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J Pharmacol Exp Ther. 2002 Oct;303(1):232-7.
Angiotensin-converting enzyme inhibitor-associated angioedema is characterized by a slower degradation of des-arginine(9)-bradykinin.

Molinaro G, Cugno M, Perez M, Lepage Y, Gervais N, Agostoni A, Adam A.

Faculte de Pharmacie, Departement de Mathematiques et de Statistique, Universite de Montreal, Canada.

Angioedema (AE) is a rare but potentially life-threatening side effect of therapy with inhibitors of angiotensin-converting enzyme (ACE), the main bradykinin (BK)- inactivating metallopeptidase in humans. The pathogenesis of ACE inhibitor (ACEi)- associated AE (AE+) is presently unknown, although there is increasing evidence of a kinin role. We analyzed the metabolism of endogenous BK (B(2) receptor agonist) and its active metabolite, des-Arg(9)-BK (B(1) receptor agonist), in the presence of an ACEi during in vitro contact activation of plasma from hypertensive patients (n = 39) who presented AE+. Kinetic parameters were compared with those measured in a control group (AE-) of hypertensive patients (n = 39) who never manifested any acute or chronic side effects while treated with an ACEi. The different kinetic parameters were analyzed using a mathematical model (y = k t(alpha) e(-beta t)) previously applied to a normal, healthy population. The slope of BK degradation, but not its formation from high-molecular-weight kininogen, was lower in AE+ patients when compared with the AE- controls. des-Arg(9)-BK accumulation during the kinetic measurements was significantly higher in AE+ plasma. This accumulation of the B(1) agonist in AE+ patients paralleled its half-life of degradation. In conclusion, our results show, for the first time, that an abnormality of endogenous des-Arg(9)-BK degradation exists in the plasma of patients with ACEi-associated AE, suggesting that its pathogenetic mechanism lies in the catabolic site of kinin metabolism.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235256&dopt=Abstract



Proc Natl Acad Sci U S A. 2002 Oct 1;99(20):13284-9. Epub 2002 Sep 16.
Familial hemiplegic migraine mutations increase Ca(2+) influx through single human CaV2.1 channels and decrease maximal CaV2.1 current density in neurons.

Tottene A, Fellin T, Pagnutti S, Luvisetto S, Striessnig J, Fletcher C, Pietrobon D.

Department of Biomedical Sciences, University of Padova, 35121 Padova, Italy.

Insights into the pathogenesis of migraine with aura may be gained from a study of human Ca(V)2.1 channels containing mutations linked to familial hemiplegic migraine (FHM). Here, we extend the previous single-channel analysis to human Ca(V)2.1 channels containing mutation V1457L. This mutation increased the channel open probability by shifting its activation to more negative voltages and reduced both the unitary conductance and the density of functional channels in the membrane. To investigate the possibility of changes in Ca(V)2.1 function common to all FHM mutations, we calculated the product of single-channel current and open probability as a measure of Ca(2+) influx through single Ca(V)2.1 channels. All five FHM mutants analyzed showed a single-channel Ca(2+) influx larger than wild type in a broad voltage range around the threshold of activation. We also expressed the FHM mutants in cerebellar granule cells from Ca(V)2.1alpha(1)-/- mice rather than HEK293 cells. The FHM mutations invariably led to a decrease of the maximal Ca(V)2.1 current density in neurons. Current densities were similar to wild type at lower voltages because of the negatively shifted activation of FHM mutants. Our data show that mutational changes of functional channel densities can be different in different cell types, and they uncover two functional effects common to all FHM mutations analyzed: increase of single-channel Ca(2+) influx and decrease of maximal Ca(V)2.1 current density in neurons. We discuss the relevance of these findings for the pathogenesis of migraine with aura.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235360&dopt=Abstract



Schmerz. 2002 Sep;16(5):404-11.
[Neurosurgical therapy of facial neuralgias]

[Article in German]

Tronnier VM, Rasche D, Hamer J, Kunze S.

Neurochirurgische Universitatsklinik Heidelberg, Germany.

INTRODUCTION: Neuralgias of the face, especially trigeminal neuralgia and glossopharyngeal neuralgia are indications for surgical interventions after failed medical therapy. In contrast to other forms of headache or atypical facial pain, where surgical measures are considered to be contraindicated, percutaneous procedures or microvascular decompression are able to produce immediate and longstanding pain relief. Careful preoperative evaluation is essential to confirm the clinical diagnosis and to rule out other causes as multiple sclerosis or tumors afflicting the cranial nerves. The following study will summarize the common surgical techniques and their role considering a mechanism-based therapy as well as document long-term results of these measures. METHODS: Between 1977 and 1997 316 thermo-controlled radiofrequency trigeminal rhizotomies (TK) and 379 microvascular decompressions (MVD) were performed in our hospital to treat trigeminal neuralgia; additional 6 MVDs for glossopharyngeal neuralgia and one MVD of the intermediate facial nerve were carried out. Questionnaires were sent out to all patients still living in 1981, 1982, 1992 and 1998. For all other patients, interviews with relatives or the general practitioners were conducted. A retrospective analysis of postoperative pain relief was performed using Kaplan-Meier curves at the latest follow-up. Additionally 80 patients underwent careful quantitative sensory testing with Von-Frey-hairs. RESULTS: 225 patients who underwent microvascular decompression and 206 with radiofrequency trigeminal rhizotomies were further analyzed. There was a 50% risk for pain recurrence two years after radiofrequency rhizotomy. On the other hand 64% of patients who underwent microvascular decompression remained painfree 20 years postoperatively. Patients with microvascular decompression without sensory deficit were painfree significantly longer than patients with postoperative hypesthesia. DISCUSSION: Etiology and pathogenesis of facial neuralgias are far from understood despite several hypotheses. Based on current models there is no explanation for the immediate pain relief especially after microvascular decompression. Some authors even discuss surgical trauma as the only cause for postoperative pain relief.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235505&dopt=Abstract



Eur Arch Otorhinolaryngol. 2002 Sep;259(8):413-8. Epub 2002 Jun 25.
Immunolocalization of inducible nitric oxide synthase and 3-nitrotyrosine in recurrently inflamed, human palatine tonsils.

Wang HW, Su WF, Lin YS, Kang BH.

Department of Otolaryngology, Tri-Service General Hospital, 325, Section 2, Cheng-Gung Road, Taipei, Taiwan 114, R.O.C.

The purpose of this study was to evaluate the possible involvement of nitric oxide and its toxic metabolite--peroxynitrite--in the pathogenesis of recurrent tonsillitis. Tonsil specimens with recurrent inflammation were obtained from patients who required tonsillectomies as surgical treatment for their conditions. The relatively normal tonsils were obtained from patients who underwent uvulo-palato-pharyngoplasty for habitual snoring or obstructive sleep apnea. The sites of inducible nitric oxide synthase (iNOS) expression in the tonsil specimens were examined with an immunohistochemical technique. The possible production of peroxynitrite was evaluated by immunolabeling of 3-nitrotyrosine (3-NT) as its biological footprint. Each section was given a score of 0 to 4 according to the labeling intensity seen, with the highest number representing the highest labeling intensity. We found that tonsils with recurrent inflammation had iNOS expression mainly in the mucosal epithelium, subepithelial regions and vascular endothelium. The parenchyma of the tonsils, where T- and B-cell clones are located, showed little iNOS immunoreactivity. The accumulation of 3-NT had a similar distribution pattern to that of iNOS expression. However, the normal tonsils showed limited iNOS expression on mucosal epithelium and rare 3-NT accumulation. Recurrently inflamed tonsils had significantly higher labeling scores for both iNOS and 3-NT compared to normal tonsils. Further, a higher iNOS score correlated with a higher 3-NT accumulation. These data suggest that iNOS expression and the formation of peroxynitrite may have an important role in the pathogenesis of recurrent tonsillitis.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235514&dopt=Abstract



Bone Marrow Transplant. 2002 Sep;30(6):375-80.
Macrophage migratory inhibitory factor (MIF) expression in acute graft-versus-host disease (GVHD) in allogeneic hemopoietic stem cell transplant recipients.

Lo JW, Leung AY, Huang XR, Lie AK, Metz C, Bucala R, Liang R, Lan HY.

Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong.

Graft-versus-host disease (GVHD) is a major complication after hemopoietic stem cell transplantation (HSCT), but its pathogenesis remains uncertain. Macrophage migratory inhibitory factor (MIF) is an important mediator in the allo-immune reaction during renal transplantation, yet its role in hemopoietic stem cell transplantation (HSCT) remains unexplored. This study investigated the potential role of MIF in acute graft-versus-host disease (aGVHD) following allogeneic HSCT. Forty-six randomly selected patients undergoing autologous or allogeneic HSCT were studied. Immunohistochemistry and in situ hybridization were performed to examine tissue MIF mRNA and protein expression on skin and colonic biopsy specimens. The associated T cell and macrophage activation was also studied by immunohistochemical studies. A semi-quantitative method was used to assess MIF staining, as well as T cell and macrophage staining. Serial blood samples were analyzed by ELISA for serum MIF levels. Immunohistochemistry and in situ hybridization performed in 15 skin and 19 colonic biopsies from 17 patients who developed moderate to severe aGVHD showed a significant increase in MIF mRNA and protein expression compared with normal controls (seven skin and five colonic biopsies). MIF was localized within the epidermis and the vascular area of skin, but diffusely expressed in the entire thickness of colon. Macrophage and T lymphocyte infiltration was confined to areas of strong MIF expression. Serial analysis by ELISA showed that only patients who developed aGVHD (n = 19) exhibited an increase (two- to three-fold) in serum MIF during HSCT, but not in the allogeneic HSCT recipients without aGVHD (n = 7) or those who received autologous HSCT (n = 8). In 14 out of 19 patients, serum MIF peaked before the onset of aGVHD. Local and systemic up-regulation of MIF expression is associated with the occurrence of acute GVHD. Its pathogenetic role remains to be further determined.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235522&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 can address all hair loss cases. Another problem is that most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.

Hair Million is an alternative solution to cope with hair loss problems. Anecdotally, it shows prositive results and improvement especially for age-related hair thinning and hair loss for a large group of people who take it as suggested. Although personal experiences and anecdotal evidences indicate that it works, we still do not understand the mechanisms of action as to how Hair Million works to help stop hair loss, and promote hair growth. There has been no clinical trials nor placebo controlled statistical analysis on the efficacy of Hair Million on hair loss and hair growth. R & D costs dearly, and no one would afford to research complex herbal ingredients, which are often not patentable at all because they are made by mother nature.












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