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Query: UMLS:C0040822 (
tremor
)
18,428
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Ftorafur is a 5-fluorouracil analogue which is slowly metabolized to 5-FU, resulting in prolonged therapeutic levels of this latter drug. Ninety-one evaluable patients with metastatic breast cancer were treated with Ftorafur, Adriamycin, cyclophosphamide, and BCG (ACFTOR-BCG), in an attempt to increase the effectiveness of the program or decrease its myelosuppressive toxicity. The results of this trial were compared to those previously reported with the combination of 5-FU, Adriamycin, cyclophosphamide, and BCG (FAC-BCG). Overall objective response rates were 65% and 76% for ACFTOR-BCG and FAC-BCG, respectively. Durations of response were 12 months and 14 months for ACFTOR-BCG and FAC-BCG (p = 0.53). The median survival of responders was 22 and 23.9 months, respectively. Substantial toxicity was observed with Ftorafur: nausea and vomiting severe enough to cause weight loss was observed in a substantially higher fraction of the patients treated with this drug than with 5-FU. Other side-effects, which were not observed with the 5-FU combination, were somnolence, dizziness, personality changes,
tremor
, ataxia, and confusion. No differences in myelosuppressive toxicity were observed between the two combinations, and the incidence of infectious complications was identical. The combination of Ftorafur, Adriamycin, cyclophosphamide and BCG did not offer any advantages with respect to increased effectiveness or reduced toxicity over the FAC-BCG regimen in breast
carcinoma
.
...
PMID:Ftorafur, adriamycin, cyclophosphamide and BCG in the treatment of metastatic breast cancer. 38 55
A very simple, rapid and reproducible method has been developed for studying the interaction of lectins with the cell surface. This involves determining the number of adherent cells after
shaking
cell suspensions in Petri dishes which have had a lectin coupled to their surface using 1-cyclohexyl-3-(2-morpholinoethyl) carbodiimide metho-p-toluene sulfonate. Using concanavalin A coupled to 60 mm diameter dishes and between 1.5 and 2 x 10(6) tumour cells, this adhesion reached a maximum after 10 min
shaking
. Maximum cell adhesion also varied according to the particular lectin used. Adhesion was absent or was very low if cells were shaken in untreated dishes, or in dishes coupled to bovine serum albumin, or in the presence of the lectin-specific sugar-competitor. Under conditions of maximum cell adhesion, the binding of two different lymphosarcoma lines to four different lectins was very similar, whereas the binding of a
carcinoma
line to these lectins was completely different from that observed for the lymphosarcomas.
...
PMID:A simple lectin-mediated cell-adhesion method for investigating the cell surface. 58 40
Two patients had ocular myasthenia gravis coexistent with Hashimoto's thyroiditis. A 37-year-old woman presented with diplopia and displayed a head
tremor
and thyroid enlargement. Thyroid function tests showed an elevated thyroid stimulating hormone (TSH). A quantitative Tensilon test yeilded a "perverse" response and a needle biopsy indicated Hashimoto's disease. A 26-year-old woman presented with diplopia and subsequently developed blepharoptosis and thyroid enlargement. Examination revealed Cogan's eyelid twitch sign, a paradoxical quantitative Tensilon test, and laboratory studies revealed normal thyroid function tests. Treatment was directed at each disease entity separately. Ocular myasthenia gravis was managed with an anticholinesterase agent in combination with oral corticosteroids that provided additional control. Suppressive therapy with desiccated thyroid hormone reduced the size of the thyroid gland, diminished the signs and symptoms of hypothyroidism, and lowered the levels of TSH, possibly decreasing the risk of thyroid
carcinoma
. Both patients showed gratifying responses to therapy.
...
PMID:Ocular myasthenia gravis and Hashimoto's thyroiditis. 117 40
A 76-year-old female patient with a large neck lump of 15-year duration, was accompanied by palpitation and
tremor
. The lump was 9 x 5cm in size and the lower half of it was not palpable because the lower pole was located in the mediastinum. Physical examination revealed two enlarged lymph nodes in the right supraclavicular area. Chest X-ray film showed a coin lesion in the right lung that seemed to be a metastasis. The patient was apparently thyrotoxic with elevated serum concentrations of 15.7 micrograms/dl thyroxin and 359 ng/dl triiodothyronine. A neck scintigraphy using 123Iodine showed a thyroid hot nodule in accordance with this lesion. A total thyroidectomy with a modified neck dissection was carried out. This was followed by 131Iodine therapy. Specimen of the primary lesion weighed 147 g. Pathology of this tumor was follicular
carcinoma
of the thyroid. The patient was doing well 14 months after surgery. In the literature, three cases of similar hyperfunctioning thyroid
carcinoma
have been reported, all of which had a large primary lesion. The histological features proved to be of follicular or papillofollicular type. The treatment in these cases was administration of an antithyroid drug followed by surgical removal.
...
PMID:[Hyperfunctioning follicular carcinoma of the thyroid. A case report]. 336 32
The effects of ranitidine hydrochloride, a histamine H2-receptor antagonist, on delivery, lactation, postnatal development of F1 generation of Crj:CD (SD) rats were examined. Ranitidine hydrochloride was intravenously administered once daily from day 17 of gestation to day 21 after delivery at dose levels of 5, 15 and 40 mg/kg in base weight respectively. All females were allowed to litter naturally, and postnatal development of offsprings was observed. Tachypnea, prone position and transient
tremor
were observed for approximately one minute directly after an intravenous administration of ranitidine in the dose of 40 mg/kg, which were probably induced by a rapid fall in blood pressure. In delivery and postpartum observation, there occurred no influence of the ranitidine administration on maternal body weight, delivery and lactation. In studies on general behavior of F1 rats, no abnormal changes were observed on postnatal development and various functions such as reflex response and learning. Ranitidine treatment did not affect reproductive performances of F1 generation. A slight inhibition in body weight gain and a slight decrease in average weight of liver were observed in F1 females of 40 mg/kg group, but no other influence attributable to the ranitidine administration was observed on the general state and development of offsprings. In necropsy of offsprings, hydronephrosis, transitional
epithelial carcinoma
, kinky tail, unilateral absence of testis and epididymis were observed in one case of ranitidine-treated groups. But they were not attributable to administration of ranitidine. In summary, it was concluded that ranitidine hydrochloride had no effects on delivery and lactation of dams, and also on viability, development and various functions of F1 generation at the dose of 40 mg/kg/day or less.
...
PMID:[Effects of intravenous administration of ranitidine hydrochloride to the female rat in perinatal and postnatal periods]. 609 58
We present three cases of the adult opsoclonus-myoclonus syndrome in patients with systemic
carcinoma
. In addition to opsoclonus and myoclonus, other clinical components of the syndrome can include ataxia,
tremor
, gait and stance dysfunction, altered mental status, and head and face dyskinesias. The most common etiologies are idiopathic, paraneoplastic, and infectious encephalitis. Radiographic and pathological studies suggest brain-stem dysfunction with associated cerebellar and/or cerebellar pathway dysfunction. In many cases, there is evidence for the involvement of immunologic and/or inflammatory processes in the pathogenesis of this syndrome. The timely recognition of this syndrome is important because of its implications for the underlying etiology and prognosis. The appearance of this syndrome should prompt the search for an occult malignancy.
...
PMID:The movement disorder of adult opsoclonus. 788 52
Sarcoidosis is a systemic chronic granulomatous disease of unknown etiology most commonly affecting young females. The disease was first described in the thyroid gland in 1938. Our patient, a 27-year-old male with known sarcoidosis, was referred to the National University Hospital for acute symptoms of thyrotoxicosis (weight loss of 6 kg,
tremor
, thyroid enlargement, and tachycardia). Laboratory findings showed suppressed serum thyrotropin (TSH, <0.03 mU/L [0.5-4.20]), increased total thyroxine (T4) (223 nmol/L, [60-140]), and triiodothyronine (T3) (8.5 nmol/L, [1.5-2.7]). Furthermore, Tc-99m pertechnetate scintigraphy disclosed diffuse accumulation of the isotope confirming the diagnosis of Graves' disease. During the next 18 months of antithyroid treatment (thiamazole, Thycapzol) hyperthyroidism was difficult to control, the thyroid gland gradually enlarged, and surgery was recommended. Initially, the patient declined surgery but after an additional 18 months, he accepted surgery. During the 36-month period of antithyroid drug treatment TSH was suppressed (<0.01 mU/L) and T3 often elevated despite high doses of thiamazole. Total thyroidectomy was performed, and histologic examination of the removed thyroid tissue confirmed the diagnosis of Graves' disease and also the presence of sarcoid granuloma and metastatic papillary adenocarcinoma with spread to neck lymph nodes. Four months later, a modified radical neck dissection was performed with removal of neck lymph nodes followed by external radiation therapy (2 Gy x 32 fractions to the neck). The concomitant presence of sarcoidosis, papillary
carcinoma
, and Graves' disease in a thyroid gland, to our knowledge, has not previously been described in the literature.
...
PMID:A case of sarcoidosis and sarcoid granuloma, papillary carcinoma, and Graves' disease in the thyroid gland. 1077 43
A 65-year-old woman was operated for gastric adenocarcinoma in 1989. Six years later, peritonitis carcinomatosa, swelling of periaortic lymphnodes and high serum CA-125 were discovered. She received chemotherapy with 5-FU and cisplatin resulting in reduction of ascites. In September, 1998, the swelling of left supraclavicular lymphnodes and the elevation of serum CA-125 reappeared. Pathological diagnosis of supraclavicular lymphnodes was adenocarcinoma. Serum CA-125 was normalized by chemotherapy using cisplatin, farumorubicin and endoxan. However, unsteadiness appeared since December 10, 1998 followed by dysarthria and involuntary movement of neck and upper limbs. These symptoms progressed subacutely. The physical examination on admission revealed swelling of left suraclavicular lymphnodes, nystagmus on lateral gaze, saccadic eye movement on smooth pursuit and severe cerebellar ataxia. In addition, resting
tremor
of 3-4 Hz was observed at right hand, left wrist and neck which tended to increase amplitude by calculation. Similar movements were seen in the left first toe, though the frequency was lower. Brain MRI revealed mild cerebellar atrophy. She was diagnosed as paraneoplastic cerebellar degeneration (PCD) by serum anti Yo antibody and clinical course. The study of HLA showed positive link to A4 without A24. The primary focus of adenocarcinoma in cervical lymphnodes was suggested to be ovary rather than stomach due to the pattern of immunostaining for cytokeratin, CEA and CA125, although no
carcinoma
was found in ovarium clinically. The feature of this case is a PCD with resting
tremor
of frequency of 3-4 Hz and negative link to HLA-A24 in Japanese.
...
PMID:[A case of paraneoplastic cerebellar degeneration with resting tremor]. 1143 63
The investigational anti-cancer drug 5,6-dimethylxanthenone-4-acetic acid (DMXAA) was developed by the Auckland Cancer Society Research Centre (ACSRC). It has recently completed Phase I trials in New Zealand and UK under the direction of the Cancer Research Campaign's Phase I/II Clinical Trials Committee. As a biological response modifier, pharmacological and toxicological properties of DMXAA are remarkably different from most conventional chemotherapeutic agents. Induction of cytokines (particularly tumour necrosis factor (TNF-alpha), serotonin and nitric oxide (NO)), anti-vascular and anti-angiogenic effects are considered to be major mechanisms of action based on in vitro and animal studies. In cancer patients of Phase I study, DMXAA also exhibited various biological effects, including induction of TNF-alpha, serotonin and NO, which are consistent with those effects observed in in vitro and animal studies. Preclinical studies indicated that DMXAA had more potent anti-tumour activity compared to flavone-8-acetic acid (FAA). In contrast to FAA that did not show anti-tumour activity in cancer patients, DMXAA (22 mg/kg by intravenous infusion over 20 min) resulted in partial response in one patient with metastatic cervical squamous
carcinoma
in a Phase I study where 65 cancer patients were enrolled in New Zealand. The maximum tolerated dose (MTD) in mouse, rabbit, rat and human was 30, 99, 330, and 99 mg/kg respectively. The dose-limiting toxicity of DMXAA in cancer patients included acute reversible
tremor
, cognitive impairment, visual disturbance, dyspnoea and anxiety. The plasma protein binding and distribution into blood cells of DMXAA are dependent on species and drug concentration. DMXAA is extensively metabolised, mainly by glucuronidation of its acetic acid side chain and 6-methylhydroxylation, giving rise to DMXAA acyl glucuronide (DMXAA-G), and 6-hydroxymethyl-5-methylxanthenone-4-acetic acid (6-OH-MXAA), which are excreted into bile and urine. DMXAA-G has been shown to be chemically reactive, undergoing hydrolysis, intramolecular migration and covalent binding. Studies have indicated that DMXAA glucuronidation is catalysed by uridine diphosphate glucuronosyltransferases (UGT1A9 and UGT2B7), and 6-methylhydroxylation by cytochrome P450 (CYP1A2). Non-linear plasma pharmacokinetics of DMXAA has been observed in animals and patients, presumably due to saturation of the elimination process and plasma protein binding. Species differences in DMXAA plasma pharmacokinetics have been observed, with the rabbit having the greatest plasma clearance, followed by the human, rat and mouse. In vivo disposition studies in these species did not provide an explanation for the differences in MTD. Co-administration of DMXAA with other drugs has been shown to result in enhanced anti-tumour activity and alterations in pharmacokinetics, as reported for the combination of DMXAA with melphalan, thalidomide, cyproheptadine, and the bioreductive agent tirapazamine, in mouse models. Species-dependent DMXAA-thalidomide pharmacokinetic interactions have been observed. Co-administration of thalidomide significantly increased the plasma area of the plasma concentration-time curve (AUC) of DMXAA in mice, but had no effect on DMXAA's pharmacokinetics in the rat. It appears that the pharmacological and toxicological properties of DMXAA as a new biological response modifier are unlikely to be predicted based on preclinical studies. Similar to many biological response modifiers, DMXAA alone did not show striking anti-tumour activity in patients. However, preclinical studies of DMXAA-drug combinations indicate that DMXAA may have a potential role in cancer treatment when co-administered with other drugs. Further studies are required to explore the molecular targets of DMXAA and mechanisms for the interactions with other drugs co-administered during combination treatment, which may allow for the optimisation of DMXAA-based chemotherapy.
...
PMID:5,6-dimethylxanthenone-4-acetic acid (DMXAA): a new biological response modifier for cancer therapy. 1220 91
Hydroquinone is used an antioxidant in the rubber industry and as a developing agent in photography. It is also an intermediate in the manufacture of rubber and food antioxidants and monomer inhibitors. Hydroquinone and products containing hydroquinone are used as depigmenting agents to lighten skin. NTP Toxicology and Carcinogenesis studies were conducted by administering hydroquinone (greater than 99% pure) in corn oil or water by gavage to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 weeks, or 2 years. Additionally, genetic toxicology studies were conducted in Salmonella typhimurium, mouse lymphoma cells, Chinese hamster ovary (CHO) cells, and Drosophila melanogaster. Preliminary 3-day dermal studies were conducted with rats and mice using sufficient hydroquinone in 95% ethanol to crystallize on the skin (4 or 40 mg per animal); conjugated metabolites of hydroquinone were detected in the urine. Fourteen-day dermal studies were conducted at doses up to 3,840 mg/kg for rats and 4,800 mg/kg for mice. No toxic effects were seen in the 3- or 14-day dermal studies. Therefore, in further evaluations of hydroquinone, the gavage route of administration was used. Results of Fourteen-Day and Thirteen-Week Studies: Fourteen-day gavage studies were conducted by administering hydroquinone in corn oil to rats at doses ranging from 63 to 1,000 mg/kg body weight and to mice at doses ranging from 31 to 500 mg/kg. All rats receiving 1,000 mg/kg and 1/5 male and 4/5 female rats receiving 500 mg/kg died before the end of the 14 days. Compound-related clinical signs in rats included tremors lasting up to 30 minutes after each dosing at 500 and 1,000 mg/kg. In the 14-day gavage studies with mice, 4/5 male mice and 5/5 female mice receiving 500 mg/kg and 3/5 males receiving 250 mg/kg died before the end of the studies.
Tremors
followed by convulsions were seen at 250 and 500 mg/kg. In the 13-week studies, doses for rats and mice ranged from 25 to 400 mg/kg. All rats receiving 400 mg/kg and 3/10 female rats receiving 200 mg/kg died before the end of the studies. The mean body weight at necropsy of male rats administered 100 or 200 mg/kg was about 8%-9% lower than that of vehicle controls. Mean body weights of vehicle control and dosed female rats at necropsy were similar.
Tremors
and convulsions were observed after dosing in most rats receiving 400 mg/kg and in several female rats receiving 200 mg/kg. Inflammation and/or epithelial hyperplasia (acanthosis) of the forestomach were seen in 4/10 male rats and 1/10 female rats receiving 200 mg/kg. Toxic nephropathy, characterized by tubular cell degeneration in the renal cortex, was seen in 7/10 male and 6/10 female rats receiving 200 mg/kg and in 1/10 females receiving 100 mg/kg. In the 13-week studies in mice, 8/10 males and 8/10 females receiving 400 mg/kg and 2/10 male mice receiving 200 mg/kg died early. Mean body weights of dosed and vehicle control mice at necropsy were similar. Liver weight to body weight ratios for dosed male mice were significantly greater than for vehicle controls. Ulceration, inflammation, or epithelial hyperplasia of the forestomach was found in 3/10 male and 2/10 female mice receiving 400 mg/kg and 1/10 females receiving 200 mg/kg. Based on these collective results, 2-year studies were conducted by administering 0, 25, or 50 mg/kg hydroquinone in deionized water by gavage to groups of 65 rats of each sex, 5 days per week. Groups of 65 mice of each sex were administered 0, 50, or 100 mg/kg on the same schedule. Ten rats and 10 mice from each group were killed after 15 months for an interim evaluation. Observations at Fifteen Months: In the rats killed at 15 months, the relative kidney weight for high dose male rats was greater than that for vehicle controls. The hematocrit value, hemoglobin concentration, and erythrocyte count for high dose female rats were decreased. Compound-related increased severity of nephropathy was observed in male rats. In mice killed at 15 months, the relative liver weights for high dose male and female mice were signif and female mice were significantly greater than those for vehicle controls. Lesions seen in the liver of male mice included increased syncytial cells and diffuse cytomegaly. Body Weights, Organ Weights, and Survival in the Two-Year Studies: Mean body weights of high dose male rats were 5%-13% lower than those of vehicle controls after week 73, and those of low dose male rats were 5%-9% lower than those of vehicle controls after week 89. Mean body weights of dosed female rats were similar to those of vehicle controls throughout the study. The relative kidney and liver weights for high dose male rats were higher than those for vehicle controls. Mean body weights of high dose male mice were 5%-8% lower than those of vehicle controls after week 93, and those of high dose female mice were 5%-14% lower after week 20. Relative liver weights were increased for dosed male and high dose female mice. No significant differences in survival were observed between any groups of rats or mice of either sex after 2 years (male rats: vehicle control, 27/55; low dose, 18/55; high dose, 18/55; female rats: 40/55; 27/55; 32/55; male mice: 33/55; 37/54; 36/55; female mice: 37/55; 39/55; 36/55). Nonneoplastic and Neoplastic Effects in the Two-Year Studies: Nearly all male rats and most female rats in all vehicle control and dosed groups had nephropathy. The severity of this disease was judged to be greater in high dose male rats. Hyperplasia of the renal pelvic transitional epithelium and renal cortical cysts, changes observed with advanced renal disease, were increased in male rats. Renal tubular hyperplasia was seen in 2 high dose male rats, and renal tubular adenomas were seen in 4/55 low dose and 8/55 high dose male rats; none was seen in vehicle controls. Mononuclear cell leukemia in female rats occurred with a positive trend, and the incidences in the dosed groups were greater than that in the vehicle controls (vehicle control, 9/55; low dose, 15/55; high dose, 22/55). The historical incidence of leukemia in water gavage vehicle control female F344/N rats is 25% ± 15% and in untreated controls is 19% ± 7%. Compound-related lesions observed in the liver of high dose male mice included anisokaryosis (0/55; 2/54; 12/55), syncytial alteration (5/55; 3/54; 25/55), and basophilic foci (2/55; 5/54; 11/55). The incidences of hepatocellular adenomas were increased in dosed male mice (9/55; 21/54; 20/55), but these increases were offset by decreases in the incidences of hepatocellular carcinomas (13/55; 11/54; 7/55). The incidences of hepatocellular neoplasms, primarily adenomas, were increased in dosed female mice (3/55; 16/55; 13/55). Follicular cell hyperplasia of the thyroid gland was increased in dosed mice (male: 5/55; 15/53; 19/54; female: 13/55; 47/55; 45/55). Follicular cell adenomas were seen in 2/55 vehicle control, 1/53 low dose, and 2/54 high dose male mice and in 3/55 vehicle control, 5/55 low dose, and 6/55 high dose female mice, a follicular cell
carcinoma
was seen in a seventh high dose female mouse. The highest observed incidence of follicular cell adenomas or carcinomas(combined) in historical water gavage vehicle control female B6C3F1 mice is 3/48 (6%). Genetic Toxicology: Hydroquinone was not mutagenic in S. typhimurium strains TA98, TA100, TA1535, or TA1537 with or without exogenous metabolic activation. It induced trifluorothymidine (Tft) resistance in mouse L5178Y/TK lymphoma cells in the presence or absence of metabolic activation. An equivocal response was obtained in tests for induction of sex-linked recessive lethal mutations in Drosophila administered hydroquinone by feeding. Hydroquinone induced sister chromatid exchanges (SCEs) in CHO cells both with or without exogenous metabolic activation and caused chromosomal aberrations in the presence of activation. Conclusions: Under the conditions of these 2-year gavage studies, there was some evidence of carcinogenic activity of hydroquinone for male F344/N rats, as shown by marked increases in tubular cell adenomas of the kidney. There was some evidence of carcinogenic activity of hydroquinone for female F344/N rats, as shown by increases in mononuclear cell leukemia. There was no evidence of carcinogenic activity of hydroquinone for male B6C3F1 mice administered 50 or 100 mg/kg in water by gavage. There was some evidence of carcinogenic activity of hydroquinone for female B6C3F1 mice, as shown by increases in hepatocellular neoplasms, mainly adenomas. Administration of hydroquinone was associated with thyroid follicular cell hyperplasia in both male and female mice and anisokaryosis, multinucleated hepatocytes, and basophilic foci of the liver in male mice. Synonyms: 1,4-benzenediol; p-benzenediol; benzohydroquinone; benzoquinol; 1,4-dihydroxybenzene; p-dihydroxybenzene; p-dioxobenzene; p-dioxybenzene; hydroquinol; hydroquinole; a-hydroquinone; p-hydroquinone; p-hydroxyphenol; quinol; b-quinol
...
PMID:NTP Toxicology and Carcinogenesis Studies of Hydroquinone (CAS No. 123-31-9) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1269 38
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