Biomedical subjects
Publications and source records attributed to F Arena.
The preparation of imidazo [1,2-a] pyrimidin-2-acetic acid by two different synthetic methods is reported. A structure is tentatively proposed for a side product.
A group of ethyl imidazo (1,2-a) and imidazo (1,2-c)pyrimidin-2-acetates was prepared, starting respectively from 2-amino- and 4-aminopyrimidines, by reaction with ethyl 4-bromoacetoacetate. From these esters the corresponding acids were prepared and their antiinflammatory activity was evaluated.
We have prepared a group of ethyl imidazo [2,1-b]thiazole-6- and imidazo[2,1-b]benzothiazole-2-acetates, starting from some substituted 2-aminothiazoles and 2-aminobenzothiazoles, by reaction with ethyl 4-bromoacetoacetate. From these esters we have obtained the corresponding acetic acids, and we have tested their anti-inflammatory activity.
A series of ethyl imidazo [1,2-a]pyridin-2-acetates was prepared by reaction between several substituted 2-aminopyridines and ethyl-4-bromoacetate. From these esters the corresponding acids were prepared and their anti-inflammatory activity was tested.
The synthesis of styrylpyridine methiodides where a hydrogen of the pyridyl moiety was replaced by the hydroxyiminomethyl group produced highly effective inhibitors of acetylcholinesterase. As starting materials 4-methylpyridine-2-aldoxime and 2-methylpyridine-4-aldoxime methiodides were prepared which, together with 4-imidazolylethenyl-pyridine-2-aldoxime methiodide, were the only substances for which some activity as reactivators of phosphorylated electric eel cholinesterase in vitro could also be found.
By reaction of suitable hydroxamic acids chlorides with beta-ketoesters, we have prepared the ethyl esters of isoxazol-4-carboxylic acids, substituted in the 3- and 5-positions with 4-pyridyl and o-chlorophenyl groups, and some of their esters and amides of pharmaceutical interest. 3-(4-Pyridyl)-5-(o-chlorophenyl)isoxazole was obtained either by decarboxylation of the acid or by oxidation of the syn and anti oximes of 3-(o-chlorophenyl)-1-(4-pyridyl)-2-propen-1-one; from the syn oxime the corresponding isoxazoline was also obtained. Pharmacological screening shows that some of the new compounds have a myolytic activity.
Some new heteroarylacetic acids were prepared. Among the products so far obtained, 2-imidazo [1,2-a] pyrazineacetic acid showed an interesting antiinflammatory activity coupled with low toxicity.
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Up to now, we have identified 77 X-linked conditions in which mental retardation is the primary or a major component manifestation. These conditions were subdivided into 2 categories, designated respectively "X-linked mental retardation syndromes" and "Non-specific X-linked mental retardation". Forty genes have been regionally mapped onto the X chromosome. However, in several instances the data were derived from a single family and most lod scores were less than 3.0.
A family in which 6 males have X-linked mental retardation has been studied with polymorphic DNA probes. The males differ from unaffected males only in impaired intellect and in smaller head size. The gene that causes mental retardation in the family appears to be located in band Xq21 on the basis of linkage with 3 markers: DXS250, DXS345 and DXS3 (theta max = 0.00; Zmax = 1.6). A multipoint lod score of 2.36 was obtain with no recombination relative to DXS326 in Xq21. This family is considered to have nonspecific X-linked mental retardation and has been given the designation MRX8.
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The immunohistochemical localization of lactoferrin (LF) was investigated in the duodenojejunal mucosa of children with untreated and treated celiac disease and in a control group of children of short stature and of children with postenteritis syndrome. In subtotal villous atrophy, LF was present in all epithelial cells of the luminal surface with a lower degree of positivity in crypts, whereas a variable degree of reactivity for LF was observed in epithelial cells of reconstituted villi and crypts. The LF mucosal distribution, however, was not specific for celiac disease since the LF pattern was similar in untreated celiac disease and also in postenteritis syndrome. Moreover, LF was detectable only in 7 of 18 duodenojejunal juice samples obtained from untreated and treated celiac patients and normal controls, the observed values being irrespective of the mucosal morphological status. We conclude that the immunohistochemical evidence of LF in the enterocyte may derive from an autochthonous production since our histochemical findings cannot be related to the concentration of LF in duodenal juice.
Mc Kusick-Kaufman Syndrome (SMK) is an autosomal recessive multiple malformation Syndrome characterized by hydrometrocolpos and polydactyly. This Syndrome is more frequent in females, whose parents are first-degree cousins (frequency 1:8 liveborn). We describe two cases of SMK: a male and a female. Patients were siblings and their parents were first cousins. The first child presented postaxial hexadactily, of the hands and feet, cardiovascular malformation and Arnold-Chiari II malformation. The baby died on the 17th day of life, for neurosurgical complications. Second baby, in which a prenatal ultrasonography showed a large cystic dilatation in the pelvis, presented with urinary hydrometrocolpos associated with persistent urogenital sinus (UGS) and polydactyly. The patient was temporary treated with intermittent vaginal catheterization. At age of 6 months she underwent reconstructive surgery via the anterior sagittal transanorectal approach (ASTRA), previous creation of a colostomy. Thirty-two months of the operation, the patient is continent for stool and urine and the vagina looks normal.
To examine features of primary vesicoureteric reflux (VUR) at birth following prenatal hydronephrosis and to describe the course of congenital damage in the first two years of life. We reviewed the records of 382 patients with prenatally diagnosed dilated urinary tracts seen during a 15-years period. When fetal hydronephrosis was confirmed at birth, voiding cystography was performed. If a VUR was diagnosed dimercaptosuccinic acid (DMSA) renography, at 1 month of age, was also performed. Cystography and DMSA renography were repeated and 1 and 2 years of age. Of 382 patients with prenatal hydronephrosis, 68 (17.8%) had primary VUR (50 male and 18 female, M:F = 3:1). VUR was unilateral in 24 patients and bilateral in 44 for a total of 112 refluxing renal units (RRUs). High-grade VUR (grade > or = 4) was found in 70 (62.5%) RRUs, and 60 (85.7%) were boys. Grade V reflux was observed in 96.5% of males. At birth, 22 (20%) RRUs had moderate impairment of renal function. In 12 (10%) RRUs (grade > or = 4) was demonstrated by a severe decrease in renal function. In all cases no focal scarring was noted. Eight infants (all males), with grade 5 degrees VUR, in the first six months of life had surgical treatment. The majority of the RRUs (110/112 = 89%) were followed medically. Mild reflux (grade I-III) had resolved in 81% RRUs, severe reflux (grade > or = 4) had resolved in 38% RRUs. Serial renal scans during the follow-up showed no progression of renal damage. VUR diagnosed at birth on prenatal ultrasonography is associated with congenital damage, with males affected more often than females. In patients without infection, after two years, modification of renal function or renal scars are very rarely observed.