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Phase II study of radiochemotherapy with vinblastine in
invasive bladder cancer.
Kragelj B, Zaletel-Kragelj L, Sedmak B, Cufer T, Cervek J.
Department of Radiation Therapy, Institute of Oncology, Ljubljana, Slovenia.
Concurrent vinablastine-based radiochemotherapy was evaluated in 84
bladder-cancer patients. It was effective in more than half: tumour-specific
survival (51% 9-year), local control rate (55% 9-year). The drawback was the
impaired function of the bladder (9-year prevalence SOMA G3-4 symptoms: 66%),
indicating the need for treatment aimed at reducing chronic morbidity.
Hair cycle-specific expression of versican in human hair
follicles.
Soma T, Tajima M, Kishimoto J.
Shiseido Life Science Research Center, 2-12-1 Fukuura, Kanazawa-ku, Yokohama
236-8643, Japan.
BACKGROUND:: Versican, a large chondroitin sulfate proteoglycan molecule, is
implicated in the induction of hair morphogenesis, the initiation of hair
regeneration, and the maintenance of hair growth in mouse species. In contrast,
in human hair follicles, the distribution and the roles of versican remains
obscure. OBJECTIVES:: To elucidate the implication of versican in normal human
hair growth. METHODS:: Versican expression was examined by in situ hybridization
(mRNA) and immunohistochemistry (protein). RESULTS:: The results clearly showed
specific versican gene expression in the dermal papilla of anagen, which
apparently decreased in the dermal papilla of catagen hair follicles. No
specific signal was detectable in telogen hair follicles. Consistent with ISH
results, versican immunoreactivity was extended over the dermal papilla of
anagen hair follicles, and again, this staining diminished in the catagen phase
of human hair follicles. Interestingly, versican proteins were deposited outside
K15-positive epithelial cells in the bulge throughout the hair cycle. Versican
immunoreactivity in the dermal papilla was almost lost in vellus-like hair
follicles affected by male pattern baldness. CONCLUSION:: Specific expression of
versican in the anagen hair follicles suggests its importance to maintain the
normal growing phase of human as well as mouse.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15871917&query_hl=1
Occlusal forces promote periodontal healing of transplanted
teeth with enhanced nitric oxide synthesis.
Chen CC, Kanno
Z, Soma K.
Graduate Student, Orthodontic Science, Department of
Orofacial Development and Function, Division of Oral Health Science, Graduate
School, Tokyo Medical and Dental University, Japan. chenorts@tmd.ac.jp
It
has been reported that occlusal forces promote periodontal healing of
transplanted teeth and prevent dentoalveolar ankylosis, although its mechanism
is still unclear. Nitric oxide (NO) produced by NO synthase (NOS) is considered
to be an important factor which is involved in wound healing, and it increases
with mechanical stimuli. The objective of this study was to examine the
relationship among occlusal stimuli, inducible NOS (iNOS) and PDL healing of
transplanted teeth. Five-week-old Sprague-Dawley male rats were used for this
study. The right maxillary first molars of rats were replanted and animals were
divided into occluded and non-occluded groups. Histologic observations were
carried out after one and two weeks. After two weeks, the non-occluded group had
clearly detectable ankylosis and obvious PDL stricture. On the other hand, the
occluded group showed an enlarged and thickened PDL without ankylosis. The
number of iNOS positive cells in the occluded group, samples significantly
increased in comparison to that of the non-occluded group. These results suggest
that occlusal stimuli enhanced the production of NO in the PDL healing process
of transplanted teeth and a favorable result could be obtained.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15868742&query_hl=1
Expression of novel keratin associated protein 5 genes in the
cuticle layer of human hair follicles.
Soma T, Iino M,
Tajima M, Kishimoto J.
Shiseido Life Science Research Center, 2-12-1
Fukuura, Kanazawa-ku, Yokohama 236-8643, Japan.
Publication Types:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15862944&query_hl=1
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