Forensic odontology with digital technologies: A systematic review.

Postmortem dental examinations play an important role in individual identification. In forensic odontology, individual identification is based on a traditional visual comparison of the antemortem dental record and dental radiographs with those obtained by postmortem examinations. Digitization in forensic odontology has recently started. The aim of this systematic review was to reveal the progress in forensic odontology by using ante/postmortem information obtained by digital technologies. Thirty-six eligible studies were included. No methods with digital technology have been accepted worldwide because of various factors such as expensive special equipment and the cost of other components. Further research should be conducted and progress should be made in the field of forensic odontology along with the progression of general digital technology.

Hyperoxia causes diffuse alveolar damage through mechanisms involving upregulation of c-Myc/Bax and enhanced production of reactive oxygen species.

BACKGROUND: Hyperoxia is a known cause of diffuse alveolar damage (DAD). We previously reported the transcript profiling of DAD induced by hyperoxia exposure in mouse lungs and showed that the gene expression of myelocytomatosis oncogene (c-Myc) was significantly upregulated whereas that of surfactant-associated protein (SP)-C was downregulated. However, the mechanism underlying hyperoxia-induced DAD is not well understood. METHODS: The hyperoxia-induced changes in SP-A/B/C/D, c-Myc, B-cell chronic lymphocytic leukemia/lymphoma (Bcl)-2, and Bcl-2-associated X protein (Bax) expression in mouse lungs were examined by cDNA microarray analysis. The expression levels of the above mentioned genes, cell viability, caspase activity, and reactive oxygen species (ROS) production were also examined in the human lung adenocarcinoma cell line A549 and mouse fibroblast-like cell line NIH/3T3. RESULTS: Hyperoxia induced a decrease in SP-C/A expression in mouse lungs, and SP-C downregulation was also confirmed in A549 cells. In addition to enhanced c-Myc expression, Bax expression also increased following exposure of the mice to hyperoxia. In vitro analysis showed that expression of these genes is regulated in a cell-type-dependent manner, i.e., upregulation of c-Myc in NIH/3T3 cells and Bax in A549 cells occurred regardless of whether there was a similar decrease in cell viability and increase in caspase-3/7 activation in response to hyperoxia. ROS production and caspase-8 activation were also observed in both cells. CONCLUSIONS: We concluded that hyperoxia induces ROS production and cell death in lung tissues through a cell-type specific mechanism involving the upregulation of c-Myc/Bax, and caspase-8 and -3/7 activation-dependent pathways, thereby leading to the development of DAD.

A palindromic CpG-containing phosphodiester oligodeoxynucleotide as a mucosal adjuvant stimulates plasmacytoid dendritic cell-mediated T(H)1 immunity.

BACKGROUND: CpG oligodeoxynucleotides (ODNs), resembling bacterial DNA, are currently tested in clinical trials as vaccine adjuvants. They have the nuclease-resistant phosphorothioate bond; the immune responses elicited differ according to the CpG ODN sequence and vaccination method. To develop a CpG ODN that can induce plasmacytoid dendritic cell (pDC)-mediated T(H)1 immunity through the mucosa, we constructed phosphodiester G9.1 comprising one palindromic CpG motif with unique polyguanosine-runs that allows degradation similar to naturally occurring bacterial DNA. METHODS: T(H)1 and T(H)2 immunity activation was evaluated by cytokine production pattern and T-bet/GATA-3 ratio in human peripheral blood mononuclear cells and mouse bone marrow cells. Adjuvanticity was evaluated in mice administered G9.1 with diphtheria toxoid (DT) through nasal vaccination. RESULTS: G9.1 exhibited stronger IFN-α-inducing activity than A-class CpG ODN2216 and increased T-bet/GATA-3 ratio by enhancing T-bet expression. Nasally administered G9.1 plus DT induced DT-specific mucosal IgA and serum IgG, but not IgE, responses with antitoxin activity in C57BL/6 and BALB/c mice, possibly due to IFN/BAFF production. Induction of T(H)1, but not T(H)2-type Abs depended completely on pDCs, the first in vivo demonstration by CpG ODNs. CONCLUSIONS: G9.1 is a promising mucosal adjuvant for induction of pDC-mediated T(H)1 immunity.

Time course of housekeeping gene expression changes in diffuse alveolar damage induced by hyperoxia exposure in mice.

We have found diffuse alveolar damage (DAD) has taken place in some patients under mechanical ventilation with high-inspired oxygen concentrations. To clarify the molecular pathophysiology of this, the time course of gene expression changes induced by hyperoxia exposure in mouse lungs was examined using real-time quantitative polymerase chain reaction (real-time qPCR). Our raw data and those normalized with glyceraldehyde 3-phosphate dehydrogenase (GAPDH) showed that: (1) there is a decrease in levels of mRNAs for surfactant-associated protein C (SFTPC), cytochrome P450, 2F2 (CYP2F2), Claudin 1 (CLDN1), membrane-associated zonula occludens protein-1 (ZO-1), lysozyme (LYZS), and this suggests alveolar dysfunction and a disruption of the immune system, (2) we confirmed apoptotic conditions, such as significant up-regulations of mRNA levels in Myc and Galectin-3, and (3) hyperoxic conditions probably yielded reactive oxygen species (ROS), which resulted in a malignant cycle of ROS production by Myc overexpression [Shimada I, Matsui K, Brinkmann B, Hohoff C, Hiraga K, Tabuchi Y, et al. Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase. Int J Legal Med 2008;122:373-83]. In this experiment, GAPDH was up-regulated when hyperoxia exposure was continued. Therefore, we reexamined our data and found that: (1) mRNA levels of other housekeeping genes, including beta(2)-microglobulin (beta2M), ribosomal protein: large P2 (RPLP2), and importin 8 (IPO8) altered to a lesser extent, (2) mRNA levels of beta2M and IPO8 were down-regulated when hyperoxia exposure was continued, and (3) our previous work was validated by normalization with these three housekeeping genes.

Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase.

Under mechanical ventilation with high-inspired oxygen concentration, diffuse alveolar damage was found to take place in some patients. To clarify the molecular pathophysiology of this condition, we investigated the time course of gene expression changes induced by hyperoxia exposure in mouse lung using real-time quantitative polymerase chain reaction (qPCR). Our results normalized by glyceraldehyde 3-phosphate dehydrogenase showed that mRNA levels of cysteine rich protein 61 (CYR61) and connective tissue growth factor (CTGF) were significantly upregulated, while those of surfactant-associated protein C (SFTPC), cytochrome P450, 2F2 (CYP2F2), Claudin 1, (CLDN1), membrane-associated zonula occludens protein-1 (ZO-1), lysozyme (LYZS), and P lysozyme structural (LZP-S) were significantly downregulated. Increasing level of mRNAs, each encoding CYR61 and CTGF, suggests a serious risk of fibrosing alveolitis. Decrease in levels of mRNAs for SFTPC, CYP2F2, CLDN1, ZO-1, LYZS, and LZP-S suggests alveolar dysfunction and disruption of the immune system. Moreover, we confirmed apoptotic conditions, such as significant upregulations of mRNA levels in Myc and Galectin-3. Hyperoxic condition probably yielded reactive oxygen species (ROS), which resulted in a malignant cycle of ROS production by Myc overexpression.

Immunohistochemical study of thyroid transcription factor-1 and surfactant-associated protein A for investigation of peripheral airway structure in perinatal fatality.

We studied histopathological findings of the lungs in four cases where there was a suspicion of infanticide whereby an autopsy was performed. All four babies were born in full term delivery. It was difficult to discern whether the peripheral airways of the lungs were open or closed with conventional histological examination. Therefore immunohistochemistry with a combination of anti-thyroid transcription factor-1 (TTF-1) and anti-surfactant-associated protein A (PE-10) was used in order to elucidate the fundamental structures of the peripheral airways. TTF-1 highlighted nuclei of Clara cells and type II alveolar cells. The findings of immunohistochemistry with TTF-1 enabled us to more objectively recognize the peripheral airways: respiratory bronchioles and alveolar ducts, even in collapsed lungs. PE-10 was expressed in the cytoplasm of Clara cells, type II alveolar cells and the substance of air space. Aspect for immunohistochemistry with PE-10 appeared to be granular in closed air space, whereas it appeared to be stretched membranously along the interalveolar septa in open air space. These findings suggest that application of immunohistochemistry with TTF-1 and PE-10 is a useful diagnostic tool in judging perinatal fatality.

Cyclooxygenase-2 in sporadic colorectal polyps: immunohistochemical study and its importance in the early stages of colorectal tumorigenesis.

Cyclooxygenase-2 (COX-2) is one of the important targets for the chemoprevention of colorectal cancer by non-steroidal anti-inflammatory drugs (NSAIDs). To evaluate the role of COX-2 in early stages of colorectal tumorigenesis, we immunohistochemically investigated the frequency and localization of COX-2 in sporadic colorectal polyps that showed various histology using a commercially available monoclonal antibody. A total of 105 colorectal polyps were examined. These included 33 low-grade adenomas (LGAs), 28 high-grade adenomas (HGAs), 32 HGAs with p53 overexpression (HGAs-p53), and 12 cases of carcinoma in adenoma (CIA). Regarding the immunohistochemical expression of p53, MIB-1, and CD63, histological classification was made for each case. COX-2 was expressed in neoplastic epithelial cells and interstitial macrophages that were distributed mainly in the superficial areas of polyps. COX-2 labeling indices (LIs) were 8.2% in LGAs, 6.3% in HGAs, 0.9% in HGAs-p53, and 0.6% in the carcinomatous components of CIAs. COX-2 LIs were significantly higher in adenomas, including LGAs and HGAs, than in HGAs-p53 and CIAs (p < 0.001). Within CIAs, significantly higher COX-2 LIs were obtained in the adenomatous components than in the carcinomatous components (p < 0.05). The size of polyps was not correlated with COX-2 expression irrespective of their histology. The results show that COX-2 might be involved in early stages of colorectal tumorigenesis. Colorectal adenomas could be a target for the chemopreventive strategy irrespective of their sizes.

Analysis of 15 short tandem repeats reveals significant differences between the Arabian populations from Morocco and Syria.

The short tandem repeat (STR) systems D3S1358, TH01, D21S11, D18S51, Penta E, D5S818, D13S317, D7S820, D16S539, CSF1PO, Penta D, vWA, D8S1179, TPOX and FGA were studied in Arabian population samples from Morocco and Syria. No significant deviation from Hardy-Weinberg equilibrium could be observed in either preparation. Comparing the Moroccan and Syrian populations using the program RxC, no similarity could be observed at all 15 loci. In the Moroccan and Syrian populations the matching probability is 1 in 1.4 x 10(17) and 1 in 2.6 x 10(17), respectively. Thus, the combination of these 15 STR loci is powerful tool for forensic identification in Arabian populations.