[Experience with LH-FSH releasing hormone in treatment of ovarian cysts within the framework of artificial insemination of cows]. / Erfahrungen mit LH-FSH-Releasinghormon bei der Behandlung der Ovariazystem im Rahmen der kuenstlichen Besaming.

PIP: 95 cows with large cystic degeneration of the ovaries were treated with luteinizing hormone-follicle stimulating hormone releasing hormone (dosages of .25-1.0 mg). 12 of the cows were treated further with repeated Lutal doses. 70 cows became pregnant, a success rate of 73.6%, which corresponds to the experiences of Bentele and Humke and Christl. The 1st venereal ardor occurred 22.8 days after Lutal injection with a standard deviation of 15.4 days. The unpredictability of the onset is a disadvantage of the therapy and use of prostaglandins should be researched in this context. Otherwise this therapy is practical and effective. No clear correlation was found with respect to effectiveness of the medication and the dosage level.^ieng

A morphometric study of Reye's syndrome. Correlation of reduced mitochondrial numbers and increased mitochondrial size with clinical manifestations.

Morphometric analysis of liver ultrastructure in 14 children with Reye's syndrome (RS) of varying morphologic severity was compared with that of 6 children with normal livers. Results showed reduced numbers of enlarged mitochondria in RS. Multivariant analysis identified correlations between increased mitochondrial size, decreased mitochondrial number, and severity of neurologic disease (stage). A disproportionate increase in mitochondrial area and perimeter in the RS cases with the most depressed mitochondrial number distinguished the 4 children with residual neurologic damage or death. Serum salicylate concentrations were negatively correlated with severity of morphologic alteration. Two cases of non-RS salicylate toxicity showed normal or near-normal mitochondrial size and number. In fatty liver from an autopsy specimen from a child, a child with carnitine deficiency, and a child on therapy for dermatomyositis, mitochondrial numbers were also normal. Decreased mitochondrial numbers are characteristic of RS and imply a pathophysiologic mechanism, possibly related to impaired mitochondrial replication. Synergism with other forms of mitochondrial injury, such as salicylates, hypoglycemia, or shock may influence clinical severity, progression, and outcome.

Abnormal lipid accumulation within the small intestinal mucosa of children with juvenile-onset diabetes mellitus.

The lipid content of the proximal jejunum, as studied by light microscopy with lipid histochemical staining methods, is determined in 14 fasting children with juvenile-onset diabetes mellitus. The results show that four children had greatly increased amounts of lipid, while six others had a mildly to moderately increased amounts of lipid present. The amount of lipid present appears to correlate most closely with the quality of control of the diabetes. These results indicate either that the clearance of exogenous lipid is impaired or that there is an increased endogenous synthesis of lipid within the intestine of the diabetic child, especially in those under poor control.

Isolation of influenza virus from liver and muscle biopsy specimens from a surviving case of Reye's syndrome.

Influenza virus (A/Ohio/7/76) was demonstrated by haemagglutination and by direct electron microscopy in chick embryo fluids inoculated with liver, muscle, cerebrospinal fluid, and nasotracheal secretions obtained from a boy with Reye's syndrome, 8 days after the onset of the upper-respiratory-tract symptoms and at the height of neurological and hepatic involvement. This finding accords with the hypothesis that Reye's syndrome may be an epiphenomenon of influenza-virus infection. It is postulated that the pathogenesis of Reye's syndrome may be related to the other influenzal eipiphenomena including influenzal pneumonia in previously healthy persons and influenza-associated myopathy, both of which, like Reye's syndrome, become clinically evident about 7 days after the first clinical signs of influenza.

Tratamiento de dislipidemias con ácido nicotínico / Treatment of dyslipidemia with Nicotinic acid

El ácido nicotínico fue el primer agente para el tratamiento de dislipidemias. Con la aparición de las estatinas su uso disminuyó ya que éstas no presentaban los efectos molestos de ruborizacioón causados por el ácido nicotínico. Las estatinas no han demostrado ser tan efectivas para la reducción de los triglicéridos y en el aumento de las lipoproteínas de alta densidad como el ácido nicotínico. Se han desarrollado dos variaciones adicionales de ácido nicotínco con el objetivo de disminuir su poder de causar ruborización y de suministrar un mejor efecto de regulación sobre esos lípidos. En el presente artículo se realiza una revisión de la literatura médica sobre el uso del ácido nicotínico como agente para el control de las dislipidemias. Las dislipidemias son un grupo de trastornos caracterizados por anomalías tanto cuantitativas como cualitativas de las lipoproteínas plasmáticas. La excesiva aucumulación de una se acompaña generalmente de una disminución en la concentración de la otra. Se pueden considerar como el resultado de defectos en el sistema catabólico por anomalías en las enzimas, receptores celulares de superficie, o bien de una estructura anormal de la partícula lipoprotéica que disminuye su capacidad para interactuar con los mecanismo catabólicos. La mayoría de las dislipidemias son poligénicas o el producto de la interacción entre factores ambientales y cierta predisposición genética.