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Basic Excision Repair Of Dna Damage (Molecular Biology Intelligence Unit)
HICKSON
Manufacturer: Chapman & Hall
ProductGroup: Book
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ASIN: 0412131617 |
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8-OxoG retards the activity of the ligase III/XRCC1 complex during the repair of a single-strand break, when present within a clustered DNA damage site [An article from: DNA Repair]
M.E. Lomax ,
S. Cunniffe , and
P. O'Neill
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
Elsevier
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ASIN: B000RQZMAA |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
Ionising radiation produces clustered DNA damage. Recent studies have established that the efficiency of excision of a lesion within clustered damage sites is reduced. This study presents evidence that the repair of clustered DNA damage is compromised, relative to that of the isolated lesions, since the lifetime of both lesions is extended by up to eight fold. Simple clustered damage sites, comprised of a single-strand break, one or five bases 3' or 5' to 8-oxoG on the opposite strand, were synthesised in oligonucleotides and repair carried out in XRS5 nuclear extracts. The rate of repair of the single-strand break within these clustered damage sites is reduced, mainly due to inhibition of the DNA ligase III/XRCC1 complex. The single-strand break, present as an isolated lesion, is repaired by short-patch base excision repair, however the mechanism of repair of the single-strand break within the clustered damage site is asymmetric. When the lesions are 5' to each other, the single-strand break is rejoined by short-patch repair whereas the rejoining of the single-strand break occurs by long-patch type repair when the lesions are 3' to one another. The retardation of DNA ligase III/XRCC1 complex, following addition of one base, is responsible for the initiation of long-patch base excision repair when the lesions are 3' to each other. The lesions within the cluster are processed sequentially, the single-strand break being repaired before excision of 8-oxoG, limiting the formation of double-strand breaks to
<2%. Stalled processing of clustered DNA damage is suggested to have implications for mutation induction by radiation.
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Alkylation damage in DNA and RNA-repair mechanisms and medical significance [An article from: DNA Repair]
F. Drablos ,
E. Feyzi ,
P.A. Aas ,
C.B. Vaagbo , and
Kavli
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
Elsevier
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ASIN: B000RR394K |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
Alkylation lesions in DNA and RNA result from endogenous compounds, environmental agents and alkylating drugs. Simple methylating agents, e.g. methylnitrosourea, tobacco-specific nitrosamines and drugs like temozolomide or streptozotocin, form adducts at N- and O-atoms in DNA bases. These lesions are mainly repaired by direct base repair, base excision repair, and to some extent by nucleotide excision repair (NER). The identified carcinogenicity of O^6-methylguanine (O^6-meG) is largely caused by its miscoding properties. Mutations from this lesion are prevented by O^6-alkylG-DNA alkyltransferase (MGMT or AGT) that repairs the base in one step. However, the genotoxicity and cytotoxicity of O^6-meG is mainly due to recognition of O^6-meG/T (or C) mispairs by the mismatch repair system (MMR) and induction of futile repair cycles, eventually resulting in cytotoxic double-strand breaks. Therefore, inactivation of the MMR system in an AGT-defective background causes resistance to the killing effects of O^6-alkylating agents, but not to the mutagenic effect. Bifunctional alkylating agents, such as chlorambucil or carmustine (BCNU), are commonly used anti-cancer drugs. DNA lesions caused by these agents are complex and require complex repair mechanisms. Thus, primary chloroethyl adducts at O^6-G are repaired by AGT, while the secondary highly cytotoxic interstrand cross-links (ICLs) require nucleotide excision repair factors (e.g. XPF-ERCC1) for incision and homologous recombination to complete repair. Recently, Escherichia coli protein AlkB and human homologues were shown to be oxidative demethylases that repair cytotoxic 1-methyladenine (1-meA) and 3-methylcytosine (3-meC) residues. Numerous AlkB homologues are found in viruses, bacteria and eukaryotes, including eight human homologues (hABH1-8). These have distinct locations in subcellular compartments and their functions are only starting to become understood. Surprisingly, AlkB and hABH3 also repair RNA. An evaluation of the biological effects of environmental mutagens, as well as understanding the mechanism of action and resistance to alkylating drugs require a detailed understanding of DNA repair processes.
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Attempted base excision repair of ionizing radiation damage in human lymphoblastoid cells produces lethal and mutagenic double strand breaks [An article from: DNA Repair]
N. Yang ,
H. Galick , and
S.S. Wallace
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
Elsevier
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ASIN: B000RQZLEW |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
A significant proportion of cellular DNA damages induced by ionizing radiation are produced in clusters, also called multiply damaged sites. It has been demonstrated by in vitro studies and in bacteria that clustered damage sites can be converted to lethal double strand breaks by oxidative DNA glycosylases during attempted base excision repair. To determine whether DNA glycosylases could produce double strand breaks at radiation-induced clustered damages in human cells, stably transformed human lymphoblastoid TK6 cells that inducibly overexpress the oxidative DNA glycosylases/AP lyases, hNTH1 and hOGG1, were assessed for their radiation responses, including survival, mutation induction and the enzymatic production of double strand breaks post-irradiation. We found that additional double strand breaks were generated during post-irradiation incubation in uninduced TK6 control cells. Moreover, overproduction of either DNA glycosylase resulted in significantly increased double strand break formation, which correlated with an elevated sensitivity to the cytotoxic and mutagenic effects of ionizing radiation. These data show that attempted repair of radiation damage, presumably at clustered damage sites, by the oxidative DNA glycosylases can lead to the formation of potentially lethal and mutagenic double strand breaks in human cells.
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Base damage and single-strand break repair: Mechanisms and functional significance of short- and long-patch repair subpathways [An article from: DNA Repair]
P. Fortini , and
E. Dogliotti
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
Elsevier
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ASIN: B000PDU1U6 |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2007. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
A large variety of DNA lesions induced by environmental agents or arising as an outcome of cellular metabolism are counteracted by a complex network of proteins that belong to the base excision repair/single strand break repair (BER/SSBR) processes. No matter whether the initial lesions are modified DNA bases or single-strand breaks with non-conventional termini these processes are completed either by replacement of a single (short-patch, SP) or more (long-patch, LP) nucleotides by different arrays of proteins. Here, the factors that are involved in the selection between SP- and LP-BER/SSBR are reviewed. The biological significance of these alternative subpathways is also presented as inferred from mutant mouse/cell models.
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Base excision repair by hNTH1 and hOGG1: A two edged sword in the processing of DNA damage in @c-irradiated human cells [An article from: DNA Repair]
N. Yang ,
M.A. Chaudhry , and
S.S. Wallace
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
Elsevier
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ASIN: B000RR6KMI |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
Using siRNA technology, we down-regulated in human B-lymphoblastoid TK6 cells the two major oxidative DNA glycosylases/AP lyases that repair free radical-induced base damages, hNTH1 and hOGG1. The down-regulation of hOGG1, the DNA glycosylase whose main substrate is the mutagenic but not cytotoxic 8-oxoguanine, resulted in reduced radiation cytotoxicity and decreased double strand break (DSB) formation post-irradiation. This supports the idea that the oxidative DNA glycosylases/AP lyases convert radiation-induced clustered DNA lesions into lethal DSBs and is in agreement with our previous finding that overexpression of hNTH1 and hOGG1 in TK6 cells increased radiation lethality, mutant frequency at the thymidine kinase locus and the enzymatic production of DSBs post-irradiation [N. Yang, H. Galick, S.S. Wallace, Attempted base excision repair of ionizing radiation damage in human lymphoblastoid cells produces lethal and mutagenic double strand breaks, DNA Repair (Amst) 3 (2004) 1323-1334]. Interestingly, cells deficient in hNTH1, the DNA glycosylase that repairs a major lethal single free radical damage, thymine glycol, were more radiosensitive but at the same time fewer DSBs were formed post-irradiation. These results indicate that hNTH1 plays two roles in the processing of radiation damages: repair of potentially lethal single lesions and generation of lethal DSBs at clustered damage sites. In contrast, in hydrogen peroxide-treated cells where the majority of free radical DNA damages are single lesions, the base excision repair pathway functioned to protect the cells. Here, overexpression of hNTH1 and hOGG1 resulted in reduced cell killing while suppression of glycosylase expression resulted in elevated cell death.
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Effects of ethylene oxide and ethylene inhalation on DNA adducts, apurinic/apyrimidinic sites and expression of base excision DNA repair genes in rat brain, ... and liver [An article from: DNA Repair]
I. Rusyn ,
S. Asakura ,
Y. Li ,
O. Kosyk ,
H. Koc , and
Nak
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
Elsevier
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ASIN: B000RR6KH8 |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in . The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
Ethylene oxide (EO) is an important industrial chemical that is classified as a known human carcinogen (IARC, Group 1). It is also a metabolite of ethylene (ET), a compound that is ubiquitous in the environment and is the most used petrochemical. ET has not produced evidence of cancer in laboratory animals and is ''not classifiable as to its carcinogenicity to humans'' (IARC, Group 3). The mechanism of carcinogenicity of EO is not well characterized, but is thought to involve the formation of DNA adducts. EO is mutagenic in a variety of in vitro and in vivo systems, whereas ET is not. Apurinic/apyrimidinic sites (AP) that result from chemical or glycosylase-mediated depurination of EO-induced DNA adducts could be an additional mechanism leading to mutations and chromosomal aberrations. This study tested the hypothesis that EO exposure results in the accumulation of AP sites and induces changes in expression of genes for base excision DNA repair (BER). Male Fisher 344 rats were exposed to EO (100ppm) or ET (40 or 3000ppm) by inhalation for 1, 3 or 20 days (6h/day, 5 days a week). Animals were sacrificed 2h after exposure for 1, 3 or 20 days as well as 6, 24 and 72h after a single-day exposure. Experiments were performed with tissues from brain and spleen, target sites for EO-induced carcinogenesis, and liver, a non-target organ. Exposure to EO resulted in time-dependent increases in N7-(2-hydroxyethyl)guanine (7-HEG) in brain, spleen, and liver and N7-(2-hydroxyethyl)valine (7-HEVal) in globin. Ethylene exposure also induced 7-HEG and 7-HEVal, but the numbers of adducts were much lower. No increase in the number of aldehydic DNA lesions, an indicator of AP sites, was detected in any of the tissues between controls and EO-, or ET-exposed animals, regardless of the duration or strength of exposure. EO exposure led to a 3-7-fold decrease in expression of 3-methyladenine-DNA glycosylase (Mpg) in brain and spleen in rats exposed to EO for 1 day. Expression of 8-oxoguanine DNA glycosylase, Mpg, AP endonuclease (Ape), polymerase @b (Pol @b) and alkylguanine methyltransferase were increased by 20-100% in livers of rats exposed to EO for 20 days. The only effects of ET on BER gene expression were observed in brain, where Ape and Pol @b expression were increased by less than 20% after 20 days of exposure to 3000ppm. These data suggest that DNA damage induced by exposure to EO is repaired without accumulation of AP sites and is associated with biologically insignificant changes in BER gene expression in target organs. We conclude that accumulation of AP sites is not a likely primary mechanism for mutagenicity and carcinogenicity of EO.
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Human AP endonuclease (APE1) demonstrates endonucleolytic activity against AP sites in single-stranded DNA [An article from: DNA Repair]
D.R. Marenstein ,
D.M. Wilson , and
G.W. Teebor
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
ASIN: B000RQZLWE |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
Human apurinic/apyrimidinic endonuclease (APE1) is an enzyme of DNA base excision repair (BER) which catalyzes endonucleolytic cleavage immediately 5' to abasic (AP) sites. APE1 has long been thought to act on AP sites only in double stranded (ds) DNA, in order to generate the appropriate site for insertion of the correct nucleotide of DNA repair synthesis effected by DNA polymerase @b. We now present evidence that APE1 also acts on AP sites in single-stranded (ss) DNA. The catalytic efficiency of this activity (defined within as k"c"a"t/Km) is ~20-fold less than the activity against AP sites in ds DNA, with the disparity stemming largely from a difference in Km. Similar to its action on AP sites in ds DNA, catalysis of endonucleolytic cleavage of ss DNA by APE1 is Mg^2^+ dependent, DNA N-glycosylase independent, and requires an active site aspartate. In contrast to its activity against AP sites in ds DNA, APE1 does not display product inhibition when acting on an AP site in ss DNA. We suggest that this novel activity is related to the processing of DNA N-glycosylase initiated BER in ss DNA perhaps during replication and/or transcription.
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Inroads into base excision repair I [An article from: DNA Repair]
T. Lindahl
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
ASIN: B000RR395O |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
DNA treated with alkylating agents is incised at sites of damage by cell extracts. A key component of this DNA repair function was shown by Verly and co-workers to be an endonuclease acting at secondary lesions, apurinic sites, rather than directly at alkylated nucleotide residues.
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The intricate structural chemistry of base excision repair machinery: Implications for DNA damage recognition, removal, and repair [An article from: DNA Repair]
K. Hitomi ,
S. Iwai , and
J.A. Tainer
Manufacturer: Elsevier
ProductGroup: Book
Binding: Digital
ASIN: B000PDU1UG |
Book Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2007. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
Three-dimensional structures of DNA N-glycosylases and N-glycosylase/apyrimidine/apurine (AP)-lyase enzymes and other critical components of base excision repair (BER) machinery including structure-specific nuclease, repair polymerase, DNA ligase, and PCNA tethering complexes reveal the overall unity of the simple cut and patch process of DNA repair for damaged bases. In general, the damage-specific excision is initiated by structurally-variable DNA glycosylases targeted to distinct base lesions. This committed excision step is followed by a subsequent damage-general processing of the resulting abasic sites and 3' termini, the insertion of the correct base by a repair DNA polymerase, and finally sealing the nicked backbone by DNA ligase. However, recent structures of protein-DNA and protein-protein complexes and other BER machinery are providing a more in-depth look into the intricate functional diversity and complexity of maintaining genomic integrity despite very high levels of constant DNA base damage from endogenous as well as environmental agents. Here we focus on key discoveries concerning BER structural biology that speak to better understanding the damage recognition, reaction mechanisms, conformational controls, coordinated handoffs, and biological activities including links to cancer. As the three-dimensional crystal and NMR structures for the protein and DNA complexes of all major components of the BER system have now been determined, we provide here a relatively complete description of the key complexes starting from DNA base damage detection and excision to the final ligation process. As our understanding of BER structural biology and the molecular basis for cancer improve, we predict that there will be multiple links joining BER enzyme mutations and cancer predispositions, such as now seen for MYH. Currently, structural results are realizing the promise that high-resolution structures provide detailed insights into how these BER proteins function to specifically recognize, remove, and repair DNA base damage without the release of toxic and mutagenic intermediates.
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- Very helpful!
- Insightful observations by thoughtful student of the game
- Provides easy to understand golf related mental tips
- Zen, existentialism, death anxiety - what else but GOLF?
- Something for All Golfers
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Golf's Mental Hazards: Overcome Them and Put an End to the Self-Destructive Round
Alan Shapiro
Manufacturer: Fireside
ProductGroup: Book
Binding: Paperback
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Zen Golf: Mastering the Mental Game
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The Golfer's Mind: Play to Play Great
ASIN: 0684804573 |
Book Description
What's Your Golf Personality?
According to Dr. Alan Shapiro, the personality traits that cause problems in your everyday life can also wreak havoc on your golf game. If you're a worrier, chances are you're also anxious at the tee. If you're a control freak, you probably overanalyze your swing and tend to freeze up over the ball. If you have a short fuse, there is a good chance you're a club thrower.
Using his experience as a psychologist and a devoted golfer, Dr. Shapiro has identified six major golf personality types or "Mental Hazards." Just take the simple, forty-eight-question quiz provided to determine your Mental Hazard Profile, then read and apply Dr. Shapiro's customized advice for overcoming the Mental Hazards that plague you on and off the course.
No matter what your handicap, the unique approach of Golf's Mental Hazards will lead to increased self-awareness and lower golf scores, finally putting an end to the self-destructive round.
Customer Reviews:
Very helpful!.......2006-03-29
The self evaluation is very insightful if you're honest with yourself.
I guess it is a little self-centered of me to think that anyone else cares where my tee shot goes. The book sure helps put things into perspective. I'm ready to read it again.
Insightful observations by thoughtful student of the game.......2002-12-06
This tightly written little gem of a book is packed full of interesting insights about the mental side of the game. Mr. Shapiro draws on material ranging from clinical psychology to zen, and from Hogan, Nicklaus & Woods to the double-digit handicappers most of us are more intimately familiar with in shaping a realistic and workable strategy for golfers of all abilities to not only get the most out of their golf games but to find more balanced lives away from the course. I highly recommend it.
Provides easy to understand golf related mental tips.......2002-09-25
This is the 3rd book on Mental Golf that I have read, and by far the best. The author provides a great test (similar to Myers-Briggs) that helps to focus on 6 areas that can be improved mentally. Each of these areas then has a chapter that has golf-related ideas (instead of some other books that provide overall life changing fixes...yuck) to get over the mental hurdles. For me, Hazard 5 (control freak) and 4 (trying to live up to other's expectations) were right on the money as far as the test scores then the anecdotes. I now have alot of new, useful golf-related ideas to try. Thanks!
Zen, existentialism, death anxiety - what else but GOLF?.......2002-01-22
One of those "little" books that turns out to be a gem of wisdom "Golf's Mental Hazards" is a book that will definitely inform your game, whether it's the game of golf or the game of life. A clincal psychologist, Dr. Shapiro employs a deft and insightful quiz to help the golfer establish his/her personality profile and then uses the profiles to point out strategies to improve the game. The book can be read as a straight "how-to" on the game of golf (and this avid duffer clearly knows and loves the game) but it also delves deeper into strategies that can inform and enhance the golfer's life when off the links, as well. Calling upon such eclectic references as Zen, Existentialist Psychology and death anxiety, Dr. Shapiro weaves together a philosophy of golf, and of living, that will expand the mind and spirit as much as it enhances the game. Delivered with both elegant insights and the rollicking style of a stand-up comic,"Golf's Mental Hazards" is a thoughtful, funny, delightful, and very helpful book, destined to become a classic in the literature of golf.
Something for All Golfers.......2001-08-10
There is something for everyone here who ever steps on the golf course. From Dr. Shapiro's simple mental profile you take to his six chapters focusing on golfers traits Dr. Shapiro will find something for everyone; even you Tiger Woods. Don't go looking for any other book to begin your journey into the mental side of golf. This is a must for every golfers library.
Average customer rating:
- The Ultimate Source
- Errata in this dictionary
- The complete dictionary
- superb dictionary
- Amazing dictionary / Not for travel
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Collins German Unabridged Dictionary 5th Edition (Harpercollins Unabridged Dictionaries)
Harpercollins Uk
Manufacturer: Collins
ProductGroup: Book
Binding: Hardcover
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German Quickly: A Grammar for Reading German
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German for Reading Knowledge
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Hammer's German Grammar and Usage
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Collins Robert French Unabridged Dictionary, 8th Edition (Harpercollins Unabridged Dictionaries)
-
The Big Yellow Book of German Verbs (Book w/CD-ROM)
ASIN: 0060733810
Release Date: 2004-09-07 |
Book Description
The
Collins German Unabridged Dictionary is simply the best German dictionary you can own. Here's why:
More than 850,000 entries and translations.
The Collins German Unabridged Dictionary gives you comprehensive coverage of both German and English and most up-to-date business, political, and technical terms. Native German and English speakers worked side by side to create a balanced treatment of both languages and to make authentic and appropriate translations.
Most consistently updated. This edition has been extensively revised and updated to cover all the vocabulary of today's German, including thousands of new phrases and indicators. In addition, the Unabridged edition includes exhaustive coverage of key words, and full treatment of irregular forms of verbs, nouns, and adjectives to create the most complete and accurate picture of real language available today.
More colloquial usage than any other German dictionary. With its emphasis on current German and English, both written and spoken, including all areas of modern life and featuring regional usage, this dictionary gives you the edge in finding the correct translations.
Customer Reviews:
The Ultimate Source.......2007-09-26
I generally use online German-English dictionaries as sources for looking up new German words while I'm performing my computer based interactive German language course. However, when these online sources give meanings that don't seem to make sense or apply (and this is becoming more apparent as my level of German language skills increase); then I refer to the Collins Unabridged German-English Dictionary, 5th Edition as the ultimate source that always has the word meaning and other helpful information that I'm looking for.
Errata in this dictionary.......2007-09-22
I was very disappointed in the dictionary. On page 502 within the blue box in the middle
it has "... träumen in ihrer Lieder ... this should be Liedern ( dative plural). Errata in other books are not so serious - but in a reference book, particularily a dictionary, a mistake like this calls into question the accuracy of the whole dictionary!!! I liked it otherwise but I feel if there is one such basic error there could be more. I have returned it to Amazon.
The complete dictionary.......2007-07-05
This is a fantastic dictionary! The incorporation of innumerable idiomatic and everyday phrases is very helpful. In addition, though this is a big dictionary, it is not as heavy as you may think. I highly recommend this lexicon to any German student at or above an intermediate level.
superb dictionary.......2007-02-15
I am a foreign language teacher and did a huge search for a German dictionary to support my self-education in German. This is the only up to date German dictionary which is easy to read and beautifully designed. The blue ink used for the words in contrast with the black ink for the text makes this dictionary very easy to use. There is a center section with very useful information, for example how to set up a business letter, an informal note, salutations and greetings, etc. It is a large book, but I am confident after my research that there is nothing better on the market which has modern updates.
Amazing dictionary / Not for travel.......2007-01-10
The wording is limitless, I work for a German company and used it while on site for mainly technical phrases. There wasn't a word that I couldn't find and that inclused a lot of slang. I will say this is not a great book for airtravel, it is gigantic and weighs about 5 lbs.
Average customer rating:
- The Best
- A Superb Series
- Yaoi at it's very best!
- kizuna
- Get this beautiful series!
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Kizuna - Bonds of Love: Book 2 (Yaoi)
Kazuma Kodaka
Manufacturer: Central Park Media - Be Beautiful
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Binding: Paperback
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Kizuna: Bonds of Love, Book 5 (Kizuna; Bonds of Love)
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Kizuna - Bonds of Love 6 (Kizuna; Bonds of Love)
ASIN: 1586649574 |
Book Description
Ranmaru and Kei were not always the perfect couple. There was a time when Ranmaru was an up-and-coming Kendo star and Kei was shy and timid scholar. What brought these two different souls together, and how did their love grow so strong? The top selling series continues to document the twists and turns of this beautiful relationship.
Customer Reviews:
The Best.......2007-03-08
This book is funny and sexy at the same time. You'll have a laugh reading it.
A Superb Series.......2006-03-08
As others have noted, Kizuna is one of the classic boys love series, and deservedly so. Characters, plot, art: it's all topnotch, and this is one of those rare manga that has something that will appeal to everyone.
Be Beautiful is to be thanked for bringing Kizuna to the English-language market, yet the translations of the first three volumes were frustratingly inconsistent and there's just no excuse for professionally published books to contain typos and misspellings. Happily, they seem to have pulled it together with Vol. 4, so you'll have nothing to distract you from the brilliance of Kodaka sensei's work.
Yaoi at it's very best!.......2006-02-24
If I could give it 6 stars I would. It is a must have for any yaoi fan. I was first introduced to this series by watching the anime years ago, and since then I've collected all the manga in Japanese. It has passion, action, attitude, and tenderness. The greatest thrill in this story comes from the slowly developing relationship with Kai and his protector, Masa.
kizuna.......2006-02-24
i heard from the interset and say that is very good and wonderful story of love.. i want to buy one and read it!!
Get this beautiful series!.......2005-07-18
Any Yaoi fan should have Kizuna. For fans who wish to purchase book 4, note that it is available in Amazon in Oct 2005 under title "Kizuna:Bond of Love" by the distributor Client Distribution Services, the new distributor engaged by the publisher "Bebeautifulmanga.com". The same goes for Embracing Love, another recommended Yaoi series.
Average customer rating:
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Kizuna - Bonds of Love: Book 2 (Yaoi)
Kazuma Kodaka
Manufacturer: Be Beautiful
ProductGroup: Book
Binding: Paperback
ASIN: B000METEDS |
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