Biomedical subjects

Lei Zhang

Publications and source records attributed to Lei Zhang.

At least 235 records · Page 13Linked to original sources

PubMed2005

Change of the cell cycle after flutamide treatment in prostate cancer cells and its molecular mechanism.

AIM: To explore the effect of androgen receptor (AR) on the expression of the cell cycle-related genes, such as CDKN1A and BTG1, in prostate cancer cell line LNCaP. METHODS: After AR antagonist flutamide treatment and confirmation of its effect by phase contrast microscope and flow cytometry, the differential expression of the cell cycle-related genes was analyzed by a cDNA microarray. The flutamide treated cells were set as the experimental group and the LNCaP cells as the control. We labeled cDNA probes of the experimental group and control group with Cy5 and Cy3 dyes, respectively, through reverse transcription. Then we hybridized the cDNA probes with cDNA microarrays, which contained 8 126 unique human cDNA sequences and the chip was scanned to get the fluorescent values of Cy5 and Cy3 on each spot. After primary analysis, reverse transcription polymerase chain reaction (RT-PCR) tests were carried out to confirm the results of the chips. RESULTS: After AR antagonist flutamide treatment, three hundred and twenty-six genes (3.93%) expressed differentially, 97 down-regulated and 219 up-regulated. Among them, eight up-regulated genes might be cell cycle-related, namely CDC10, NRAS, BTG1, Wee1, CLK3, DKFZP564A122, CDKN1A and BTG2. The CDKN1A and BTG1 gene mRNA expression was confirmed to be higher in the experimental group by RT-PCR, while p53 mRNA expression had no significant changes. CONCLUSION: Flutamide treatment might up-regulate CDKN1A and BTG1 expression in prostate cancer cells. The protein expressions of CDKN1A and BTG1 play an important role in inhibiting the proliferation of cancer cells. CDKN1A has a great impact on the cell cycle of prostate cancer cells and may play a role in the cancer cells in a p53-independent pathway. The prostate cancer cells might affect the cell cycle-related genes by activating AR and thus break the cell cycle control.

Androgen Receptor Antagonists↗

PubMed2005

Gene transcription profile in mice vaccinated with ultraviolet-attenuated cercariae of Schistosoma japonicum reveals molecules contributing to elevated IFN-gamma levels.

Vaccination with ultraviolet-attenuated cercariae of Schistosoma japonicum induced protective immunity against challenge infection in experimental animal models. Our preliminary study on the transcription levels of IFN-gamma and IL-4 in splenic CD4+ T cells revealed that attenuated cercariae elicited predominantly a Th1 response in mice at the early stage, whereas normal cercariae stimulated primarily Th2-dependent responses. Further analysis on the gene profile of the skin-draining lymph nodes demonstrated that the levels of IFN-gamma were significantly higher in vaccinated mice than those in infected mice at day 4, 7 and 14 post-vaccination or post-infection. However, for IL-12 and IL-4, the potent inducers of Th1 and Th2 responses, respectively, as well as IL-10, there were no differences over the course of the experiment between the infected and vaccinated mice. To explore the underlying factors that may potentially contribute to elevated IFN-gamma in vaccinated mice, the mRNA profiles of the skin-draining lymph nodes at day 4 post-exposure were compared using oligonucleotide microarrays. Within the 847 probe sets with increased signal values, we focused on chemokines, cytokines and relevant receptors, which were validated by semi-quantitative RT-PCR. A comprehensive understanding of the immune mechanisms of attenuated cercariae-induced protection may contribute to developing efficient vaccination strategies against S. japonicum, especially during the early stage of infection.

Animals↗

PubMed2005

Violence-related behaviors on school property among Mississippi Public High School students, 1993--2003.

Researchers examined trends and compared subgroup differences in violence-related behaviors on school property among Mississippi public high school students from 1993 to 2003. Findings are based on data from the Mississippi Youth Risk Behavior Surveillance System (YRBSS), a representative sample (N = 9,058) of Mississippi high school students. Males, non-Hispanic Whites, heavy smokers, and binge drinkers reported violence-related behaviors on school property more frequently than their counterparts. A statistically significant linear decrease occurred during 1993--2003 in the percent of students carrying a weapon (p < 0.0001) and having a physical fight (p < 0.0001). The percent of students threatened or injured with a weapon on school grounds did not decrease significantly (p = 0.2800). Violence-related behaviors were reported somewhat less frequently among 12th graders but overall, grade was not a statistically significant factor. Trends observed in Mississippi appear to be occurring throughout the United States and perhaps globally. Parents, school officials, and community administrators are committed to reducing violence-related behavior on school property. Although the decreases are encouraging, the percent of students who reported violence-related behaviors remains at a level that causes serious concern. Efforts must continue and perhaps increase to curb behaviors that may lead to school violence. Future studies should elucidate mechanisms associated with the self-reported decreasing behaviors so intervention programs can be properly focused.

Adolescent↗

PubMed2005

Sphingosine kinase regulates the sensitivity of Dictyostelium discoideum cells to the anticancer drug cisplatin.

The drug cisplatin is widely used to treat a number of tumor types. However, resistance to the drug, which remains poorly understood, limits its usefulness. Previous work using Dictyostelium discoideum as a model for studying drug resistance showed that mutants lacking sphingosine-1-phosphate (S-1-P) lyase, the enzyme that degrades S-1-P, had increased resistance to cisplatin, whereas mutants overexpressing the enzyme were more sensitive to the drug. S-1-P is synthesized from sphingosine and ATP by the enzyme sphingosine kinase. We have identified two sphingosine kinase genes in D. discoideum--sgkA and sgkB--that are homologous to those of other species. The biochemical properties of the SgkA and SgkB enzymes suggest that they are the equivalent of the human Sphk1 and Sphk2 enzymes, respectively. Disruption of the kinases by homologous recombination (both single and double mutants) or overexpression of the sgkA gene resulted in altered growth rates and altered response to cisplatin. The null mutants showed increased sensitivity to cisplatin, whereas mutants overexpressing the sphingosine kinase resulted in increased resistance compared to the parental cells. The results indicate that both the SgkA and the SgkB enzymes function in regulating cisplatin sensitivity. The increase in sensitivity of the sphingosine kinase-null mutants was reversed by the addition of S-1-P, and the increased resistance of the sphingosine kinase overexpressor mutant was reversed by the inhibitor N,N-dimethylsphingosine. Parallel changes in sensitivity of the null mutants are seen with the platinum-based drug carboplatin but not with doxorubicin, 5-fluorouracil, and etoposide. This pattern of specificity is similar to that observed with the S-1-P lyase mutants and should be useful in designing therapeutic schemes involving more than one drug. This study identifies the sphingosine kinases as new drug targets for modulating the sensitivity to platinum-based drugs.

Adenosine Triphosphate↗

PubMed2005

High-potency human immunodeficiency virus vaccination leads to delayed and reduced CD8+ T-cell expansion but improved virus control.

CD8(+) T lymphocytes are thought to play an important role in the control of acute and chronic human immunodeficiency virus infections. However, there is a significant delay between infection and the first observed increase in virus-specific CD8(+) T-cell numbers. Prior to this time, viral kinetics are not significantly different between controls and vaccinees. Surprisingly, higher initial virus-specific CD8(+) T-cell numbers lead to a longer delay prior to initial CD8(+) T-cell expansion, and slower CD8(+) T-cell increases. Nevertheless, higher initial CD8(+) T-cell numbers were associated with reduced peak and chronic viral loads and reduced CD4(+) T-cell depletion.

AIDS Vaccines↗

PubMed2005

The noncatalytic amino terminus of mitogen-activated protein kinase phosphatase 1 directs nuclear targeting and serum response element transcriptional regulation.

The mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1) is an immediate-early gene comprised of a dual-specificity phosphatase domain and a noncatalytic NH(2) terminus. Here, we show that the NH(2) terminus of MKP-1, containing the cdc25 homology domains A (CH2A) and B (CH2B), mediates MKP-1 nuclear targeting and modulates MAPK-mediated gene expression. An LXXLL motif which is known to mediate protein-protein interactions with nuclear-targeted hormone receptors was identified proximal to the CH2A domain of MKP-1. The NH(2) terminus alone of MKP-1 containing this LXXLL motif was sufficient to direct nuclear targeting, and mutating this motif to LXXAA resulted in the exclusion of MKP-1 from the nucleus. We found that the LXXLL motif proximal to the CH2A domain was present in other nuclear-localized MKPs but was absent in MKPs that localized to the cytoplasm. These data suggest that this LXXLL motif confers nuclear targeting properties to the MKPs. The NH(2) terminus of MKP-1 was also found to inhibit the activation of the serum response element (SRE) by preventing MAPK-mediated phosphorylation of the regulatory serine 383 residue on Elk-1. Moreover, we show that MKP-1 plays a major role in the attenuation of serum-induced SRE activity, since MKP-1 null fibroblasts exhibited enhanced SRE activity in response to serum compared with wild-type fibroblasts. The NH(2) terminus of MKP-1, when reconstituted into MKP-1 null fibroblasts to levels similar to endogenous MKP-1 following serum stimulation, reduced serum-mediated SRE activity. Collectively, these data reveal novel roles for the NH(2) terminus of MKP-1 in nuclear targeting and transcriptional regulation.

Active Transport, Cell Nucleus↗

PubMed2005

Membrane insertion by anthrax protective antigen in cultured cells.

The enzymatic moieties of anthrax toxin enter the cytosol of mammalian cells via a pore in the endosomal membrane formed by the protective antigen (PA) moiety. Pore formation involves an acidic pH-induced conformational rearrangement of a heptameric precursor (the prepore), in which the seven 2beta2-2beta3 loops interact to generate a 14-strand transmembrane beta-barrel. To investigate this model in vivo, we labeled PA with the fluorophore 7-nitrobenz-2-oxa-1,3-diazole (NBD) at cysteine residues introduced into the 2beta2-2beta3 loop. Each labeled PA was bound to CHO cells, and NBD fluorescence was monitored over time in stirred cell suspensions or by confocal microscopy. A strong increase was observed with NBD at positions 305, 307, 309, and 311, sites where side chains are predicted to face the bilayer, and little change was seen at residues 304, 306, 308, 310, and 312, sites where side chains are predicted to face the pore lumen. The increase at position 305 was inhibited by membrane-restricted quenchers, low temperature, or various reagents known to affect toxin action. Of the 24 NBD attachment sites examined, all but three gave results qualitatively consistent with the beta-barrel model. Besides supporting the beta-barrel model of membrane insertion, our results describe the time course of insertion and identify PA residues where NBD gives a strong signal upon membrane insertion in vivo.

4-Chloro-7-nitrobenzofurazan↗

PubMed2005

Sphingosine-1-phosphate lyase regulates sensitivity of human cells to select chemotherapy drugs in a p38-dependent manner.

Resistance to cisplatin is a common problem that limits its usefulness in cancer therapy. Molecular genetic studies in the model organism Dictyostelium discoideum have established that modulation of sphingosine kinase or sphingosine-1-phosphate (S-1-P) lyase, by disruption or overexpression, results in altered cellular sensitivity to this widely used drug. Parallel changes in sensitivity were observed for the related compound carboplatin but not for other chemotherapy drugs tested. Sensitivity to cisplatin could also be potentiated pharmacologically with dimethylsphingosine, a sphingosine kinase inhibitor. We now have validated these studies in cultured human cell lines. HEK293 or A549 lung cancer cells expressing human S-1-P lyase (hSPL) show an increase in sensitivity to cisplatin and carboplatin as predicted from the earlier model studies. The hSPL-overexpressing cells were also more sensitive to doxorubicin but not to vincristine or chlorambucil. Studies using inhibitors to specific mitogen-activated protein kinases (MAPK) show that the increased cisplatin sensitivity in the hSPL-overexpressing cells is mediated by p38 and to a lesser extent by c-Jun NH2-terminal kinase MAPKs. p38 is not involved in vincristine or chlorambucil cytotoxicity. Measurements of MAPK phosphorylation and enzyme activity as well as small interfering RNA inhibition studies show that the response to the drug is accompanied by up-regulation of p38 and c-Jun NH2-terminal kinase and the lack of extracellular signal-regulated kinase up-regulation. These studies confirm an earlier model proposing a mechanism for the drug specificity observed in the studies with D. discoideum and support the idea that the sphingosine kinases and S-1-P lyase are potential targets for improving the efficacy of cisplatin therapy for human tumors.

Aldehyde-Lyases↗

PubMed2005

Increased expression of aquaporin-4 in human traumatic brain injury and brain tumors.

OBJECTIVE: To characterize the expression of aquaporin-4 (AQP4), one of the aquaporins (AQPs), in human brain specimens from patients with traumatic brain injury or brain tumors. METHODS: Nineteen human brain specimens were obtained from the patients with traumatic brain injury, brain tumors, benign meningioma or early stage hemorrhagic stroke. MRI or CT imaging was used to assess brain edema. Hematoxylin and eosin staining were used to evaluate cell damage. Immunohistochemistry was used to detect the AQP4 expression. RESULTS: AQP4 expression was increased from 15 h to at least 8 d after injury. AQP4 immunoreactivity was strong around astrocytomas, ganglioglioma and metastatic adenocarcinoma. However, AQP4 immunoreactivity was only found in the centers of astrocytomas and ganglioglioma, but not in metastatic adenocarcinoma derived from lung. CONCLUSION: AQP4 expression increases in human brains after traumatic brain injury, within brain-derived tumors, and around brain tumors.

Adult↗

PubMed2005

Effects of Compound Dan-shen Root Dropping Pill on hemorheology in high-fat diet induced hyperlipidemia in dogs.

The purpose of this study was to examine the effects of Compound Dan-shen Root Dropping Pill (CDRDP) (Tasly Group, Tianjing, China) on hemorheology and biorheology of dogs suffering from hyperlipidemia induced by high-fat diet. Eighteen dogs were randomly divided into two groups: the high-fat diet group (H group); the control group (C group), fed with a standard laboratory diet. Six month later, six dogs in the H group were chosen as the drug-taking group (D group), to which CDRDP was administered, fed with the same diet as H group. In the 4th month, blood was taken from the veins of the dogs, and blood triglyceride (TG), total cholesterol (TC), RBC hemorheological indexes as well as malondialdehyde (MDA), glutathione transferase (GSH-ST) and superoxide dismutase (SOD) activities in plasma and erythrocytes were measured. Compared with H group, TC, TG, plasma MDA levels, the whole blood viscosity, RBC osmotic fragility and the value of CHOL (cholesterol)/PL (phospholipid) of the membrane of D group decreased, however, erythrocyte GSH-ST, histopathological changes in liver, deformation index (DI), orientation index (DI)or, small deformation index (DI)d, electrophoresis ratio and microfluidity of the membrane lipid bilayer of RBCs, increased distinctly. CDRDP can improve micro-hemorheological characteristics, therefore has a significant therapy application of hyperlipidemia.

Animals↗

PubMed2005

Prevention of central cell damage to isolated islets of Langerhans in hamsters by low temperature preconditioning.

BACKGROUND: The efficacy of clinical islet transplantation has been demonstrated with autografts, and although islet allografts have established insulin independence in a small number of IDDM patients, the treatment is confounded by the necessity of central cell damage immunosuppression, the lack of donor tissue, and recurring islet immunogenicity. These limitations underscore a need to develop therapies to serve the large population of diabetic patients. This study was designed to document central cell damage to isolated islets of Langerhans in hamsters and its prevention. METHODS: Islets were cultured at 37 degree centigrade for 7-14 days after isolation, and then at 26 degree centigrade for 2,4 and 7 days before additional culture at 37 degree centigrade for an additional 7 days. Central cell damage in the isolated islets was monitored by video-microscopy and analyzed quantitatively by a computer-assisted image analysis system. The analysis included daily measurement of the diameter and the area of the isolated islets and the area of the central cell damage that developed in those islets over time during culture. Histological examination and TdT-mediated dUTP-biotin nick end labeling (TUNEL) assay were used to characterize cell damage and to monitor islet function. RESULTS: Microscopic analysis showed that during the 7 to 14 days of culture at 37 degree centigrade, central cell damage appeared in the larger islets with diameters greater than 200 microm, which included both necrotic and apoptotic cell death. Low temperature (26 degree centigrade) culture prevented central cell damage of isolated islets. The 7-day culture procedure at 26 degree centigrade could inhibit most of the central cell (excluding diameters greater than 300 microm) damage when the islets were rewarmed to 37 degree centigrade. CONCLUSIONS: Our results indicate that central cell damage to isolated islets of Langerhans correlates with the size of the islets. Low temperature (26 degree centigrade) culture can prevent central cell damage to the isolated islets, and is capable to successfully precondition these islets for 37 degree centigrade culture. These novel findings may help to understand the pathophysiology of early loss of islet tissue after transplantation, and may provide a new strategy to improve graft function in the clinical setting of islet transplantation.

Animals↗

PubMed2005

Co-expression and immunity of Legionella pneumophila mip gene and immunoadjuvant ctxB gene.

The mip gene of Legionella pneumophila and the ctxB gene of Vibrio cholerae were amplified by PCR respectively. The amplified cDNA was ligated to the pcDNA3.1(+) vector. The recombinant plasmids pcDNA3.1-mip and pcDNA3.1-ctxB were identified by restriction analysis and PCR, and further confirmed by sequencing analysis. NIH3T3 cells were transfected with pcDNA3.1-mip and pcDNA3.1-ctxB according to the Lipofection method. Transient and stable products of the co-expression of the mip gene and ctxB gene were detected by immunofluorescence and Western blotting. The results showed that NIH3T3 cells were successfully transfected, and that the transiently and stably co-expressed products can be detected in the transfected cells. To detect the humoral and cellular immune response in immunized mice induced by the co-mmunization of the mip and ctxB genes, female BALB/c mice were immunized intramuscularly with pcDNA3.1-mip and pcDNA3.1-ctxB. The results showed that the specific antibody titer and the cytotoxic T-lymphocyte response for pcDNA3.1-mip immunization and co-immunization were increased compared with that of pcDNA3.1(+) immunization. Furthermore, the specific antibody titer and cytotoxic T-lymphocyte response for co-immunization were increased compared with that of pcDNA3.1-mip immunization. Statistical analysis using one-way analysis of variance (ANOVA) showed that there was a significant difference between the groups (P<0.01). The results indicated that the ctxB gene enhanced the humoral and cellular immune response to the mip gene immunization. These findings provide experimental evidence to support the development of the L. pneumophila DNA vaccine.

Adjuvants, Immunologic↗

PubMed2005

[Brain activities during maximum voluntary clenching with soft occlusal pad in healthy adults by functional magnetic resonance imaging].

OBJECTIVE: Using functional magnetic resonance imaging (fMRI) to detect the cerebral cortical somatotopy during maximum voluntary clenching with soft occlusal pad in healthy adults. By comparing with the cerebral cortical activation during clenching with and without soft occlusal pad we try to detect the central mechanism of the rule of the occlusal pad. METHODS: Ten healthy subjects were selected and scanned by Elscint/GE 2.0 Tesla MR system. Block design was used and the movement pattern was maximum voluntary clenching with soft occlusal pad. The fMRI data were analyzed by SPM99 software and group map analysis was done. RESULTS: The activation areas were found in bilateral or unilateral motor cortex, somatosensory cortex, prefrontal cortex, temporal cortex, premotor cortex, insula, frontal operculum, basal ganglia (putamen), parietal cortex and cingulate. Group map analysis showed activation in bilateral motor cortex, right somatosensory cortex, bilateral basal ganglia, and bilateral insula. The activation of left motor cortex was significantly higher than right side. Compared with cortical activation without occlusal pad, the motor and somatosensory cortex changed a lot. CONCLUSION: The changes of the activation of motor and somatosensory cortex during clenching after wearing the soft occlusal pad might be the central mechanism of the rule of the occlusal pad.

Adult↗

PubMed2005

[T-type calcium channel gene-CACNA1H is a susceptibility gene to childhood absence epilepsy].

OBJECTIVE: Childhood absence epilepsy (CAE) is one of the most frequently recognized syndromes among the idiopathic generalized epilepsies (IGEs). It is considered to be a hereditary disease. The possible inheritance pattern of CAE is polygenic. The genes responsible for CAE, however, have not yet been identified. The aim of this study was to further investigate based on the authors' recent work whether or not T-type calcium channel gene-CACNA1H is a susceptibility gene to childhood absence epilepsy. METHODS: The authors conducted the mutation screening of the exons 6-12 and the nearby partial introns of the CACNA1H gene using the method of direct sequencing of PCR products in 48 newly found CAE patients. RESULTS: The authors found 13 single nucleotide polymorphisms (SNPs). They also found 4 mutations which only existed in CAE patients. Both G773D and H515Y mutations were heterozygous. The mutation of H515Y has never been reported previously. The patient inherited the mutation from his mother. The authors found two CAE patients with the mutation of G773D previously. This is the third time that the authors found one more CAE family with this G773D mutation, and the patient with the mutation G773D inherited the mutation from his father. CONCLUSION: T-type calcium channel gene-CACNA1H might be a susceptibility gene to childhood absence epilepsy.

Amino Acid Sequence↗

PubMed2005

[The interaction of vascular endothelial growth factor and interleukin-6 in multiple myeloma].

OBJECTIVE: To study the interaction between human multiple myeloma (MM) cell line and MM-bone marrow stromal cells (BMSCs) modulated by mutual stimulation of vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6), and to analyze the role of VEGF and IL-6 in the pathogenesis of MM. METHODS: MM patient (MM-BMSCs) and normal donor-BMSCs (N-BMSCs) were established from the MNCs of MM and normal bone marrow. ELISA was performed to detect the expression of VEGF and IL-6 in culture supernatants of human MM cell lines U266, MM-BMSCs, N-BMSCs, and co-cultures of U266 and BMSCs in vitro. VEGF and IL-6 were detected in culture supernatants with or without IL-6, anti-IL-6, VEGF, anti-VEGF antibody. RESULTS: Human MM cell line U266 secreted VEGF, but did not secrete IL-6. BMSCs from MM patients and normal donors secreted both VEGF and IL-6. BMSCs stimulated with recombinant human VEGF induced a time and dose-dependent increase in IL-6 secretion. The effects of VEGF were canceled by monoclonal anti-VEGF antibody. Exogenous IL-6 stimulated VEGF secretion of BMSCs. Importantly, when U266 cell were adhered to BMSCs, there was significant increase of VEGF (2.5 - 5.0 fold, P < 0.05) and IL-6 (5.5 - 9.0 fold, P < 0.05) secretion. The secretion of VEGF or IL-6 in BMSCs alone or co-cultures of BMSCs with U266 were inhibited by anti-human IL-6 or anti-human VEGF antibody. U266 cell stimulated with recombinant human IL-6 induced a dose-dependent increase in VEGF secretion, which was inhibited in the presence of a monoclonal antihuman IL-6 antibody. CONCLUSIONS: The interaction between myeloma cells and marrow stromal cells modulates the secretion of VEGF and IL-6, facilitates myeloma cells growth and angiogenesis in MM. It plays an important role in the pathogenesis of MM. This study provides a theoretic basis for target therapy in the treatment of bone marrow microenvironment.

Aged↗

PubMed2005

[Clinicopathologic analysis of pulmonary lymphangioleiomyomatosis].

OBJECTIVE: To investigate the clinicopathological features of pulmonary lymphangioleiomyomatosis (PLAM). METHODS: By means of HE and immunohistochemistry (SP method) studies, the clinical and pathological features of 5 PLAM cases were analyzed and the related literature reviewed. RESULTS: PLAM was a rare lung disease of unknown etiology and was restricted to females who were generally pre-menopausal. Pathological features showed abnormal smooth muscle cells (LAM cells) line the airways, lymphatics and blood vesssels leading to airflow obstruction and replacement of the lung parenchyma by cysts. LAM cells were positive for HMB45. Clinically the disease was categorized by dyspnoea, haemoptysis, recurrent pneumothoraces and chylous effusions. CONCLUSIONS: PLAM should be considered when recurrent pneumothorax, haemoptysis and dyspnoea occur in females. Pathologic examination of lung tissue biopsy is required for confirmation of PLAM diagnosis.

Actins↗

PubMed2005

[Ribosomal protein genes highly expressed in swamp eel gonads].

8 cDNA clones have been isolated from a cDNA library prepared from swamp eel testies by macroarray. DNA sequence analysis and database search showed that they encode 8 proteins which are highly homologous to 40S ribosomal proteins S4,S9,S16,S17,S20 and 60S riobosomal proteins L7, L18a,L29. Phylogenetic trees (ML) based on ribosomal protein genes from swamp eel and other organisms has been reconstructed, which showed that ribosomal protein genes were highly conserved during evolution. These results suggested that ribosomal protein genes as house keeping genes may play roles in developmental regulation such as sexual differentiation and can also be used as markers for the study of molecular evolution.

Amino Acid Sequence↗

PubMed2005

[Raman spectra of cell from breast cancer patients].

Raman spectra of normal and cancer cell from breast cancer patients a represented. It is reported that all of the Ramanlines become weak. The intensities of Raman lines 782 and 1 084 cm(-1) of DNA phosphate group and 1 155 and 1 262 cm(-1) of deoxyribosephosphate decrease. The spectral lines 812 cm(-1) of A-type DNA and 979 and 668 cm(-1) disappear, and the 905 cm(-1) peak is shifted to lower frequency by 6 cm(-1). This means that the phosphate backbone of DNA is destroyed to a certain extent and the fissiparity of cancer cell can't be controlled effectively. In addition, the authors found a kind of Raman line 960 cm(-1) concerning calcificationand sclerosis of cancer cell. The results indicate that Raman spectra may offer the experiment basis for the cancer diagnosis and treatment.

Breast Neoplasms↗