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  1. Rajandram R, Ong TA, Razack AH, MacIver B, Zeidel M, Yu W
    Am J Physiol Renal Physiol, 2016 05 01;310(9):F885-94.
    PMID: 26911853 DOI: 10.1152/ajprenal.00483.2015
    Ketamine is a popular choice for young drug abusers. Ketamine abuse causes lower urinary tract symptoms, with the underlying pathophysiology poorly understood. Disruption of urothelial barrier function has been hypothesized to be a major mechanism for ketamine cystitis, yet the direct evidence of impaired urothelial barrier function is still lacking. To address this question, 8-wk-old female C57BL/6J mice were injected intraperitoneally with 30 mg·kg(-1)·day(-1) ketamine for 12 wk to induce ketamine cystitis. A spontaneous voiding spot assay showed that ketamine-treated mice had increased primary voiding spot numbers and smaller primary voiding spot sizes than control mice (P < 0.05), indicating a contracted bladder and bladder overactivity. Consistently, significantly increased voiding frequency was observed in ketamine-treated mice on cystometrograms. These functional experiments indicate that ketamine induces voiding dysfunction in mice. Surprisingly, urothelial permeability in ketamine-treated mice was not changed when measured using an Ussing chamber system with isotopic urea and water. Mouse urothelial structure was also not altered, and intact umbrella cell structure was observed by both transmission and scanning electron microscopy. Furthermore, immunostaining and confocal microscopy confirmed the presence of a well-defined distribution of zonula occuldens-1 in tight junctions and uroplakin in umbrella cells. In conclusion, these data indicate that ketamine injection induces voiding dysfunction in mice but does not necessarily disrupt mouse bladder barrier function. Disruption of urothelial barrier function may not be the major mechanism in ketamine cystitis.
    Matched MeSH terms: Urinary Bladder/physiopathology; Cystitis/pathology*; Urothelium/pathology*; Urinary Bladder, Overactive/physiopathology
  2. Marafi F, Sasikumar A, Aldaas M, Esmail A
    Clin Nucl Med, 2021 Jan;46(1):e65-e67.
    PMID: 33181733 DOI: 10.1097/RLU.0000000000003354
    A 46-year-old man with end-stage renal disease and renal cell carcinoma underwent F-FDG PET/CT for initial staging followed by F-PSMA-1007 PET/CT. Unlike F-FDG, which undergoes renal clearance, F-PSMA-1007 undergoes hepatobiliary clearance and thus generates superior quality images. F-PSMA-1007 PET/CT showed intense tracer-avid left renal mass lesion (FDG nonavid); lytic bone lesions (FDG avid) and single liver lesion (FDG nonavid). This case highlights the superiority of F-PSMA-1007 over F-FDG PET/CT in identifying primary lesion as well as metastatic sites in case of renal cell carcinoma even in the presence of end-stage renal disease.
    Matched MeSH terms: Carcinoma, Renal Cell/pathology*; Kidney Neoplasms/pathology*
  3. Ameli F, Ghafourina Nassab F, Masir N, Kahtib F
    Asian Pac J Cancer Prev, 2021 Aug 01;22(8):2603-2609.
    PMID: 34452576 DOI: 10.31557/APJCP.2021.22.8.2603
    INTRODUCTION: Breast carcinoma is the most common malignancy and the leading cause of cancer death in women. Matrix metalloproteinase-13 (MMP-13) is a hypothetical prognostic marker in invasive breast cancer. This study aimed to determine MMP-13 expression in benign and malignant breast lesions and to evaluate the correlation between MMP-13 expression and tumor characteristics in invasive ductal carcinoma (IDC).

    MATERIALS AND METHOD: We evaluated cytoplasmic expression of MMP-13 based on staining index using immunohistochemistry (IHC) in epithelial cells, stromal fibroblasts of IDC (n=90) and benign epithelial breast (n=90) lesions. Correlation between IHC and tumor size, lymph node status, distance metastasis, estrogen receptor (ER), progesterone receptor (PR) and Her-2/neu was assessed.

    RESULTS: MMP-13 expression was 45% and 38.8% in malignant epithelial cells and peritumoral fibroblasts, respectively. Only low level of MMP-13 expression was seen in benign breast lesions (8.8% in epithelial component and 2.2% in stromal fibroblasts), while high level of MMP-13 expression was noted in malignant tumors, mainly grade II or III. Cytoplasmic MMP-13 expressions in epithelial tumor cells was correlated significantly with peritumoral fibroblasts. MMP-13 expression was directly correlated with distant metastasis and tumor stage in epithelial tumoral cells and was inversely correlated with progesterone expression in both tumoral and stromal cells.

    CONCLUSION: This study showed that MMP-13 was a moderator for tumor invasion and metastasis and could be an independent predictor of poor prognosis in breast cancer. The role of MMP-13 in predicting the risk of malignant transformation in benign lesions should be further investigated.

    Matched MeSH terms: Breast Neoplasms/pathology*; Neoplasms/pathology*
  4. Ng SC, Hilmi IN, Blake A, Bhayat F, Adsul S, Khan QR, et al.
    Inflamm Bowel Dis, 2018 Oct 12;24(11):2431-2441.
    PMID: 30312414 DOI: 10.1093/ibd/izy153
    BACKGROUND: Vedolizumab (ENTYVIO) is a humanized α4β7 integrin antagonist approved for the treatment of inflammatory bowel disease, which selectively blocks gut-specific lymphocyte trafficking. We evaluated the risk of opportunistic infections of interest in patients treated with vedolizumab.

    METHODS: We determined the frequency of opportunistic infections and tuberculosis in patients receiving vedolizumab in phase 3 clinical trials and post-marketing settings. We also evaluated adverse events reported in the post-marketing setting in patients with a history of or concurrent hepatitis B/C virus infection.

    RESULTS: The incidence of opportunistic infections in patients receiving vedolizumab was 0.7 (GEMINI 1 and 2 clinical trials) and 1.0 (long-term safety study) per 100 patient-years, with 217 events reported in approximately 114,071 patient-years of exposure (post-marketing setting). Most opportunistic infections were nonserious and the majority of patients continued treatment with vedolizumab. Clostridium difficile was the most commonly reported infection, with an incidence rate of 0.5 per 100 patient-years (clinical trials). Tuberculosis was reported at 0.1 per 100 patient-years (clinical trials), with 7 events in the post-marketing setting. No tuberculosis-related deaths were reported in either setting. No cases of progressive multifocal leukoencephalopathy were reported. In 29 patients with a history of or concurrent hepatitis B/C infection in the post-marketing setting, no viral reactivation was observed.

    CONCLUSIONS: Clinical trials and post-marketing data showed that the rate of serious opportunistic infections in patients receiving vedolizumab was low and most patients could continue vedolizumab treatment. The frequency of tuberculosis infection was also low and no hepatitis B/C viral reactivation was reported.

    Matched MeSH terms: Opportunistic Infections/pathology; Tuberculosis/pathology
  5. Mohd Ali NA, Nasaruddin AF, Mohamed SS, Wan Rahman WF
    Asian Pac J Cancer Prev, 2020 Sep 01;21(9):2653-2659.
    PMID: 32986365 DOI: 10.31557/APJCP.2020.21.9.2653
    OBJECTIVE: Phyllodes tumour (PT) is a rare fibroepithelial neoplasm of the breast that carries a risk of malignancy. Histopathological examination remains a gold standard for diagnosis. The usage of the immunohistochemical markers of Ki67 and p53 acts as a supplement method, particularly for the malignant PT. We aim here to study the expression of these markers in PT and to see their relation to the tumour grading.

    METHODOLOGY: We conducted a retrospective cross-sectional study on 57 archived formalin-fixed paraffin-embedded tissue blocks of PT from the years 2015 to 2018 from two hospitals in East Coast Malaysia. The histopathological examination and immunohistochemical stain for Ki67 and p53 were analysed.

    RESULTS: There was an association between clinical descriptive data of skin changes, lump size of more than 3 cm, cytological atypia, stromal hypercellularity, mitosis and immunohistochemistry with the clinical diagnosis of PT. Both marked expression of Ki67 and p53 were seen in borderline and malignant PT. Our study showed that in the presence of high mitotic figures, marked expression of Ki67 was only seen in cases of malignant PT.

    CONCLUSION: We found a significant association of Ki67 and p53 expressions, high mitosis and other descriptive histopathological features in malignant PT. Further study with larger sample size is recommended to predict tumour grade and prognosis as well as the disease-free survival of the tumour. 
    .

    Matched MeSH terms: Breast Neoplasms/pathology*; Phyllodes Tumor/pathology*
  6. Amran AZ, Jantan I, Dianita R, Buang F
    Pharm Biol, 2015;53(12):1795-802.
    PMID: 25868620 DOI: 10.3109/13880209.2015.1008147
    CONTEXT: Ginger [Zingiber officinale Roscoe. (Zingiberaceae)] has been universally used as a spice as well as for its health benefits.

    OBJECTIVE: The present study evaluates the protective effect of the standardized extract of ginger against isoproterenol (ISO)-induced myocardial infarction (MI) in rats.

    MATERIALS AND METHODS: Wistar rats were pretreated orally with three doses of standardized ginger extract (100, 200, and 400 mg/kg of body weight) or propranolol (5 mg/mL) for 28 d prior to ISO (85 mg/kg) induced MI in two doses on days 29 and 30. The rats were sacrificed 48 h after the first induction; serum and hearts were collected for biochemical and histopathological analysis.

    RESULTS: Gingerols and shogaols were identified and quantitatively analyzed in the extracts using validated reversed phase HPLC methods. Pretreatment with ginger extract at 400 mg/kg showed a significant decrease (p 

    Matched MeSH terms: Myocardial Infarction/pathology*; Myocardium/pathology
  7. Kong YC, Bhoo-Pathy N, O'Rorke M, Subramaniam S, Bhoo-Pathy NT, See MH, et al.
    Medicine (Baltimore), 2020 Feb;99(6):e19093.
    PMID: 32028433 DOI: 10.1097/MD.0000000000019093
    Percutaneous biopsy in breast cancer has been associated with an increased risk of malignant cell seeding. However, the importance of these observations remains obscure due to lack of corroborating evidence from clinical studies. We determined whether method of biopsy is associated with breast cancer survival. This hospital registry-based cohort study included 3416 non-metastatic breast cancer patients diagnosed from 1993 to 2011 in a tertiary setting. Factors associated with biopsy methods were assessed. Multivariable Cox regression analysis was used to determine the independent prognostic impact of method of biopsy. Overall, 990 patients were diagnosed by core needle biopsy (CNB), 1364 by fine needle aspiration cytology (FNAC), and 1062 by excision biopsy. Excision biopsy was significantly associated with more favorable tumor characteristics. Radiotherapy modified the prognostic impact of biopsy method (Pinteraction 
    Matched MeSH terms: Breast/pathology; Breast Neoplasms/pathology
  8. Adebayo IA, Arsad H, Gagman HA, Ismail NZ, Samian MR
    Asian Pac J Cancer Prev, 2020 May 01;21(5):1247-1252.
    PMID: 32458629 DOI: 10.31557/APJCP.2020.21.5.1247
    BACKGROUND: Recently, nanoparticle synthesis by eco-friendly methods has received tremendous attention due to the method advantages and also because of the application of the nanoparticles in cancer research. Therefore, in this study, we synthesized silver nanoparticles from Detarium microcarpum leaf phytochemicals and evaluated its inhibitory effect on pancreatic and cervical cancer cells.

    MATERIALS AND METHODS: Silver nanoparticles (dAgNps) were synthesized by reacting phytochemicals of D. microcarpum leaves with silver nitrate for 12 hours. Cell viability assay was carried out to investigate the cytotoxic effect of dAgNps on HeLa and PANC-1 cells.

    RESULTS: Scanning electron microscopy (SEM) and transmission electron microscopy(TEM) results revealed the average sizes of dAgNps are 81 nm and 84 nm respectively. The x-ray diffraction (XRD) pattern of dAgNps was similar to that of face centered cubic(fcc) structure of silver as reported by joint committee on powder diffraction standards (JCPDS) and fourier-transform infrared spectroscopy (FTIR) analysis showed that some phytochemicals of D. microcarpum such as polyphenols and flavonoids were likely involved in the reduction of Ag+ to form nanoparticles. Finally, cell viability assay revealed dAgNps inhibited PANC-1 and HeLa cell proliferations with IC50 values of 84 and 31.5 µg/ml respectively.

    CONCLUSION: In conclusion, the synthesized nanoparticles from D. microcarpum leaves (dAgNps) have inhibitory effect on pancreatic and cervical cancer cells.

    Matched MeSH terms: Uterine Cervical Neoplasms/pathology; Pancreatic Neoplasms/pathology
  9. Thompson CW, Phelps KL, Allard MW, Cook JA, Dunnum JL, Ferguson AW, et al.
    mBio, 2021 Jan 12;12(1).
    PMID: 33436435 DOI: 10.1128/mBio.02698-20
    Despite being nearly 10 months into the COVID-19 (coronavirus disease 2019) pandemic, the definitive animal host for SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), the causal agent of COVID-19, remains unknown. Unfortunately, similar problems exist for other betacoronaviruses, and no vouchered specimens exist to corroborate host species identification for most of these pathogens. This most basic information is critical to the full understanding and mitigation of emerging zoonotic diseases. To overcome this hurdle, we recommend that host-pathogen researchers adopt vouchering practices and collaborate with natural history collections to permanently archive microbiological samples and host specimens. Vouchered specimens and associated samples provide both repeatability and extension to host-pathogen studies, and using them mobilizes a large workforce (i.e., biodiversity scientists) to assist in pandemic preparedness. We review several well-known examples that successfully integrate host-pathogen research with natural history collections (e.g., yellow fever, hantaviruses, helminths). However, vouchering remains an underutilized practice in such studies. Using an online survey, we assessed vouchering practices used by microbiologists (e.g., bacteriologists, parasitologists, virologists) in host-pathogen research. A much greater number of respondents permanently archive microbiological samples than archive host specimens, and less than half of respondents voucher host specimens from which microbiological samples were lethally collected. To foster collaborations between microbiologists and natural history collections, we provide recommendations for integrating vouchering techniques and archiving of microbiological samples into host-pathogen studies. This integrative approach exemplifies the premise underlying One Health initiatives, providing critical infrastructure for addressing related issues ranging from public health to global climate change and the biodiversity crisis.
    Matched MeSH terms: Communicable Diseases/pathology*; Zoonoses/pathology*
  10. Nuge T, Liu Z, Liu X, Ang BC, Andriyana A, Metselaar HSC, et al.
    Molecules, 2021 Jan 29;26(3).
    PMID: 33572728 DOI: 10.3390/molecules26030699
    Volumetric Muscle Loss (VML) is associated with muscle loss function and often untreated and considered part of the natural sequelae of trauma. Various types of biomaterials with different physical and properties have been developed to treat VML. However, much work remains yet to be done before the scaffolds can pass from the bench to the bedside. The present review aims to provide a comprehensive summary of the latest developments in the construction and application of natural polymers-based tissue scaffolding for volumetric muscle injury. Here, the tissue engineering approaches for treating volumetric muscle loss injury are highlighted and recent advances in cell-based therapies using various sources of stem cells are elaborated in detail. An overview of different strategies of tissue scaffolding and their efficacy on skeletal muscle cells regeneration and migration are presented. Furthermore, the present paper discusses a wide range of natural polymers with a special focus on proteins and polysaccharides that are major components of the extracellular matrices. The natural polymers are biologically active and excellently promote cell adhesion and growth. These bio-characteristics justify natural polymers as one of the most attractive options for developing scaffolds for muscle cell regeneration.
    Matched MeSH terms: Muscular Diseases/pathology; Muscle, Skeletal/pathology
  11. Kotyla PJ, Engelmann M, Giemza-Stokłosa J, Wnuk B, Islam MA
    Int J Mol Sci, 2021 Feb 28;22(5).
    PMID: 33671049 DOI: 10.3390/ijms22052449
    Recent advances in immunology enabled the characterization of several signal transmitting pathways responsible for proper cytokine and chemokine signaling. Among them, Janus kinases (JAKs) are essential components of receptor activation systems. The discovery of JAK kinases enabled the synthesis of JAK kinase inhibitors (JAKi or Jakinibs), which have proven to be efficacious in the treatment of hematologic malignancies and several rheumatological disorders and continue to be investigated in many clinical indications. Blocking multiple cytokines belonging to several cytokine families with a single small molecule may, however, create a potential risk for the patients. Recently, a higher risk of thromboembolic complications, namely, deep vein thrombosis and pulmonary embolism, has been recognized as the main concern during treatment with Jakinibs. At present, it is not entirely clear whether this increased risk is related to direct cytokine blockade, the presence of concomitant diseases in treated patients or other unknown circumstances that work together to increase the risk of this side effect. In this review, we discuss data on the risk of thromboembolic side effects, with special emphasis on the mechanism that may be responsible for this increased risk. Many indirect data indicate that higher thromboembolic risk may be related to the specificity of JAK inhibitor action, such that preferentially blocking one signaling pathway upsets the balance between pro and anti-thrombotic activities.
    Matched MeSH terms: Thromboembolism/pathology*; Drug-Related Side Effects and Adverse Reactions/pathology*
  12. Smith ES, Smith DR, Eyring C, Braileanu M, Smith-Connor KS, Ei Tan Y, et al.
    Neurobiol Learn Mem, 2019 Nov;165:106962.
    PMID: 30502397 DOI: 10.1016/j.nlm.2018.11.007
    Rett Syndrome (RTT) is a genetic disorder that is caused by mutations in the x-linked gene coding for methyl-CpG-biding-protein 2 (MECP2) and that mainly affects females. Male and female transgenic mouse models of RTT have been studied extensively, and we have learned a great deal regarding RTT neuropathology and how MeCP2 deficiency may be influencing brain function and maturation. In this manuscript we review what is known concerning structural and coinciding functional and behavioral deficits in RTT and in mouse models of MeCP2 deficiency. We also introduce our own corroborating data regarding behavioral phenotype and morphological alterations in volume of the cortex and striatum and the density of neurons, aberrations in experience-dependent plasticity within the barrel cortex and the impact of MeCP2 loss on glial structure. We conclude that regional structural changes in genetic models of RTT show great similarity to the alterations in brain structure of patients with RTT. These region-specific modifications often coincide with phenotype onset and contribute to larger issues of circuit connectivity, progression, and severity. Although the alterations seen in mouse models of RTT appear to be primarily due to cell-autonomous effects, there are also non-cell autonomous mechanisms including those caused by MeCP2-deficient glia that negatively impact healthy neuronal function. Collectively, this body of work has provided a solid foundation on which to continue to build our understanding of the role of MeCP2 on neuronal and glial structure and function, its greater impact on neural development, and potential new therapeutic avenues.
    Matched MeSH terms: Motor Disorders/physiopathology; Basal Ganglia/pathology; Brain/physiopathology; Hippocampus/pathology; Rett Syndrome/physiopathology
  13. Campa D, Barrdahl M, Santoro A, Severi G, Baglietto L, Omichessan H, et al.
    Breast Cancer Res, 2018 04 17;20(1):29.
    PMID: 29665866 DOI: 10.1186/s13058-018-0955-5
    BACKGROUND: Leukocyte telomere length (LTL) and mitochondrial genome (mtDNA) copy number and deletions have been proposed as risk markers for various cancer types, including breast cancer (BC).

    METHODS: To gain a more comprehensive picture on how these markers can modulate BC risk, alone or in conjunction, we performed simultaneous measurements of LTL and mtDNA copy number in up to 570 BC cases and 538 controls from the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. As a first step, we measured LTL and mtDNA copy number in 96 individuals for which a blood sample had been collected twice with an interval of 15 years.

    RESULTS: According to the intraclass correlation (ICC), we found very good stability over the time period for both measurements, with ICCs of 0.63 for LTL and 0.60 for mtDNA copy number. In the analysis of the entire study sample, we observed that longer LTL was strongly associated with increased risk of BC (OR 2.71, 95% CI 1.58-4.65, p = 3.07 × 10- 4 for highest vs. lowest quartile; OR 3.20, 95% CI 1.57-6.55, p = 1.41 × 10- 3 as a continuous variable). We did not find any association between mtDNA copy number and BC risk; however, when considering only the functional copies, we observed an increased risk of developing estrogen receptor-positive BC (OR 2.47, 95% CI 1.05-5.80, p = 0.04 for highest vs. lowest quartile).

    CONCLUSIONS: We observed a very good correlation between the markers over a period of 15 years. We confirm a role of LTL in BC carcinogenesis and suggest an effect of mtDNA copy number on BC risk.

    Matched MeSH terms: Breast Neoplasms/pathology; Leukocytes/pathology
  14. Fu YP, Kohaar I, Moore LE, Lenz P, Figueroa JD, Tang W, et al.
    Cancer Res, 2014 Oct 15;74(20):5808-18.
    PMID: 25320178 DOI: 10.1158/0008-5472.CAN-14-1531
    A genome-wide association study (GWAS) of bladder cancer identified a genetic marker rs8102137 within the 19q12 region as a novel susceptibility variant. This marker is located upstream of the CCNE1 gene, which encodes cyclin E, a cell-cycle protein. We performed genetic fine-mapping analysis of the CCNE1 region using data from two bladder cancer GWAS (5,942 cases and 10,857 controls). We found that the original GWAS marker rs8102137 represents a group of 47 linked SNPs (with r(2) ≥ 0.7) associated with increased bladder cancer risk. From this group, we selected a functional promoter variant rs7257330, which showed strong allele-specific binding of nuclear proteins in several cell lines. In both GWASs, rs7257330 was associated only with aggressive bladder cancer, with a combined per-allele OR = 1.18 [95% confidence interval (CI), 1.09-1.27, P = 4.67 × 10(-5)] versus OR = 1.01 (95% CI, 0.93-1.10, P = 0.79) for nonaggressive disease, with P = 0.0015 for case-only analysis. Cyclin E protein expression analyzed in 265 bladder tumors was increased in aggressive tumors (P = 0.013) and, independently, with each rs7257330-A risk allele (P(trend) = 0.024). Overexpression of recombinant cyclin E in cell lines caused significant acceleration of cell cycle. In conclusion, we defined the 19q12 signal as the first GWAS signal specific for aggressive bladder cancer. Molecular mechanisms of this genetic association may be related to cyclin E overexpression and alteration of cell cycle in carriers of CCNE1 risk variants. In combination with established bladder cancer risk factors and other somatic and germline genetic markers, the CCNE1 variants could be useful for inclusion into bladder cancer risk prediction models.
    Matched MeSH terms: Urinary Bladder/pathology; Urinary Bladder Neoplasms/pathology
  15. Fortner RT, Ose J, Merritt MA, Schock H, Tjønneland A, Hansen L, et al.
    Int J Cancer, 2015 Sep 01;137(5):1196-208.
    PMID: 25656413 DOI: 10.1002/ijc.29471
    Whether risk factors for epithelial ovarian cancer (EOC) differ by subtype (i.e., dualistic pathway of carcinogenesis, histologic subtype) is not well understood; however, data to date suggest risk factor differences. We examined associations between reproductive and hormone-related risk factors for EOC by subtype in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Among 334,126 women with data on reproductive and hormone-related risk factors (follow-up: 1992-2010), 1,245 incident cases of EOC with known histology and invasiveness were identified. Data on tumor histology, grade, and invasiveness, were available from cancer registries and pathology record review. We observed significant heterogeneity by the dualistic model (i.e., type I [low grade serous or endometrioid, mucinous, clear cell, malignant Brenner] vs. type II [high grade serous or endometrioid]) for full-term pregnancy (phet  = 0.02). Full-term pregnancy was more strongly inversely associated with type I than type II tumors (ever vs. never: type I: relative risk (RR) 0.47 [95% confidence interval (CI): 0.33-0.69]; type II, RR: 0.81 [0.61-1.06]). We observed no significant differences in risk in analyses by major histologic subtypes of invasive EOC (serous, mucinous, endometrioid, clear cell). None of the investigated factors were associated with borderline tumors. Established protective factors, including duration of oral contraceptive use and full term pregnancy, were consistently inversely associated with risk across histologic subtypes (e.g., ever full-term pregnancy: serous, RR: 0.73 [0.58-0.92]; mucinous, RR: 0.53 [0.30-0.95]; endometrioid, RR: 0.65 [0.40-1.06]; clear cell, RR: 0.34 [0.18-0.64]; phet  = 0.16). These results suggest limited heterogeneity between reproductive and hormone-related risk factors and EOC subtypes.
    Matched MeSH terms: Neoplasms, Glandular and Epithelial/pathology*; Ovarian Neoplasms/pathology*
  16. Zamora-Ros R, Rinaldi S, Tsilidis KK, Weiderpass E, Boutron-Ruault MC, Rostgaard-Hansen AL, et al.
    Int J Cancer, 2016 Jan 01;138(1):65-73.
    PMID: 26190646 DOI: 10.1002/ijc.29693
    Incidence rates of differentiated thyroid carcinoma (TC) have increased in many countries. Adiposity and dietary risk factors may play a role, but little is known on the influence of energy intake and macronutrient composition. The aim of this study was to investigate the associations between TC and the intake of energy, macronutrients, glycemic index (GI) and glycemic load in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. The study included 477,274 middle-age participants (70.2% women) from ten European countries. Dietary data were collected using country-specific validated dietary questionnaires. Total carbohydrates, proteins, fats, saturated, monounsaturated and polyunsaturated fats (PUFA), starch, sugar, and fiber were computed as g/1,000 kcal. Multivariable Cox regression was used to calculate multivariable adjusted hazard ratios (HR) and 95% confidence interval (CI) by intake quartile (Q). After a mean follow-up time of 11 years, differentiated TC was diagnosed in 556 participants (90% women). Overall, we found significant associations only with total energy (HRQ4 vs .Q1 , 1.29; 95% CI, 1.00-1.68) and PUFA intakes (HRQ4 vs .Q1 , 0.74; 95% CI, 0.57-0.95). However, the associations with starch and sugar intake and GI were significantly heterogeneous across body mass index (BMI) groups, i.e., positive associations with starch and GI were found in participants with a BMI ≥ 25 and with sugar intake in those with BMI 
    Matched MeSH terms: Carcinoma/pathology; Thyroid Neoplasms/pathology
  17. Schmidt JA, Fensom GK, Rinaldi S, Scalbert A, Appleby PN, Achaintre D, et al.
    Int J Cancer, 2020 Feb 01;146(3):720-730.
    PMID: 30951192 DOI: 10.1002/ijc.32314
    Metabolomics may reveal novel insights into the etiology of prostate cancer, for which few risk factors are established. We investigated the association between patterns in baseline plasma metabolite profile and subsequent prostate cancer risk, using data from 3,057 matched case-control sets from the European Prospective Investigation into Cancer and Nutrition (EPIC). We measured 119 metabolite concentrations in plasma samples, collected on average 9.4 years before diagnosis, by mass spectrometry (AbsoluteIDQ p180 Kit, Biocrates Life Sciences AG). Metabolite patterns were identified using treelet transform, a statistical method for identification of groups of correlated metabolites. Associations of metabolite patterns with prostate cancer risk (OR1SD ) were estimated by conditional logistic regression. Supplementary analyses were conducted for metabolite patterns derived using principal component analysis and for individual metabolites. Men with metabolite profiles characterized by higher concentrations of either phosphatidylcholines or hydroxysphingomyelins (OR1SD  = 0.77, 95% confidence interval 0.66-0.89), acylcarnitines C18:1 and C18:2, glutamate, ornithine and taurine (OR1SD  = 0.72, 0.57-0.90), or lysophosphatidylcholines (OR1SD  = 0.81, 0.69-0.95) had lower risk of advanced stage prostate cancer at diagnosis, with no evidence of heterogeneity by follow-up time. Similar associations were observed for the two former patterns with aggressive disease risk (the more aggressive subset of advanced stage), while the latter pattern was inversely related to risk of prostate cancer death (OR1SD  = 0.77, 0.61-0.96). No associations were observed for prostate cancer overall or less aggressive tumor subtypes. In conclusion, metabolite patterns may be related to lower risk of more aggressive prostate tumors and prostate cancer death, and might be relevant to etiology of advanced stage prostate cancer.
    Matched MeSH terms: Prostate/pathology; Prostatic Neoplasms/pathology*
  18. Chuah YY, Lee YY
    Med J Aust, 2021 03;214(4):164.
    PMID: 33458825 DOI: 10.5694/mja2.50924
    Matched MeSH terms: Liver/pathology; Peritoneum/pathology
  19. Gopinath VK, Al-Salihi KA, Yean CY, Ann MC, Ravichandran M
    J Clin Pediatr Dent, 2004;28(4):319-22.
    PMID: 15366620
    Amelogenesis imperfecta (AI) is a hereditary disorder resulting in generalized defects in the enamel. The case reported here is of a seven-year-old male child with yellow color of all his teeth. Two of his primary molars were extracted due to dental abscess with advanced root resorption. Histologically hypoplastic enamel layer, positively birefringent, generalized pitting, roughness with irregular general cracked borders were observed. Scanning electron microscope, revealed extensive irregular, disorganized rough superficial enamel layer. The enamel was irregularly decussate with filamentous prisms accompanied by small rounded formations. The morphological and histological examination of the tooth revealed that this patient has the features of AI. For genetic study blood sample were collected from the patient and PCR analysis revealed that there is no mutation in exons 1-7 of AMELX gene on the X chromosome of the patient. Hence, it is probable that the AI of this patient is not X-linked. It is more likely to be an autosomal mutation.
    Matched MeSH terms: Amelogenesis Imperfecta/pathology*; Dental Enamel Hypoplasia/pathology
  20. Mohamad Shah NS, Sulong S, Wan Sulaiman WA, Halim AS
    Mol Genet Genomic Med, 2019 May;7(5):e635.
    PMID: 30924295 DOI: 10.1002/mgg3.635
    BACKGROUND: Nonsyndromic cleft lip and/or palate is one of the most common human birth defects worldwide that affects the lip and/or palate. The incidence of clefts varies among populations through ethnic, race, or geographical differences. The focus on Malay nonsyndromic cleft lip and/or palate (NSCL/P) is because of a scarce report on genetic study in relation to this deformity in Malaysia. We are interested to discuss about the genes that are susceptible to cause orofacial cleft formation in the family.

    METHODS: Genome-wide linkage analysis was carried out on eight large extended families of NSCL/P with the total of 91 individuals among Malay population using microarray platform. Based on linkage analyses findings, copy number variation (CNV) of LPHN2, SATB2, PVRL3, COL21A1, and TOX3 were identified in four large extended families that showed linkage evidence using quantitative polymerase chain reaction (qPCR) as for a validation purpose. Copy number calculated (CNC) for each genes were determined with Applied Biosystems CopyCallerTM Software v2.0. Normal CNC of the target sequence expected was set at two.

    RESULTS: Genome-wide linkage analysis had discovered several genes including TOX3 and COL21A1 in four different loci 4p15.2-p16.1, 6p11.2-p12.3, 14q13-q21, and 16q12.1. There was significant decreased, p 

    Matched MeSH terms: Cleft Lip/pathology; Cleft Palate/pathology
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