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Biomedical subjects

O Frank

Publications and source records attributed to O Frank.

At least 55 records · Page 3Linked to original sources
PubMed1991

Role of 5'-deoxy-5'-methylthioadenosine in growth of several microbial B12 requirers.

5'-Deoxy-5'-Methylthioadenosine (MTA) figures in cellular methionine and polyamine syntheses. It replaces B12 for growth of the chrysomonad protozoan Poteriochromonas malhamensis at a ratio of MTA:B12 of approximatly 10,000,000:1 (by weight). MTA does not replace B12 for other B12-requirers, e.g.: Euglena gracilis, Lactobacillus leichmannii, and Escherichia coli 113-3. The methionine synergism for P. malhamensis growth is also negated when B12 activity is annulled by alkali treatment; MTA is not inactivated by such treatment. The growth promoting activity of various deoxynucloesides and deoxynucloetides for P. malhamensis and other B12-requirers is reported here due to contamination by cobalamins. Ethionine antagonizes the growth-enhancing effect of MTA, methionine, and B12, individually and collectively -evidence that MTA plays a role in supplying methionine for P. malhamensis growth. MTA concentrations in body fluids and mammalian tissues are too low to interfere with the use of P. malhamensis for estimating only metabolically active B12.

Adenosine↗
PubMed1991

Effect of short- and long-term diabetes on carnitine and myo-inositol in rats.

1. The effect of short- (2 wk) and long-term (20 wk) streptozotocin diabetes was studied on urine, blood, liver, heart, brain, skeletal muscle, pancreas and kidney concentrations of acid-soluble carnitine and free myo-inositol. 2. Short-term diabetic rats excreted significantly higher concentrations of carnitine as well as myoinositol than normal rats. Blood carnitine and myo-inositol were not different between normal and diabetic rats. Diabetes caused a decrease in liver, brain and pancreatic carnitine, but not in heart, skeletal muscle and kidney. Myo-inositol concentration was decreased in liver, heart and kidney but not in brain, pancreas and skeletal muscle. 3. Long-term diabetic rats had higher urinary excretions of both carnitine and myo-inositol. Blood carnitine did not change; however, myo-inositol was higher in diabetic than in normal rats. Diabetes caused a significant increase in liver and a decrease in heart, brain, skeletal muscle and pancreatic content of carnitine; no difference in kidney carnitine was noted. Myo-inositol content was elevated only in liver of diabetic rats. 4. We suggest that carnitine and myo-inositol concentrations are influenced both by short- and long-term diabetes through changes in tissue metabolism.

Acute Disease↗
PubMed1991

Hypovitaminosis C in patients treated with high-dose interleukin 2 and lymphokine-activated killer cells.

Patients (n = 15) with metastatic malignant melanoma, hypernephroma, and colon carcinoma received a three-phase adoptive immunotherapy protocol: phase 1, 10(5) units (high-dose) interleukin-2 (IL-2) iv every 8 h or 1 mg/m2 continuous intravenous infusion; phase 2, 6.5 d rest + leukapheresis; phase 3, 4 d of high-dose IL-2 plus three infusions of autologous lymphokine-activated killer cells. Toxicities of treatment included fever, chills, tachycardia, hypotension, vomiting, diarrhea, and fluid retention. Patients entering the trial were not malnourished, and mean plasma ascorbic acid concentrations before therapy were normal (36.3 +/- 14.2 mumol/L). Mean concentrations dropped by 80% after the first phase of treatment with high-dose IL-2 alone (to 7.4 +/- 4.5 mumol/L). Mean plasma ascorbic acid concentrations remained severely depleted (between 4.5 and 7.4 mumol/L) throughout the remainder of the 15-d treatment. Ascorbic acid concentrations became undetectable (less than 2.8 mumol/L) in 12/15 patients during this time. Blood pantothenate and plasma vitamin E concentrations remained within normal limits in all patients tested throughout the phases of therapy.

Adult↗
PubMed1991

Branched-chain amino acids overcome cycloleucine growth inhibition in B12 and non-B12-requiring microorganisms.

Because cycloleucine (CL) inhibits methionine, and probably B12, we studied CL activity in some B12 or methionine dependent microorganisms to determine whether methionine or other amino acids are targeted by CL. We found that branched-chain amino acids, valine in particular, effectively annulled CL growth inhibition, whereas B12 was ineffective. alpha-Ketoisovalerate was the only intermediate in pathways of branched-chain amino acids catabolism that overcome CL toxicity; propionate, methylmalonate, succinate, alpha-ketoisocaproate and alpha-ketoglutarate were inactive by themselves or in combination. This study suggests that CL antagonizes the action of not only B12 and methionine but also branched-chain amino acids. Results seem comparable to those with B12-deficient fruit bats having neurologic involvement.

Amino Acids↗
PubMed1990

Excess vitamin A injures the liver.

Chronic vitamin A intoxication in a 56-year-old female is reported. Some abnormal blood chemistries included elevated transaminase and alkaline phosphatase, increased cerebrospinal fluid and portal pressure, and elevated vitamin A in blood and liver. A liver biopsy indicated histologic evidence of perisinusoidal collagen deposition and noncoalescent fat droplets in Ito cells. Caution against the misdiagnosis of alcoholic cirrhosis for vitamin A intoxication is recommended.

Diagnosis, Differential↗
PubMed1990

Effect of genetic diabetes and alcohol on tissue carnitine and inositol concentrations in mice.

Concentrations of acid-soluble L-carnitine and inositol were determined in heart, kidney, muscle, pancreas, liver, brain and blood of genetically diabetic obese db/db and their nondiabetic control C57BL/6J (CBL) mice. Results were compared to a group of diabetic and CBL mice fed ethanol (ETOH) 4 g/kg daily for 58-64 days. In CBL and db/db mice, heart muscle was found to have the greatest and brain the least content of carnitine. Diabetes caused a significant decrease in hepatic concentration of carnitine but did not affect carnitine concentration of heart, kidney, skeletal muscle, brain and pancreas. ETOH intake had no effect on carnitine content of any of the tissues studied. Free inositol content was highest in brain and lowest in skeletal muscle of CBL and db/db mice; diabetes or ETOH intake did not affect tissue inositol content. Except for liver, neither diabetes nor ETOH intake affects tissue carnitine or inositol concentration.

Alcohol Drinking↗
PubMed1990

Micronutrient status and human immunodeficiency virus (HIV) infection.

This study surveyed serum concentrations of vitamins, electrolytes, and trace elements in subjects seropositive for HIV-1 by ELISA and confirmatory Western blot. Thirty subjects (26 males, 4 females) were recruited at a hospital clinic. Seventeen were classified as having mild or severe ARC (AIDS-related complex), 7 had AIDS, and 6 were asymptomatic. Eight had experienced weight loss of 10 pounds or more in the past 6 months. Most (93%) were anergic to skin test antigens. Percentages of subjects with below normal plasma concentrations include: zinc-30%, calcium-27%, magnesium-30%, carotenes-31%, total choline-50%, and ascorbate-27%. Eighty-seven percent of the subjects had at least one abnormally low value. Percentages with above normal values include: folate-37% and carnitine-37%. Some subjects with above normal values for plasma vitamins reported self-supplementation, usually with large doses. The results suggest that one or more abnormally low concentrations of the plasma micronutrients studied here are likely to be present in the majority of HIV seropositive patients.

AIDS-Related Complex↗
PubMed1990

Riboflavin excretion in normal and diabetic rats.

Twenty-four hour urinary excretion of riboflavin was determined in normal and short-term and long-term streptozotocin diabetic rats. Compared to non-diabetic rats (controls), short-term (1 week) diabetic rats had no increased urinary riboflavin. In contrast, long-term (20 week) diabetic rats excreted significantly elevated levels of urinary riboflavin. Results suggest that the reported riboflavin deficiency seen in chronic diabetes may be related to augmented urinary excretion of riboflavin.

Animals↗
PubMed1989

Interleukin-2 enhances biopterins and catecholamines production during adoptive immunotherapy for various cancers.

Biopterins production during three different protocols for adoptive immunotherapy for human cancer was investigated. Adoptive immunotherapy treatment with interleukin-2 (IL-2) was carried out for 13 patients with malignant melanoma; eight with metastatic renal cell carcinoma; and three with metastatic colon cancer. The authors estimated total biopterins in plasma and lymphokine (IL-2)-activated killer cells (LAK) from these patients before and during various treatment phases to determine if increased biopterins production reflects leukocyte activation by IL-2 or antitumor activity. They noted an increased synthesis of total "biopterins," i.e., biopterin; 7,8-dehydrobiopterin; and L-neopterin in LAK cells and plasma which correlated with IL-2 exposure. Mean plasma biopterins were normal (1.2 +/- 0.5 ng/ml) before therapy; in contrast, biopterins increased significantly to 3.4 +/- 1.9 ng/ml and 3.9 +/- 1.9 ng/ml during IL-2 and IL-2 + LAK treatment each, respectively. Similar biopterin elevations were noted irrespective of the different adoptive immunotherapy protocols used. Elevated biopterins decreased to normal levels (1.2 +/- 0.7 ng/ml) when IL-2 treatment was omitted. Tumor regression with adoptive immunotherapy did not correlate with increased plasma biopterins. Increased biopterins production was also associated with increase in plasma catecholamine after IL-2 treatment during adoptive immunotherapy. Conceivably increased biopterins, induced by IL-2 activation of a leukocyte population, is a cell-mediated consequence not necessarily serving as a signal for the antitumor effect associated with adoptive immunotherapy.

Adult↗
PubMed1989

Pyridoxal phosphate annuls acetaldehyde inhibition of uridine uptake by hepatocytes.

Methods were evaluated for depressing the acetaldehyde (AcH) inhibition of uridine uptake by Chang liver cells and isolated autologous liver cells, obtained by percutaneous liver biopsy from cases of alcoholic hepatitis. Hepatocytes so obtained were significantly more susceptible to AcH-induced inhibition of uridine uptake than hepatocytes from normal liver, alcoholic fatty liver, stable alcoholic cirrhosis and acute viral hepatitis. Benzylamine (an aldehyde buffer) and pyridoxal-5' phosphate (PLP) counteracted the inhibition of uridine uptake by AcH in vitro. We suggest that benzylamine neutralizes AcH toxicity through a Schiff-base condensation with AcH thus taking AcH out of the field of action. PLP protects against AcH-induced inhibition of uridine uptake by probably forming a Schiff base with cellular amino acids thus blocking further condensation of these amino groups with AcH. In this manner, uridine uptake by liver cells for RNA synthesis can proceed without interference by AcH.

Acetaldehyde↗
PubMed1988

Vitamins and other metabolites in various sera commonly used for cell culturing.

Many cell culture media use different sera to enhance growth. We assayed vitamins and some related metabolites in different sera and identified the concentration of: thiamin, biotin, folates, riboflavin, pantothenates, nicotinates, vitamins B6, B12, A, E, C, and carotenes and some related metabolites: biopterins, free inositol, free and total choline, total carnitines in chicken, horse, rabbit, goat, pig, calf, newborn calf, fetal calf and human sera. Results indicate that vitamin and metabolite content of different sera vary. Such variations could produce fluctuant effects on cell culturings if the metabolite content of the serum is not documented.

Animals↗
PubMed1988

Biotin supplementation improves glucose and insulin tolerances in genetically diabetic KK mice.

Because biotin treatment may lower blood glucose in insulin-dependent diabetes, we chose to study such an effect in non-insulin dependent diabetes. Twenty-six diabetic KK mice, moderately hyperglycemic and insulin resistant, were treated for 10 weeks: 9 animals with 2 mg of biotin/Kg, 8 with 4 mg of biotin/Kg, and 9 with saline (controls). Blood glucose levels, oral glucose tolerance, insulin response to oral glucose, and blood glucose decrease in response to insulin were quantitated. Compared to controls, biotin treatment lowered post-prandial glucose levels, and improved tolerance to glucose and insulin resistance. Serum immunoreactive insulin levels in biotin-treated mice were like the controls.

Animals↗
PubMed1987

Severe hypovitaminosis C occurring as the result of adoptive immunotherapy with high-dose interleukin 2 and lymphokine-activated killer cells.

Adoptive immunotherapy of human cancer was investigated in our institution as part of a National Cancer Institute extramural group study. This treatment, for patients with metastatic malignant melanoma, hypernephroma, and colon carcinoma, consisted of three phases: (a) 5 days of i.v. high-dose (10(5) units/kg every 8 h) interleukin 2, (b) 6 1/2 days of rest plus leukapheresis; and (c) 4 days of high-dose interleukin 2 plus three infusions of autologous lymphokine-activated killer cells. Toxicities included fever, chills, tachycardia, hypotension, vomiting, diarrhea, and fluid retention. Ascorbic acid is known to be important to cell-mediated immunity, and it has been reported to be depleted during physiologically stressful events. Therefore, we determined plasma ascorbic acid levels in patients (n = 11) before adoptive immunotherapy and before and after Phases 1, 2, and 3 of treatment. Patients entering the trial were not malnourished. Mean plasma ascorbic acid levels were normal (0.64 +/- 0.25 mg/dl) before therapy. Mean levels dropped by 80% after the first phase of treatment with high-dose interleukin 2 alone (0.13 +/- 0.08 mg/dl). Mean plasma ascorbic acid levels remained severely depleted (0.08 to 0.13 mg/dl) throughout the remainder of the treatment, becoming undetectable (less than 0.05 mg/dl) in eight of 11 patients during this time. Values obtained from 24-h urine collections on two of two patients indicated that ascorbate was not excreted in the urine. Plasma ascorbic acid normalized in three of three patients tested 1 mo after the completion of treatment. Unlike the results for ascorbic acid, blood pantothenate and plasma vitamin E remained within normal limits in all 11 patients throughout the phases of therapy. Responders (n = 3) differed from nonresponders (n = 8) in that plasma ascorbate levels in the former recovered to at least 0.1 mg/dl (frank clinical scurvy) during Phases 2 and 3, whereas levels in the latter fell below this level.

Adult↗
PubMed1987

Vitamin status in patients undergoing single or multiple plasmapheresis.

Folate, thiamin, nicotinate, biotin, riboflavin, pantothenate, vitamins A, B6, B12, C, E, and beta-carotene were determined in: (a) eight patients before and after one plasma exchange; (b) in one patient after five consecutive treatments; (c) in three patients before and 2-8 weeks after plasmapheresis. Vitamin B12, beta-carotene, vitamin B6, and vitamins A, C, E were depressed after acute or chronic plasmapheresis. Concentrations of folate, thiamin, nicotinate, biotin, riboflavin, and pantothenate were essentially unchanged after one plasma exchange.

Adult↗
PubMed1987

Effect of folate on phenytoin hyperplasia.

There have been some reports that folic acid inhibits phenytoin-induced gingival hyperplasia. The purpose of this double-blind study was to quantify clinically the effects of both systemic and topical administration of folic acid on phenytoin-induced gingival overgrowth in man. For a period of 6 months, one group of phenytoin patients received 2 daily topical applications of a folate solution. An additional group received 2 daily doses of systemic folate while a control group received placebo medication. Results indicate that throughout the 180-day period of the study, the topical folate significantly inhibited gingival hyperplasia to a greater extent than either systemic folate or placebo groups.

Administration, Oral↗
PubMed1987

Plasma vitamin B12 titres as indicators of disease severity and mortality of patients with alcoholic hepatitis.

Patients with alcoholic hepatitis with plasma B12 levels above 800 pg/ml have overt clinical manifestations of liver disease including severe hepatocellular damage. High plasma B12 levels significantly correlate (P less than 0.0001) with standard liver function tests, e.g. bilirubin, cholylglycine, alkaline phosphatase, AST and prothrombin time as an index of the severity of hepatic damage. Decrease in plasma B12 to normal titres implies a decrease in the severity of alcoholic liver disease, whereas increased plasma B12 levels relate to increased severity and mortality.

Hepatitis, Alcoholic↗