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Biomedical subjects

J Nei

Publications and source records attributed to J Nei.

14 recordsLinked to original sources
PubMed2001

Problems and pitfalls in cardiac drug therapy.

Medical errors in the care of patients may account for 44,000 to 98,000 deaths per year, and 7,000 deaths per year are attributed to medication errors alone. Increasing awareness among health care providers of potential errors is a critical step toward improving the safety of medical care. Because today's medications are increasingly complex, approved at an accelerated rate, and often have a narrow therapeutic window with only a small margin of safety, patient and provider education is critical in assuring optimal therapeutic outcomes. Providers can use electronic resources such as Web sites to keep informed on drug-drug, drug-food, and drug-nutritional supplements interactions.

California↗
PubMed2000

GVHD after transfusion of stored RBC concentrates in a solution of mannitol, adenine, phosphate, citrate, glucose, and NaCl following trauma.

BACKGROUND: It has not previously been reported that WBC-reduced RBC preparations can cause transfusion-associated GVHD, even in an immunocompetent individual. CASE REPORT: A 74-year-old man suffered a hemorrhage from the mesentery of the transverse colon after a traffic accident. During surgery, he received 10 units of RBCs from 10 donors in a solution containing mannitol, adenine, phosphate, citrate, glucose and NaCl (MAP). MAP RBCs had been stored for 7 to 8 days before use. On the 27th day after surgery, an erythematous, pruritic rash appeared over the face, neck, and trunk, which was associated with low-grade fever and pancytopenia. Transfusion-associated GVHD was strongly suspected and was confirmed by skin biopsy. To determine the origin of lymphocytes causing GVHD, several microsatellite loci were amplified from DNA of the patient's nails and blood and from blood samples of all 10 RBC donors by using PCR. Amplified alleles derived from the patient's blood were identical to those from one of the 10 samples. CONCLUSION: These findings indicate that transfusions of MAP-RBCs can cause transfusion-associated GVHD in an elderly but immunocompetent host.

Accidents, Traffic↗
PubMed1987

Effects of malotilate on ethanol-inhibited hepatocyte regeneration in rats.

The effects of malotilate, a hepatotrophic drug, on the inhibition of hepatocyte regeneration induced by ethanol were studied in rats. Following acute ethanol administration, both DNA synthesis and commencement of the S phase of the cell cycle in hepatocytes after partial hepatectomy were delayed. Malotilate prevents this ethanol-induced delay. Upon chronic ethanol administration, DNA synthesis after partial hepatectomy was reduced and commencement of the S phase was retarded. Treatment with malotilate clearly lessened the reduction in DNA synthesis in the resected liver, and retardation of the cell cycle was partially inhibited. These results indicate that malotilate prevents the ethanol-induced inhibition of hepatocyte regeneration at the dose tested and that this drug may be effective for the treatment of alcoholic liver disease.

Animals↗
PubMed1983

Chronic hepatitis induced by alcohol.

Fifteen heavy drinkers with the histological features of chronic hepatitis were studied. Chronic hepatitis observed in heavy drinkers can be divided into two categories. One is caused by alcohol, and the other is not etiologically related to alcohol. Chronic hepatitis caused by alcohol showed a definite improvement of clinical features following abstinence, as well as significantly high serum GOT/GPT ratios and high glutamate dehydrogenase activities on admission. These clinical features are distinctly different from chronic hepatitis without etiological relation to alcohol and resemble the other types of alcoholic liver injury. The leukocyte migration inhibition test by ethanol was more frequently positive in chronic hepatitis induced by alcohol than in the other types of alcoholic liver injury except for alcoholic hepatitis. Histological characteristics of the liver in chronic hepatitis induced by alcohol included the coexistence of features of both chronic hepatitis and alcoholic fibrosis. Three of four cases of chronic hepatitis induced by alcohol developed cirrhosis during the follow-up period. These results suggest that chronic hepatitis induced by alcohol is a type of alcoholic liver disease with an immunopathological etiology. It is a step toward the development of liver cirrhosis.

Adult↗
PubMed1982

Clinicopathological study of alcoholic fibrosis.

Among 112 patients with alcoholic liver injury, 45 had alcoholic fibrosis. The incidence of alcoholic fibrosis was 40.2% which was the highest among various types of alcoholic liver injury (fatty liver; 3.6%, alcoholic hepatitis; 2.7% and liver cirrhosis; 31.3%). Clinical features of alcoholic fibrosis were milder than those of liver cirrhosis and more severe than those of fatty liver. The mean laboratory values in alcoholic fibrosis were significantly different from those in fatty liver and liver cirrhosis. The laboratory data were well correlated with the presence of pericellular fibrosis and thickening of the terminal hepatic venule, but only partially with hepatic cell necrosis and not with fatty metamorphosis. Two patients with alcoholic fibrosis who developed cirrhosis without any clinical and histological features of hepatitis were observed during 5-yr follow-up. These results indicate that alcoholic fibrosis is the most common type of alcoholic liver injury in Japan and is an independent clinicopathological entity distinct from the classical types of alcoholic liver injury. Pericellular fibrosis and thickening of the terminal hepatic venule which are the main histological features of alcoholic fibrosis may play an important role in its transition to liver cirrhosis.

Aged↗
PubMedDate not supplied

Effects of ethanol on experimental hepatocarcinogenesis.

Although primary hepatoma is not very frequent in alcoholics, the incidence of hepatoma in cases of hepatitis B infection combined with heavy alcohol drinking is high. In the present study, the effects of chronic alcohol administration on the development of chemical-induced hepatic cancer in rats were analyzed. In 70% hepatectomized Wistar strain male rats, a single dose (1 mg per 100 gm body weight) of diethylnitrosamine was injected intraperitoneally. Eight weeks after the injection, 20% alcohol-10% sucrose solution (diethylnitrosamine-alcohol group), 0.1% sodium phenobarbital solution (diethylnitrosamine-phenobarbital group), 10% sucrose solution (diethylnitrosamine-sucrose group) or tap water (diethylnitrosamine-alone group) was given as drinking water for 32 weeks. The numbers of visible nodules per liver were significantly greater in the diethylnitrosamine-alcohol and diethylnitrosamine-phenobarbital groups compared to the diethylnitrosamine-alone and diethylnitrosamine-sucrose groups. The numbers of enzyme-altered foci which were positive to gamma-glutamyl transpeptidase staining per square centimeter of liver section were also greater in the diethylnitrosamine-alcohol and diethylnitrosamine-phenobarbital groups than in the diethylnitrosamine-alone and diethylnitrosamine-sucrose groups, although the numbers of nodules and enzyme-altered foci were significantly larger in the diethylnitrosamine-phenobarbital group than in the diethylnitrosamine-alcohol group. The enzyme-altered foci areas calculated by gamma-glutamyl transpeptidase staining were significantly larger in the diethylnitrosamine-alcohol and diethylnitrosamine-phenobarbital groups than in the diethylnitrosamine-alone and diethylnitrosamine-sucrose groups. Histologically, visible nodules observed in diethylnitrosamine-phenobarbital and diethylnitrosamine-alcohol groups showed characteristic features of neoplastic nodules. These results indicate that alcohol has a promoter action on the development of chemically induced hepatic cancer like phenobarbital.

Animals↗