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J Infect Dis. 2002 Oct 1;186(7):1039-42. Epub 2002 Sep 13.
Are quinolone-resistant uropathogenic Escherichia coli less virulent?

Vila J, Simon K, Ruiz J, Horcajada JP, Velasco M, Barranco M, Moreno A, Mensa J.

Servei de Microbiologia, Instiutu Clinic Infeccions i Immunologia, Hospital Clinic-IDIBAPS, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain. viledicina.ub.es

The prevalence of hemolysin, type 1 fimbriae, P fimbriae, cytotoxic necrotizing factor-1 (CNF-1), aerobactin, and autotransporter toxin (sat) was analyzed by polymerase chain reaction and phenotypic assays of 42 epidemiologically unrelated Escherichia coli strains causing acute pyelonephritis in women (21 nalidixic acid-susceptible and 21 nalidixic acid-resistant strains) and 58 E. coli strains causing cystitis in women (29 nalidixic acid-susceptible and 29 nalidixic acid-resistant strains). Hemolysin and CNF-1 were less prevalent (P<.05) in nalidixic acid-resistant than in nalidixic acid-susceptible E. coli strains from patients with either pyelonephritis (14.3% vs. 52.4%) or cystitis (0% vs. 31.0%). Among E. coli strains causing cystitis, type 1 fimbriae expression was less prevalent (P<.05) in the nalidixic acid-resistant group (55.2%) than in the nalidixic acid-susceptible group (86.2%). None of the nalidixic acid-resistant and 20.7% of the nalidixic acid-susceptible strains causing cystitis showed the proteolytic toxin Sat (P<.05). These results suggest that resistance to quinolones may be associated with a decrease in the presence or the expression of some virulence factors in uropathogenic E. coli.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12232848&dopt=Abstract



Pest Manag Sci. 2002 Sep;58(9):859-67.
Mechanisms influencing the evolution of resistance to Qo inhibitor fungicides.

Gisi U, Sierotzki H, Cook A, McCaffery A.

SYNGENTA Crop Protection, Research, Product Biology, WRO-1060, CH-4002 Basel, Switzerland. ulrich.gisyngenta.com

Fungicides inhibiting the mitochondrial respiration of plant pathogens by binding to the cytochrome bc1 enzyme complex (complex III) at the Qo site (Qo inhibitors, QoIs) were first introduced to the market in 1996. After a short time period, isolates resistant to QoIs were detected in field populations of a range of important plant pathogens including Blumeria graminis Speer f sp tritici, Sphaerotheca fuliginea (Schlecht ex Fr) Poll, Plasmopara viticola (Berk & MA Curtis ex de Bary) Berl & de Toni, Pseudoperonospora cubensis (Berk & MA Curtis) Rost, Mycosphaerella fijiensis Morelet and Venturia inaequalis (Cooke) Wint. In most cases, resistance was conferred by a point mutation in the mitochondrial cytochrome b (cyt b) gene leading to an amino-acid change from glycine to alanine at position 143 (G143A), although additional mutations and mechanisms have been claimed in a number of organisms. Transformation of sensitive protoplasts of M fijiensis with a DNA fragment of a resistant M fijiensis isolate containing the mutation yielded fully resistant transformants, demonstrating that the G143A substitution may be the most powerful transversion in the cyt b gene conferring resistance. The G143A substitution is claimed not to affect the activity of the enzyme, suggesting that resistant individuals may not suffer from a significant fitness penalty, as was demonstrated in B graminis f sp tritici. It is not known whether this observation applies also for other pathogen species expressing the G143A substitution. Since fungal cells contain a large number of mitochondria, early mitotic events in the evolution of resistance to QoIs have to be considered, such as mutation frequency (claimed to be higher in mitochondrial than nuclear DNA), intracellular proliferation of mitochondria in the heteroplasmatic cell stage, and cell to cell donation of mutated mitochondria. Since the cyt b gene is located in the mitochondrial genome, inheritance of resistance in filamentous fungi is expected to be non-Mendelian and, therefore, in most species uniparental. In the isogamous fungus B graminis f sp tritici, crosses of sensitive and resistant parents yielded cleistothecia containing either sensitive or resistant ascospores and the segregation pattern for resistance in the F1 progeny population was 1:1. In the anisogamous fungus V inaequalis, donation of resistance was maternal and the segregation ratio 1:0. In random mating populations, the sex ratio (mating type distribution) is generally assumed to be 1:1. Therefore, the overall proportion of sensitive and resistant individuals in unselected populations is expected to be 1:1. Evolution of resistance to QoIs will depend mainly on early mitotic events; the selection process for resistant mutants in populations exposed to QoI treatments may follow mechanisms similar to those described for resistance controlled by single nuclear genes in other fungicide classes. It will remain important to understand how the mitochondrial nature of QoI resistance and factors such as mutation, recombination, selection and migration might influence the evolution of QoI resistance in different plant pathogens.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12233175&dopt=Abstract [PubMed - in process]



Mycoses. 2002 Dec;45(11-12):488-91.
Fungal flora of human toe webs.

Oyeka CA, Ugwu LO.

Department of Applied Microbiology and Brewing, Faculty of Natural Sciences, Nnamdi Azikiwe University, Awka, Anambra State, Nigeria.

A total of 100 young adults (67 males and 33 females) participated in the study. Clinical evaluation showed that only 10 of the volunteers showed some scaling, fissuring and peeling of the toe webs. Four of these complained of occasional itching. Fourteen different genera of fungi were recovered from 78 of the 100 youths screened. Yeasts were recovered from 21 (27%) of the positive cases, nondermatophytes from 38 (49%) and dermatophytes from 19 (24%). Microsporum gypseum was the most commonly recovered dermatophyte. Rhizopus stolonifer and Trichosporon cutanueum were the most frequently recovered nondermatophytic mould and yeast, respectively. More males (62.8%) harboured these organisms than females (37.2%). The study further showed that human toe webs that are apparently healthy harbour a variety of fungi, that may be potential pathogens.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12472726&dopt=Abstract



Pest Manag Sci. 2002 Sep;58(9):908-16.
A non-Mendelian inheritance of resistance to strobilurin fungicides in Ustilago maydis.

Ziogas BN, Markoglou AN, Tzima A.

Laboratory of Plant Pathology, Agricultural University of Athens, Votanikos, 118 55 Athens, Greece. ziuadec.aua.gr

Mutants of Ustilago maydis (DC) Corda with high resistance to azoxystrobin (RF 164 to 4714, based on EC50 values), an inhibitor of mitochondrial electron transport at the cytochrome bc1 complex, were isolated in a mutation frequency of 2.3 x 10(-7) after nitrosoguanidine mutagenesis and selection on media containing 1 microgram ml-1 azoxystrobin in addition to 0.5 mM salicylhydroxamate (SHAM), a specific inhibitor of cyanide-resistant (alternative) respiration. Oxygen uptake in whole cells was strongly inhibited in the wild-type strains by azoxystrobin (1.5 micrograms ml-1) in addition to SHAM (1 mM), but not in the mutant isolates. Genetic analysis with nine such mutant isolates resulted in progeny phenotypes which did not follow Mendelian segregation, but satisfied the criteria of non-Mendelian (cytoplasmic) heredity. In crosses between three mutant isolates with the compatible wild-type strains, the sensitivity was inherited by progeny maternally from the wild-type parent strain (criterion of uniparental inheritance). In crosses between wild-type strains and remaining mutant isolates, a continuous distribution of sensitivity in the progeny was found (criterion of vegetative segregation). The third criterion of cytoplasmic resistance (criterion of intracellular selection) was fulfilled by experiments on the stability of resistance phenotypes. With two exceptions, a reduction of resistance was observed in the mutant strains when they were grown on inhibitor-free medium. Recovery of the high resistance level was observed after they were returned to the selection medium. Cross-resistance studies with other fungicides, which also inhibit electron transport through complex III of respiratory chain, showed that mutations for resistance to azoxystrobin were also responsible for reduced sensitivity to kresoxim-methyl (RF 18 to 1199) and to antimycin-A (RF 20 to 305), which act at the Qo and Qi sites of the cytochrome bc1 complex, respectively. Studies of the fitness of azoxystrobin-resistant isolates showed that these mutations appeared to be pleiotropic, having significant adverse effects on growth in liquid culture and pathogenicity on young corn plants.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12233180&dopt=Abstract [PubMed - in process]



Pest Manag Sci. 2002 Sep;58(9):944-50.
Phytophthora infestans: populations, pathogenicity and phenylamides.

Shattock RC.

School of Biological Sciences, University of Wales, Bangor, Gwynedd LL57 2UW, UK. r.c.shattocangor.ac.uk

Isolates of Phytophthora infestans (Mont) de Bary (the potato and tomato late blight pathogen) resistant to phenylamides appeared in Europe and North America in the late 1970s and early 1990s respectively. Concurrent, but coincidentally, with both these events there were radical structural shifts in the pathogen populations as immigrant genotypes from Mexico displaced the indigenous populations. Both A1 and A2 mating type isolates are now present in blighted crops, permitting alternative inoculum via germinating sexually produced oospores to influence dynamics of late blight populations. Studies of inheritance of ploidy, host-specific pathogenicity, mating type and resistance to antibiotics and phenylamide fungicides have provided insight into mechanisms of variation in this potent pathogen.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12233186&dopt=Abstract [PubMed - in process]








The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer an essential part of our body, just like appendix. What little hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

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