and older generation music fans, The Trimms are a kick, no better way to put it. They have that certain je ne sais quoi, a rock and sock and roll spirit worth acknowledging. They are, you know, the kind of band that come with searing guitar licks and all of that good stuff drenched in copious amounts of ice-cold Bud Light (which fits, being a sponsor).
Though playing many (well-selected) covers as a traditional-looking rock outfit, this motley trio played bombastic songs that stood out in their performance spirit. Each band member had a great amount of energy onstage, which translated into standout talent, and vice versa. ALEXA CRENSHAW
The Trimms: I really liked these newcomers. The power trio was a little White Stripes-heavy, but they had energy for days and had an enthusiastic crowd up front and wailing during their Lucky's Pub set. They were also handing out free discs featuring a live set from a few shows back, so that should be getting some rotation around these parts.
It's refreshing to see band members interacting with one another, and not setting themselves into little islands onstage. The Trimms were really good at invading each other's space. CRAIG HLAVATY
Leah White & the Magic Mirrors: I saw a lot of great loud, heavy music on Sunday yet of all of the things I decided to take a chance on Leah White & the Magic Mirrors bring the biggest grin to my face.
Knowing nothing about them gave rise to tons of questions (Are these novelty songs? Is this a crazy/genius gimmick?) but the important part is this: Whether she's singing about a local library, being an astronaut or art cars, the songs are really good. I'm just glad there's room at the HPMAs for facemelting (hi Floorbound) and kids' songs. CORY GARCIA
Follow Rocks Off on Facebook and on Twitter at @HPRocksOff.
HPMA
Houston Music