Parotid glands

Adverse effects with bretylium include hypotension, nausea, vomiting, parotid gland tenderness, and arrhythmogenesis (1,2). [Pg.121]

Ohr-speicheldriise, /. parotid gland, -stein, m. otolith, -trommel,/, eardrum, -trompete,/. (Anat.) Eustachian tube, -wachs, n. ear wax, cerumen, -wasser, n. endolymph. [Pg.326]

By extraction of animal lymph glands, parotid glands, pancreas, liver, milt and blood serum with diluted acetic acid-ethanol-mixtures upon removal of fat and proteins. [Pg.134]

Magert H., Cieslak A., Alkan O., Luscher B., et al. (1999). The golden hamster aphrodisin gene — stmcture, expression in parotid glands of female animals, and comparison with a similar murine gene. J Biol Chem 274, 444-450. [Pg.226]

Mumps is an acute viral infection transmitted by airborne droplets. Mumps is considered to be a childhood infection affecting those between 5 and 15 years of age. Classic symptoms of mumps include fever, chills, malaise, and enlargement of the parotid glands, which may be unilateral or bilateral. The swelling of the parotid glands may result in the patient experiencing a dry mouth because saliva flow is blocked. [Pg.78]

Mehansho, H., Hagerman, A., Clements, S., etal. (1983). Modulation of proline-rich protein biosynthesis in rat parotid glands by sorghums with high tannin levels. Proceedings ofthe National Academy of Sciences USA 80, 3948-3952. [Pg.488]

Aniello, F., ColeDa, G., Muscariello, G., Lanza, A., Ferrara, D., Branno, M. and Minucd, S. (2006) Expression of four histone lysine-methyltransferases in parotid gland tumors. Anticancer Research, 26, 2063-2067. [Pg.267]

Signs of respiratory irritation have been reported in animals acutely exposed to cresol vapors and aerosols, although the levels associated with irritation have not been reliably documented (Campbell 1941 Uzhdavini et al. 1972). Mucosal irritation, as shown by parotid gland secretions, occurred in cats during 30-minute exposures to 5-9 mg/m of o-cresol (Uzhdavini et al. 1972). An assortment of... [Pg.15]

Nielsen M, Albrechtsen R, Johnson NJ, et al. 1979. Carcinoma of the parotid gland following sialography with Thorotrast. Acta Otolaryngol 88 462-467. [Pg.147]

Parotid gland swelling may occur with prolonged use. [Pg.653]

Rats poisoned by subcutaneous injection of VX at twice the LD50 were kept alive for 20 min with artificial ventilation of the lungs when necessary.At 20 min after the dose of VX, some rats were given intraperitoneal injections of either atropine sulfate (7 mg/kg) or atropine sulfate plus 2-PAM I (17.5 mg/kg). Untreated rats were killed 20 min after injection of VX samples of parotid gland, gastrocnemius muscle, and brain were collected for examination for cholinesterase activity. The treated rats were killed 3 h after treatment. Organ samples were collected and analyzed for cholinesterase activity. Reactivation of cholinesterase was calculated as 100 times the ratio of the difference between cholinesterase activities 3 h after therapy and 20 min after VX to the difference between cholinesterase activities in unpoisoned rats and in poisoned rats 20 min after VX it is shown in Table 3 for the two modes of therapy. [Pg.282]

Because atropine has never been found to have reactivating activity in vitro, the reactivation that occurred in the rats treated with atropine sulfate is assumed to be spontaneous. It is apparent from Table 3 that addition of 2-PAM I to atropine increased cholinesterase reactivation by 40.5% in the parotid gland, by 127.8% in the gastrocnemius muscle, and by 8.2% in the brain. The especially large change in cholinesterase activity in skeletal muscle suggests that this may be the principal site at which 2-PAM I antagonizes inhibition of cholinesterase. [Pg.282]

Recovery of Cholinesterase Activity in Parotid Glands, Gastrocnemius Muscles, and Brains of Rats Poisoned with Subcutaneous VX at 40 ug/kg and Treated 20 Min Later with Intraperitoneal Atropine Sulfate at 7 mg/kg or with Intraperitoneal Atropine Sulfate and 2-PAM I at 17.5 mg/kga... [Pg.283]

Bufotenine was isolated from skin and parotid gland of the toad Bufo vulgaris in 1893, and from plants and mushrooms. It is also foimd in the toad Bufo marinus that lives in the southern part of the United States and the Caribbean, and in Bufo alvarius, found in the southwestern United States. Amazon explorers had described poisoning by toad and mushroom preparations more than 400 years ago. Street names include black stone, Chan Su, Chinese love stones, cohoba, rock hard. Stud 100, and toad. [Pg.96]

Catecholamines Muscle, liver, spleen, kidney, brain pineal gland, adipose, pancreatic islets, erythrocytes, leukocytes, thymocytes, fat cell, lung fibroblasts, parotid gland, endothelium, peritoneal macrophages... [Pg.207]

Fig. 3. Immunohistochemical expression of (a) hK7 by the epithelium of eccrine glands of the skin (monoclonal antibody, clone 73.2), (b) hK13 by the epithelium of the bronchus (monoclonal antibody, clone IIC1), (c) hK5 by the ductal epithelium of the parotid gland (polyclonal antibody), (d) hK7 by the esophageal glands (monoclonal antibody, clone 73.2), (e) hK13 by the gastric mucosa (monoclonal antibody, clone 2-17), (f) hK6 by the large intestine mucosa (polyclonal antibody), (g) hK10 in an islet of Langerhans in the pancreas (monoclonal antibody, clone 5D3), (h) hKll by the epithelium of the urinary tubuli (monoclonal antibody), (i) hKll by a papillary renal cell carcinoma (monoclonal antibody).

The biochemical mechanisms by which cAMP-dependent phosphorylation leads to enhanced IR-PTH release remain to be determined. It is of interest, however, that isoproterenol activates phosphorylation of proteins of similar molecular weight in the rat parotid gland (22), while glucagon stimulates phosphorylation of a protein of molecular weight 19,000 in calcitonin-secreting cultured cells from a medullary carcinoma of the rat thyroid (22) It is conceivable that in all three tissues, activation of exocytosis results from a cAMP-dependent phosphorylation of a critical cellular substrate. [Pg.13]

The predominant sites of failure with tamoxifen at the start of EM-800 administration were in decreasing order of incidence rate bone (28), nodes (15), liver (11), skin (8), lung (7), breast (2), and parotid gland (1). Progression was present at one site in 20 patients, at two sites in 17 patients, and at three sites in 6 patients at the start of treatment with the antiestrogen. [Pg.353]

Parotid glands may present with parotids following treatment with 1-ASP... [Pg.242]

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