scholarly journals Postradiation Matrix Metalloproteinase-20 Expression and Its Impact on Dental Micromorphology and Radiation-Related Caries

2017 ◽  
Vol 51 (3) ◽  
pp. 216-224 ◽  
Author(s):  
Wagner Gomes-Silva ◽  
Ana Carolina Prado-Ribeiro ◽  
Thaís Bianca Brandão ◽  
Karina Morais-Faria ◽  
Gilberto de Castro Junior ◽  
...  

Recent evidence suggests that head-and-neck radiotherapy (HNRT) increases active forms of matrix metalloproteinase-20 (MMP-20) in human tooth crowns, degrading the dentin-enamel junction (DEJ) and leading to enamel delamination, which is a pivotal step in the formation of radiation-related caries (RRC). Additional participation of enzymatic degradation of organic matrix components in caries progression was attributed to MMP-20 in dentin. Therefore, the current study tested the hypothesis that MMP-20 is overexpressed in the DEJ, dentin-pulp complex components, and carious dentin of post-HNRT patients, leading to detectable micromorphological changes to the enamel and dentin. Thirty-six teeth were studied, including 19 post-HNRT specimens and 17 nonirradiated controls. Optical light microscopy was used to investigate the micromorphological components of the DEJ, dentin-pulp complex components, and carious dentin. The samples were divided into 2 subgroups: nondemineralized ground sections (n = 20) and demineralized histological sections (n = 16). In addition, immunohistochemical analysis using the immunoperoxidase technique was conducted to semiquantitatively assess MMP-20 expression in the DEJ, dentin-pulp complex components, and carious dentin. No apparent damage to the DEJ microstructure or other dentin-pulp complex components was observed and no statistically significant differences were detected in MMP-20 expression (p > 0.05) between the irradiated and control groups. This study rejected the hypothesis that MMP-20 is overexpressed in the DEJ, dentin-pulp complex components, and carious dentin of post-HNRT patients, leading to detectable micromorphological changes. Hence, direct effects of radiation may not be regarded as an independent factor to explain aggressive clinical patterns of RRC.

2002 ◽  
Vol 14 (2) ◽  
pp. 85 ◽  
Author(s):  
Mary Tolcos ◽  
Sandra Rees ◽  
Hugh McGregor ◽  
David Walker

The purpose of this study was to determine the effects of prenatal growth restriction on the ventilatory and thermoregulatory responses to asphyxia and hypercapnia in the newborn guinea-pig. Spontaneously growth-restricted (SGR) animals born to unoperated dams, and growth-retarded (GR) neonates born to dams in which a uterine artery had been ligated at mid gestation, were studied and compared with control neonates. Ventilatory responses to progressive asphyxia and steady-state hypercapnia were tested at 3–6 days of age using a barometric plethysmograph. The animals were then killed and the brains prepared for histological and immunohistochemical analysis. During progressive asphyxia, SGR neonates (n = 5) had a significantly increased minute ventilation compared with both control (n = 6) and GR (n = 5) neonates. Rectal temperature fell significantly in GR and SGR neonates after progressive asphyxia, but was unchanged in control neonates. The ventilatory responses to steady-state hypercapnia were not different in the GR, SGR and control neonates. The immunoreactive expression of glial fibrillary acidic protein, tyrosine hydroxylase, substance P and met-enkephalin in the medulla was also not different between the three groups. It was concluded that prenatal growth restriction is associated with alterations in the respiratory and thermoregulatory responses to asphyxia and hypercapnia, with greater effects observed when in utero growth restriction arises spontaneously, compared with that produced experimentally over approximately the last half of gestation.


2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Catherine Langevin ◽  
Lysanne Normandeau ◽  
Mickael Bouin

Background. Because of the chronic and relapsing nature of inflammatory bowel disease (IBD), which often requires characterization with CT scan, IBD patients might be exposed to a large amount of radiation. As a cumulative effective dose (CED) ≥ 100 mSv is considered significant for stochastic risks of cancer, it is important to monitor and control the radiation exposure of the IBD patients. In the present work, we aimed to quantify the mean CED in IBD patients to assess any harmful effects of radiation. Methods. This study includes 200 IBD patients, identified retrospectively, from the outpatient clinics of the Centre Hospitalier de l’Université de Montréal between January 1, 2010, and February 15, 2017, from the gastroenterologists’ patients lists. The number and type of each radiology test performed were listed for each patient during the study period and the CED was calculated using our institution’s dose index when available and standardized tables. Results. Among the 200 IBD patients, 157 patients had Crohn’s disease (CD), 41 had ulcerative colitis (UC), and 2 had indeterminate colitis. The mean CED for IBD patients was 23.1 ± 45.2 mSv during a mean follow-up duration of 4.3 years. CED was higher among patients with CD than with UC (27.5 ± 49.5 versus 6.8 ± 14.8 mSv; p<0.01). Six patients were exposed to a high CED (>100 mSv) and all had CD. Conclusion. While potentially harmful levels of radiation exposure are of concern in only a small number of patients, strategies to limit such exposure are encouraged when clinically appropriate.


Author(s):  
Fatemeh Vafashoar ◽  
Kazem Mousavizadeh ◽  
Hadi Poormoghim ◽  
Abbas Tavasoli ◽  
Tahereh Musavi Shabestari ◽  
...  

Systemic sclerosis is a fibrotic autoimmune disease in which aberrant remodeling of the extracellular matrix in organs disturbs their functionalities. The aim of this study was to investigate the expression of gelatinases on systemic sclerosis. Consequently, a mouse model of systemic sclerosis was employed and the gelatinolytic activity of gelatinases was evaluated on the fibrotic tissues of this model. Two groups of ten mice were considered in this work: a group of systemic sclerosis model and control group. For the generation of systemic sclerosis model, mice received bleomycin, while the control group was subjected to phosphate buffered saline (PBS) reception. Mice were tested for fibrosis by using trichrome staining, hydroxyproline measurement and α-SMA detection in tissue sections. Additionally, the gelatinolytic activity of matrix metalloproteinase 2 and matrix metalloproteinase 9 were measured using gelatin zymography in lungs and skin tissue homogenates. The obtained results indicated that subcutaneous injection of bleomycin-induced fibrosis in skin and lung tissues of mice. Pro and active forms of matrix methaloproteinase 9 were increased in fibrotic lung tissues (p<0.05 and p<0.01, respectively), while, the gelatinolytic activity of MMP2 was unaffected in these tissues. Additionally, in skin tissues of bleomycin-treated animals, both pro and active forms of MMP9 and MMP2 were increased (p<0.05). Pro and active forms of gelatinases increase differently in skin and lung tissues of bleomycin-induced scleroderma.  


Genetics ◽  
1973 ◽  
Vol 75 (1) ◽  
pp. 93-111
Author(s):  
Seaward A Sand ◽  
Harold H Smith

ABSTRACT Somatic effects of radiation intensity on the mutable V and stable R genes were detected in plants of a heterozygous clone (vS3/vs, R/r) subjected to the same dose at four rates. The effects were compared by counting speckled and purple sectors in flowers from irradiated and control plants. Response curves were estimated from the mutant sector averages, observed over a period of transient response for successive mature flowers. A structure for integrating the mutational contributions from different flowers was provided by models. The average control mutation rates are 8,110 per 107 cells for the V gene, and 49.45 for R. At a constant intensity of 4320 roentgens/hour, average induced mutation rates per 107 cells per roentgen for V increase from 194 (at 24 r total dose) to 1,116 (at 3 r dose); the corresponding rates for R increase from 7.24 to 27.65. With these responses as standards, both genes at corresponding total doses yield lower rates at lower intensities. For the series of intensities 1.2, 0.6, 0.3 and 0.15 roentgens/hour, the decreases in mutation rate for the V gene are, respectively, 66, 148, 315, and 617 per 107 cells per roentgen. The corresponding decrements for R are 4.86, 8.70, 14.61, and 23.51. These effects are non-linear functions of intensity for both genes, but V is at least 13 times as sensitive as R. Radiation operating to extinguish a buffering system against final mutation can account for the dose and dose-rate effects observed.


2021 ◽  
Author(s):  
Catherine Davis ◽  
Theirno Bah ◽  
Wenri Zhang ◽  
Jonathan Nelson ◽  
Kirsti Golgotiu ◽  
...  

INTRODUCTION: The pathogenesis of vascular cognitive impairment (VCI) is not fully understood. GPR39, an orphan G-protein coupled receptor, is implicated in neurological disorders but its role in VCI is unknown. METHODS: We performed GPR39 immunohistochemical analysis in postmortem brain samples from mild cognitive impairment (MCI) and control subjects. DNA was analyzed for GPR39 SNPs, and correlated with white matter hyperintensity (WMH) burden on premortem MRI. RESULTS: GPR39 is expressed in aged human dorsolateral prefrontal cortex, localized to microglia and peri-capillary cells resembling pericytes. GPR39-capillary colocalization, and density of GPR39-expressing microglia was increased in aged brains compared to young. SNP distribution was equivalent between groups; however, homozygous SNP carriers were present only in the MCI group, and had higher WMH volume than WT or heterozygous SNP carriers. DISCUSSION: GPR39 may play a role in aging-related VCI, and may serve as a therapeutic target and biomarker for the risk of developing VCI.


2004 ◽  
Vol 45 (4-5) ◽  
pp. 231-237 ◽  
Author(s):  
Merja Sulkala ◽  
Virve Pääkkönen ◽  
Markku Larmas ◽  
Tuula Salo ◽  
Leo Tjäderhane

2020 ◽  
Vol 79 (5) ◽  
pp. 551-561
Author(s):  
Meirong Liu ◽  
Ling Li ◽  
Tingjun Dai ◽  
Ying Hou ◽  
Wei Li ◽  
...  

Abstract Different mechanisms have been proposed to explain the pathological basis of perifascicular atrophy (PFA), a pathognomonic histologic feature of dermatomyositis (DM); however, the detailed mechanisms remain to be elucidated. There is mitochondrial dysfunction in PFA and expression of mitochondrial apoptosis molecules has been reported in DM. Overexpression of gasdermin E (GSDME) can turn mitochondrial apoptosis to mitochondrial pyroptosis, a newly characterized form of programmed cell death. We determined the expression of proteins involved in the caspase-3- and GSDME-dependent mitochondrial pyroptotic pathway, including BAX, BAK, cytochrome C, caspase-9, caspase-3, GSDME, and IL-1α, in biopsied muscles from DM and control patients. Immunohistochemical analysis showed that those markers were expressed in most fibers in PFA in DM. GSDME-positive and IL-1α-positive staining was mainly localized around punched-out vacuoles or sarcolemma. These markers were significantly upregulated at the protein and mRNA levels in DM versus controls. Our results suggest that caspase-3- and GSDME-dependent mitochondrial pyroptosis are involved in the pathogenetic mechanisms of PFA in DM and that targeting GSDME-dependent mitochondrial pyroptosis may be an effective therapeutic approach for this condition.


1986 ◽  
Vol 111 (1) ◽  
pp. 128-132 ◽  
Author(s):  
Outi Hovatta ◽  
I. Huhtaniemi ◽  
T. Wahlström

Abstract. The localisation of endogenous FSH and LH was studied in 4 inguinal adult human testes by the immunoperoxidase technique utilising antisera against the β-subunits of human FSH and LH. The content of available FSH and LH receptors was determined by radioreceptor assay. The Sertoli cells and about 10% of cells in the intersitium the Leydig cells, possibly the testicular macrophages, were similarly FSH-positive in cryptorchidism and control testes. The FSH receptor levels per testis were significantly lower in cryptorchidism than in control testes. Also the localisation of LH in Leydig cells in cryptorchidism was similar to the control testes, but the LH receptor level was significantly lower. These data bring further evidence for Leydig and Sertoli cell malfunction in the inguinal human testis.


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