DreamPharm Products:
Lutein-20||Herbs for headache, fever, and migraine ||
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
KSU.edu.sa
BACKGROUND/AIMS: T lymphocytes are present in increased numbers in the conjunctiva of patients with vernal keratoconjunctivitis (VKC) and their activation has a central role in the pathogenesis of the chronic allergic inflammatory reactions seen in VKC. The aims of this study were to examine the expression of three recently described potent T lymphocyte chemoattractants, PARC (pulmonary and activation regulated chemokine), macrophage derived chemokine (MDC), and I-309, the MDC receptor CCR4, and T lymphocyte activation markers, CD25, CD26, CD62L, CD71, and CD30, and to correlate them with the counts of CD3(+) T lymphocytes in the conjunctiva of patients with VKC. METHOD: Conjunctival biopsy specimens from 11 patients with active VKC, and eight control subjects were studied by immunohistochemical techniques using a panel of monoclonal and polyclonal antibodies directed against PARC, MDC, I-309, CCR4, CD25, CD26, CD62L, CD71, and CD30. The numbers of positively stained cells were counted. The phenotype of inflammatory cells expressing chemokines was examined by double immunohistochemistry. RESULTS: In the normal conjunctiva, vascular endothelial cells in the upper substantia propria showed weak immunoreactivity for CD26. There was no immunoreactivity for the other antibodies. VKC specimens showed inflammatory cells expressing PARC, MDC, and I-309. The numbers of PARC(+) inflammatory cells were higher than the numbers of MDC(+) and I-309(+) inflammatory cells and the mean values of the three groups differed significantly (17.0 (SD 10.1); 9.5 (9.9), and 4.3 (7.9), respectively, p = 0.0117, ANOVA). The numbers of PARC(+) inflammatory cells had the strongest correlation with the numbers of CD3(+) T lymphocytes. Few CCR4(+) inflammatory cells were observed in only three specimens. Double immunohistochemistry revealed that all inflammatory cells expressing chemokines were CD68(+) monocytes/macrophages. The numbers of CD25(+) T lymphocytes were higher than the numbers of CD26(+), CD62L(+), CD71(+), and CD30(+) T lymphocytes and the mean values of the five groups differed significantly (46.2 (27.9), 30.7 (16.0), 20.1 (8.6), 7.8 (7.7), and 6.5 (4.0), respectively, p <0.001, ANOVA). The numbers of CD25(+) T lymphocytes had the strongest correlation with the numbers of CD3(+) T lymphocytes. CONCLUSION: These results suggest a potential role for PARC, MDC, and I-309 in attracting T lymphocytes into conjunctiva in VKC. T lymphocytes in VKC are activated and express several activation markers which might contribute to the pathogenesis of VKC.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12234902&dopt=Abstract
Gut. 2002 Oct;51(4):485-9.
Impact of Helicobacter pylori infection and mucosal atrophy on gastric lesions in patients with familial adenomatous polyposis.
Nakamura S, Matsumoto T, Kobori Y, Iida M.
Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. shonakntmed2.med.kyushu-u.ac.jp
BACKGROUND AND AIMS: The role of Helicobacter pylori and atrophic gastritis in the pathogenesis of gastric lesions in familial adenomatous polyposis (FAP) has not been clarified. PATIENTS: Thirty one patients with FAP. METHODS: The presence of fundic gland polyposis (FGP) and gastric adenoma (GA) was determined by upper endoscopy with biopsies. The degree of gastric mucosal atrophy and H pylori status were determined by serological and histological findings. Germline mutation in the adenomatous polyposis coli (APC) gene was determined by polymerase chain reaction based single strand conformation polymorphism and direct sequencing. RESULTS: Gastric lesions were detected in 23 patients (74%). FGP and GA were found in 52% and 39%, respectively. APC gene mutation was identified in 22 of 30 patients. Patients with FGP were less frequently infected with H pylori than those without FGP (13% v 67%). The former patients had a lower degree of atrophy than the latter. Patients with GA tended to be more frequently infected with H pylori and they had higher degrees of atrophy than those without GA. When subjects were subdivided by gastric lesions (FGP alone, FGP+GA, GA alone, and negative groups), the GA alone group had the lowest pepsinogen I/II ratio and the highest seropositivity for H pylori. GA was found more frequently in patients positive for the APC mutation whereas no such a trend was observed in FGP. CONCLUSIONS: In FAP, H pylori associated atrophic gastritis contributes negatively to FGP. It seems to contribute positively to GA, especially in patients with truncating APC gene mutation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235068&dopt=Abstract
Gut. 2002 Oct;51(4):567-73.
Cigarette smoking, appendectomy, and tonsillectomy as risk factors for the development of primary sclerosing cholangitis: a case control study.
Mitchell SA, Thyssen M, Orchard TR, Jewell DP, Fleming KA, Chapman RW.
Department of Gastroenterology, Oxford Radcliffe Hospital, Oxford, UK.
BACKGROUND AND AIMS: The strong clinical association between primary sclerosing cholangitis (PSC) and ulcerative colitis (UC) suggests common factors in their pathogenesis. Smoking, previous appendectomy, and tonsillectomy have been associated with a decreased risk of developing UC. In this study, our aim was to examine these risk factors in patients with PSC with and without underlying inflammatory bowel disease (IBD). METHODS: The smoking habits and history of previous appendectomy and/or tonsillectomy of 170 patients with PSC, 41 without underlying IBD, 170 patients with UC but normal liver function tests, and 170 age and sex matched community controls were obtained by questionnaire. RESULTS: A total of 112 PSC patients (66%) had never smoked compared with 66 controls (39%). Only 12 PSC patients (7%) were current smokers versus 43 controls (25%). The resultant odds ratio of having PSC was 0.17 (95% confidence interval (CI) 0.08-0.35) among current smokers and 0.33 (95% CI 0.21-0.52) among ever (former+current) smokers. Among former smokers, the odds of having PSC were also significantly decreased (odds ratio 0.45, 95% CI 0.26-0.73; p<0.05). In the subgroup of PSC patients without IBD, only 5% were current smokers versus 26% of matched controls, and never smokers were overrepresented (68% v 37%). The rate of previous appendectomy was similar in all three study groups (14%, 12%, and 13%) but the frequency of tonsillectomy was reduced in the PSC group (21% v 31%; p=0.05). CONCLUSION: PSC, like UC, is a disease of non-smokers as the odds of having PSC was significantly decreased among current and former smokers. The association between non-smoking and PSC was independent of whether the PSC patient had underlying IBD. Previous tonsillectomy but not appendectomy may also be associated with a decreased risk of PSC but this warrants further study.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235082&dopt=Abstract
J Clin Invest. 2002 Sep;110(6):793-800.
Testing the NKT cell hypothesis of human IDDM pathogenesis.
Lee PT, Putnam A, Benlagha K, Teyton L, Gottlieb PA, Bendelac A.
Department of Molecular Biology, Princeton University, Princeton, New Jersey, USA.
Defects in IL-4-producing CD1d-autoreactive NKT cells have been implicated in numerous Th1-mediated autoimmune diseases, including diabetes, multiple sclerosis, rheumatoid arthritis, lupus, and systemic sclerosis. Particular attention has been focused on autoimmune insulin-dependent diabetes mellitus (IDDM) because nonobese diabetic (NOD) mice and humans with IDDM are both reported to express severe deficiencies in the frequency and Th2 functions of NKT cells. Furthermore, experimental manipulations of the NKT defect in the NOD mouse induced corresponding changes in disease. Taken together, these converging studies suggested a general role of NKT cells in natural protection against destructive autoimmunity. However, in previous reports the identification of NKT cells was based on indirect methods. We have now devised a direct, highly specific CD1d tetramer-based methodology to test whether humans with IDDM have associated NKT cell defects. Surprisingly, although we find marked and stable differences in NKT cells between individuals, our study of IDDM patients and healthy controls, including discordant twin pairs, demonstrates that NKT cell frequency and IL-4 production are conserved during the course of IDDM. These results contradict previous conclusions and refute the hypothesis that NKT cell defects underlie most autoimmune diseases.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235110&dopt=Abstract
J Clin Invest. 2002 Sep;110(6):835-42.
TNF-alpha mediates chemokine and cytokine expression and renal injury in cisplatin nephrotoxicity.
Ramesh G, Reeves WB.
Division of Nephrology, Penn State College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania 17033, USA.
The purpose of these studies was to examine the role of cytokines in the pathogenesis of cisplatin nephrotoxicity. Injection of mice with cisplatin (20 mg/kg) led to severe renal failure. The expression of cytokines, chemokines, and ICAM-1 in kidney was measured by ribonuclease protection assays and RT-PCR. We found significant upregulation of TNF-alpha, TGF-beta, RANTES, MIP-2, MCP-1, TCA3, IL-1beta, and ICAM-1 in kidneys from cisplatin-treated animals. In addition, serum, kidney, and urine levels of TNF-alpha measured by ELISA were increased by cisplatin. Inhibitors of TNF-alpha production (GM6001, pentoxifylline) and TNF-alpha Ab's reduced serum and kidney TNF-alpha protein levels and also blunted the cisplatin-induced increases in TNF-alpha, TGF-beta, RANTES, MIP-2, MCP-1, and IL-1beta, but not ICAM-1, mRNA. In addition, the TNF-alpha inhibitors also ameliorated cisplatin-induced renal dysfunction and reduced cisplatin-induced structural damage. Likewise, TNF-alpha-deficient mice were resistant to cisplatin nephrotoxicity. These results indicate cisplatin nephrotoxicity is characterized by activation of proinflammatory cytokines and chemokines. TNF-alpha appears to play a central role in the activation of this cytokine response and also in the pathogenesis of cisplatin renal injury.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12235115&dopt=Abstract
Hair loss is a problem in modern soceity. Examining the factors of hair growth may
shed light on how hair loss might occur.
How long can hair grow before it stops growing eventually if it does?
Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of
hair growth as well as
hair loss.
The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.
DHEA is a natural hormone, and it is produced in our body by the adrenal glands.
DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones)
or estrogens (female hormones) in the cells.
DreamPharm Online Healthy Supplements ||
Lutein ||
Progesterone Cream ||
Natural herbal formula for hair loss problems ||