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Chemical Compound Review

AC1NRATB     (2S)-2-amino-3- (dimethylcarbamoyl)propanoi...

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Disease relevance of DMH

  • In this investigation we found the addition of 0.5 or 0.1% semipurified BBI or 0.1% purified BBI to the diet of DMH-treated mice resulted in a statistically significant suppression of angiosarcomas and nodular hyperplasia of the liver and adenomatous tumors of the gastrointestinal tract [1].
  • In addition, we used a cell-mediated mutagenesis assay to test rat colon epithelial cells grown from tissue explants for their ability to metabolize DMH into products mutagenic for human P3 teratoma cells [2].
  • Precipitation tests using properly absorbed rabbit antisera revealed that PCA extracts of DMH-induced rat jejunal and colonic adenocarcinomas contain an antigen that is not detectable in extracts of normal rat tissue or other rat tumors [3].
  • At 12 mo, glomerular hypertension persisted in DMC and DMH rats but was still absent in DME rats [4].
  • Progressive albuminuria occurred in DMC and DMH but not in DME rats [4].

Psychiatry related information on DMH

  • DMH and VMH lesions significantly advanced the onset of maternal behavior (5-6 days vs. 0-1 day before parturition) in first-time pregnant rats [5].
  • Consistently, food deprivation lowered, while refeeding normalized endogenous cAMP content in DMH and VMH, but not in LH areas [6].
  • Those people who had previously been patients of the Department of Mental Health of Missouri who died in the three year period 1972 through 1974 and whose deaths were designated as suicide or "undetermined whether purposely or accidentally inflicted," were identified by matching statewide death tapes against the DMH data base [7].

High impact information on DMH

  • Our results indicate that the colon itself contains epithelial cell types capable of effectively converting DMH into mutagenic (and presumably carcinogenic) products without necessarily involving intermediary metabolism by hepatocytes as previously thought [2].
  • Cocultivation of the colon cells with the P3 cells in the cell-mediated assay resulted in mutagenesis, whereas in the absence of the colon cells, no mutagenesis by DMH was observed [2].
  • From this work, we conclude that the majority of inputs to the DMH arise in the hypothalamus, although there are a few significant projections from the telencephalon and brainstem [8].
  • Ascending inputs arrive through a midbrain periventricular pathway that travels adjacent to the cerebral aqueduct in the periaqueductal gray, and through a brainstem lateral pathway that travels through central and ventral midbrain tegmental fields and enters the hypothalamus, and then the DMH from more lateral parts of the medial forebrain bundle [8].
  • Leptin treatment significantly reduced NPY concentrations by 20-50% (P < 0.05) in the ARC, PVN, and DMH and significantly decreased hypothalamic NPY mRNA levels (0.61 +/- 0.02 vs. 0.78 +/- 0.03 arbitrary units; P < 0.01) [9].

Chemical compound and disease context of DMH

  • The effect of Se treatment on DMH-induced large-bowel carcinogenesis confirms previous findings and proves that the opposite effect on fibroadenoma development is not due to differences in e.g. effective dose, animal strains or condition of the animals [10].
  • Influence of dietary cis and trans fats on DMH-induced colon tumors, steroid excretion, and eicosanoid production in rats prone to colon cancer [11].
  • The objective of the present study was to determine if neurotoxic lesions of the dorsomedial (DMH) and ventromedial nuclei (VMH) of the hypothalamus will advance the onset of maternal behavior in primigravid rats [5].
  • The animals were given weekly injections of N,N'-dimethylhydrazine (DMH, 10 mg/kg body weight) for the initial 10 weeks to induce colon carcinogenesis, and then fed on diet with or without 5% MAK for 10 weeks [12].
  • Luteolin (0.2 mg/kg body weight/everyday p.o.) was given to the DMH-treated rats at the initiation and post-initiation stages of carcinogenesis [13].

Biological context of DMH


Anatomical context of DMH

  • With few exceptions, each major nucleus and area of the hypothalamus provides inputs to the DMH [8].
  • RIA data indicated that both orexin A and orexin B peptide levels were significantly elevated (45-54%; P < 0.01) in the dorsomedial nucleus (DMH) of the nicotine-treated rats compared with either solvent-only or pair-fed controls [17].
  • Normal and DMH-treated male rats aged 18-20 weeks underwent surgical transection and anastomosis of the transverse colon [15].
  • We found double-labeled neurons surrounding the median eminence and in the RCA, Arc, VMH, DMH, and PMV [18].
  • A similar leukocyte migration pattern was seen after i.p. injection of the alkali-insoluble fraction (F1) from DYH (F1Y) and F1 from DMH (F1M) this being more active than former [19].

Associations of DMH with other chemical compounds

  • Unlike previous studies, that have used relatively short-term (2-5 weeks) treatment with one of the alkylating agents 1,2,-dimethylhydrazine (DMH) or azoxymethane, we have investigated the mutational spectrum of the beta-catenin gene in a panel of rat colon tumors induced by long-term (20 weeks) DMH-treatment [20].
  • These results indicate that both NMDA and non-NMDA glutamate receptors in the RPa play a significant role in mediating the excitatory synaptic transmission producing the activation of BAT thermogenesis following disinhibition of DMH neurons [21].
  • 4. LT seems to be the principal mediator of leukocyte migration in response to LYH, DYH or DMH or to beta-glucan [19].
  • By using double-labeling immunohistochemistry or immunohistochemistry coupled with in situ hybridization, leptin-activated neurons were found that contained cocaine- and amphetamine-regulated transcript mRNA in several hypothalamic nuclei, including the RCA, Arc, DMH, and PMV [18].
  • In experiment 1, male 6-week-old F344 rats were administered N,N'-dimethylhydrazine (DMH) 20 mg/kg s.c. once a week 4 times [22].

Gene context of DMH


Analytical, diagnostic and therapeutic context of DMH


  1. Suppression of dimethylhydrazine-induced carcinogenesis in mice by dietary addition of the Bowman-Birk protease inhibitor. St Clair, W.H., Billings, P.C., Carew, J.A., Keller-McGandy, C., Newberne, P., Kennedy, A.R. Cancer Res. (1990) [Pubmed]
  2. Activation of the colon carcinogen 1,2-dimethylhydrazine in a rat colon cell-mediated mutagenesis assay. Oravec, C.T., Jones, C.A., Huberman, E. Cancer Res. (1986) [Pubmed]
  3. A thermostable antigen characteristic for carcinogen-induced rat intestinal tumors. Abeyounis, C.J., Milgrom, F. J. Immunol. (1976) [Pubmed]
  4. Glomerular abnormalities in long-term experimental diabetes. Role of hemodynamic and nonhemodynamic factors and effects of antihypertensive therapy. Fujihara, C.K., Padilha, R.M., Zatz, R. Diabetes (1992) [Pubmed]
  5. Disinhibition of maternal behavior following neurotoxic lesions of the hypothalamus in primigravid rats. Mann, P.E., Babb, J.A. Brain Res. (2004) [Pubmed]
  6. Hypothalamic administration of cAMP agonist/PKA activator inhibits both schedule feeding and NPY-induced feeding in rats. Sheriff, S., Chance, W.T., Iqbal, S., Rizvi, T.A., Xiao, C., Kasckow, J.W., Balasubramaniam, A. Peptides (2003) [Pubmed]
  7. A comparison of suicide and undetermined deaths in psychiatric patients. Nuttall, E.A., Evenson, R.C., Cho, D.W. Suicide & life-threatening behavior. (1980) [Pubmed]
  8. Organization of inputs to the dorsomedial nucleus of the hypothalamus: a reexamination with Fluorogold and PHAL in the rat. Thompson, R.H., Swanson, L.W. Brain Res. Brain Res. Rev. (1998) [Pubmed]
  9. Interactions between leptin and hypothalamic neuropeptide Y neurons in the control of food intake and energy homeostasis in the rat. Wang, Q., Bing, C., Al-Barazanji, K., Mossakowaska, D.E., Wang, X.M., McBay, D.L., Neville, W.A., Taddayon, M., Pickavance, L., Dryden, S., Thomas, M.E., McHale, M.T., Gloyer, I.S., Wilson, S., Buckingham, R., Arch, J.R., Trayhurn, P., Williams, G. Diabetes (1997) [Pubmed]
  10. Effect of selenium on the induction of breast fibroadenomas by adenovirus type 9 and 1,2-dimethylhydrazine-induced bowel carcinogenesis in rats. Ankerst, J., Sjögren, H.O. Int. J. Cancer (1982) [Pubmed]
  11. Influence of dietary cis and trans fats on DMH-induced colon tumors, steroid excretion, and eicosanoid production in rats prone to colon cancer. Sugano, M., Watanabe, M., Yoshida, K., Tomioka, M., Miyamoto, M., Kritchevsky, D. Nutrition and cancer. (1989) [Pubmed]
  12. Prevention of development of N,N'-dimethylhydrazine-induced colon tumors by a water-soluble extract from cultured medium of Ganoderma lucidum (Rei-shi) mycelia in male ICR mice. Lu, H., Kyo, E., Uesaka, T., Katoh, O., Watanabe, H. Int. J. Mol. Med. (2002) [Pubmed]
  13. Rat colonic lipid peroxidation and antioxidant status: the effects of dietary luteolin on 1,2-dimethylhydrazine challenge. Manju, V., Balasubramaniyan, V., Nalini, N. Cell. Mol. Biol. Lett. (2005) [Pubmed]
  14. Non-steroidal anti-inflammatory drugs with activity against either cyclooxygenase 1 or cyclooxygenase 2 inhibit colorectal cancer in a DMH rodent model by inducing apoptosis and inhibiting cell proliferation. Brown, W.A., Skinner, S.A., Malcontenti-Wilson, C., Vogiagis, D., O'Brien, P.E. Gut (2001) [Pubmed]
  15. The influence of surgical transection and anastomosis on the rate of cell proliferation in the colonic epithelium of normal and DMH-treated rats. Barkla, D.H., Tutton, P.M. Carcinogenesis (1983) [Pubmed]
  16. Cardiovascular regulation through hypothalamic GABA(A) receptors in a genetic absence epilepsy model in rat. Aker, R.G., Onat, F.Y. Epilepsia (2002) [Pubmed]
  17. Nicotine up-regulates expression of orexin and its receptors in rat brain. Kane, J.K., Parker, S.L., Matta, S.G., Fu, Y., Sharp, B.M., Li, M.D. Endocrinology (2000) [Pubmed]
  18. Chemical characterization of leptin-activated neurons in the rat brain. Elias, C.F., Kelly, J.F., Lee, C.E., Ahima, R.S., Drucker, D.J., Saper, C.B., Elmquist, J.K. J. Comp. Neurol. (2000) [Pubmed]
  19. Leukotrienes are involved in leukocyte recruitment induced by live Histoplasma capsulatum or by the beta-glucan present in their cell wall. Medeiros, A.I., Silva, C.L., Malheiro, A., Maffei, C.M., Faccioli, L.H. Br. J. Pharmacol. (1999) [Pubmed]
  20. Predominant mutation of codon 41 of the beta-catenin proto-oncogene in rat colon tumors induced by 1,2-dimethylhydrazine using a complete carcinogenic protocol. Koesters, R., Hans, M.A., Benner, A., Prosst, R., Boehm, J., Gahlen, J., Doeberitz, M.K. Carcinogenesis (2001) [Pubmed]
  21. Glutamate receptors in the raphe pallidus mediate brown adipose tissue thermogenesis evoked by activation of dorsomedial hypothalamic neurons. Cao, W.H., Morrison, S.F. Neuropharmacology (2006) [Pubmed]
  22. Inhibition of development of N,N'-dimethylhydrazine-induced rat colonic aberrant crypt foci by pre, post and simultaneous treatments with 24R,25-dihydroxyvitamin D3. Salim, E.I., Wanibuchi, H., Taniyama, T., Yano, Y., Morimura, K., Yamamoto, S., Otani, S., Nishizawa, Y., Morii, H., Fukushima, S. Jpn. J. Cancer Res. (1997) [Pubmed]
  23. Evidence of altered hypothalamic pro-opiomelanocortin/ neuropeptide Y mRNA expression in tubby mice. Guan, X.M., Yu, H., Van der Ploeg, L.H. Brain Res. Mol. Brain Res. (1998) [Pubmed]
  24. Chemopreventive potential of luteolin during colon carcinogenesis induced by 1,2-dimethylhydrazine. Manju, V., Nalini, N. Ital. J. Biochem. (2005) [Pubmed]
  25. Induction of neuropeptide Y expression in dorsomedial hypothalamus of diet-induced obese mice. Guan, X.M., Yu, H., Trumbauer, M., Frazier, E., Van der Ploeg, L.H., Chen, H. Neuroreport (1998) [Pubmed]
  26. Bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione (a curcumin analog) ameliorates DMH-induced hepatic oxidative stress during colon carcinogenesis. Devasena, T., Rajasekaran, K.N., Menon, V.P. Pharmacol. Res. (2002) [Pubmed]
  27. Comparison of 7-medG formation in white blood cells, liver and target organs in rats treated with methylating carcinogens. Bianchini, F., Wild, C.P. Carcinogenesis (1994) [Pubmed]
  28. The role of amygdala and hypothalamus in GABAA antagonist bicuculline-induced cardiovascular responses in conscious rats. Gören, Z., Aslan, N., Berkman, K., Oktay, S., Onat, F. Brain Res. (1996) [Pubmed]
  29. An assessment of the risk of neoplasia in long-term ileal reservoirs using the DMH rodent model. Heppell, J., De Zubiria, M., Brais, M.F., Durh, M.A., Carioto, S., Boivin, Y., Potvin, C. Dis. Colon Rectum (1990) [Pubmed]
  30. Changes in cell proliferation and morphology in the large intestine of normal and DMH-treated rats following colostomy. Barkla, D.H., Tutton, P.J. Dis. Colon Rectum (1987) [Pubmed]
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