| Number |
Title |
Comments |
| ...1... |
- Glucosamine [see comments]
|
An excellent overview of the use of glucosamine |
| ...2... |
- Enhanced synovial production of hyaluronic acid may explain rapid clinical
response to high-dose glucosamine in osteoarthritis.
|
|
| ...3... |
- An evaluation of the potential side-effects of alpha-glucosidase inhibitors
used for the management of diabetes mellitus.
|
|
| ...4... |
- Type 2 diabetes: glycemic targets and oral therapies for older patients.
|
|
| ...5... |
- Potential of alpha-glucosidase inhibitors in elderly patients with diabetes
mellitus and impaired glucose tolerance.
|
|
| ...6... |
- Glucosamine sulfate for osteoarthritis [see comments]
|
|
| ...7... |
- The role of glucosamine sulfate and chondroitin sulfates in the treatment of
degenerative joint disease.
|
Successful treatment of osteoarthritis must effectively control pain, and
should slow down or reverse progression of the disease. Biochemical and
pharmacological data combined with animal and human studies demonstrate
glucosamine sulfate is capable of satisfying these criteria. |
| ...8... |
- Pharmacology of alpha-glucosidase inhibition.
|
|
| ...9... |
- The neglect of glucosamine as a treatment for osteoarthritis--a personal
perspective.
|
. . . medical researchers and
physicians in the US have totally ignored this rational and safe therapeutic
strategy. |
| ...10... |
- Glucosamine for psoriasis?
|
|
| Menu
Position #10 |
| ...11... |
- Glucosamine may retard atherogenesis by promoting endothelial production of
heparan sulfate proteoglycans.
|
It is reasonable to
speculate that exogenous glucosamine will likewise enhance heparan sulfate
proteoglycans production by vascular endothelial cells, and, when administered
orally in regimens comparable to those effective in osteoarthritis, will thereby
act to retard atherogenesis. |
| ...12... |
- Conservative management of spinal osteoarthritis with glucosamine sulfate
and chiropractic treatment.
|
CONCLUSION: The rationales for using NSAIDs in the treatment of
osteoarthritis is controversial and openly contested. Given the detrimental
effects of NSAIDs on joints and other organs, their use should be discouraged
and their classification as a first choice conservative treatment should be
abolished. A truly effective and conservative approach to the treatment of
osteoarthritis should include chiropractic manipulation, essential nutrient
supplementation, exogenous administration of glucosamine sulfate and
rehabilitative stretches and exercises to maintain joint function. Because there
is no correlation between pain levels and the extent of degeneration detected by
radiographic or physical examination, conservative treatment should be initiated
and sustained based on functional, objective findings and not strictly on how
the patient feels. The use of NSAIDs should be limited to the treatment of gross
inflammation and analgesics should only be used in the short-term when
absolutely necessary for pain palliation. The present conservative approach
could lead not only to a better quality of life but also to the saving of health
care dollars by reducing the iatrogenic morbidity and mortality associated with
NSAID use. |
| ...13... |
- Drug treatment of arthritis. Update on conventional and less conventional
methods.
|
|
| ...14... |
- Severe rheumatoid arthritis: current options in drug therapy.
|
|
| ...15... |
- The actions of parathyroid hormone on bone: relation to bone remodeling and
turnover, calcium homeostasis, and metabolic bone diseases. II. PTH and bone
cells: bone turnover and plasma calcium regulation.
|
|
| ...16... |
- Carbohydrate metabolism and the glucoreceptor mechanism.
|
|
| ...17... |
- Aspartylglycosaminuria: an inborn error of glycoprotein catabolism.
|
|
| ...18... |
- Clinical research in osteoarthritis: design and results of short-term and
long-term trials with disease-modifying drugs.
|
|
| ...19... |
- Structure-activity relationships in lipopolysaccharides of Bacteroides
fragilis.
|
|
| ...20... |
- Heparan sulphate in the binding and activation of basic fibroblast growth
factor.
|
|
| Menu
Position #20 |
| ...21... |
- Prostate-specific antigen and history of its discovery.
|
|
| ...22... |
- The role of phosphometabolites in cell proliferation, energy metabolism, and
tumor therapy.
|
|
| ...23... |
- How does hyperglycaemia predispose to diabetic nephropathy?
|
|
| ...24... |
- Interactions of human malaria parasites, Plasmodium vivax and P.falciparum,
with the midgut of Anopheles mosquitoes.
|
|
| ...25... |
- Shedding of CD9 antigen in acute lymphoblastic leukemia.
|
|
| ...26... |
- Ectodomain interactions of leukocyte integrins and pro-inflammatory
GPI-linked membrane proteins.
|
|
| ...27... |
- Effect of low molecular weight heparin preparations on the inhibition of
thrombin by heparin cofactor II.
|
|
| ...28... |
- The PIG-A gene somatic mutation responsible for paroxysmal nocturnal
hemoglobinuria.
|
|
| ...29... |
- Mucin glycoproteins as tumor markers.
|
|
| ...30... |
- Involvement of heparan sulfate and related molecules in sequestration and
growth promoting activity of fibroblast growth factor.
|
|
| Menu
Position #30 |
| ...31... |
- Oral adhesion of yeasts.
|
|
| ...32... |
- Proposal for a pathway to mediate the metabolic effects of insulin.
|
|
| ...33... |
- Diagnostic procedures in immunodermatology.
|
|
| ...34... |
- Stimulation of fibroblast biosynthetic activity by serum of patients with
pretibial myxedema.
|
|
| ...35... |
- Basement membranes: current concepts of structure and synthesis.
|
|
| ...36... |
- Biochemistry and lectin binding properties of mammalian salivary mucous
glycoproteins.
|
|
| ...37... |
- Interactions between cells of the immune system and hyaluronate synthesis by
human dermal fibroblasts.
|
|
| ...38... |
- Evidence for multidrug-resistant cells in human tumor cell populations.
|
|
| ...39... |
- Glycolipid membrane-binding domain of human erythrocyte
acetylcholinesterase.
|
|
| ...40... |
- Invasion of erythrocytes by malaria merozoites: evidence for specific
receptors involved in attachment and entry.
|
|
| Menu
Position #40 |
| ...41... |
- Receptors and recognition mechanisms of Trypanosoma cruzi.
|
|
| ...42... |
- Studies on the biochemical basis of the interaction of the merozoites of
Plasmodium falciparum and the human red cell.
|
|
|
Record 1 from database: MEDLINE
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- Title
- Glucosamine [see comments]
- Author
- Barclay TS; Tsourounis C; McCart GM
- Address
- School of Pharmacy, University of California, San Francisco 94143, USA.
- Source
- Ann Pharmacother, 1998 May, 32:5, 574-9
- Abstract
- OBJECTIVE: To review the pharmacology and pharmacokinetics of glucosamine
and critically evaluate currently available literature regarding its safety and
efficacy. DATA SOURCE: A MEDLINE search was conducted between January 1965 and
May 1997. Key words used in the search were osteoarthritis, osteoarthrosis,
gonarthrosis, and glucosamine. In addition, references cited in articles
obtained from the MEDLINE search were reviewed for additional literature. STUDY
SELECTION AND DATA EXTRACTION: All articles were considered for inclusion in the
review. Articles were excluded from critical evaluation for lack of
randomization, lack of a control group, 30 or fewer study participants,
inconsistent treatment regimen, incomplete dosing information, or incomplete
reporting of results. DATA SYNTHESIS: Osteoarthritis affects approximately 12%
of the US population; the incidence increases with increasing age. Currently
used pharmacologic treatments, including acetaminophen and nonsteroidal
antiinflammatory drugs, do not slow or reverse the degenerative process in
osteoarthritis. Glucosamine has recently received a great deal of attention from
the public as a potential treatment of osteoarthritis, prompting healthcare
professionals to investigate its clinical usefulness and potential for adverse
effects. The drug has been proposed to stop and possibly reverse the
degenerative process in osteoarthritis. Following absorption of an oral dose,
glucosamine is incorporated into plasma proteins during first-pass metabolism,
resulting in 26% bioavailability. Unbound glucosamine is concentrated in the
articular cartilage. Each of the three critically evaluated studies reported a
decrease in the symptoms of osteoarthritis (e.g., decreased Lequesne index,
decreased pain severity, increased range of motion) for the glucosamine group,
which was greater than that obtained in the control group. Flaws in study
design, however, prevent the use of these results in modifying current clinical
practice. Reported short-term adverse effects include mild gastrointestinal
problems, drowsiness, skin reactions, and headache. CONCLUSIONS: Improvement in
the symptoms of osteoarthritis associated with the use of glucosamine has been
observed in clinical trials; however, those trials have flaws in design and data
analysis. Further research needs to be conducted before glucosamine can be
recommended as a treatment for osteoarthritis.
- Language of Publication
- English
- Unique Identifier
- 98269324
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- MeSH Heading (Major)
- Glucosamine|AD/AE/*PD/PK; Osteoarthritis|*DT/ME
- MeSH Heading
- Clinical Trials; Human; Metabolic Clearance Rate
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1060-0280
- Country of Publication
- UNITED STATES
Record 2 from database: MEDLINE
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- Title
- Enhanced synovial production of hyaluronic acid may explain rapid clinical
response to high-dose glucosamine in osteoarthritis.
- Author
- McCarty MF
- Address
- Nutrition 21, San Diego, CA 92109, USA.
- Source
- Med Hypotheses, 1998 Jun, 50:6, 507-10
- Abstract
- Anecdotal reports of rapid symptomatic response to high-dose glucosamine in
osteoarthritis are not credibly explained by the traditional view that
glucosamine promotes synthesis of cartilage proteoglycans. An alternative or
additional possibility is that glucosamine stimulates synovial production of
hyaluronic acid (HA), which is primarily responsible for the lubricating and
shock-absorbing properties of synovial fluid. Many clinical and veterinary
studies have shown that intra-articular injections of high-molecular-weight HA
produce rapid pain relief and improved mobility in osteoarthritis. HA has
anti-inflammatory and analgesic properties, and promotes anabolic behavior in
chondrocytes. The concentration and molecular weight of synovial fluid HA are
decreased in osteoarthritis; by reversing this abnormality, high-dose
glucosamine may provide rapid symptomatic benefit, and in the longer term aid
the repair of damaged cartilage.
- Language of Publication
- English
- Unique Identifier
- 98374099
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- MeSH Heading (Major)
- Glucosamine|AD/*TU; Hyaluronic Acid|*BI; Osteoarthritis|*DT; Synovial
Membrane|DE/*ME
- MeSH Heading
- Animal; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0306-9877
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 3416-24-8 (Glucosamine); 9004-61-9 (Hyaluronic Acid)
Record 3 from database: MEDLINE
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- Title
- An evaluation of the potential side-effects of alpha-glucosidase inhibitors
used for the management of diabetes mellitus.
- Author
- Reuser AJ; Wisselaar HA
- Address
- Department of Clinical Genetics, Erasmus University Rotterdam, The
Netherlands.
- Source
- Eur J Clin Invest, 1994 Aug, 24 Suppl 3:, 19-24
- Abstract
- Orally taken alpha-glucosidase inhibitors are used for the management of
diabetes mellitus. These drugs can prevent the postprandial rise of the blood
glucose level by inhibiting the enzymatic digestion of carbohydrates in the
intestinal lumen. Non-absorbable inhibitors such as acarbose are expected to
function exclusively in the intestine, but absorbable inhibitors such as
miglitol may exert an inhibitory effect on non-intestinal alpha-glucosidases
present in the various cell types of the body. The potential side-effects of
absorbable inhibitors are evaluated in this literature review. It is concluded
that there is little risk of inducing unwanted side-effects when miglitol is
taken in an oral dose of approximately 1 mg kg-1 body weight. The use of
absorbable inhibitors is, however, not advised in case of kidney dysfunction.
- Language of Publication
- English
- Unique Identifier
- 95094871
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- MeSH Heading (Major)
- alpha-Glucosidases|*AI; Diabetes Mellitus|BL/*DT; Glucosamine|*AA/AE/PD;
Hypoglycemic Agents|AE/CT/*PD; Trisaccharides|*AE/PD
- MeSH Heading
- Administration, Oral; Animal; Blood Glucose|DE/ME; Carbohydrate Sequence;
Diabetic Nephropathies|PP; Glycogen|ME; Glycogen Storage Disease|ME;
Glycoproteins|BI/CH; Human; Molecular Sequence Data; Sucrase-Isomaltase
Complex|DF
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0014-2972
- Country of Publication
- ENGLAND
Record 4 from database: MEDLINE
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- Title
- Type 2 diabetes: glycemic targets and oral therapies for older patients.
- Author
- Lardinois CK
- Address
- University of Nevada School of Medicine, USA.
- Source
- Geriatrics, 1998 Nov, 53:11, 22-3, 27-8, 33-4 passim
- Abstract
- In older patients with type 2 diabetes, life expectancy and the presence of
microvascular complications determine the appropriate intensity of glucose
control. The available antidiabetic agents offer many options for achieving
glycemic targets, based on the needs of the individual patient. New stimulators
of insulin secretion include glimepiride (a sulfonylurea) and repaglinide (a
meglitinide). The biguanide metformin is especially useful in obese,
insulin-resistant patients. Alpha-glucosidase inhibitors such as acarbose and
miglitol act locally in the GI tract to reduce postprandial excursion in glucose
levels. The insulin-sensitizing drug troglitazone enhances insulin-mediated
glucose disposal. When troglitazone is used, careful monitoring of patients'
liver function is required.
- Language of Publication
- English
- Unique Identifier
- 99042415
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- MeSH Heading (Major)
- Diabetes Mellitus, Non-Insulin-Dependent|CO/*DT/ME; Hypoglycemic
Agents|CL/PD/*TU
- MeSH Heading
- Age Factors; Aged; Blood Glucose|AN; Carbamates|TU; Glucosamine|AA/TU;
Human; Metformin|TU; Piperidines|TU; Sulfonylurea Compounds|TU;
Trisaccharides|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0016-867X
- Country of Publication
- UNITED STATES
Record 5 from database: MEDLINE
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- Title
- Potential of alpha-glucosidase inhibitors in elderly patients with diabetes
mellitus and impaired glucose tolerance.
- Author
- Rabasa Lhoret R; Chiasson JL
- Address
- Research Group on Diabetes and Metabolic Regulation Research Center, Centre
Hospitalier de l'UniversitÆe de MontrÆeal, Campus HÈotel-Dieu, MontrÆeal,
QuÆebec, Canada.
- Source
- Drugs Aging, 1998 Aug, 13:2, 131-43
- Abstract
- The prevalence of diabetes mellitus (DM) among the elderly, who constitute
> 20% of the population in developed countries, is high (up to 40%). Indeed,
elderly people represent the bulk (approximately 50%) of the diabetic
population. There is much evidence that better glycaemic control can reduce the
morbidity associated with this disease. alpha-Glucosidase inhibitors are well
tolerated in the treatment of DM in this population. They reduce postprandial
hyperglycaemia and have a moderate effect on fastign plasma glucose levels,
resulting in a significant reduction in glycated haemoglobin (HbA1C) levels.
alpha-Glucosidase inhibitors can be used either as monotherapy or in combination
with other oral hypoglycaemic agents or insulin. The good safety profile of
these drugs makes them suitable for use in elderly patients with type 2
(non-insulin-dependent) DM, because they can achieve substantial metabolic
improvements without any additional risks. Thus, the use of alpha-glucosidase
inhibitors should be considered: (i) as a first-choice treatment in newly
diagnosed patients; (ii) in individuals whose DM is not well controlled with any
other type of treatment; (iii) as an alternative to sulphonylureas or biguanides
in patients at risk from hypoglycaemia or lactic acidosis, respectively. Despite
the numerous potential advantages of alpha-glucosidase inhibitors in elderly
patients with type 2 DM, there is a lack of studies focusing specifically on
that population. However, such studies are under way. In addition, the potential
of alpha-glucosidase inhibitors in the prevention of type 2 DM and/or on
macrovascular disease is currently under study.
- Language of Publication
- English
- Unique Identifier
- 98411819
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- MeSH Heading (Major)
- alpha-Glucosidases|*AI; Diabetes Mellitus,
Non-Insulin-Dependent|CO/DH/*DT/PC; Enzyme Inhibitors|*TU; Glucose
Intolerance|*CO; Hypoglycemic Agents|AE/*TU
- MeSH Heading
- Aged; Body Weight|DE; Cognition|DE; Glucosamine|AA/TU; Human;
Trisaccharides|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1170-229X
- Country of Publication
- NEW ZEALAND
Record 6 from database: MEDLINE
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- Title
- Glucosamine sulfate for osteoarthritis [see comments]
- Author
- da Camara CC; Dowless GV
- Address
- School of Pharmacy, Campbell University, Buies Creek, NC, USA.
- Source
- Ann Pharmacother, 1998 May, 32:5, 580-7
- Abstract
- OBJECTIVE: To characterize the usefulness of glucosamine sulfate in the
treatment of patients with osteoarthritis (OA). DATA SOURCES AND STUDY
SELECTION: Pertinent citations were identified via a MEDLINE search (January
1975-March 1997). Only trials available in the English language involving human
subjects, OA, and glucosamine sulfate were selected for review. DATA SYNTHESIS:
OA is the most common form of arthritis and represents a major cause of
morbidity and disability in the elderly. The main symptom of OA is pain and most
of the commonly prescribed medications (e.g. acetaminophen, nonsteroidal
antiinflammatory drugs) have been targeted at relieving the pain. Some of these
medications have serious adverse effects and do not necessarily change the
natural course of the disease. Glucosamine sulfate, a nutritional supplement,
has recently emerged as an alternative treatment option for patients with OA.
The beneficial effects of this chondroprotective agent have been reported to
reverse or at least stop the progression of the disease without inducing serious
adverse effects. Limited data from short-term human trials suggest that
glucosamine sulfate administered orally, intravenously, intramuscularly, and
intraarticularly may produce a gradual and progressive reduction in joint pain
and tenderness, as well as improved range of motion and walking speed. Results
of the trials have also shown that glucosamine has produced consistent benefits
(> 50% overall improvement in symptom scores) in patients with OA and that,
in some cases, it may be equal or superior to ibuprofen in controlling symptoms.
CONCLUSIONS: There is evidence that glucosamine sulfate may provide pain relief,
reduce tenderness, and improve mobility in patients with OA. Most of the current
data, however, are derived from the European and Asian literature and there are
no studies supporting the use of this agent in the US. The studies published to
date have been done in small numbers of patients; adequate long-term trials
examining the safety, efficacy, and optimal dosage requirements of glucosamine
sulfate are lacking. Most of the available clinical data are difficult to
interpret due to serious deficiencies in study design. Furthermore, studies
evaluating the appropriate place of glucosamine sulfate in the therapeutic
armamentarium of OA remain to be done.
- Language of Publication
- English
- Unique Identifier
- 98269325
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- MeSH Heading (Major)
- Glucosamine|AE/*TU; Osteoarthritis|*DT
- MeSH Heading
- Anti-Inflammatory Agents, Non-Steroidal|TU; Clinical Trials; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1060-0280
- Country of Publication
- UNITED STATES
Record 7 from database: MEDLINE
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- Title
- The role of glucosamine sulfate and chondroitin sulfates in the treatment of
degenerative joint disease.
- Author
- Kelly GS
- Address
-
- Source
- Altern Med Rev, 1998 Feb, 3:1, 27-39
- Abstract
- Successful treatment of osteoarthritis must effectively control pain, and
should slow down or reverse progression of the disease. Biochemical and
pharmacological data combined with animal and human studies demonstrate
glucosamine sulfate is capable of satisfying these criteria. Glucosamine
sulfate's primary biological role in halting or reversing joint degeneration
appears to be directly due to its ability to act as an essential substrate for,
and to stimulate the biosynthesis of, the glycosaminoglycans and the hyaluronic
acid backbone needed for the formation of proteoglycans found in the structural
matrix of joints. Chondroitin sulfates, whether they are absorbed intact or
broken into their constituent components, similarly provide additional
substrates for the formation of a healthy joint matrix. Evidence also supports
the oral administration of chondroitin sulfates for joint disease, both as an
agent to slowly reduce symptoms and to reduce the need for non-steroidal
anti-inflammatory drugs. The combined use of glucosamine sulfate and chondroitin
sulfates in the treatment of degenerative joint disease has become an extremely
popular supplementation protocol in arthritic conditions of the joints. Although
glucosamine sulfate and chondroitin sulfates are often administered together,
there is no information available to demonstrate the combination produces better
results than glucosamine sulfate alone.
- Language of Publication
- English
- Unique Identifier
- 98262758
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- MeSH Heading (Major)
- Chondroitin Sulfates|CH/ME/*TU; Glucosamine|ME/*TU; Osteoarthritis|*DT
- MeSH Heading
- Drug Therapy, Combination; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1089-5159
- Country of Publication
- UNITED STATES
Record 8 from database: MEDLINE
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- Title
- Pharmacology of alpha-glucosidase inhibition.
- Author
- Bischoff H
- Address
- Institute for Cardiovascular and Arteriosclerosis Research, Wuppertal,
Germany.
- Source
- Eur J Clin Invest, 1994 Aug, 24 Suppl 3:, 3-10
- Abstract
- The development of alpha-amylase and brush-border alpha-glucosidase
inhibitors is reviewed. The mode of action as well as pharmacological and
pharmacodynamic properties of selected inhibitors with special regard to the
most thoroughly investigated alpha-glucosidase inhibitor acarbose are discussed.
Inhibition of intestinal alpha-glucosidases delays the digestion of starch and
sucrose, flattens the postprandial blood glucose excursions, and thus mimics the
effects of dieting on hyperglycaemia, hyperinsulinaemia and
hypertriglyceridaemia. Therefore, the mechanism of alpha-glucosidase inhibition
represents the pharmacological optimization of the dietary principle of delayed
carbohydrate absorption. In pre-clinical studies using diabetic animals the oral
administration of acarbose improved the metabolic state and reduced the blood
glucose area under the curve. As a consequence, the process of non-enzymatic
glycation of proteins was retarded as indicated by reduced glycated haemoglobin,
glomerular basement membranes or advanced glycation end-products (AGEs) in
collagen. These improved biochemical parameters correlated with beneficial
effects against the development of diabetic nephropathy and neuropathy. Thus,
the treatment of diabetic animals with acarbose does not only improve the
metabolic state but has also the potential to delay, or possibly prevent, the
development of diabetic complications.
- Language of Publication
- English
- Unique Identifier
- 95094873
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- MeSH Heading (Major)
- alpha-Glucosidases|*AI; Dietary Carbohydrates|*; Hypoglycemic Agents|*PD;
Trisaccharides|CH/*PD/TU
- MeSH Heading
- Animal; Blood Glucose|DE/ME; Carbohydrate Sequence; Diabetes Mellitus,
Experimental|DT; Diabetic Nephropathies|PC; Diabetic Neuropathies|PC; Digestion;
Glucosamine|AA/PD; Glycosylation End Products, Advanced|AI; Human; Insulin|BL;
Molecular Sequence Data
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0014-2972
- Country of Publication
- ENGLAND
Record 9 from database: MEDLINE
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- Title
- The neglect of glucosamine as a treatment for osteoarthritis--a personal
perspective.
- Author
- McCarty MF
- Address
-
- Source
- Med Hypotheses, 1994 May, 42:5, 323-7
- Abstract
- Osteoarthritis results from progressive catabolic loss of cartilage
proteoglycans, owing to an imbalance between synthesis and degradation. Standard
drug therapy is only of palliative benefit and may exacerbate loss of cartilage.
Glucosamine is an intermediate in mucopolysaccharide synthesis, and its
availability in cartilage tissue culture can be rate-limiting for proteoglycan
production. A number of double-blind studies dating from the early 1980s
demonstrate that oral glucosamine decreases pain and improves mobility in
osteoarthritis, without side effects. Nevertheless, medical researchers and
physicians in the US have totally ignored this rational and safe therapeutic
strategy. By mechanisms that are still unclear, the natural methyl donor
S-adenosylmethionine also promotes production of cartilage proteoglycans, and is
therapeutically beneficial in osteoarthritis in well-tolerated oral doses. These
and other safe nutritional measures supporting proteoglycan synthesis, may offer
a practical means of preventing or postponing the onset of osteoarthritis in
older people or athletes.
- Language of Publication
- English
- Unique Identifier
- 95020811
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- MeSH Heading (Major)
- Glucosamine|AE/*TU; Osteoarthritis|*DT/ME
- MeSH Heading
- Animal; Cartilage|DE/ME; Clinical Trials; Controlled Clinical Trials; Drug
Tolerance; Human; Models, Biological; Proteoglycans|ME; S-Adenosylmethionine|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0306-9877
- Country of Publication
- ENGLAND
Record 10 from database: MEDLINE
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- Title
- Glucosamine for psoriasis?
- Author
- McCarty MF
- Address
-
- Source
- Med Hypotheses, 1997 May, 48:5, 437-41
- Abstract
- Amphiregulin and transforming growth factor-alpha, agonists for the
epidermal growth factor receptor, are the major autocrine growth factors for
cultured keratinocytes, and their substantial overexpression in psoriatic
lesions suggests that they are crucial to the basal hyperplasia that
characterizes psoriasis. Amphiregulin binds to heparin and related highly
sulfated polysaccharides, and exogenous heparin blocks its growth factor
activity, rationalizing previous reports that psoriasis responds to heparin
therapy. Differentiating keratinocytes produce increased amounts of
protein-bound as well as free-chain heparan sulfates, which may function
physiologically as amphiregulin antagonists. By promoting keratinocyte synthesis
of these heparan sulfates, glucosamine administration may inhibit amphiregulin
function and thus provide therapeutic benefit in psoriasis. Concurrent ingestion
of fish oil, by impeding the excessive activation of protein kinase C, may
decrease keratinocyte production of amphiregulin and other autocrine growth
factors, thus complementing the postulated benefits of glucosamine.
- Language of Publication
- English
- Unique Identifier
- 97328595
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- MeSH Heading (Major)
- Glucosamine|AD/*TU; Psoriasis|*DT/ET/PP
- MeSH Heading
- Fish Oils|AD; Glycoproteins|PH; Growth Substances|PH; Heparitin Sulfate|PH;
Human; Models, Biological; Receptors, Epidermal Growth Factor-Urogastrone|PH;
Transforming Growth Factor alpha|PH
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0306-9877
- Country of Publication
- ENGLAND
Record 11 from database: MEDLINE
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- Title
- Glucosamine may retard atherogenesis by promoting endothelial production of
heparan sulfate proteoglycans.
- Author
- McCarty MF
- Address
- Nutrition 21, San Diego, CA 92109, USA.
- Source
- Med Hypotheses, 1997 Mar, 48:3, 245-51
- Abstract
- Heparan sulfate proteoglycans produced by vascular endothelium may function
physiologically to restrain the migration, multiplication, and phenotypic
transition of vascular smooth-muscle cells, and to maintain an anticoagulant
luminal surface by bonding and activating antithrombin III. Thus, ample
production of heparan sulfate proteoglycans may act to prevent atherosclerosis
and its thrombotic complications. The ability of exogenous heparin to stimulate
synthesis of heparan sulfate proteoglycans by vascular endothelium may be
largely responsible for the positive outcomes of most controlled evaluations of
low-dose heparin as a long-term therapy for coronary disease. Glucosamine, a
biosynthetic precursor of mucopolysaccharides, can substantially enhance
mucopolysaccharide production when added to cultured fibroblasts or
chondrocytes; the clinical utility of oral glucosamine in osteoarthritis may
reflect increased synthesis of cartilage proteoglycans. It is reasonable to
speculate that exogenous glucosamine will likewise enhance heparan sulfate
proteoglycans production by vascular endothelial cells, and, when administered
orally in regimens comparable to those effective in osteoarthritis, will thereby
act to retard atherogenesis.
- Language of Publication
- English
- Unique Identifier
- 97285672
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- MeSH Heading (Major)
- Atherosclerosis|*PC/PP; Endothelium, Vascular|DE/*ME; Glucosamine|*PD/*TU;
Heparitin Sulfate|*BI; Models, Cardiovascular|*; Proteoglycans|*BI
- MeSH Heading
- Animal; Cartilage|DE/ME; Cells, Cultured; Coronary Disease|DT;
Fibroblasts|DE/ME; Glycosaminoglycans|BI; Heparin|TU; Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0306-9877
- Country of Publication
- ENGLAND
Record 12 from database: MEDLINE
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- Title
- Conservative management of spinal osteoarthritis with glucosamine sulfate
and chiropractic treatment.
- Author
- Gottlieb MS
- Address
-
- Source
- J Manipulative Physiol Ther, 1997 Jul, 20:6, 400-14
- Abstract
- OBJECTIVE: To evaluate the rationale behind the most commonly used
treatments of osteoarthritis, including nonsteroidal anti-inflammatory drugs
(NSAIDs), and to assess more effective conservative treatment options. SUMMARY
OF BACKGROUND DATA: This review includes a description of the pathophysiology
and prevalence of osteoarthritis, joint physiology and NSAID treatment of
osteoarthritis, as well as side effects on joints, the gastrointestinal tract,
kidneys and livers. Several studies of conservative treatment, consisting of
supplementation of glucosamine sulfate (which occurs naturally in the human
body), exercise, and the use of chiropractic treatment for maintaining joint
function and preventing further destruction, are reviewed. DATA SOURCES: A
computerized search of Medline using the key indexing terms osteoarthritis,
degenerative joint disease, nonsteroidal anti-inflammatory drugs, glucosamine
sulfate, chiropractic and manipulation. RESULTS: Numerous studies wee obtained
under each subheading and reviewed by category. Human and animal-model studies
are described. CONCLUSION: The rationales for using NSAIDs in the treatment of
osteoarthritis is controversial and openly contested. Given the detrimental
effects of NSAIDs on joints and other organs, their use should be discouraged
and their classification as a first choice conservative treatment should be
abolished. A truly effective and conservative approach to the treatment of
osteoarthritis should include chiropractic manipulation, essential nutrient
supplementation, exogenous administration of glucosamine sulfate and
rehabilitative stretches and exercises to maintain joint function. Because there
is no correlation between pain levels and the extent of degeneration detected by
radiographic or physical examination, conservative treatment should be initiated
and sustained based on functional, objective findings and not strictly on how
the patient feels. The use of NSAIDs should be limited to the treatment of gross
inflammation and analgesics should only be used in the short-term when
absolutely necessary for pain palliation. The present conservative approach
could lead not only to a better quality of life but also to the saving of health
care dollars by reducing the iatrogenic morbidity and mortality associated with
NSAID use.
- Language of Publication
- English
- Unique Identifier
- 97418499
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- MeSH Heading (Major)
- Anti-Inflammatory Agents, Non-Steroidal|*TU; Chiropractic|*;
Glucosamine|*TU; Osteoarthritis|DT/PP/*TH; Spinal Diseases|DT/*TH
- MeSH Heading
- Combined Modality Therapy; Diet; Glycosaminoglycans|ME; Human; Joints|DE/PH
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0161-4754
- Country of Publication
- UNITED STATES
Record 13 from database: MEDLINE
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- Title
- Drug treatment of arthritis. Update on conventional and less conventional
methods.
- Author
- Spencer-Green G
- Address
- Dartmouth-Hitchcock Medical Center, Lebanon, NH 03756.
- Source
- Postgrad Med, 1993 May 15, 93:7, 129-40
- Abstract
- Nonsteroidal anti-inflammatory drugs comprise an important class of
medications that reduce the signs and symptoms of osteoarthritis and rheumatoid
arthritis. They bring relief to millions of people but do not eliminate
underlying disease. Disease-modifying antirheumatic drugs also bring relief, but
these drugs are often ineffective and not well tolerated. Failure to provide
long-term benefits combined with the high toxicity of most of the
disease-modifying agents has prompted a search for more effective treatments.
New methods using modern technologies have generated much enthusiasm and hold
promise for the future. In the meantime, administration of nonsteroidal
anti-inflammatory drugs and judicious use of disease-modifying agents remain the
cornerstone of therapy for arthritis.
- Language of Publication
- English
- Unique Identifier
- 93261929
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- MeSH Heading (Major)
- Anti-Inflammatory Agents, Non-Steroidal|PD/*TU; Arthritis, Rheumatoid|*DT;
Osteoarthritis|*DT
- MeSH Heading
- Adrenal Cortex Hormones|TU; Aurothioglucose|TU; Azathioprine|TU;
Glucosamine|AA/TU; Gold Sodium Thiomalate|TU; Human; Hydroxychloroquine|TU;
Methotrexate|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0032-5481
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Adrenal Cortex Hormones); 0 (Anti-Inflammatory Agents, Non-Steroidal);
118-42-3 (Hydroxychloroquine); 12192-57-3 (Aurothioglucose); 12244-57-4 (Gold
Sodium Thiomalate); 3416-24-8 (Glucosamine); 446-86-6 (Azathioprine); 56824-20-5
(amiprilose); 59-05-2 (Methotrexate)
Record 14 from database: MEDLINE
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- Title
- Severe rheumatoid arthritis: current options in drug therapy.
- Author
- Kremer JM
- Address
- Division of Rheumatology, Albany Medical College, New York.
- Source
- Geriatrics, 1990 Dec, 45:12, 43-8
- Abstract
- Therapeutic advances have been made in rheumatoid arthritis (RA), but
patients (and sometimes physicians) may become frustrated at the apparent lack
of breakthrough treatments. The latest advances in the treatment of severe RA
are discussed, along with what investigators are using experimentally both in
combination with other drugs and alone to treat RA now and, possibly, in the
future. These agents include methotrexate, cyclosporine, gamma-interferon, and
omega-3 fatty acids.
- Language of Publication
- English
- Unique Identifier
- 91071618
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- MeSH Heading (Major)
- Arthritis, Rheumatoid|*DT/TH; Clinical Protocols|*ST
- MeSH Heading
- Anti-Inflammatory Agents, Non-Steroidal|TU; Antibodies, Monoclonal|TU;
Aspirin|TU; Cyclosporins|TU; Drug Therapy, Combination; Fatty Acids, Omega-3|TU;
Glucosamine|AA/TU; Human; Hydroxychloroquine|TU; Interferon Type II|TU;
Methotrexate|TU
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0016-867X
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antibodies, Monoclonal); 0 (Cyclosporins); 0 (Fatty Acids, Omega-3);
118-42-3 (Hydroxychloroquine); 3416-24-8 (Glucosamine); 50-78-2 (Aspirin);
56824-20-5 (amiprilose); 59-05-2 (Methotrexate); 82115-62-6 (Interferon Type II)
Record 15 from database: MEDLINE
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- Title
- The actions of parathyroid hormone on bone: relation to bone remodeling and
turnover, calcium homeostasis, and metabolic bone diseases. II. PTH and bone
cells: bone turnover and plasma calcium regulation.
- Author
- Parfitt AM
- Address
-
- Source
- Metabolism, 1976 Aug, 25:8, 909-55
- Abstract
- Kinetic and morphologic studies in patients with parathyroid disease, and a
wide variety of studies in experimental animals indicate that one major effect
of PTH is to increase the proliferation of osteoprogenitor cells into
osteoclasts and so to increase bone turnover. PTH stimulates bone cells by
increasing cell membrane permeability to calcium and consequently increasing
calcium influx and by activating membrane-bound adenyl-cyclase. It is likely
that the former event precedes the latter and that calcium is the second
messenger and cyclic AMP the third messenger. PTH increases the production by
bone cells of lactate, citric and carbonic acids, lysosomal enzymes,
collagenase, and hyaluronic acid, some or all of which are concerned in the
mechanism of bone resorption. With the exception of lactate which probably comes
mainly from osteocytes, the increase in metabolic activity is largely due to the
increase in the number of osteoclasts. There is also ultrastructural,
biochemical, and biophysical evidence that PTH stimulates existing osteoclasts,
but this most likely represents the transformation of inactive cells into an
active state, and is a transient and nonsustainable effect. As yet, there is no
evidence that either increased osteoprogenitor cell proliferation or increased
osteoclast activity is mediated by adenyl-cyclase activation. PTH also acts on
the deep osteocyte to cause rapid mobilization of calcium from the zone of
hypomineralized metabolically active perilacunar bone. This effect is mediated
by adenyl-cyclase activation and is preceded by a slight fall in plasma calcium
probably due to the movement of calcium into bone cells. The function of this
rapid hypercalcemic response to PTH is correct errors in the prevailing
steady-state level of plasma calcium...
- Language of Publication
- English
- Unique Identifier
- 76242326
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- MeSH Heading (Major)
- Bone and Bones|DE/*PH; Calcium|BL/*ME/PD; Parathyroid Hormones|*PH
- MeSH Heading
- Animal; Bone Development; Bone Resorption; Carbonic Acid|ME; Glucosamine|ME;
Homeostasis; Human; Hypercalcemia|ET; Hyperparathyroidism|ME;
Hypoparathyroidism|ME; Lysosomes|EN; Mast Cells|PH; Microbial Collagenase|ME;
Models, Biological; Osteoclasts|PH; Osteocytes|PH; Parathyroid Glands|PH;
Phosphates|PH
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0026-0495
- Country of Publication
- UNITED STATES
Record 16 from database: MEDLINE
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- Title
- Carbohydrate metabolism and the glucoreceptor mechanism.
- Author
- Ashcroft SJ; Sugden MC; Williams IH
- Address
-
- Source
- Horm Metab Res Suppl, 1980, Suppl 10:, 1-7
- Abstract
- Current views on the recognition of sugars as signals for insulin
biosynthesis and release are discussed. Evidence is presented that the initial
steps in the metabolism of N-acetyl-glucosamine differ from those in glucose
metabolism in that for the former transport into the islet represents the
rate-limiting step. Different enzymes phosphorylate these two sugar, but it is
suggested that N-acetylglucosamine and glucose enter the beta-cell via the same
carrier since 3-O-methylglucose is shown to be a competitive inhibitor of
N-acetylglucosamine oxidation. Inhibitory effects on N-acetylglucosamine
oxidation are also observed with caffeine, 3-isobutyl-methylxanthine and
phloretin. Inhibition of N-acetylglucosamine metabolism is associated with
inhibition of N-acetylglucosamine-stimulated insulin release and biosynthesis.
Methylxanthines also inhibit uptake of 45Ca2+ by islet mitochondria. The
possible physiological role of islet mitochondrial Ca2+ uptake in the regulation
of beta-cell cytosolic Ca2+ concentration is discussed.
- Language of Publication
- English
- Unique Identifier
- 81092241
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- MeSH Heading (Major)
- Acetylglucosamine|*ME; Glucosamine|*AA; Glucose|*ME; Islets of
Langerhans|DE/*ME; Receptors, Cell Surface|*ME
- MeSH Heading
- Animal; Caffeine|PD; Calcium|ME; Cyclic AMP|ME; Human; Insulin|ME;
Mitochondria|ME; Support, Non-U.S. Gov't; 1-Methyl-3-isobutylxanthine|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0018-5043
- Country of Publication
- GERMANY, WEST
- CAS Registry/EC Number
- 0 (glucose receptor); 0 (Receptors, Cell Surface); 11061-68-0 (Insulin);
28822-58-4 (1-Methyl-3-isobutylxanthine); 3416-24-8 (Glucosamine); 50-99-7
(Glucose); 58-08-2 (Caffeine); 60-92-4 (Cyclic AMP); 7440-70-2 (Calcium);
7512-17-6 (Acetylglucosamine)
Record 17 from database: MEDLINE
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- Title
- Aspartylglycosaminuria: an inborn error of glycoprotein catabolism.
- Author
- Maury CP
- Address
-
- Source
- J Inherit Metab Dis, 1982, 5:4, 192-6
- Abstract
- Aspartylglycosaminuria (AGU, McKusick 20840) is a metabolic disorder
affecting the catabolism of glycoproteins. It was first described in 1967, by
Jenner and Pollitt, in two mentally retarded English siblings. Subsequently
several cases were reported from Finland (Palo and Mattsson, 1970; Autio, 1972;
Autio et al., 1973). Today the number of known cases is about 140, most of them
Finnish or of Finnish origin (Aula et al., 1980). The incidence of AGU in
Finland has been estimated to be approximately 1:26000 and the disease is
inherited as an autosomal recessive trait (Autio et al., 1973). Clinical
manifestations include progressive mental retardation, coarse gargoyle-like
facial features, skeletal abnormalities and recurrent infections. Early
development of the patients is usually normal, but by the age of 5-15 years they
are already severely retarded (Autio, 1972; Autio et al., 1973). Morphologically
AGU is a generalized storage disease (Haltia et al., 1975). Affected tissues
show enlarged lysosomes. Vacuolization is a prominent feature of liver and nerve
cells (Haltia et al., 1975) and of peripheral lymphocytes (Aula et al., 1975).
- Language of Publication
- English
- Unique Identifier
- 83190526
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- MeSH Heading (Major)
- Acetylglucosamine|*AA/PH/UR; Glucosamine|*AA; Glycoproteins|*ME; Metabolism,
Inborn Errors|DI/*ME/UR
- MeSH Heading
- Brain|ME; Human; Liver|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW
- ISSN
- 0141-8955
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (Glycoproteins); 2776-93-4 (N-acetylglucosaminylasparagine); 3416-24-8
(Glucosamine); 7512-17-6 (Acetylglucosamine)
Record 18 from database: MEDLINE
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- Title
- Clinical research in osteoarthritis: design and results of short-term and
long-term trials with disease-modifying drugs.
- Author
- Rovati LC
- Address
- Department of Clinical Pharmacology, Rotta Research Laboratorium S.p.A.,
Monza, Italy.
- Source
- Int J Tissue React, 1992, 14:5, 243-51
- Abstract
- Putative disease-modifying drugs are usually clinically used in
osteoarthritis with two main aims: not only stopping or reducing the cartilage
degenerative process after a long-term treatment, but also controlling the
symptoms of the disease within a few days or weeks, thus avoiding or diminishing
the use of symptomatic medications. Due to the difficulties of implementing the
first aim, the latter aim was more often investigated, even if most often with
inadequate study design and insufficient numbers of patients. We have recently
carried out three double-blind, controlled, parallel groups, randomized, 4-6
week trials of glucosamine sulphate versus placebo or the NSAID ibuprofen on a
total of 606 gonarthrosic out-patients. Movement limitation and pain were scored
according to the Lequesne index, and the efficacy goals were strictly
pre-determined. Access to other medications was not allowed. Glucosamine was
significantly more effective than placebo, while no difference was detected in
comparison with the NSAID (p < 0.025 and p = 0.77, respectively: Fisher's
two-tailed exact test). On the other hand, glucosamine was as well tolerated as
placebo, while the percentage of patients suffering adverse drug reactions was
higher in the ibuprofen group (37% vs 7%: p < 0.001). Long-term trials are in
progress and several aspects are to be considered in their design: they must be
double-blind, placebo-controlled, randomized, continued for a period of years
and (most importantly) with the careful use of imaging and biochemical
techniques capable of generating objective evaluation criteria.
- Language of Publication
- English
- Unique Identifier
- 93239409
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- MeSH Heading (Major)
- Osteoarthritis|*DT; Research Design|*
- MeSH Heading
- Clinical Trials; Double-Blind Method; Drug Administration Schedule; Human;
Randomized Controlled Trials; Time Factors
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0250-0868
- Country of Publication
- SWITZERLAND
Record 19 from database: MEDLINE
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- Title
- Structure-activity relationships in lipopolysaccharides of Bacteroides
fragilis.
- Author
- Lindberg AA; Weintraub A; Zähringer U; Rietschel ET
- Address
- Department of Clinical Bacteriology, Karolinska Institute, Huddinge
University Hospital, Sweden.
- Source
- Rev Infect Dis, 1990 Jan-Feb, 12 Suppl 2:, S133-41
- Abstract
- The endotoxic activity of lipopolysaccharide (LPS) extracted from the
envelope of Bacteroides fragilis is low compared with that of LPS from
Escherichia coli, Salmonella, and other Enterobacteriaceae. Thus, pyrogenicity,
the ability to prepare for or provoke the local Shwartzman reaction, and the
ability to induce the production of interleukin 1 are reduced by 100- to
1,000-fold. Structural analyses of characterized B. fragilis LPS have shown that
its lipid A is composed of a beta 1,6-linked D-glucosamine disaccharide that has
the following properties: (1) a phosphate group on C1 of the reducing amino
sugar, (2) amide- and ester-linked 3-hydroxylated branched and nonbranched
long-chain (C15-C17) fatty acids, (3) an average of five fatty acids per
glucosamine disaccharide, and (4) the core and O-antigenic saccharide chain
linked to C6 of the nonreducing glucosamine residue. Although structurally
similar to lipid A of E. coli, the lipid A of B. fragilis differs by its lack of
the phosphate group on C4 of the nonreducing amino sugar and by the presence of
fewer and different fatty acids. These differences explain the low endotoxic
activity of B. fragilis LPS. The core and O-antigenic chain are linked to lipid
A via a phosphorylated 2-keto-3-deoxyoctonate (KDO) residue. The saccharide
chain is short and is composed of L-rhamnose, D-glucose, and D-galactose, with
the O-antigenic specificity determined by a beta 1,6-linked D-galactose
oligomer. This O-antigenic specificity was present in 14 of 17 strains of B.
fragilis that were investigated.
- Language of Publication
- English
- Unique Identifier
- 90161741
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- MeSH Heading (Major)
- Bacteroides fragilis|*; Lipopolysaccharides|*AN/TO
- MeSH Heading
- Animal; Carbohydrate Conformation; Carbohydrate Sequence; Human; Lipid
A|AN/TO; Molecular Sequence Data; Monosaccharides|AN; Structure-Activity
Relationship; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0162-0886
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Lipid A); 0 (Lipopolysaccharides); 0 (Monosaccharides)
Record 20 from database: MEDLINE
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- Title
- Heparan sulphate in the binding and activation of basic fibroblast growth
factor.
- Author
- Gallagher JT; Turnbull JE
- Address
- Department of Medical Oncology, Christie Hospital NHS Trust, Manchester, UK.
- Source
- Glycobiology, 1992 Dec, 2:6, 523-8
- Abstract
- Heparan sulphate proteoglycans (HSPGs) are widely distributed in animal
tissues, but their most prominent locations are cell surface membranes and
basement membranes. Their influence on various fundamental aspects of cell
behaviour (e.g. cell adhesion, growth and morphogenesis) are dependent on the
specific binding properties of the heparan sulphate (HS) chains. These
polysaccharides are complex structures in which N-sulphated glucosamine and
ester sulphate groups tend to be clustered in discrete regions of the chain
separated by sequences enriched in N-acetylglucosamine residues, but with a low
sulphate concentration. The sulphated domains contain the sugar residue
sequences for interaction with specific proteins essential for HS function. In
this review, we describe the plasma membrane HSPGs and their role in regulating
the activity of basic fibroblast growth factor (bFGF).
- Language of Publication
- English
- Unique Identifier
- 93113099
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- MeSH Heading (Major)
- Fibroblast Growth Factor, Basic|*ME; Heparitin Sulfate|BI/CH/*ME
- MeSH Heading
- Animal; Binding Sites; Carbohydrate Sequence; Cell Membrane|ME; Human;
Molecular Sequence Data; Proteoglycans|CH/ME; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0959-6658
- Country of Publication
- ENGLAND
- CAS Registry/EC Number
- 0 (heparan sulfate proteoglycan); 0 (Fibroblast Growth Factor, Basic); 0
(Proteoglycans); 9050-30-0 (Heparitin Sulfate)
Record 21 from database: MEDLINE
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- Title
- Prostate-specific antigen and history of its discovery.
- Author
- Zaviacic M
- Address
- Institute of Pathology, School of Medicine, Comenius University, Bratislava.
Zaviacic@fmed.uniba.sk
- Source
- Bratisl Lek Listy, 1997 Dec, 98:12, 659-62
- Abstract
- In contradistinction to prostatic acid phosphatase (PAcP), prostate-specific
antigen (PSA) is currently the most reliable and most frequently used marker for
identification of normal and pathologically altered prostatic tissues both in
the male and female. In clinical practice, it has become an appreciated serum
marker in the assessment and management of prostate carcinoma in the male,
although it is far from being a perfect "tumor" marker. Our knowledge
on female PSA is expected to be broadened by the introduction of novel highly
sensitive serological methods (IMMULITE--immunochemiluminiscent third-generation
PSA assay and others), which in some females have already demonstrated
surprisingly high values. Biochemically, PSA in seminal fluid in its free form
has a molecular weight of about 30,000 daltons, while in serum, where it occurs
in the complex form with alpha1-chymotrypsin, its molecular weight is
approximately 100,000 daltons being comparable to that of PAcP. On
immunohistochemical examination, PSA is expressed in the highly specialized
apically-superficial layer of male and female secretory (luminal) cells of the
prostatic glands, as well as at other sites of the urogenital tract, frequently
coinciding with glucosamine glucans, glycoproteins and numerous enzyme proteins.
With regard to the increasing interest in PSA evidenced in urology,
gynecological urology, in the orthology and pathology of male and female
prostates, the interest in the history of discovery of this exceptional
prostatic marker appears to be justified. PSA was discovered by Richard Ablin
and co-workers in the USA, who published their pioneer work in the Journal of
Reproduction and Fertility and in the Journal of Immunology as early as in 1970.
Thus their results had been available nine years before the publication of Wang
et al. appeared in Investigative Urology (1979), on the basis of which the
latter are frequently incorrectly considered and cited as the authors of PSA
discovery. (Ref. 46.)
- Language of Publication
- English
- Unique Identifier
- 98185775
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- MeSH Heading (Major)
- Prostate-Specific Antigen|*/HI/ME/PH
- MeSH Heading
- Female; History of Medicine, 20th Cent.; Human; Male; Prostatic
Neoplasms|DI; Urethra|ME
- Publication Type
- HISTORICAL ARTICLE; JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0006-9248
- Country of Publication
- SLOVAKIA
Record 22 from database: MEDLINE
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- Title
- The role of phosphometabolites in cell proliferation, energy metabolism, and
tumor therapy.
- Author
- Mazurek S; Boschek CB; Eigenbrodt E
- Address
- Institute for Biochemistry and Endocrinology, Veterinary Faculty, University
of Giessen, Germany.
- Source
- J Bioenerg Biomembr, 1997 Aug, 29:4, 315-30
- Abstract
- A common characteristic of tumor cells is the constant overexpression of
glycolytic and glutaminolytic enzymes. In tumor cells the hyperactive hexokinase
and the partly inactive pyruvate kinase lead to an expansion of all
phosphometabolites from glucose 6-phosphate to phosphoenolpyruvate. In addition
to the glycolytic phosphometabolites, synthesis of their metabolic derivatives
such as P-ribose-PP, NADH, NADPH, UTP, CTP, and UDP-N-acetyl glucosamine is also
enhanced during cell proliferation. Another phosphometabolite derived from
P-ribose-PP, AMP, inhibits cell proliferation. The accumulation of AMP inhibits
both P-ribose-PP-synthetase and the increase in concentration of
phosphometabolites derived from P-ribose-PP. In cells with low glycerol
3-phosphate and malate-aspartate shuttle capacities the inhibition of the
lactate dehydrogenase by low NADH levels leads to an inhibition of glycolytic
ATP production. Several tumor-therapeutic drugs reduce NAD and NADH levels,
thereby inhibiting glycolytic energy production. The role of AMP, NADH, and
NADPH levels in the success of chemotherapeutic treatment is discussed.
- Language of Publication
- English
- Unique Identifier
- 98048333
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- MeSH Heading (Major)
- Cell Division|*; Energy Metabolism|*/DE; Neoplasms|DT/*ME/PA; Phosphates|*ME
- MeSH Heading
- Antineoplastic Agents|PD; Apoptosis; Glutamine|ME; Glycolysis; Human;
Neoplasm Metastasis; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0145-479X
- Country of Publication
- UNITED STATES
Record 23 from database: MEDLINE
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- Title
- How does hyperglycaemia predispose to diabetic nephropathy?
- Author
- Wardle EN
- Address
-
- Source
- QJM, 1996 Dec, 89:12, 943-51
- Abstract
- Diabetic nephropathy is preceded by 'hyperfiltration' mediated by dilatation
of the afferent arterioles to the glomeruli by means of IGF-1, prostaglandins,
bradykinin, nitric oxide and atrial natriuretic peptide, together with
constriction of the efferent arterioles by local thromboxane A2. Raised
glomerular intracapillary pressures might then contribute to glomerulosclerosis,
but in any case there is permeability of the vascular endothelium. AGEPs and
lipid peroxides can explain this. AGEPs, or simply intermittently high levels of
glucose, also account for synthesis of extracellular matrix proteins that lead
to thickening of the basement membrane and glomerulosclerosis. Another glucose
product, glucosamine-6-phosphate, is formed when there is hexosamine flux along
with insulin resistance in tissues, and is implicated in glomerulosclerosis,
since it also stimulates TGF-beta transcription. In seeking to explain
proteinuria, depletion of heparan sulphates from the endothelial cells and GBM
is now established as a principal cause. In addition to a high glucose reducing
the synthesis of heparan sulphates, it has now been shown that high glucose may
depress the synthesis of heparin sulphate proteoglycan.
- Language of Publication
- English
- Unique Identifier
- 97167871
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- MeSH Heading (Major)
- Diabetic Nephropathies|*ET/ME/PA; Hyperglycemia|*CO/ME/PA
- MeSH Heading
- Enzyme Activation; Glycosylation; Heparin|ME; Human; Kidney|PA; Protein
Kinase C|ME; Thromboxane A2|ME
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- Country of Publication
- ENGLAND
Record 24 from database: MEDLINE
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- Title
- Interactions of human malaria parasites, Plasmodium vivax and P.falciparum,
with the midgut of Anopheles mosquitoes.
- Author
- Ramasamy MS; Kulasekera R; Wanniarachchi IC; Srikrishnaraj KA; Ramasamy R
- Address
- Division of Life Sciences, Institute of Fundamental Studies, Kandy, Sri
Lanka.
- Source
- Med Vet Entomol, 1997 Jul, 11:3, 290-6
- Abstract
- Present understanding of the development of sexual stages of the human
malaria parasites Plasmodium vivax and P.falciparum in the Anopheles vector is
reviewed, with particular reference to the role of the mosquito midgut in
establishing an infection. The sexual stages of the parasite, the gametocytes,
are formed in human erythrocytes. The changes in temperature and pH encountered
by the gametocyte induce gametogenesis in the lumen of the midgut.
Macromolecules derived from mosquito tissue and second messenger pathways
regulate events leading to fertilization. In An.tessellatus the movement of the
ookinete from the lumen to the midgut epithelium is linked to the release of
trypsin in the midgut and the peritrophic matrix is not a firm barrier to this
movement. The passage of the P.vivax ookinete through the peritrophic matrix may
take place before the latter is fully formed. The late ookinete development in
P.falciparum requires chitinase to facilitate penetration of the peritrophic
matrix. Recognition sites for the ookinetes are present on the midgut epithelial
cells. N-acetyl glucosamine residues in the oligosaccharide side chains of
An.tessellatus midgut glycoproteins and peritrophic matrix proteoglycan may
function as recognition sites for P.vivax and P.falciparum ookinetes. It is
possible that ookinetes penetrating epithelial cells produce stress in the
vector. Mosquito molecules may be involved in oocyst development in the basal
lamina, and encapsulation of the parasite occurs in vectors that are refractory
to the parasite. Detailed knowledge of vector-parasite interactions,
particularly in the midgut and the identification of critical mosquito molecules
offers prospects for manipulating the vector for the control of malaria.
- Language of Publication
- English
- Unique Identifier
- 97471321
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- MeSH Heading (Major)
- Anopheles|*PS; Digestive System|*PS; Plasmodium falciparum|*PH; Plasmodium
vivax|*PH
- MeSH Heading
- Animal; Erythrocytes|PH; Host-Parasite Relations; Human; Life Cycle Stages;
Reproduction; Support, Non-U.S. Gov't
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0269-283X
- Country of Publication
- ENGLAND
Record 25 from database: MEDLINE
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- Title
- Shedding of CD9 antigen in acute lymphoblastic leukemia.
- Author
- Komada Y; Sakurai M
- Address
- Department of Pediatrics, Mie University School of Medicine, Japan.
- Source
- Leuk Lymphoma, 1994 Feb, 12:5-6, 365-72
- Abstract
- A leukemia-associated CD9 glycoprotein antigen released into the
extracellular milieu from acute lymphoblastic leukemia cells has been detected
using a unique lectin-monoclonal antibody immunoassay. It has been demonstrated
that the release of CD9 antigen is an active process and is associated with
active cell growth. In addition, the difference of carbohydrate moiety, and
hence glycosylation, in the CD9 antigen derived from lymphoblasts and
neuroblasts was verified using lectin affinity chromatography. The lectin
affinity of the carbohydrate moiety of lymphoblast CD9 antigen would indicate
the presence of N-linked oligosaccharide chains having groups of N-acetyl
glucosamine residues, a mannose core and a terminal D-galactose. The soluble CD9
antigen is specifically detected in plasma from ALL patients at the time of
diagnosis, in cerebrospinal fluid from patients with central nervous system
involvement, and spent medium from CD9-positive leukemic blasts obtained at the
time of diagnosis. Interestingly when bone marrow cells taken from patients in
complete remission were studied, a distinct amount of CD9 antigen was released
into spent medium in some of the cases. All of these patients have subsequently
developed hematological relapse. The present data suggest that shedding of CD9
antigen by leukemic cells may enable the clinical monitoring of residual
leukemic cell burden.
- Language of Publication
- English
- Unique Identifier
- 94236127
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- MeSH Heading (Major)
- Antigens, CD|*AN/CF; Leukemia, Lymphocytic, Acute|*IM
- MeSH Heading
- Human
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 1042-8194
- Country of Publication
- SWITZERLAND
Record 26 from database: MEDLINE
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- Title
- Ectodomain interactions of leukocyte integrins and pro-inflammatory
GPI-linked membrane proteins.
- Author
- Petty HR; Kindzelskii AL; Adachi Y; Todd RF 3rd
- Address
- Department of Biological Sciences, Wayne State University, Detroit, MI
48202, USA.
- Source
- J Pharm Biomed Anal, 1997 Jun, 15:9-10, 1405-16
- Abstract
- Although glycosylphosphatidyl-inositol (GPI) linked membrane proteins do not
possess transmembrane or cytosolic sequences they elicit transmembrane signals.
Using microscopic fluorescence imaging and resonance energy transfer (RET)
techniques we have shown that certain pro-inflammatory GPI-linked membrane
proteins can interact with leukocyte beta 2 integrins (complement receptor type
3 (CR3) and 4 (CR4) and the leukocyte function-associated antigen-1 (LFA-1)).
For example, physical associations between CR3 and Fc gamma RIIIB, CR3 and
urokinase receptors, and CR3 and CD14 (lipopolysaccharide receptor) have been
found. Although Fc gamma RIIIB appears to be constitutively associated with CR3,
urokinase receptors and CD14 associations with CR3 are influenced by their
ligation status and cell function (e.g. adherence and locomotion).
CR3-to-urokinase receptor interactions have been confirmed by
immunoprecipitation techniques. Immunoprecipitation of CR3 from Brij-58 lysates
after biotinylation of neutrophil membranes revealed proteins of M(r) = 40,000,
50,000, 74,000 and 120,000, in addition to bands corresponding to the integrin
alpha and beta chains. Cell functions such as transmembrane signaling and
superoxide release/priming have been linked to these interactions. Importantly,
reagents that affect the lectin-like site of CR3, such as
N-acetyl-D-glucosamine, alpha-methyl-D-mannoside and beta-glucan alter these
interactions and, in parallel, leukocyte functions. Thus, the interactions of
GPI-linked proteins and integrins can be highly dynamic events linked to cell
activities. Our studies suggest that it may be possible to develop new drugs
directed at the lectin-like site of beta 2 integrins that block GPI-linked
protein-to-integrin coupling thereby controlling inflammatory cell processes
including cell adherence, locomotion and activation. Such drugs may be useful in
clinical conditions such as ischemia-reperfusion injury, sepsis, arthritis and
others.
- Language of Publication
- English
- Unique Identifier
- 97370194
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- MeSH Heading (Major)
- Antigens, CD18|*BL; Glycosylphosphatidylinositols|*CH; Inflammation
Mediators|*CH; Leukocytes|*CH; Membrane Proteins|*CH; Protein Structure,
Tertiary|*
- MeSH Heading
- Carbohydrate Conformation; Human; Macrophage-1 Antigen|BL; Support, Non-U.S.
Gov't; Support, U.S. Gov't, P.H.S.
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0731-7085
- Country of Publication
- ENGLAND
Record 27 from database: MEDLINE
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- Title
- Effect of low molecular weight heparin preparations on the inhibition of
thrombin by heparin cofactor II.
- Author
- Tollefsen DM; Sugimori T; Maimone MM
- Address
- Department of Medicine, Washington University School of Medicine, St. Louis,
Missouri 63110.
- Source
- Semin Thromb Hemost, 1990 Oct, 16 Suppl:, 66-70
- Abstract
- 1. Heparin molecules approximately 24 to 30 residues in length are required
to catalyze the thrombin-HC II reaction. The requirement for heparin molecules
of this length is consistent with a model for catalysis in which heparin binds
HC II and thrombin simultaneously to form a ternary complex in a manner similar
to that proposed for the thrombin-AT III reaction. Smaller molecules (18 or more
monosaccharide units in length) are required to catalyze the thrombin-AT III
reaction. 2. The specific AT III-binding pentasaccharide containing 3-O-sulfated
glucosamine is not required for activity with HC II. 3. Some low molecular
weight heparin preparations have significant activity with HC II (approximately
10 to 20% that of standard heparin). This is probably related to the presence of
species with molecular weights greater than 6000 to 7500 (24 to 30
monosaccharide units) in these preparations.
- Language of Publication
- English
- Unique Identifier
- 91142784
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- MeSH Heading (Major)
- Heparin Cofactor II|*PH; Heparin, Low-Molecular-Weight|*PD; Thrombin|*AI
- MeSH Heading
- Antithrombin III|PH; Human; Oligosaccharides|PD
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0094-6176
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- EC 3.4.21.5 (Thrombin); 0 (Heparin, Low-Molecular-Weight); 0
(Oligosaccharides); 81604-65-1 (Heparin Cofactor II); 9000-94-6 (Antithrombin
III)
Record 28 from database: MEDLINE
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- Title
- The PIG-A gene somatic mutation responsible for paroxysmal nocturnal
hemoglobinuria.
- Author
- Rotoli B; Boccuni P
- Address
- Division of Hematology, Federico II University Medical School, Naples,
Italy.
- Source
- Haematologica, 1995 Nov, 80:6, 539-45
- Abstract
- Paroxysmal nocturnal hemoglobinuria is the first example of a non neoplastic
human disease caused by the somatic mutation of an X-linked gene. The PIG-A gene
maps to Xp22.1 and is required for the transfer of N-acetyl glucosamine to
phosphoinositol, an early step in the production of the GPI anchor. A deficiency
of GPI-linked proteins on the cell surface is responsible for the PNH cell
defect, which can be detected by flow cytometry not only on red cells, but also
on myeloid cells and in some patients even on lymphoid cells. Its location on
the X-chromosome explains how a single recessive mutation can cause the
appearance of the abnormal clone. A number of patients may have more than one
PNH clone, suggesting that the expansion of GPI-deficient clones occurs under
the pressure of a selection mechanism.
- Language of Publication
- English
- Unique Identifier
- 96226664
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- MeSH Heading (Major)
- Hemoglobinuria, Paroxysmal|*GE; Point Mutation|*
- MeSH Heading
- Human; Linkage (Genetics); Support, Non-U.S. Gov't; X Chromosome
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL
- ISSN
- 0390-6078
- Country of Publication
- ITALY
Record 29 from database: MEDLINE
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- Title
- Mucin glycoproteins as tumor markers.
- Author
- Feller WF; Henslee JG; Kinders RJ; Manderino GL; Tomita JT; Rittenhouse HG
- Address
- Georgetown University School of Medicine, Washington, D.C.
- Source
- Immunol Ser, 1990, 53:, 631-72
- Abstract
- Extensive biochemical studies have shown that mucin tumor antigens have a
range of molecular sizes from 200 to greater than 1000 kDa. The molecular size
of mucin antigens can be dramatically affected by the source and method of
purification. Mucin antigens vary from 24 to 80% in carbohydrate content and
their density is usually greater than 1.40 g/ml. Galactose and N-acetyl
glucosamine are the predominant sugar residues in many mucins, whereas mannose
is usually present in low levels or absent. The amino acids serine, threonine,
alanine, glycine, and proline are abundant in mucins. An O-glycosidic linkage
between the carbohydrate and protein of mucins is the most common linkage
encountered. The gene encoding the core peptide for at least one mucin tumor
marker, HMFG, has been identified, sequenced, and expressed. These findings may
lead to a better understanding of the multiepitope nature of mucin tumor
markers. The advent of hybridoma technology has yielded several monoclonal
antibodies that have been used to identify the presence of tumor-associated
mucins in the sera of cancer patients. Elevated levels of mucin antigens have
been found in the serum of most patients with advanced adenocarcinomas. Many
studies have shown that tumor-associated markers are useful in monitoring
patients following cancer treatment. Clinically useful immunoassays have been
developed for monitoring patients with ovarian, breast, and pancreatic
adenocarcinomas. Although individual mucin tumor markers show limited utility in
detecting early adenocarcinoma, recent studies using multiple mucin markers have
suggested that early detection, at sensitivities greater than 50%, can be
achieved.
- Language of Publication
- English
- Unique Identifier
- 91308321
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- MeSH Heading (Major)
- Antigens, Neoplasm|*AN; Glycoproteins|*AN/BI/IM; Mucins|*AN/IM; Neoplasm
Proteins|*AN/BI/IM; Neoplasms|*DI; Tumor Markers, Biological|*AN
- MeSH Heading
- Animal; Antibodies, Monoclonal|DU; Female; Glycosylation; Human; Male;
Predictive Value of Tests; Protein Processing, Post-Translational; Species
Specificity
- Publication Type
- JOURNAL ARTICLE; REVIEW; REVIEW, ACADEMIC
- ISSN
- 0092-6019
- Country of Publication
- UNITED STATES
- CAS Registry/EC Number
- 0 (Antibodies, Monoclonal); 0 (Antigens, Neoplasm); 0 (Glycoproteins); 0
(Mucins); 0 (Neoplasm Proteins); 0 (Tumor Markers, Biological)
Record 30 from database: MEDLINE
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