Persistence of Mammary Artery Branches and Blood Supply to the Left Anterior Descending Artery

Background. Partial harvesting of the left internal mammary artery (LIMA) is a widespread technique used during minimally invasive coronary operations performed through a left anterior small thoracotomy. The influence of persisting LIMA branches was investigated to evaluate their effect on the blood flow of the left anterior descending artery.

Methods. Thirty patients, 15 with totally (group A) and 15 with partially (group B) harvested LIMAs, were evaluated. All the patients underwent postoperative angiography, during which a flow map of the LIMA was performed. The average peak velocity and the diastolic-to-systolic peak velocity ratio were recorded. The LIMA graft flow pattern was recorded in the proximal and distal thirds of the artery. Intramammary adenosine (12 to 14 μg) was injected and the average peak velocities before and after injection were calculated.

Results. The average peak velocity was similar in both groups in the proximal and distal thirds of the LIMA (25 ± 7 and 26 ± 5 cm/sec, respectively, in group A versus 27 ± 5 and 25 ± 5 cm/sec, respectively in group B; p = NS). The diastolic-to-systolic peak velocity ratio was similar proximally (0.78 ± 0.3 in group A versus 0.69 ± 0.3 cm/s in group B; p = NS), but not distally (1.72 ± 0.1 in group A versus 0.97 ± 0.3 in group B; p < 0.0005). The LIMA graft flow reserve was similar both proximally and distally (2.6 ± 0.6 and 2.5 ± 0.3 cm/s, respectively, in group A versus 2.6 ± 0.5 and 2.6 ± 0.3 cm/s, respectively, in group B; p = NS).

Conclusions. The persistence of LIMA branches does not influence the blood flow of the left anterior descending artery after acute adenosine-induced myocardial hyperemia. If a left anterior small thoracotomy is used in left anterior descending artery direct revascularization, complete LIMA harvesting is not mandatory and depends on the personal preference of the surgeon.     

Visual function in Huntington's disease patients and presymptomatic gene carriers.

Disturbances of visual cognition, visuomotor performance, and visual memory have been described frequently in Huntington's disease (HD). Early stage visual abnormalities could contribute to these deficits. We evaluated visual processing in 20 control subjects who were non-gene carriers at risk for HD, nine presymptomatic gene-positive subjects, and eight subjects with a recent diagnosis of Huntington's disease. Visual perceptual tests of contrast sensitivity and motion discrimination were used to probe early stage visual processing. Extraocular movements were evaluated in a neurologic examination, and the Digit Symbol test was used to test visual motor performance. Contrast sensitivity did not differ among the three groups. Motion discrimination was impaired in HD subjects but not in the presymptomatic gene carriers when compared to gene noncarriers. Among gene carriers, impaired motion discrimination performance was associated with poorer Digit Symbol performance and extraocular abnormalities. These findings suggest that the early stages of HD are associated with disturbances of motion perception as well as disruptions of visual motor and ocular motor performance.     

Anal polypoid tumor formation as the form of presentation of rectal gastric heterotopia]

Heterotopic gastric epithelium occurs in all portions of the alimentary tract, but it is extremely rare in the rectum. The authors report the finding of a pedunculated anal polyp in a 9-year-old girl with a six-month history of rectal bleeding. Microscopically, the polyp consisted of epithelium of the fundic type. Both the age of the patient and the finding of heterotopic epithelium of the fundic type alone supports a congenital malformation and not an inflammatory condition.     

Short-term synaptic plasticity, simulation of nerve terminal dynamics, and the effects of protein kinase C activation in rat hippocampus

Phorbol esters are hypothesised to produce a protein kinase C (PKC)-dependent increase in the probability of transmitter release via two mechanisms: facilitation of vesicle fusion or increases in synaptic vesicle number and replenishment. We used a combination of electrophysiology and computer simulation to distinguish these possibilities. We constructed a stochastic model of the presynaptic contacts between a pair of hippocampal pyramidal cells that used biologically realistic processes and was constrained by electrophysiological data. The model reproduced faithfully several forms of short-term synaptic plasticity, including short-term synaptic depression (STD), and allowed us to manipulate several experimentally inaccessible processes. Simulation of an increase in the size of the readily releasable vesicle pool and the time of vesicle replenishment decreased STD, whereas simulation of a facilitation of vesicle fusion downstream of Ca²⁺ influx enhanced STD. Because activation of protein kinase C with phorbol ester enhanced STD of EPSCs in rat hippocampal slice cultures, we conclude that an increase in the sensitivity of the release process for Ca²⁺ underlies the potentiation of neurotransmitter release by PKC.     

Two novel mutations at exon 8 of the Sequestosome 1 (SQSTM1) gene in an Italian series of patients affected by Paget's disease of bone (PDB).

PDB is genetically heterogeneous. Mutations of the sequestosome1 gene have been reported in sporadic and familial forms of Paget's in patients of French Canadian and British descent. Mutational analyses in different ethnic groups are needed to accurately investigate hereditary diseases. We describe two novel mutations of sequestosome1 in 62 Italian sporadic patients, confirming the role of the encoded protein in this disorder. INTRODUCTION: Paget's disease of bone (PDB) is a relatively common disease of bone metabolism reported to affect up to 3% of whites over 55 years of age. The disorder is genetically heterogeneous, and at present, there is scientific evidence that at least eight different human chromosomal loci are correlated with its pathogenesis. Mutations of the sequestosome1 (SQSTM1) gene were identified as responsible for most of the sporadic and familial forms of Paget in patients of French Canadian and British descent. Such mutations were located at exon 7 and 8 levels, encoding for the ubiquitin protein-binding domain (UBA) and representing a mutational hot spot area. MATERIALS AND METHODS: To verify the involvement of this gene in Italian subjects affected by PDB, we performed mutational analysis in 62 sporadic PDB cases. RESULTS: We described three different mutations at exon 8 level: P392L, already described in the French Canadian population and families predominantly of British descendent, and two novel mutations consisting of the amino acid substitutions M404V and G425R. No significant differences in the clinical history of PDB have been observed in patients with SQSTM1 mutations in respect to those without. CONCLUSIONS: Even though our findings suggest a minor involvement of the SQSTM1 gene in the pathogenesis of sporadic Italian Paget's cases, the identification of different significant mutations within the SQSTM1 gene in unrelated, but clinically similar individuals, offers extremely convincing evidence for a causal relationship between this gene and PDB. Longitudinal studies are needed to assess the penetrance of genotype/phenotype correlations. Our findings confirm the evidence of a clustered mutation area at this level in this disorder.     

Neridronate prevents bone loss in patients receiving androgen deprivation therapy for prostate cancer.

Today, androgen deprivation therapy is a cornerstone of treatment for advanced prostate cancer, although it presents important complications such as osteoporosis. Neridronate, a relatively new bisphosphonate, is able to prevent bone loss in patients with prostate cancer during androgen ablation. INTRODUCTION: Androgen-deprivation therapy (ADT) is a cornerstone of treatment for advanced prostate cancer. This therapy has iatrogenic complications, such as osteoporosis. The aim of our study was to evaluate the efficacy of neridronate, a relatively new bisphosphonate, to prevent bone loss during androgen ablation. MATERIALS AND METHODS: Forty-eight osteoporotic patients with prostate cancer, treated with 3-month depot triptorelina, were enrolled and randomly assigned to two different treatment groups: group A (n = 24) was treated with a daily calcium and cholecalciferol supplement (500 mg of elemental calcium and 400 IU cholecalciferol), and group B (n = 24) received in addition to the same daily calcium and cholecalciferol supplement, 25 mg of neridronate given intramuscularly every month. All patients also received bicalutamide for 4 weeks. Lumbar and femoral BMD was evaluated by DXA at baseline and after 1 year of therapy; moreover, deoxypyridinoline (DPD) and bone alkaline phosphatase (BALP) were determined at the beginning, midway through, and at the end of the study. RESULTS: After 6 and 12 months, whereas patients treated only with calcium and cholecalciferol (group A) showed a marked bone loss, with increased levels of DPD and BALP compared with baseline values, patients treated also with neridronate (group B) had substantially unchanged levels of these markers. After 1 year of treatment, lumbar and total hip BMD decreased significantly in patients treated only with calcium and cholecalciferol (group A), whereas it did not change significantly at any skeletal site in patients treated also with neridronate (group B). No relevant side effects were recorded during our study. CONCLUSIONS: Neridronate is an effective treatment in preventing bone loss in the hip and lumbar spine in men receiving ADT for prostate cancer.     

Stability of risk factors for cardiovascular diseases in Portuguese children and adolescents from the Porto area.

An important aspect of preventive medicine is to identify subjects at risk as soon as possible, so preventive strategies can be introduced at early ages. The justification for this strategy is twofold: firstly, the assumption that children maintain a particular high value of a risk factor for disease throughout life; and secondly, the assumption that lowering the level of the risk factor in early life will have a greater impact on the disease than will risk factor changes in later life. In epidemiology the analysis of such factors over time is referred to as tracking. Tracking analysis has been applied to risk factors for cardiovascular diseases (CVD) in pediatric years. The aims of this study were: I) to analyze the stability of biological risk factors [high blood pressure (BP), high percentage of fat mass (%FM) and high total cholesterol (TC)] and lifestyle risk factors [low physical activity index (PAI)] in isolation; and II) to analyze the stability of zero, one, two or three biological risk factors. There were two evaluations in 692 children and adolescents (325 boys and 367 girls), aged between 8 and 15 years. The quartiles, adjusted for age and gender, were the criterion used to identify subjects with biological risk factors (fourth quartile) and with lifestyle risk factors (first quartile) for CVD. The stability was calculated through the relative frequency of subjects who maintained or changed quartile between the two evaluations. There is stability for biological risk factors as well as for behavioral and/or lifestyle risk factors. However, the highest stability is seen in biological risk factors.     

Temazepam impairs effortful but not automatic processing of stimulus elements

The experiment investigated the effects in healthy volunteers of a single dose of temazepam (30 mg, oral) on effortful and automatic processing, by measuring memory for information and its context. Effortful processing was impaired, as shown by significant impairments in free recall of an 18-item list, but automatic processing was spared, as evidenced by no impairments in recall of the frequency of presentation, the colour, size or form of the items. In a second task, temazepam significantly impaired both recognition and recency memory of 30 items, although these scores were not correlated. Temazepam caused significant sedation, measured by an objective test and by subjective ratings, but this did not correlate with the memory impairments. The pattern of results is discussed with reference to the hypothesis that the memory impairments resulting from benzodiazepines are due to a reduction in information processing resources and thus affect effortful processing more than automatic processing.     

Hepatoprotective effects of diethylcarbamazine in acute liver damage induced by carbon tetrachloride in rats

This research was carried out to determine a potential role of leukotrienes in the acute hepatotoxicity induced by CC14 in rats. An inhibitor of leukotrienes biosynthesis, diethylcarbamazine (DEC, 25 and 50 mg ·kg-1 ip) exerted hepatoprotective effects, decreasing the activity of alanine aminotransfer-ase in serum and the concentration of liver triglycerides. DEC reduced histological damage of liver evidenced by electron microscopy. The hepatoprotective effects of DEC were dose-dependent. The results favor the role of leukotrienes in CC14 hepatotoxicity.