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Natl Toxicol Program Tech Rep Ser. 1986 Oct;257:1-222.
NTP Toxicology and Carcinogenesis Studies of Diglycidyl Resorcinol Ether (Technical Grade) (CAS No. 101-90-6) In F344/N Rats and B6C3F1 Mice (Gavage Studies).

National Toxicology Program.

Diglycidyl resorcinol ether (DGRE), a pale, yellow, translucent, amorphous solid at room temperature, is used as a liquid spray epoxy resin, as a diluent in the production of other epoxy resins used in electrical, tooling, adhesive, and laminating applications, and as a curing agent for polysulfide rubber. Approximately 3,000 workers are exposed to DGRE. The quantity of DGRE produced in the United States is not known. Toxicology and carcinogenesis studies of technical grade diglycidyl resorcinol ether (81% pure) were conducted by administering the chemical in corn oil by gavage to groups of 50 male and 50 female F344/N rats at doses of 25 or 50 mg/kg and to groups of 50 male and female B6C3F1 mice at doses of 50 or 100 mg/kg. A supplemental study of similar design in male and female rats (0 or 12 mg/kg) was started approximately 12 months later because of high mortality in the 50 mg/kg dose groups. Doses were administered five times per week for 103 weeks. Groups of 50 rats and 50 mice of each sex received corn oil by gavage on the same dosing schedule and served as vehicle controls. Throughout most of the primary study, mean body weights of high dose male and female rats and female mice were lower than those of the corresponding vehicle controls. In the supplemental study, body weights of both sexes of the dosed rats were unaffected by administration of DGRE. Survival of dosed rats of each sex in the primary study was dose related and was shorter (P<0.001) than that of the vehicle controls. No high dose male rats and only 1/50 high dose female rats lived to the end of the study. Bronchopneumonia was the most frequent cause of early death among the rats and may have resulted from the animals' aspiration of corn oil containing diglycidyl resorcinol ether. Survival of the dosed male rats in the supplemental study was reduced (P<0.005) when compared to controls. There was no significant difference in survival between dosed and control female rats in the supplemental study. Survival of dosed and control mice was comparable but poorer in females, with 20/50 (40%) of the controls, 13/50 (26%) of the low dose, and 10/50 (20%) of the high dose groups alive at the end of 2 years. These early deaths were due to suppurative and necrotizing inflammation of the reproductive tract, possibly caused by a Klebsiella sp. infection. The incidences of rats and mice with hyperkeratosis and hyperplasia of the forestomach were compound related. For rats and mice of each sex, incidences of animals with squamous cell papillomas, squamous cell carcinomas, or both occurred with statistically significant positive trends and the incidences observed in other organs in dosed groups relative to the controls. An audit of the experimental data was conducted for the 2-year studies of diglycidyl resorcinol ether. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies, technical grade diglycidyl resorcinol ether caused hyperkeratosis and hyperplasia of the forestomach in rats and mice. DGRE was carcinogenic for male and female F344/N rats and for male and female B6C3F1 mice, causing both benign and malignant neoplasms of the forestomach. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Positive Female Mice: Positive Synonym: DGRE

PMID:_12748690 [PubMed - as supplied by publisher] Natl Toxicol Program Tech Rep Ser. 1986 Aug;251:1-194.
NTP Toxicology and Carcinogenesis Studies of Commercial Grade 2,4 (80%)- and 2,6 (20%)- Toluene Diisocyanate (CAS No. 26471-62-5) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

National Toxicology Program.

Toluene diisocyanate (TDI) is commercially produced as an approximate 80:20 mixture of the 2,4- and 2,6-isomers. In 1980, 580,000 pounds of this chemical were produced in the United States, primarily for use in the manufacture of flexible polyurethane foams. These foam elastomers are found in furniture and automobile cushions, carpet underlays, pillow filling, mattresses, insulation, shoes, purses, and toys. TDI is also used to produce polyurethane coatings for lacquers and wood finishes. Groups of 50 female F344/N rats and 50 B6C3F1 mice were administered commercial grade toluene diisocyanate (80% 2,4- and 20% 2,6-) in corn oil by gavage at doses of 60 or 120 mg/kg body weight, 5 days per week for 105 or 106 weeks. Groups of 50 male F344/N rats received 30 or 60 mg/kg and groups of 50 male B6C3F1 mice received 120 or 240 mg/kg on the same schedule. Dosage analyses of toluene diisocyanate indicated that the chemical had reacted in the corn oil vehicle, resulting in actual gavage concentrations 77% to 90% of theoretical values. Groups of 50 rats and 50 mice of each sex received corn oil only and served as vehicle controls. Survival in all groups of dosed rats in the 2-year studies were shorter (P</=0.005) than that of the controls; depressions of the mean body weight gain relative to controls were greater than 10% in all dosed rat groups throughout most of the study. A dose-dependent pattern of cumulative toxicity began at 70 weeks and culminated in excessive mortality, indicating the estimated tolerated dose had been exceeded for rats. Acute bronchopneumonia occurred at increased incidences in groups of dosed male and female rats (males: control, 2/50; low dose, 6/50; high dose, 14/50; females: 1/50, 10/50, 25/49). Subcutaneous tissue fibromas or fibrosarcomas (combined) in male rats occurred with a positive trend (P<0.01; 3/50, 6/50, 12/50). The incidence in the high dose group was higher than that in the controls (P</=0.01). The same tumor comparisons were significant (P<0.001) in female rats by the life table analysis. Mammary gland fibroadenomas in female rats occurred with a positive trend (P<0.001), and the incidences in low and high dose groups were significantly higher than that in controls (P</=0.01). Pancreatic acinar cell adenomas in male rats occurred with a positive trend (P<0.05; 1/47, 3/47, 7/49). The incidence in the high dose group was higher than that in the controls (P<0.05). The incidences of pancreatic islet cell adenomas in female rats were higher by the incidental tumor test (P</=0.01) in low dose (6/49) and high dose (2/47) groups than in controls (0/50). An islet cell carcinoma was also observed in a low dose female rat. The incidences of female rats with neoplastic nodules in the liver occurred with a positive trend (P<0.05; 3/50, 8/50, 8/48), and the incidence in the high dose group was higher (P<0.05) than that in the controls. Survival of high dose male mice in the 2-year study was significantly shorter than that of the controls (P<0.001). During the second year of the study, mean body weight gains of high dose male mice were less than those of the controls. Cytomegaly of kidney tubular epithelium was found in 45/48 (94%) low dose male mice and 41/50 (82%) high dose male mice but not in any of the controls. Hemangiomas or hemangiosarcomas (combined) of the circulatory system in female mice occurred with a positive trend (P</=0.01; control, 0/50; low dose, 1/50; high dose, 5/50). The incidence in the high dose group was significantly higher than that in the controls (P<0.05). Hepatocellular adenomas in female mice occurred with a positive trend (P</=0.001; 2/50, 3/50, 12/50), and the incidence in the high dose group was higher than that in the controls (P<0.01). Toluene diisocyanate was mutagenic in Salmonella typhimurium strains TA98 and TA100 in the presence (but not the absence) of Aroclor 1254-induced male Sprague-Dawley rat or male Syrian hamster liver S9; it was not mutagenic in strains TA 1535 or 1537. An audit of the experimental data for these 2-year toxicological and carcinogenicity An audit of the experimental data for these 2-year toxicological and carcinogenicity studies on commercial grade 2,4- and 2,6-toluene diisocyanate was conducted. There were no data discrepancies that influenced the final interpretations. Under the conditions of these gavage studies, commercial grade toluene diisocyanate in corn oil was carcinogenic for F344/N rats, causing subcutaneous fibromas and fibrosarcomas (combined) in males and females, pancreatic acinar cell adenomas in males, and pancreatic islet cell adenomas, neoplastic nodules of the liver, and mammary gland fibroadenomas in females. Toluene diisocyanate was not carcinogenic for male B6C3F1 mice. TDI was carcinogenic for female B6C3F1 mice, causing hemangiomas or hemangiosarcomas (combined), as well as hepatocellular adenomas. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Negative Female Mice: Positive Synonym: TDI

PMID:_12748694 [PubMed - as supplied by publisher] Natl Toxicol Program Tech Rep Ser. 1986 Jan;281:1-184.
NTP Toxicology and Carcinogenesis Studies of HC Red No. 3 [2,((Amino-2-nitrophenyl)amino)ethanol] (CAS No. 2871-01-4) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

National Toxicology Program.

oxicology and carcinogenesis studies of HC Red No. 3 (97% pure), a semipermanent hair dye, were conducted by administering the chemical in corn oil by gavage for 105 weeks to groups of 50 male and 50 female F344/N rats and for 104 weeks to groups of 50 male and 50 female B6C3F1 mice. The dosage regimen used for rats was 0, 250, or 500 mg/kg per day and for mice, 0, 125. or 250 mg/kg per day. Doses were administered 5 days per week. In prior 13-week studies, these doses produced no signs of toxicity when administered 5 days per week. In the 2-year studies, the administration of HC Red No. 3 did not affect body weight gains of male or female rats or mice. Body weight gains by all groups of female mice were reduced because of a reproductive tract infection. Survival of male and female rats and mice was not reduced by administration of HC Red No. 3. The survival of female mice, including vehicle controls, was reduced relative to historical survival rates due to a reproductive tract infection. The infection, accompanied by weight loss, high mortality, and suppurative inflammation of multiple organs, was found in 36/50 vehicle control, 32/50 low dose, and 29/50 high dose female mice. Klebsiella pneumoniae was isolated from infected tissues. Pigmentation of various tissues in both rats and mice was a common observation in both the 13-week and the 2-year studies. The pigment was not identified but was presumed to be a derivative of HC Red No. 3. Very minimal nephropathy was found in dosed female rats, but its relationship to HC Red No. 3 is equivocal. Mild nephrosis was found in dosed female mice, but this effect may have been secondary to the infection of the genital tract. There was an increase in the incidence of mammary gland fibroadenomas or cystadenomas in low dose female rats. The incidence of this lesion in high dose female rats was not increased (vehicle control, 14/50, 28%; low dose, 25/50, 50%; high dose, 11/50, 22%). Largely because of the lack of a dose response, the increased incidence in the low dose females was not considered to be due to HC Red No. 3. No increased incidences of neoplasms were seen in male rats. Transitional cell papillomas of the urinary bladder were detected in one high dose male rat, two low dose female rats, and one high dose female rat; none was observed in the vehicle controls. These uncommon neoplasms were found in animals that survived to the termination of the study and were not accompanied by other proliferative lesions. The incidence of hepatocellular adenomas or carcinomas (combined) was increased in high dose male mice, whereas the incidence of these neoplasms in low dose male mice was significantly lower than that in the vehicle controls (25/50; 15/50; 35/50). Hepatocellular carcinomas in three vehicle control, one low dose, and five high dose male mice metastasized to the lung. The incidences of liver neoplasms in dosed female mice were not significantly different from those in the vehicle control group. HC Red No. 3 was mutagenic in Salmonella typhimurium strains TA97, TA98, and TA100, but not in TA1535, in the presence or absence of Aroclor 1254-induced male Sprague-Dawley rat or male Syrian hamster liver S9 when tested by the preincubational protocol. An audit of the experimental data was conducted for these 2-year toxicology and carcinogenesis studies on HC Red No. 3. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year gavage studies of HC Red No. 3, there was no evidence of carcinogenicity for male or female F344/N rats given 250 or 500 mg/kg per day. There was equivocal evidence of carcinogenicity for male B6C3F1 mice as indicated by an increased incidence of hepatocellular adenomas or carcinomas (combined) in the 250 mg/kg dose group. Poor survival coupled with lack of significant findings rendered the study in female B6C3F1 mice an inadequate study of carcinogenicity. Both sexes of both species may have been able to tolerate higher doses of HC Red No. 3. Therefore, the sensitivity of these studies for detecting chese studies for detecting carcinogenesis may have been limited. Synonym: 2,((amino-2-nitrophenyl)amino)ethanol

PMID:_12748698 [PubMed - as supplied by publisher] Natl Toxicol Program Tech Rep Ser. 1985 Nov;287:1-180.
NTP Toxicology and Carcinogenesis Studies of Dimethyl Hydrogen Phosphite (CAS No. 868-85-9) in F344/N Rats and B6C3F1 Mice (Gavage Studies).

National Toxicology Program.

Dimethyl hydrogen phosphite (DMHP) is used as an intermediate in the production of insecticides and herbicides, as an additive to lubricants, and as a stabilizer in oil and plaster and was considered for use as a chemical to simulate the physical (but not the biologic) properties of anticholinesterase agents. Results of 13-week gavage studies in F344/N rats (0-400 mg DMHP/kg body weight) and in B6C3F1 mice (0-1,500 mg DMHP/kg body weight) were used to identify short-term toxicity and to establish doses for the 2-year toxicology and carcinogenesis studies. In these studies, dimethyl hydrogen phosphite (greater than 97% pure) was administered for 103 weeks in corn oil by gavage to groups of 50 male F344/N rats and to groups of 50 male and female B6C3F1 mice at doses of 0, 100, or 200 mg/kg and to groups of 50 female F344/N rats at doses of 0, 50, or 100 mg/kg. In the 2-year studies, survival of high dose male rats and high dose male mice was lower (P<0.05) than that of the vehicle controls (male rats: vehicle control, 39/50; low dose, 29/50; high dose, 23/50; male mice: 42/50; 34/50; 32/50). At the end of the studies, mean body weights were lower than those of the corresponding vehicle controls for high dose male rats (-15%), for high dose female rats (-5%), and for high dose male mice (-5%). Dimethyl hydrogen phosphite caused dose-related increases in nonneoplastic and neoplastic lesions of the lung in male and female rats. In high dose male rats, there were increased incidences of lung neoplasms, including squamous cell carcinomas (0/50; 0/50; 5/50), alveolar/bronchiolar adenomas (0/50; 0/50; 5/50), and alveolar/bronchiolar carcinomas (0/50; 1/50; 20/50). In high dose female rats, there was a marginal increase in the incidence of alveolar/bronchiolar carcinomas of the lung (0/50; 1/49; 3/50). Hyperplasia of the lung and chronic interstitial pneumonia were increased in dosed male rats and in high dose female rats. Dimethyl hydrogen phosphite caused increases in forestomach lesions in male and female rats. In male rats, there was an increased incidence of forestomach neoplasms, including squamous cell papillomas (0/50; 1/50; 3/50) and squamous cell carcinomas (0/50; 0/50; 3/50). High dose male rats had increased incidences of hyperkeratosis and hyperplasia of the forestomach. In high dose female rats, the incidence of forestomach hyperplasia was increased. Neoplastic lesions of the forestomach (a squamous cell papilloma and a squamous cell carcinoma) were found in two high dose female rats. Mineralization of the cerebellum was seen in high dose male rats (12/49) and in no other group. Focal calcification of the testis occurred at increased incidence in dosed male mice in the 2-year studies (2/50; 9/47; 24/50). Compound-related testicular atrophy was seen in male mice in the 13-week study. Dimethyl hydrogen phosphite did not induce any neoplasms in male or female mice. Dimethyl hydrogen phosphite was not mutagenic in Salmonella typhimurium strains TA98, TA100, TA1535, or TA1537 in the presence or absence of Aroclor 1254-induced male Sprague-Dawley rat or Syrian hamster liver S9. This chemical did not induce sex-linked recessive lethal mutations in Drosophila melanogaster. An audit of the experimental data was conducted for these carcinogenic studies on dimethyl hydrogen phosphite. No data discrepancies were found that influenced the final interpretations. Under the conditions of these gavage studies, there was clear evidence of carcinogenicity in male rats receiving dimethyl hydrogen phosphite, as shown by increased incidences of alveolar/bronchiolar adenomas, alveolar/bronchiolar carcinomas, and squamous cell carcinomas of the lung and of neoplasms of the forestomach. There was equivocal evidence of carcinogenicity in female F344/N rats receiving dimethyl hydrogen phosphite, as shown by marginally increased incidences of alveolar/bronchiolar carcinomas of the lung and of neoplasms of the stomach. There was no evidence of carcinogenicity in male or female B6C3F1 mice receiving dimethyl hydrogen phosphite at doses of 100 ogen phosphite at doses of 100 or 200 mg/kg for 103 weeks. Synonyms: phosphonic acid, dimethyl ester (9CI); dimethyl phosphite; dimethyl phosphorus acid; methyl phosphonate; dimethyl phosphonate; dimethoxyphosphine oxide; TL 585; DMHP; phosphorous acid, dimethyl ester; dimethylphosphite; dimethyl phosphonate; dimethylphosphorous acid; bis(hydroxymethyl) phosphine oxide

PMID:_12748716 [PubMed - as supplied by publisher] Am J Trop Med Hyg. 2003 Apr;68(4 Suppl):30-7.
Comparison of government statistics and demographic surveillance to monitor mortality in children less than five years old in rural western Kenya.

Arudo J, Gimnig JE, ter Kuile FO, Kachur SP, Slutsker L, Kolczak MS, Hawley WA, Orago AS, Nahlen BL, Phillips-Howard PA.

Centre for Vector Biology and Control Research, Kenya Medical Research Institute, Centers for Disease Control and Prevention, Kisumu, Kenya.

Estimates of mortality in children less than five years old using government civil registration statistics (passive surveillance) were compared against statistics generated by active demographic surveillance during a randomized controlled trial of permethrin-treated bed nets (ITNs) in western Kenya. Mortality rates were two-fold lower when estimated through civil registration compared with active prospective surveillance (rate ratio [RR] = 0.51, 95% confidence interval [CI] = 0.44-0.59). While civil registration underestimated deaths, particularly in the neonatal period, the age distribution of deaths in children 1-59 months of age was the same as with active surveillance. Seasonal mortality trends were also similar. There was no agreement between cause of death recorded by active and passive surveillance. Verbal autopsy estimated that half of all deaths were associated with malaria and pneumonia, but civil registration markedly under-reported these illnesses; incidence RR (95% CI) = 0.18 (0.14-0.24), and 0.05 (0.03-0.08), respectively, while over-reporting deaths due to measles (RR = 15.5 [95% CI = 7.3-33.2]). Government statistics under-represent mortality, particularly neonatal mortality, in children less than five years of age in rural areas of Kenya. They can provide accurate information on the age-distribution of deaths among children 1-59 months old, and on seasonal trends, but not on disease-specific mortality.

PMID:_12749483

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