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Biomedical subjects

S L Ford

Publications and source records attributed to S L Ford.

At least 19 recordsLinked to original sources
PubMed2001

Dragon's Blood incense: misbranded as a drug of abuse?

An unknown red substance was being sold and used with other drugs of abuse in Virginia (often being used in conjunction with marihuana). The red substance was identified as Dragon's Blood incense from Daemonorops draco. In bioassays, Dragon's Blood incense exhibited a low, but measurable cytotoxicity in in vitro cell lines. Dragon's Blood incense or Volatilized Dragon's Blood had no adverse effect on mouse motor performance based on the inclined screen and rotorod tests. delta(9)-Tetrahydrocannibinol (THC) produced a dose-related decline in mouse performance on the rotorod test. The combination of Dragon's Blood incense or Volatilized Dragon's Blood with delta(9)-THC did not contribute further to the impairment of the mice on the rotorod. This data suggests that the abuse potential for Dragon's Blood incense alone or in combination with marihuana is minimal.

Animals↗
PubMed1999

Pregnenolone synthesis in immature rat Sertoli cells.

It has been reported that testicular Sertoli cells can be induced to synthesize the steroidogenic acute regulatory (StAR) protein. StAR mediates the rate-limiting step of steroidogenesis, which is the transfer of cholesterol to the inner mitochondrial membrane. Since Sertoli cells are thought to be unable to utilize cholesterol for the synthesis of steroids the role of StAR in these cells was questioned. In the present studies we have corroborated the induction of StAR protein in immature cultured Sertoli cells in response to either trophic hormone or cAMP analog stimulation. Further, we have shown that long term stimulation of Sertoli cells with cAMP analog results in the induction of P450scc enzyme and increased pregnenolone production. In this manner, the Sertoli cell may resemble its ovarian homolog, the granulosa cell, more closely than previously thought with regards to its steroidogenic capacity. Thus, StAR may play the same role in Sertoli cells as it does in other steroidogenic tissues.

Animals↗
PubMed1998

Effect of dietary insoluble fiber on control of glycemia in dogs with naturally acquired diabetes mellitus.

OBJECTIVE: To evaluate the effect of a high insoluble-fiber (HF) diet containing 12% cellulose in dry matter and a low insoluble-fiber (LF) diet on control of glycemia in dogs with naturally acquired insulin-dependent diabetes mellitus. DESIGN: Prospective randomized crossover controlled trial. ANIMALS: 11 dogs with naturally acquired diabetes mellitus. PROCEDURE: Dogs were fed HF and LF diets for 8 months each in 1 of 2 randomly assigned diet sequences. Caloric intake and insulin treatment were adjusted as needed to maintain stable body weight and control of glycemia, respectively. After a 2-month adaptation period, control of glycemia was evaluated every 6 weeks for 6 months. Variables assessed included serum glucose concentration measured during the preprandial state, blood glycosylated hemoglobin concentration, serum glucose concentration measured every 2 hours for 24 hours beginning at the time of the morning insulin injection, 24-hour mean serum glucose concentration, mean serum glucose concentration fluctuation from the 24-hour mean serum glucose concentration, and 24-hour urinary excretion of glucose. RESULTS: Significant differences in mean daily caloric intake, body weight, or daily insulin dosage among dogs fed HF and LF diets were not found. Mean preprandial serum glucose concentration, most postprandial serum glucose concentrations, 24-hour mean serum glucose concentration, and 24-hour urinary excretion of glucose were significantly lower in dogs fed the HF diet, compared with the LF diet. CLINICAL IMPLICATIONS: Results of this study support feeding of commercially available insoluble fiber diets to dogs with naturally acquired diabetes mellitus.

Animals↗
PubMed1997

Electrical permeabilization of rat luteal cells: in situ phosphorylation of endogenous protein.

Progesterone synthesis in the corpus luteum is regulated primarily by luteinizing hormone which acts via the adenylate cyclase/cyclic AMP/protein kinase A signalling cascade. Protein phosphorylation therefore plays a key role in the regulation of steroidogenesis, but there are relatively few studies of the in situ phosphorylation of luteal cell substrates. This may in part reflect the difficulties inherent in measuring changes in protein phosphorylation in intact cells preloaded with 32P and difficulties in interpreting data obtained using broken cell preparations. We have now applied a method of stable permeabilization of luteal cell plasma membranes by exposure of cell populations to a high intensity electric field. Under optimum conditions (5 kV/cm, six discharges) electrical permeabilization reproducibly produced populations of luteal cells in which 70-80% of the cells were permeabilized, as assessed by Trypan blue exclusion and [14C] sucrose space measurements. Pores were stable for at least 1 h, and there were no ultrastructural changes to the cells that could be detected by transmission electron microscopy. Permeabilized cells showed rapid cyclic AMP-induced changes in phosphorylation of endogenous proteins when provided with [gamma - 32 P] ATP. Our results demonstrate that the electricity permeabilized luteal cell offers a useful model for studying intracellular events in steroidogenic stimulus-response coupling cascades.

Animals↗
PubMed1996

Role of phosphoprotein phosphatases in the corpus luteum: I identification and characterisation of serine/threonine phosphoprotein phosphatases in isolated rat luteal cells.

Although the role of protein kinases and phosphorylation in steroidogenesis has received much attention, very little is known about the activities of phosphoprotein phosphatases (PP) and dephosphorylation in steroidogenic tissues. The aims of the present study were therefore to identify which of those serine/threonine PPs more commonly involved in intracellular signalling are expressed in rat luteal cells; to quantify, in vitro, the effects of inhibitors on PP activity extracted from purified rat luteal cells; and to measure the effects of PP inhibitors on the phosphorylation of endogenous luteal cell proteins. Polyclonal antibodies raised against the catalytic subunits of PP types 1 and 2A, and a monoclonal antibody raised against the Ca(2+)-binding subunit of PP2B, were used to identify immunoreactive proteins that migrated on SDS-PAGE with approximate molecular masses of 37, 34 and 16 kDa, corresponding well with the reported molecular mass of PP1, PP2A and PP2B respectively. Five selective inhibitors of PP1/PP2A: okadaic acid, calyculin A, cantharidin, tautomycin and microcystin-RR, each caused a dose-dependent decrease in the activity of PPs in luteal cell homogenates, and also enhanced 32P incorporation into numerous luteal cell proteins; most notably, proteins with approximate molecular masses of 20 and 22 kDa. The results of this study suggest that PPs may play an important role in the regulation of rat luteal cell functions.

Animals↗
PubMed1996

Role of phosphoprotein phosphatases in the corpus luteum: II control of progesterone secretion by isolated rat luteal cells.

The key role of protein kinases and protein phosphorylation in the regulation of luteal steroidogenesis is well documented. However the role of phosphoprotein phosphatases (PP) and dephosphorylation in the regulation of luteal cell progesterone secretion is as yet unknown. We have recently demonstrated the presence and activity of PP1 and PP2A in rat luteal cells and the present study was undertaken to determine the consequences of inhibiting PP activity in terms of progesterone secretion. Three structurally dissimilar inhibitors of PP1/2A, okadaic acid, calyculin A and cantharidin each caused a dose-dependent inhibition of LH-induced progesterone secretion without affecting cyclic AMP accumulation. The less potent derivative of okadaic acid, norokadaone, had no effect on either parameter, suggesting that the inhibitory actions on progesterone secretion are due to their specific actions on PP activity and that this inhibition occurs principally at a locus which is distal to the generation of cyclic AMP. In contrast to the inhibitory effects of PP1/2A inhibitors on progesterone biosynthesis, a PP2B inhibitor, cypermethrin, had no effect on LH-stimulated steroidogenesis. The three PP1/2A inhibitors also caused a concentration-dependent inhibition of dibutyryl cyclic AMP-stimulated progesterone secretion. However, none of the inhibitors affected 22R-hydroxycholesterol-supported steroidogenesis, clearly demonstrating that the inhibitors did not interfere with the activity of steroidogenic enzymes. These results suggest that cycles of phosphorylation/dephosphorylation of specific proteins are required for the sustained production of progesterone. Whilst the precise location and function of putative PP substrates is uncertain, the present results indicate that they are involved in regulating the availability of free cholesterol to steroidogenic enzymes within mitochondria.

Animals↗
PubMed1995

Skeletal changes in the ovariectomised ewe and subsequent response to treatment with 17 beta oestradiol.

The ewe has been suggested as a suitable large animal model for assessment of therapeutic agents for the treatment of osteoporosis. In this study we asses the response of ewe bone mineral parameters, using dual energy x ray absorptiometry (DXA), after ovariectomy. Regular DXA analysis was performed over a period of 75 weeks followed by a period of dosing with 17 beta oestradiol. Total body bone mineral density (BMD) was reduced in ovariectomised animals 15 weeks post operatively. BMD remained lower than control animals for the entire pre dose period. Subsequently, dosing with 17 beta oestradiol prevented further loss of bone over a period of 38 weeks. Several complicating factors were noted during the study including seasonal BMD variation, a correlation between fat/lean ratio and total body BMD together with a reversible reduction in bone mineral content as a result of lactation. Also changes in BMD were associated with age at ovariectomy.

Absorptiometry, Photon↗
PubMed1995

NIDDM in the cat: treatment with the oral hypoglycemic medication, glipizide.

The oral hypoglycemic medication, glipizide, provides a viable therapeutic alternative to conventional insulin therapy with a positive therapeutic response in approximately 50% of diabetic cats with non-insulin-dependent disease. Response to glipizide therapy or lack thereof usually is evident within the first 4 to 6 weeks of treatment. Adverse side effects occurred in less than 10% of patients. The existence of residual beta cell function is necessary for response to glipizide therapy. Predictors of response to glipizide therapy were not found. Identification and correction or control of existing insulin antagonistic disease processes, as well as, discontinuation of diabetogenic medications that may be contributing to insulin resistance is also important.

Administration, Oral↗
PubMed1993

Effect of an orally administered sulfonylurea, glipizide, for treatment of diabetes mellitus in cats.

An orally administered sulfonylurea drug, glipizide, was evaluated for treatment of diabetes mellitus. Confirmation of diabetes was based on evidence of appropriate clinical signs, persistent hyperglycemia, and glucosuria. Glipizide (5 mg, PO, q 12 h) was administered to each cat. Sixteen cats were fed a commercial high-fiber diet and 4 cats were fed a commercial low-fiber diet. Insulin was not administered to any cat during the study. Each cat was evaluated 2, 4, 8, and 12 weeks after initiation of treatment. Three clinical responses to glipizide treatment were identified. Mean preprandial blood glucose concentration and mean blood glucose concentration during an 8-hour postprandial period decreased to < 200 mg/dl in 5 of 20 (25%) cats. In these 5 cats, glucosuria was no longer detected and clinical signs resolved by the 4-week reevaluation. Euglycemia was maintained after discontinuing glipizide treatment in 2 of these 5 cats. Glycemic control has been maintained in 2 of 5 of the responding cats for 5 and 7 months of glipizide treatment. One of 5 of the responding cats developed insulin-requiring diabetes mellitus after 6 months of glipizide treatment. Seven of 20 (35%) cats failed to respond to treatment. Mean preprandial blood glucose concentration and mean blood glucose concentration during an 8-hour postprandial period did not change from pretreatment values after 2 +/- 1 months; glucosuria persisted and clinical signs progressively worsened. Insulin treatment was required to establish glycemic control in these 7 cats. Eight of 20 (40%) cats partially responded to glipizide treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1993

Insulin resistance in three dogs with hypothyroidism and diabetes mellitus.

Insulin resistance resolved in 3 dogs with hypothyroidism and diabetes mellitus after treatment with sodium levothyroxine. A thorough diagnostic evaluation failed to identify any other cause of insulin resistance in these dogs. Hypothyroidism was diagnosed in each dog on the basis of clinical signs, physical findings, hyperlipidemia, and results of thyrotropin or thyrotropin-releasing hormone stimulation test. Hypoglycemia was documented in each dog within 2 weeks of starting sodium levothyroxine administration. The insulin dosage was decreased by 60 to 62% during the ensuing months and good glycemic control was obtained at these lower insulin dosages in all dogs. These findings would suggest hypothyroidism-induced insulin resistance in these dogs.

Animals↗
PubMed1993

Hyperadrenocorticism caused by bilateral adrenocortical neoplasia in dogs: four cases (1983-1988).

Hyperadrenocorticism caused by bilateral adrenocortical neoplasia was diagnosed in 4 dogs. Three dogs had bilateral adrenocortical adenomas, and 1 dog had bilateral adrenocortical carcinomas. The history, physical findings, clinicopathologic abnormalities, and results of ACTH stimulation and low-dose dexamethasone suppression tests were compatible with diagnosis of hyperadrenocorticism. Adrenocortical neoplasia was differentiated from pituitary-dependent hyperadrenocorticism on the basis of a combination of test results, including lack of suppression of plasma cortisol after being given a high dose dexamethasone (n = 4), undetectable (< 20 pg/ml) plasma endogenous ACTH concentration (n = 4), identification of a single mineralized adrenal mass by abdominal radiography (n = 2) and abdominal ultrasonography (n = 1), and identification of bilateral nonmineralized adrenal masses by ultrasonography (n = 1). A left adrenal mass was excised from 1 dog. Clinical signs persisted and administration of mitotane was initiated. One dog was treated only with mitotane. Treatment with ketoconazole was attempted in 2 dogs. All dogs died or were euthanatized because of persistent hyperadrenocorticism. Necropsy and histologic evaluation of the pituitary and adrenal tissue confirmed bilateral adrenocortical neoplasia in all dogs. Bilateral adrenocortical neoplasia should be considered as an uncommon, but possible, cause of bilaterally large adrenal glands in dogs with hyperadrenocorticism.

Adenoma↗
PubMed1984

Diphyllobothriasis associated with salmon consumption in Pacific Coast states.

A review of requests for niclosamide ( Niclocide or Yomesan ) made to the Centers for Disease Control Parasitic Diseases Drug Service indicated that an outbreak of diphyllobothriasis occurred in west coast states in 1980, and in the Los Angeles area in 1981. Our investigation of 52 infections that occurred in 1980 implicates fresh salmon (Oncorhynchus spp.) as the host for the Diphyllobothrium parasite in 82% of the persons interviewed. We describe here common symptoms of the infection, methods of fish preparation employed by infected individuals, and epidemiologic data. We suggest that changes in fish marketing practices and the popularity of uncooked or slightly cooked fresh salmon were responsible for this epidemic. We recommend that salmon be either cooked or frozen before it is eaten.

Alaska↗
PubMedDate not supplied

Ethane dimethane sulfonate and NNN'N'-tetrakis-(2-pyridylmethyl)ethylenediamine inhibit steroidogenic acute regulatory (StAR) protein expression in MA-10 Leydig cells and rat Sertoli cells.

Apoptosis inhibits steroid biosynthesis, but it is not clear how the Steroidogenic Acute Regulatory (StAR) protein, is affected. To characterize StAR expression during apoptosis, mouse MA-10 Leydig tumor cells were treated with ethane dimethane sulfonate (EDS), an inducer of apoptosis, and the metal ion chelator NNN'N'-tetrakis-(2-pyridylmethyl)ethylenediamine (TPEN), an inducer of cell death. Both chemicals induced cell death and similarly inhibited dbcAMP-stimulated steroidogenesis and accumulation of the 30 kDa form of StAR. Utilizing the dye JC-1, it was found that TPEN and EDS also impaired the mitochondrial electrochemical potential (delta psi). In Sertoli cells, which also express StAR, EDS induced cell death and attenuated StAR expression. We conclude 1) steroidogenesis and accumulation of mature StAR protein are inhibited as a consequence of the induction of apoptosis; 2) reduced levels of StAR may be partially attributed to inhibition of import because of the loss of delta psi; 3) loss of steroidogenesis is probably due to loss of StAR synthesis and disruption of delta psi.

Animals↗
PubMedDate not supplied

Acute, flaccid quadriplegia in three cats with suspected coral snake envenomation.

Three cats were evaluated for acute, ascending, flaccid quadriplegia; depression; and reduced nociception. Complete or partial neuromuscular junction blockade was found on nerve stimulation studies during electromyographic examinations. Two of the cases had wounds on the chin or paw compatible with coral snake bites. Although a coral snake was found in only one case, coral snake envenomation was suspected because potential for exposure, clinical signs, and electrodiagnostic findings were similar to dogs reported with this condition and to cats with tiger snake envenomation. Only one case received coral snake antivenin. All cases recovered within seven-to-10 days.

Acute Disease↗
PubMedDate not supplied

Hypercalcemia in a dog: a challenging case.

An 18-month-old, spayed female, mixed-breed dog was referred for investigation of persistent hypercalcemia. After extensive diagnostic evaluation, a tentative diagnosis of occult lymphosarcoma (LSA) was made and the dog was euthanized. At necropsy, infection with Heterobilharzia americana was diagnosed. In endemic areas, schistosomiasis should be included in the differential diagnosis of hypercalcemia, and a fecal examination should be performed in every dog with a hypercalcemia of unknown origin.

Animals↗
PubMedDate not supplied

Transient clinical diabetes mellitus in cats: 10 cases (1989-1991).

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.

Animals↗