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H Ho

Publications and source records attributed to H Ho.

15 recordsLinked to original sources
PubMed1992

Renal vascular hypertension does not lead to hyperinsulinemia in Sprague-Dawley rats.

The effect of renal vascular hypertension on blood pressure and plasma glucose, insulin, and triglyceride concentration was studied in Sprague-Dawley rats. Three weeks after the induction of renal artery sterosis, mean (+/- SEM) blood pressure was significantly greater (153 +/- 3 v 117 +/- 2 mm Hg, P less than .001) compared with that in sham-operated rats. However, the two groups were similar in terms of plasma glucose (140 +/- 3 v 140 +/- 2 mg/dL), insulin (27 +/- 3 v 23 +/- 2 microU/mL), and triglyceride (89 +/- 8 v 95 +/- 6 mg/dL) concentrations. Furthermore, blood pressure increased to a similar degree in the two groups of rats (22 +/- 4 v 24 +/- 2 mm Hg), as did plasma insulin (47 +/- 5 v 44 +/- 4 microU/mL) and triglyceride (407 +/- 50 v 381 +/- 46 mg/dL) concentrations, after 2 weeks of a high-fructose diet. These data indicate that experimental induction of renal vascular hypertension in normal rats was not associated with an increase in either plasma insulin or triglyceride concentration. Furthermore, the response of rats with renal vascular hypertension to a high-fructose diet was similar to that of the sham-operated group. These data support the view that hypertension, per se, does not lead to hyperinsulinemia and hypertriglyceridemia in normal rats.

Animals↗
PubMed1992

Recurrent Salmonella arizona infection after treatment for metastatic carcinoma.

Serious Salmonella arizona infection may be acquired through the ingestion of rattlesnake meat used as a folk medicine remedy. We report a patient with metastatic carcinoma and a remote history of rattlesnake meat ingestion who developed recurrent S. arizona bacteremia and reactivation of tuberculosis after receiving corticosteroid and radiation therapy. Physicians should be aware of the potential for rattlesnake-associated S. arizona infection to occur as either the presenting manifestation or as a complication in immunosuppressed patients who may take folk remedies, especially Hispanics who live along the United States-Mexico border.

Animals↗
PubMed1991

A prospective controlled study of the risk of bacteremia in emergency sclerotherapy of esophageal varices.

Reported incidences of bacteremia after endoscopy with esophageal variceal sclerotherapy are conflicting. A prospective controlled study was conducted to determine the frequency of bacteremia after emergency endoscopy with esophageal variceal sclerotherapy compared with frequency after elective esophageal variceal sclerotherapy and after emergency endoscopy in patients with upper gastrointestinal bleeding from nonvariceal sources. A total of 126 endoscopies were studied in 72 patients. Groups consisted of (a) emergency endoscopy without esophageal variceal sclerotherapy, 37 sessions with 36 patients; (b) elective esophageal variceal sclerotherapy, 33 sessions with 14 patients; and (c) emergency esophageal variceal sclerotherapy, 56 sessions with 36 patients. Blood cultures were obtained before and 5 and 30 minutes after endoscopy. There was a higher frequency of preendoscopic bacteremia in emergency esophageal variceal sclerotherapy (13%) than in emergency endoscopy alone (0%) (P = 0.02). Clinically significant bacteremia in emergency esophageal variceal sclerotherapy was observed in 7 of 56 (13%) sessions, compared with 0 of 33 in elective esophageal variceal sclerotherapy (P = 0.03) and 1 of 36 (3%) in emergency endoscopy alone (P = 0.45). Of these cases, 3 (5.4%) were potentially caused by emergency esophageal variceal sclerotherapy, but not clinically significant postendoscopic bacteremia was attributable to the procedure in the other groups.

Adult↗
PubMed1991

Low-dose streptozotocin-induced diabetes in the spontaneously hypertensive rat.

Streptozotocin (STZ, 35 mg/kg body weight) was injected into spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, and plasma glucose and triglyceride concentrations measured 10 days later. Neither mean (+/- SEM) plasma glucose (130 +/- 3 v 136 +/- 3 mg/dL) nor triglyceride (93 +/- 6 v 108 +/- 7 mg/dL) concentrations increased in WKY rats. In contrast, both plasma glucose (141 +/- 3 v 262 +/- 36) and triglyceride (121 +/- 8 v 196 +/- 7 mg/dL) concentrations increased significantly (P less than .01) following administration of STZ in SHR. Furthermore, when SHR previously injected with STZ were fed a diet enriched in fructose, they had a further increase (P less than .01) in both plasma glucose (343 +/- 38 mg/dL) and triglyceride (774 +/- 57 mg/dL) concentrations. Plasma triglyceride concentration also increased significantly (P less than .05) when STZ-injected WKY rats ingested the fructose-enriched diet, but plasma glucose levels still remained within the normal range (152 +/- 5 mg/dL). These results indicate that SHR were more sensitive to the effects of a decrease in pancreatic beta-cell function (STZ) and an increase in insulin resistance (fructose feeding) than WKY rats.

Animals↗
PubMed1991

Sugar-induced hypertension in Sprague-Dawley rats.

Male Sprague-Dawley rats were fed either conventional rat chow, or a diet in which vegetable starch was replaced with either glucose or sucrose for two weeks. At the end of this period, measurements were made of weight, blood pressure, and plasma glucose, insulin, and triglyceride concentrations. The average weight gain over the dietary period was approximately 75 g, and did not vary between the three groups. Mean (+/- SEM) blood pressure remained stable in the rats fed conventional chow (124 +/- 2 to 127 +/- 3 mm Hg), but increased significantly in rats fed the glucose-enriched diet (122 +/- 1 to 134 +/- 2 mm Hg, P less than .02, compared to chow-fed rats). The increase in blood pressure was even greater in rats fed the sucrose-enriched diet (122 +/- 2 to 144 +/- 2), and was significantly greater (P less than .005) than in rats fed either conventional chow or the glucose-enriched diet. Plasma glucose concentrations did not change in any of the groups, but plasma insulin concentration approximately doubled in rats fed either the glucose-enriched or sucrose-enriched diets. Finally, plasma triglyceride concentrations also were significantly higher (P less than .002) in both glucose-fed and sucrose-fed rats than in the control group. However, the increase was greatest in the sucrose-fed rats, and was significantly higher than in rats fed the glucose-enriched diet (P less than .002).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of a fructose-enriched diet on plasma insulin and triglyceride concentration in SHR and WKY rats.

Significant increases (P less than 0.001) in plasma insulin and triglyceride concentrations and in blood pressure were seen when SHR and WKY rats ate a fructose-enriched diet for 14 days. However, all of the changes were significantly accentuated (P less than 0.02-0.001) in SHR rats. Specifically the increment in plasma insulin concentration following the fructose-enriched diet was 42 +/- 4 microU/ml in SHR as compared to 25 +/- 4 microU/ml in WKY rats (P less than 0.001). Plasma triglyceride concentrations also increased to a greater degree in response to fructose in SHR rats (260 +/- 24 vs. 136 +/- 20 mg/dl, P less than 0.001). Finally, the fructose-induced increase in blood pressure of 29 +/- 4 mm of Hg in SHR rats was greater (P less than 0.02) than that seen in WKY rats (19 +/- 2 mm of Hg). There was no change in plasma glucose concentration in response to the fructose diet. WKY rats gained more weight than did the SHR rats. Thus, although plasma triglyceride and insulin concentration and blood pressure increased when either WKY or SHR rats consumed a fructose enriched diet, the magnitude of these changes was greater in SHR rats.

Animals↗
PubMed1990

Survey of H2-antagonist usage in acute upper gastrointestinal hemorrhage.

H2-antagonists are frequently used in the management of upper gastrointestinal (UGI) hemorrhage despite their lack of proven efficacy. In order to determine the pattern of H2-antagonist usage for this indication, we retrospectively reviewed the charts of 137 patients admitted with acute UGI bleeding over a 1-year period at two teaching hospitals in West Texas. An H2-antagonist was ordered in 89% of patients (77%) intravenous, 12% oral). It was administered within 2 h of admission in 25% of these patients, within 4 h in 54%, and within 8 h in 78%. An H2-antagonist was ordered among the initial six orders in 49% and among the initial 10 orders in 77% of patients. Considering orders for specific therapies, an H2-antagonist was in the initial three orders in 60% of patients and among the initial six orders in 97%. Of the patients who were prescribed an H2-antagonist and who also had upper endoscopy, the drug was ordered prior to endoscopy in 86%. This review of H2-antagonist usage in the management of acute UGI bleeding has identified a prescribing pattern of writing for these drugs early in the sequence of order writing, with the drugs being given early in the course of hospitalization.

Adult↗
PubMed1990

Frequency of recovery of Blastocystis hominis in clinical practice.

We examined the frequency of isolation of Blastocystis hominis from stools of patients seen in an indigent-care teaching hospital. Over a 2-year period, 2,744 stool specimens were examined prospectively. B. hominis was found in 262 stools (9.5% of all stool specimens and 53.5% of the positive specimens). Clinical data were obtained from 80 patients with stools positive for B. hominis. B. hominis was the only parasite isolated in 39 of 47 (83%) of the adults, compared with 17 of 33 (52%) of the children (p = 0.006). All but 2 of 52 patients without concomitant parasitic infection or bacterial pathogens in stool had gastrointestinal symptoms (41 abdominal pain, 26 diarrhea, and 5 vomiting), but no association was seen with fever, peripheral leukocytosis, stool occult blood, fecal leukocytes, or endoscopic or radiologic evidence of colitis. Therefore, B. hominis was frequently recovered from stools examined in a hospital clinical parasitology laboratory. The clinical presentations of patients in our series did not suggest that B. hominis was invasive. Most patients with B. hominis probably do not require treatment since they will either have spontaneous resolution of symptoms or will be found to have an alternative explanation for their problem.

Adolescent↗
PubMed1989

Somatostatin inhibition of fructose-induced hypertension.

The role of insulin resistance and hyperinsulinemia in the etiology of fructose-induced hypertension was studied in male Sprague-Dawley rats. Rats consumed a fructose-enriched diet (containing 66% of total calories as fructose) for 11 days and were infused continuously during the last 7 days with either a somatostatin analogue or vehicle. At the end of this period, rats receiving the somatostatin analogue had a lower plasma insulin concentration (52 +/- 4 vs. 70 +/- 6 microunits/ml, p less than 0.01) and a lower blood pressure (133 +/- 2 vs. 150 +/- 2 mm Hg) than did the rats infused with the control solution. In addition, the increase in plasma triglyceride concentration in response to the fructose-enriched diet was significantly attenuated (p less than 0.001) in the rats infused with somatostatin. These data provide further support that the increase in blood pressure that occurs when normal rats are fed a high fructose diet is dependent on the ability of this intervention to cause insulin resistance and hyperinsulinemia.

Animals↗
PubMed1976

The regulation of mouse liver ornithine decarboxylase by metabolites.

The enzyme ornithine decarboxylase (L-Ornithine carboxy-lyase, EC 4.1.1.17), has been partially purified from the livers of mice subjected to partial hepatectomy (6-8 h previously). Mouse liver ornithine decarboxylase requires pyridoxal phosphate, and dithiothreitol for maximal activity. The enzyme has a pH optimum of 7.3, it is inhibited in the presence of 0.3 M phosphate, glycine, Tricine and Tris. It shows no dependence on metal ions and is inhibited by high salt concentrations, particularly ammonium salts. The kinetics of the enzyme have been studied with putrescine (and analogs), spermidine and spermine, in the presence of both high and low levels of pyridoxal phosphate. High concentrations of pyridoxal phosphate inhibit the enzyme. The enzyme is also inhibited by low concentrations of putrescine (1 mM). As the concentration of putrescine increased to 10 mM, non-competitive inhibition was observed, this could be reversed by addition of higher levels of pyridoxal phosphate. Spermidine and spermine inhibit (noncompetitively) only at high concentrations (10 mM). Ornithine inhibits at high concentrations (2 mM). Spectral studies have shown that the observed kinetics of competitive inhibition at low concentrations of polyamine changing to noncompetitive inhibition at high polyamine concentrations are due to competition between enzyme and substrate (or inhibitor) for free (non-enzyme bound) pyridoxal phosphate. Noncompetitive inhibition arises through the formation of transient Schiff base complexes between amines and free pyridoxal phosphate. It also appears that the binding of substrate to the active site takes place through Schiff base formation with enzyme bound pyridoxal phosphate.

Animals↗
PubMed1976

The relation of dose rate of microwave radiation to the time of death and total absorbed dose in the mouse.

This experiment demonstrates that for microwave radiation, absorbed dose determination alone is not dosimetrically sufficient. The average absorbed dose to death in this experiment increases as the rate of absorption decreases. This observation is not surprising since microwave energy produces heating of the biological tissues. Hence, with a higher rate of heating the body of an animal, the less it is able to retain homeostasis through metabolic regulation than with a lower rate of heating. The absorbed dose rate and the duration of exposure must both be determined in any microwave biological effects experiments.

Animals↗