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Milk thistle||Saw palmetto||
Triple B Super Vision||Garlic, Ginger, and Grapeseed Extract||
Ginseng and Ginkgo||Hair Million||
DHEA||Coenzyme Q10||
Sleep Aid herbal formula - natural sleep aid||Herbal Breath - herbs for bad breath problems.||
Weight loss herbal formula for menopause and pms||Ginkgo biloba||
Colon cleansing, Laxative||ViaVita, Lecithin for healthy liver
Fatty acids resources:
Fatty acids research abs 1 || Fatty acids research abs 2 || Fatty acids research abs 3 || Fatty acids research abs 4 || Fatty acids research abs 5
J Neurochem. 2002 Jun;81(5):1061-72.
Transglutaminase overexpression sensitizes neuronal cell lines to apoptosis by increasing mitochondrial membrane potential and cellular oxidative stress.
Piacentini M, Farrace MG, Piredda L, Matarrese P, Ciccosanti F, Falasca L, Rodolfo C, Giammarioli AM, Verderio E, Griffin M, Malorni W.
Department of Biology, University of Rome Tor Vergata Rome, Italy.
'Tissue' transglutaminase (tTG) selectively accumulates in cells undergoing apoptosis both in vivo and in vitro. Considering the central role played by mitochondria in apoptosis, we investigated the relationships existing amongst tTG expression, apoptosis and mitochondrial function. To this aim we studied the mechanisms of apoptosis in a neuronal cell line (SK-N-BE (2)) in which the tTG-expression was driven by a constitutive promoter. Furthermore, a tet-off inducible promoter was also used in 3T3 fibroblastic cells used as control. Both cell lines, when expressing tTG, appeared 'sensitized' to apoptosis. Strikingly, we found major differences in the morphological features of mitochondria among cell lines in the absence of apoptotic stimuli. In addition, these ultrastructural characteristics were associated with specific functional features: (i) constitutively hyperpolarized mitochondria and (ii) increased reactive oxygen intermediates production. Importantly, after mitochondrial-mediated apoptosis by staurosporine, a rapid loss of mitochondrial membrane potential was found in tTG cells only. Taken together, these results seem to suggest that, via hyperpolarization, tTG might act as a 'sensitizer' towards apoptotic stimuli specifically targeted to mitochondria. These results could also be of pathogenetic relevance for those diseases that are characterized by increased tTG and apoptotic rate together with impaired mitochondrial function, e.g. in some neurodegenerative disease.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065619&dopt=Abstract
J Neurochem. 2002 May;81(4):814-9.
Modification of tyrosine hydroxylase activity by chloral derived beta-carbolines in vitro.
Riederer F, Luborzewski A, God R, Bringmann G, Scholz J, Feineis D, Moser A.
Neurochemical Research Group, Department of Neurology, Medical University of Lubeck, Ratzeburger Allee 160, D-23538 Lubeck, Germany.
Beta-carbolines have been suggested to be involved in the pathogenesis of Parkinson's disease as a result of their structural similarity to the neurotoxin N -methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The chloral-derived beta-carboline derivative 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) causes cell loss in neuronal and glial cell cultures and induces a slowly developing neurodegenerative process in rats. In our experiments, effects of TaClo and its derivatives 2-methyl-TaClo (2-Me-TaClo), and 1-dichloromethylene-1,2,3,4-tetrahydro-beta-carboline (1-CCl(2) -THbetaC) on tyrosine hydroxylase (TH) activity were investigated in TH assays using homogenate preparations of the rat nucleus accumbens and recombinant human TH (hTH1). TH activity was determined in vitro by measuring l-DOPA production with HPLC-ECD. Using homogenate preparations, TaClo, 2-Me-TaClo, and 1-CCl(2) -THbetaC inhibited TH in concentrations of 0.1 mm, while 1-CCl(2) -THbetaC in low concentrations enhanced TH activity. When TH was activated by PACAP-27, TaClo, 2-Me-TaClo, or 1-CCl(2) -THbetaC also inhibited activated enzyme activity in high concentrations. However, in the case of 2-Me-TaClo and 1-CCl(2) -THbetaC a biphasic effect was observed with a marked increase of TH activity in the nanomolar range. In our experiments using recombinant hTH1, TaClo, 2-Me-TaClo, or 1-CCl(2) -THbetaC did not modify enzyme activity. After activation of hTH1 by PKA all the tetrahydro-beta-carbolines investigated in this study decreased l-DOPA formation. We suggest that these beta-carbolines modulate dopamine synthesis by interacting with a protein kinase TH-activating system.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065640&dopt=Abstract
J Neurosurg. 2002 Nov;97(5):1212-6.
Endoscopic endonasal treatment of a spontaneous temporosphenoidal encephalocele with a detachable silicone balloon. Case report.
Alfieri A, Schettino R, Taborelli A, Pontiggia M, Reganati P, Ballarini V, Monolo L.
Department of Neurosurgery, "A. Manzoni" Hospital, Lecco, Italy. alessandralfierahoo.it
Temporosphenoidal encephaloceles are rare entities that occur when the temporal lobe herniates into the sphenoid sinus through a skull base defect of the temporal bone. Both an iatrogenic and a traumatic pathogenesis have been proposed. The authors describe a spontaneously occurring temporosphenoidal encephalocele in a 63-year-old woman who had a 4-year history of rhinorrhea. Spiral computerized tomography (CT) scanning revealed a bone defect located inside the ophthalmomaxillary triangle. The intrasphenoidal encephalocele had a heterogeneously hypointense signal compared with cerebrospinal fluid (CSF) on T1-weighted magnetic resonance (MR) images and a hyperintense signal compared with CSF on T2-weighted MR images. Two previous endonasal endoscopic procedures, performed by ear, nose, and throat surgeons, had been unsuccessful. The authors performed an endoscopic endonasal right nostril procedure by using 0 degrees and 45 degrees rigid-lens endoscopes that were 4 mm in diameter and 18 cm long. The encephalocele in the sphenoid sinus was partially removed. DuraGen and fat graft were positioned in the bone defect. Two No. 2 French detachable silicone balloons (1.5 cm3 volume) inflated with surgical glue were introduced into the skull defect and into the sphenoid sinus, respectively. The CSF leakage stopped immediately. No nasal packing or postoperative CSF lumbar drainage was necessary. The patient did well. Postoperative CT and MR imaging, obtained at 24 hours and at 3 months, demonstrated that the balloon and the fat graft filled the bone defect and the sphenoid sinus. Eight months postprocedure no CSF leakage was observed. This appears to be the first case reported in the literature of a temporosphenoidal encephalocele successfully treated by an endoscopic endonasal technique involving packing of the defect with inflated detachable balloons.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12450047&dopt=Abstract
J Neurochem. 2002 May;81(3):615-23.
Impact of endogenous nitric oxide on microglial cell energy metabolism and labile iron pool.
Chenais B, Morjani H, Drapier JC.
Institut de Chimie des Substances Naturelles, CNRS, Gif-sur-Yvette, France.
Microglial activation is common in several neurodegenerative disorders. In the present study, we used the murine BV-2 microglial cell line stimulated with gamma-interferon and lipopolysaccharide to gain new insights into the effects of endogenously produced NO on mitochondrial respiratory capacity, iron regulatory protein activity, and redox-active iron level. Using polarographic measurement of respiration of both intact and digitonin-permeabilized cells, and spectrophotometric determination of individual respiratory chain complex activity, we showed that in addition to the reversible inhibition of cytochrome-c oxidase, long-term endogenous NO production reduced complex-I and complex-II activities in an irreversible manner. As a consequence, the cellular ATP level was decreased in NO-producing cells, whereas ATPase activity was unaffected. We show that NO up-regulates RNA-binding of iron regulatory protein 1 in microglial cells, and strongly reduces the labile iron pool. Together these results point to a contribution of NO derived from inflammatory microglia to the misregulation of energy-producing reactions and iron metabolism, often associated with the pathogenesis of neurodegenerative disorders.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065670&dopt=Abstract
Lab Invest. 2002 Jun;82(6):673-86.
Mechanisms of chronic renal allograft rejection. II. Progressive allograft glomerulopathy in miniature swine.
Shimizu A, Yamada K, Sachs DH, Colvin RB.
Department of Pathology, Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02114, USA.
We have reported that in thymectomized miniature swine treated with a 12-day course of cyclosporin A that major histocompatibility complex class I-mismatched renal allografts either progress to chronic rejection (progression group; n = 4) or tolerance after acute rejection (recovery group; n = 4). Two types of glomerulopathies, termed acute and chronic allograft glomerulopathy, occur in allografts in this model. Morphological and immunohistochemical studies were performed on serial renal biopsies from both groups to examine the pathogenic mechanisms of acute and chronic allograft glomerulopathy. In acute rejection, acute allograft glomerulopathy developed in both groups by Day 18, with antibody deposition and T cell and macrophage infiltration. In situ DNA nick end-labeling (TUNEL)+ injured glomerular endothelial cells appeared from the early phase, followed by destruction of the glomerular capillary network with segmental mesangiolysis. Thereafter, in the progression group, acute allograft glomerulopathy progressed to chronic allograft glomerulopathy during the development of chronic rejection. This process was associated with persistent T cell and macrophage infiltration, antibody deposition, and TUNEL+ glomerular endothelial injury in the glomeruli. Impaired capillary repair, mesangial cell proliferation, and activation were still noted at Day 100, together with accumulation of mesangial matrix and duplication of glomerular basement membrane. In contrast, in the recovery group, acute allograft glomerulopathy recovered by Day 100, associated with the resolution of cellular infiltration and reduction of antibody deposition. We conclude that the acute and persistent cell- and antibody-mediated rejection against glomerular endothelial cells is the key pathogenic determinant of acute allograft glomerulopathy and progression toward chronic allograft glomerulopathy. Impaired capillary repair and phenotypic change of endothelial and mesangial cells also contribute to the development of chronic allograft glomerulopathy. With the development of tolerance, substantial recovery of acute allograft glomerulopathy can occur after the resolution of glomerular inflammation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12065677&dopt=Abstract
Beautiful, dense hair is a dream for many people.
Hair growth is a sophisticated biological process, which has not yet been understood.
A multitude of therapeutic measures, including drugs, surgery, and suppelements have been developed.
However, due to the diversity of the problems underlying hair loss, there is no single solution that
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Hair Million is an alternative solution to cope with hair loss problems.
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