Design and optimization of a support system for large aperture wedge prisms based on an integrated opto-mechanical analysis.

A stable and reliable support system for large aperture wedge prisms is the priority of the atmospheric dispersion corrector (ADC). The prism is not a rotationally symmetric component, and the stress distribution on large aperture wedge prisms caused by the support system is different compared with the rotationally symmetric mirror. A scheme of support forces passing through the prism center of gravity (COG) is proposed in this paper. Comparing with the scheme of support force passing through the prism geometry center of rotation (COR) under the same conditions, the root-mean-square (RMS) value of the optical surface shape error shows that the proposed scheme obtains better optical surface quality when the prism rotates from 0° to 360° under the conditions of gravity coupling at 2°C and 42°C. In addition, based on the proposed scheme, a multi-island genetic algorithm (MIGA) is used to optimize the position parameters of the supports. The results show that the RMS value of the optical surface deformation of the wedge prism decreases effectively. Under the conditions of gravity coupling at temperatures of 2°C and 42°C, the RMS value decreases from 260.7 nm to 107.8 nm with 58.6% and from 108.6 nm to 69.5 nm with 36.0%, respectively.

Ginkgo biloba Extract EGb761 Attenuates Bleomycin-Induced Experimental Pulmonary Fibrosis in Mice by Regulating the Balance of M1/M2 Macrophages and Nuclear Factor Kappa B (NF-κB)-Mediated Cellular Apoptosis.

BACKGROUND The aim of this study was to show whether the standardized Ginkgo biloba extract EGb761, a traditional Chinese medicine, has a therapeutic effect on pulmonary fibrosis (PF). MATERIAL AND METHODS Bleomycin (BLM) was used for establishing the PF mouse model. The mice were treated with a gradient of EGb761 for 28 days to determine an appropriate drug dose. On day 28, the effect of EGb761 on lung injury and inflammation was confirmed by hematoxylin and eosin and Masson staining and evaluated by pulmonary alveolitis and Ashcroft score. The balance of M1/M2 macrophages was evaluated with the respective markers inducible nitric oxide synthase and and interleukin-10 by real-time polymerase chain reaction. Furthermore, the expressions of fibrosis-associated protein alpha-smooth muscle actin (SMA), related inflammatory protein transforming growth factor (TGF)-ß1, the apoptosis-related proteins B-cell lymphoma-associated X protein (Bax), B-cell lymphoma (Bcl)-2, caspase-3, caspase-9, and phosphorylated nuclear factor (NF)-kappaB (p65) were assessed by western blot. RESULTS On day 28, PF was induced by treating with BLM, whereas EGb761 suppressed the PF of lung tissue. The BLM-induced imbalance of M1/M2 macrophages was reduced by EGb761. Furthermore, the increasing amounts of alpha-SMA and TGF-ß1 induced by BLM were suppressed by EGb761. In addition, the protein or messenger ribonucleic acid expression levels of phosphorylated NF-kappaB (p65), caspase-3, and caspase-9 were upregulated, whereas Bax and Bcl-2 were downregulated. Treatment with EGb761 restored the levels of these proteins except for caspase-9. CONCLUSIONS This study illustrated the protective effect of EGb761 on BLM-induced PF by regulating the balance of M1/M2 macrophages and NF-kappaB (p65)-mediated apoptosis. The results demonstrated the potential clinical therapeutic effect of EGb761, providing a novel possibility for curing PF.

Chronic hepatitis B virus infection and occurrence of hepatocellular carcinoma in tree shrews (Tupaia belangeri chinensis).

BACKGROUND: Hepatitis B virus (HBV) infection has been believed as a major cause of hepatocellular carcinoma (HCC) for a long time, however, the evidences of which are mostly from clinical and epidemiological investigations while there is no evidence from animal experiments. Tree shrew (Tupaia) is a small animal closely related to primates evolutionarily, with about 8 years of lifespan. Our previous study proved that tree shrews can be chronically HBV-infected after being inoculated neonatally with HBV. The present study reports the further results from the longer-term observation of these animals. METHODS: Neonatal tree shrews were inoculated with sera from HBV-infected patient or tree shrew. Their serum samples and liver biopsies were collected periodically for detection of HBV markers as well as for histopathological and immunohistochemical examinations. Group A consisted of six tree shrews with chronic HBV-infection, and group B consisted of nine tree shrews without chronic HBV infection. RESULTS: Periodical examinations on serum and liver biopsies of the animals in group A showed the progress of HBV infection, and two cases of HCC occurred at their late stage of life. The courses of HBV infection and the hepatic histopathological and immunohistochemical changes in the tree shrews were similar to those in humans. In contrast, neither HCC nor obvious hepatitis histopathological change was found among the tree shrews in group B. CONCLUSIONS: The course of HBV infection and the features of HCC discovered in tree shrews are similar to those of chronically HBV-infected humans. The tree shrew model might be used to investigate the underlying mechanisms favoring susceptibility for chronic HBV infection and disease progression.

Histopathological changes in the liver of tree shrew (Tupaia belangeri chinensis) persistently infected with hepatitis B virus.

BACKGROUND: An animal model for HBV that more closely approximates the disease in humans is needed. The tree shrew (Tupaia belangeri) is closely related to primates and susceptible to HBV. We previously established that neonatal tree shrews can be persistently infected with HBV in vivo, and here present a six year follow-up histopathological study of these animals. METHODS: Group A consists of six tree shrews with persistent HBV infection, group B consists of three tree shrews with suspected persistent HBV infection, while group C consists of four tree shrews free of HBV infection. Serum and liver tissues samples were collected periodically from all animals. HBV antigen and HBV antibodies were detected by ELISA and/or TRFIA. HBV DNA in serum and in liver biopsies was measured by FQ-PCR. Liver biopsies were applied for general histopathologic observation and scoring, immunohistochemical detections of HBsAg and HBcAg, and ultrastructural observation with electron microscope technique. RESULTS: Hydropic, fatty and eosinophilic degeneration of hepatocytes, lymphocytic infiltration and hyperplasia of small bile ducts in the portal area were observed in group A. One animal infected with HBV for over six years showed multiple necrotic areas which had fused to form bridging necrosis and fibrosis, and megalocytosis. The hepatic histopathological scores of group A were higher than those of group B and C. The histopathological score correlated positively with the duration of infection. CONCLUSIONS: Hepatic histopathological changes observed in chronically HBV-infected tree shrews are similar to those observed in HBV-infected humans. The tree shrew may represent a novel animal model for HBV infection.

Comparative observations on the squamous-columnar junction of Von Ebner's glandular duct at the bottom of vallate papillae in dogs, rats, mice and human.

BACKGROUND: This paper aims to comparatively observe similarities of squamous-columnar junction (SCJ) at the opening of Von Ebner's glandular ducts at the vallate papillae in dogs, mice, rats and humans, lay a foundation for the selection of the model in future study of the carcinogenesis in SCJ at vallate papillae. MATERIALS AND METHODS: The localization of the vallate papillae in three laboratory animals and humans was comparatively observed. The differences of SCJ at vallate papillae were comparatively observed by Alcian blue, immunohistochemistry and HE staining. RESULTS: Anatomically, the canine vallate papillae were most similar to those of humans in location, whereas mice and rats only had a single, Ω-shaped, vallate papilla lying directly anterior to the posterior border of the intermolar eminence. In histology, the SCJ of dogs lacked a transition zone similar to that of the human SCJ, and there was glandular epithelium secreting acidic mucus at the opening of the rats' Von Ebner's glandular ducts. All of this suggested that the histological structure of SCJ in rats and dogs is more distinct from that of humans, whereas the histological structure of SCJ at vallate papilla in mice was more similar. CONCLUSIONS: The structure of SCJ at vallate papilla in mice is most similar to that of humans, so we conclude that mouse is the most suitable model for studying tumorigenesis in SCJ at vallate papillae in these three common laboratory animals.

Experimental chronic hepatitis B infection of neonatal tree shrews (Tupaia belangeri chinensis): a model to study molecular causes for susceptibility and disease progression to chronic hepatitis in humans.

BACKGROUND: Hepatitis B virus (HBV) infection continues to be an escalating global health problem. Feasible and effective animal models for HBV infection are the prerequisite for developing novel therapies for this disease. The tree shrew (Tupaia) is a small animal species evolutionary closely related to humans, and thus is permissive to certain human viral pathogens. Whether tree shrews could be chronically infected with HBV in vivo has been controversial for decades. Most published research has been reported on adult tree shrews, and only small numbers of HBV infected newborn tree shrews had been observed over short time periods. We investigated susceptibility of newborn tree shrews to experimental HBV infection as well as viral clearance over a protracted time period. RESULTS: Forty-six newborn tree shrews were inoculated with the sera from HBV-infected patients or tree shrews. Serum and liver samples of the inoculated animals were periodically collected and analyzed using fluorescence quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, Southern blot, and immunohistochemistry. Six tree shrews were confirmed and four were suspected as chronically HBV-infected for more than 48 (up to 228) weeks after inoculation, including three that had been inoculated with serum from a confirmed HBV-infected tree shrew. CONCLUSIONS: Outbred neonatal tree shrews can be long-term chronically infected with HBV at a frequency comparable to humans. The model resembles human disease where also a smaller proportion of infected individuals develop chronic HBV related disease. This model might enable genetic and immunologic investigations which would allow determination of underlying molecular causes favoring susceptibility for chronic HBV infection and disease establishment vs. viral clearance.

Monitoring dynamic reactions of red blood cells to UHF electromagnetic waves radiation using a novel micro-imaging technology.

Multiple state-of-the-art techniques, such as multi-dimensional micro-imaging, fast multi-channel micro-spetrophotometry, and dynamic micro-imaging analysis, were used to dynamically investigate various effects of cell under the 900 MHz electromagnetic radiation. Cell changes in shape, size, and parameters of Hb absorption spectrum under different power density electromagnetic waves radiation were presented in this article. Experimental results indicated that the isolated human red blood cells (RBCs) do not have obviously real-time responses to the ultra-low density (15 µW/cm(2), 31 µW/cm(2)) electromagnetic wave radiation when the radiation time is not more than 30 min; however, the cells do have significant reactions in shape, size, and the like, to the electromagnetic waves radiation with power densities of 1 mW/cm(2) and 5 mW/cm(2). The data also reveal the possible influences and statistical relationships among living human cell functions, radiation amount, and exposure time with high-frequency electromagnetic waves. The results of this study may be significant on protection of human being and other living organisms against possible radiation affections of the high-frequency electromagnetic waves.

[Factors influencing long-term hepatitis B virus infection of the tree shrew (Tupaia belangeri chinensis) as an in vivo model of chronic hepatitis B].

OBJECTIVE: To determine the methods for establishing an in vivo model of long-term hepatitis B virus (HBV) infection in the Chinese tree shrew (Tupaia belangeri chinensis). METHODS: Seventy-seven neonate (1-3 days old) and 49 young adult (2 weeks to 1 year old) tree shrews were inoculated with different HBV sources (chronic hepatitis B (CHB) human patient serum, single or pooled; HBV-infected tree shrew serum, single only; HBV-infected HepG2.2.15 cells' culture medium supernatant; HBV genome-transfected HepG2.2.15 cells' culture medium supernatant) through various routes of injection (subcutaneous, intraperitoneal, and direct liver via abdominal skin; adults also received intravenous and indirect liver via spleen). Serum and liver biopsies were collected from the animals at various time points post-inoculation for detection of HBV markers by fluorescence quantitative polymerase chain reaction, enzyme-linked immunosorbent assay, time-resolved immunofluorescence, Southern blotting, dot blotting, immunohistochemistry, and microscopy. RESULTS: Among the neonatal group of tree shrews, six (7.8%) were confirmed as HBV-infected for more than 72 (up to 228) weeks after inoculation and another seven (9.1%) were suspected of persistent infections. None of the young adult tree shrews developed persistent infection. Inoculation with single-source serum from either CHB humans or tree shrews were responsible for the most cases of infections, and the subcutaneous injection produced more infections than the other inoculation routes. The most reliable methods of determining HBV infection status were detection of serum HBV immunoreactive markers and intrahepatic HBV DNA. CONCLUSION: In order to establish an in vivo model of CHB in the tree shrew, the animals should be inoculated in the neonatal period using subcutaneous injection.

Squamous-columnar junction of Von Ebner's glands may be a significant origin of squamous cell carcinomas in the base of the tongue.

Objectives: The histological origin of base of the tongue (BOT) carcinomas is still elusive, and most studies have been focusing on the lingual tonsil. In this study, we sought to identify the existence of the squamous-columnar junction (SCJ) in the human Von Ebner's glandular duct and explored the potential of that in forming squamous cell carcinomas in BOT. Materials and methods: The specific genomes of BOT carcinoma were acquired and screened out by The Cancer Genome Atlas (TCGA) database analysis. The 4-nitroquinoline-1-oxide (4-NQO)-treated mouse model was used to explore the transformation of SCJ during cancerization. We used immunohistochemistry to confirm the characteristics of SCJ in human Von Ebner's gland, which were further compared with those in the anus and cervix. Results: The SCJ in the human Von Ebner's glandular duct was found to be similar to that of the cervix and anus. The transformation zone in the 4-NQO-treated mouse model had a multilayered epithelium structure similar to that of HPV16-transgenic mice. In human, the transformation zone of Von Ebner's gland is also similar to that of the cervix and anus. Conclusion: It is the first time that the existence of SCJ in the opening of the human Von Ebner's glandular duct was confirmed. The SCJ of Von Ebner's glands may be a significant origin of squamous cell carcinomas in BOT.

Characterization of conserved combined T and B cell epitopes in Leptospira interrogans major outer membrane proteins OmpL1 and LipL41.

BACKGROUND: Leptospira interrogans are bacterial pathogens of animal that cause zoonotic infections in human. Outer membrane proteins of leptospire are among the most effective antigens which can stimulate remarkable immune responses during the infection processes, and thus are currently considered leading candidate vaccine antigens. The objective of the present study is to predict and confirm major combined B and T cell epitopes of leptospiral outer membrane proteins OmpL1 and LipL41, as well as to evaluate their capacity in the induction of immune responses in BALB/c mice. RESULTS: In this study, four epitopes from OmpL1 and four from LipL41 conserved regions were evaluated for their potential utilization in leptospire vaccines. Firstly, combined B and T cell epitopes were predicted by softwares and expressed using a phage display system. OmpL1 residues 87-98 and 173-191 (OmpL187-98 and OmpL1173-191) and LipL4130-48, LipL41233-256 of LipL41 were identified as immunodominant B cell epitopes by Western blot. Epitopes OmpL1173-191, OmpL1297-320 of OmpL1 and LipL41233-256, LipL41263-282 of LipL41 were identified as immunodominant CD4+ T cell epitopes through proliferation analysis of splenocytes from recombinant OmpL1 (rOmpL1) or recombinant LipL41 (rLipL41)-immunized BALB/c (H-2d) mice. These epitopes induced responses of CD4+ T cells and Th1 (T helper cells) type cytokine responses during the infection. CONCLUSION: This work identified combined T and B cell immunodominant epitopes in outer membrane proteins OmpL1 and LipL41 of Leptospira interrogans. OmpL1173-191 of OmpL1 and LipL41233-256 of LipL41 could be useful in a vaccine against Leptospira. The findings could also contribute to the development of effective cross-protective vaccine strategies for leptospirosis.

Occupational Radiation Exposure and Changes in Thyroid Hormones in a Cohort of Chinese Medical Radiation Workers.

OBJECTIVE: This study aimed to evaluate the association between occupational radiation exposure and changes in thyroid hormone levels among medical radiation workers. METHODS: This retrospective cohort study included 2,946 radiation workers from 20 Guangzhou hospitals. Data on general characteristics, participant radiation dosimetry, and thyroid function test results [thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroid hormone (T4)] were extracted from dosimetry and medical records. The generalized estimating equation was used to evaluate the trend of changes in thyroid hormone levels over time and was adjusted for age, gender, and occupation. RESULTS: The average annual effective dose was very low and showed a general downward trend. During the follow-up period, changes in T3 and T4 levels among radiation workers were -0.015 [95% confidence interval ( CI) -0.018 to -0.012] nmol/L per year and -2.294 (95% CI -2.426 to -2.162) nmol/L per year, respectively. Thyroid hormone levels were significantly different between males and females. T3 levels in the group of upper quartile of dose were significantly higher than in the lower quartile group ( P = 0.006). No significant decreased trend in thyroid hormone levels was observed with increasing average effective doses. CONCLUSION: Thyroid hormone secretion might be affected even in low-dose radiation exposure environments.

Vibrio vulnificus cytolysin induces apoptosis in HUVEC, SGC-7901 and SMMC-7721 cells via caspase-9/3-dependent pathway.

Vibrio vulnificus cytolysin (VVC) is known to be a pore-forming toxin which shows cytotoxicity for mammalian cells in culture and induces apoptosis in endothelial cells. In order to determine whether VVC induces apoptosis in vascular endothelial cells and tumor cells, the cytotoxicity induced by recombinant VVC (rVVC) and its potential mechanism in HUVEC, SGC-7901 and SMMC-7721 cells were investigated. Our study demonstrated that rVVC induced the release of intracellular K(+) from all the target cells, yet lactate dehydrogenase was not released by rVVC. It indicates that osmotic lysis might not contribute to the cytolysin-induced cytotoxicity. The study also demonstrated that rVVC induced apoptosis in HUVEC, SGC-7901 and SMMC-7721 cells in time- and dosage-dependent manners, which was associated with the activation of caspase-9 and -3, but not caspase-8. During the apoptotic process of the target cells, rVVC labeled with FITC was monitored to attach initially to the surface of the cells and entered the cytoplasma subsequently. These findings suggest that VVC may be not only a pore-forming toxin, but also a transmembrane toxin with powerful ability to induce apoptosis in human vascular endothelial cells and tumor cells.

An age-dependent association of mannose-binding lectin-2 genetic variants on HIV-1-related disease in children.

BACKGROUND: Mannose-binding lectin (MBL) is part of the lectin pathway of complement activation against various pathogens; however, its role in innate immune responses against HIV-1 infection in children is unknown. OBJECTIVE: This study evaluated the effects of mannose-binding lectin-2 (MBL2) alleles on HIV-1 disease progression and central nervous system (CNS) impairment in children. METHODS: A cohort of 1037 HIV-1-infected children enrolled in Pediatrics AIDS Clinical Trial Group protocols P152 and P300 before the availability of effective antiretroviral therapy was genotyped for MBL2 and evaluated for disease progression. RESULTS: Children with the homozygous variant MBL2-O/O genotype were more likely to experience rapid disease progression and CNS impairment than those with the wild-type AA genotype. The effects were predominantly observed in children younger than 2 years. In unadjusted Cox proportional hazards models, children younger than 2 years with MBL2-O/O experienced more rapid disease progression (O/O vs AA: relative hazard [RH], 1.54; 95% CI, 1.07-2.22; P = .02; O/O vs A/O: RH, 2.28; 95% CI, 1.09-4.79; P = .029). Similarly, children with MBL2-O/O were more likely to experience rapid progression to CNS impairment (O/O vs A/A: RH, 2.78; 95% CI, 1.06-2.69, P = .027; O/O vs A/O: RH, 1.69; 95% CI, 1.07-7.21; P = .035). The effects remained significant after adjustment for CD4(+) lymphocyte count, plasma HIV-1 RNA, and other genotypes. CONCLUSIONS: MBL2-O/O genotypes, which result in lower expression of MBL, are associated with more rapid HIV-1-related disease progression, including CNS impairment, predominantly in children younger than 2 years. These data suggest that MBL2 variants are associated with altered HIV-1 disease progression, particularly in young children.

[Association of fliR gene in Leptospira interrogans with adhesion and pathogenicity to host cells].

OBJECTIVE: To investigate the pathogenicity of Leptospira interrogans fliR gene to J774A.1 cells. METHODS: fliR gene from L. interrogans serogroup Icterohaemorrhagiae serovar lai strain 56601 and kana gene from plasmid pET42a were amplified by PCR. Suicide plasmid of fliR gene was constructed; and specific siRNA for fliR gene was designed and synthesized. fliR gene mutants were constructed by gene knock-out with suicide plasmid (56601fliR-Kana) and gene silencing with siRNA (56601siRNA-R2). The mutants were identified by PCR, sequencing and semi-quantitative RT-PCR. Adhesion to mouse mononuclear-macrophage J774A.1 and induction of cell necrosis and apoptosis by 56601fliR-Kana and 56601siRNA-R2 were examined by adhesion test and flow cytometry, respectively. RESULT: The nucleotide and putative amino acid sequences of cloned fliR gene had 99.9% and 100% similarities to those of reported sequences in GenBank. The nucleotide sequence of the cloned kana gene was identical to the corresponding sequence in pET42a map. The results of PCR and sequencing confirmed that kana gene was inserted in the sequence of 56601fliR-Kana fliR gene. The mRNA level of fliR gene in 56601fliR-Kana was remarkably decreased (P<0.01) while the mRNA level of fliR gene in 56601siRNA-R2 was much lower than that in wild strain 56601 (P<0.05). 56601fliR-Kana and 56601siRNA-R2 lost the ability to adhere J774A.1 cells; and their ability to induce cell necrosis and apoptosis was markedly weakened (P<0.01). CONCLUSION: fliR is a virulence-associated gene of L. interrogans and the function of the gene is closely related to adhesion, induction of cell necrosis and apoptosis of the microbe.

Spectroscopic and molecular modeling approaches to investigate the interaction of bisphenol A, bisphenol F and their diglycidyl ethers with PPARα.

A fluorescence polarization (FP) assay for the simultaneous determination of bisphenol A (BPA), bisphenol F (BPF), bisphenol A diglycidyl ether (BADGE) and bisphenol F diglycidyl ether (BFDGE) was developed. The method was based on the competition between bisphenols (BPs) and fluorescein-labeled dexamethasone derivative (Dex-fl) for mouse peroxisome proliferator-activated receptor α ligand binding domain (mPPARα-LBD). A recombinant soluble protein derivative mPPARα-LBD* was prepared, then in vitro binding of 4 BPs to mPPARα-LBD* was investigated. Fluorescence polarization assay showed that these compounds exhibited different binding potencies with mPPARα-LBD*. Additionally, molecular dynamics simulations were performed to further understand the mechanism of BPs binding affinity for mPPARα-LBD*. Docking results elucidated that the driving forces for the binding of BPs to mPPARα-LBD* were predominantly dependent on hydrophobic and hydrogen-bonding interactions. Comparison of the calculated binding energies vs. experimental binding affinities yielded a good correlation (R2 = 0.7258). The proposed method has potential for multi-residue detection of BPA, BPF, BADGE, and BFDGE.

Spermidine/spermine N1-acetyltransferase regulates cell growth and metastasis via AKT/ß-catenin signaling pathways in hepatocellular and colorectal carcinoma cells.

Hepatocellular carcinoma (HCC) and colorectal cancer (CRC) are among the most common cancers across the world. Therefore, identifying the potential molecular mechanisms that promote HCC and CRC progression and metastasis are urgently needed. Spermidine/spermine N1-acetyltransferase (SSAT) is a catabolic enzyme that acetylates the high-order polyamines spermine and spermidine, thus decreasing the cellular content of polyamines. Several publications have suggested that depletion of intracellular polyamines inhibited tumor progression and metastasis in various cancer cells. However, whether and how SSAT regulates cell growth, migration and invasion in hepatocellular and colorectal carcinoma cells remains unclear. In this study, depletion of polyamines mediated by SSAT not only attenuated the tumor cell proliferation but also dramatically inhibited cell migration and invasion in hepatocellular and colorectal carcinoma cells. Subsequent investigations revealed introduction of SSAT into HepG2, SMMC7721 hepatocellular carcinoma cells and HCT116 colorectal carcinoma cells significantly suppressed p-AKT, p-GSK3ß expression as well as ß-catenin nuclear translocation, while inhibition of GSK3ß activity or exogenous polyamines could restore SSAT-induced decreases in the protein expression of p-AKT, p-GSK3ß and ß-catenin. Conversely, knockdown of SSAT in Bel7402 hepatocellular carcinoma cells and HT-29 colorectal carcinoma cells which expressed high levels of SSAT endogenously significantly promoted the expression of p-AKT, p-GSK3ß as well as ß-catenin nuclear translocation. Taken together, our results indicated depletion of polyamines by SSAT significantly inhibited cell proliferation, migration and invasion through AKT/GSK3ß/ß-catenin signaling pathway in hepatocellular carcinoma and colorectal cancer cells.

The impact of the HbA1c level of type 2 diabetics on the structure of haemoglobin.

This study explores the impact of HbA1c levels on the structure of haemoglobin (Hb) in patients with type 2 diabetes. Seventy-four diabetic patients were classified into the following two groups based on their level of HbA1c: group A, patients with good glycaemic control (HbA1c < 7.0%, n = 36); group B, patients with persistent hyperglycaemia (HbA1c ≥ 9.0%, n = 38). Thirty-four healthy people served as controls (group H). Hb structure was examined by Fourier transform infrared spectroscopy (FTIR), and diabetic erythrocytes were modelled to estimate the impact of glucose on these cells and Hb. Increasing glucose concentrations altered both erythrocyte parameters and the Hb secondary structure. Group B differed significantly from group H (p < 0.05): in the former, the ordered Hb secondary structure had a strong tendency to transform into a disordered secondary structure, decreasing structural stability. We presumed here that high HbA1c levels might be a factor contributing to Hb structural modifications in diabetic patients. FTIR spectral analysis can provide a novel way to investigate the pathogenesis of type 2 diabetes mellitus.

[Expressions of PTEN and FHIT in oral squamous cell carcinoma and their relations with cyclin D1].

OBJECTIVE: To study the expressions of PTEN, FHIT and cyclin D1 in normal oral mucosa and oral squamous cell carcinoma (OSCC), and analyze the relationship between PTEN/FHIT and cyclin D1. METHODS: Immunohistochemical staining with SP methods was used to detect the expression of PTEN, FHIT and cyclin D1 in OSCC tissues in 62 cases and normal oral mucosa in 12 cases. RESULTS: The positivity rates of PTEN and FHIT were both 100% (12/12) in the normal oral mucosa, while in 62 cases of OSCC, 24.2% (15/62) and 17.7% (11/62) were negative for (or with low expression of) PTEN and FHIT, respectively. In normal oral mucosa, 91.7% (11/12) cases had negative or low cyclin D1 expression, while 53.2% (33/62) of the OSCC cases were positive for cyclin D1 expression. In all the cases, when PTEN and FHIT were strongly expressed, 37.8% (28/74) of the cases had negative or low expression of cyclin D1, including 11 normal cases. CONCLUSION: The tumor suppressor genes PTEN and FHIT play a role in the pathogenesis of OSCC, and PTEN and FHIT can down-regulate the expression of cyclin D1.

[Expressions of FHIT and cyclin D1/CDK4 in oral cancer and oral precancerous lesions].

OBJECTIVE: To detect the expressions of fragile histidine triad (FHIT) and cyclin D1/CDK4 in oral squamous cell carcinoma (OSCC) and oral precancerous lesions and investigate the relationship between the expressions and the histopathological changes. METHODS: Immunohistochemical staining by SP methods was utilized to detect the expression of FHIT and cyclin D1/CDK4 in 64 cases of OSCC, 39 oral precancerous lesions and 12 normal oral mucosa specimens. RESULTS: The rate of the negative or low FHIT expression in OSCC was 17% (11/64), which was remarkably lower than that in normal oral membrane and oral precancerous lesions (P<0.01). Significantly higher levels of cyclin D1/CDK4 expressed in OSCC than in normal oral membrane and precancerous lesions (P<0.01). There was no significant correlation between FHIT and cyclin D1/CDK4, and positive correlation between cyclin D1 and CDK4 was observed. CONCLUSION: FHIT, cyclin D1 and CDK4 may play a role in the pathogenesis of OSCC, and FHIT can down-regulate the expression of cyclin D1.

[Expression and significance of fragile histidine triad in oral cancer and precancerous lesions].

OBJECTIVE: To detect the expression of fragile histidine triad (FHIT) in oral cancer and oral precancerous lesions and investigate the relationship between the FHIT expression and the histopathological changes. METHODS: Immunohistochemical staining by SP methods was utilized to detect the expression of FHIT in 64 cases of oral squamous cell carcinoma, 39 oral precancerous lesions and 12 normal oral mucosa specimens. RESULTS: The positivity rate of FHIT in normal oral membrane was 100% (12/12), and medium and high FHIT expression levels were detected in oral precancerous lesions but without significant difference from that in normal oral mucosa. In 64 oral squamous cell carcinoma specimens, 3 were negative for FHIT expression, 8 had low expression, and the other 43 had moderate and high expression. The rate of negative or low FHIT expression in the oral squamous cell carcinoma was 17% (11/64), which was significantly different from that in the normal oral mucosa and oral precancerous lesions, but the rate was not correlated to the differentiation of the cancer. CONCLUSION: The tumor suppressor gene FHIT plays a role in the pathogenesis of oral squamous cell carcinoma.