Results obtained with piracetam in foetal distress during labour

A double-blind study was performed on ninety-six parturients of the Lima Maternity Hospital, Peru, with some evidence of foetal distress who were given indistinguishably piracetam or a placebo at random in order to investigate the effects of the drug on the foetus. The conditions of the new-born babies who had received piracetam were superior to those of the babies treated with the placebo, as evaluated with the Apgar at 1, 5 and 10 minutes after birth and on the basis of the neurological and clinical examination as from 24 hours until they were released. In addition, the reduction of the duration of the labour in the patients treated with piracetam as compared with the control group was obvious.     

Evaluation of a new mineral and trace metal supplement for use with synthetic diets

In an earlier study (Alexander et al., 1974) it was shown that the mineral mixture used in association with a synthetic diet was deficient in zinc, copper, iron, and manganese. A new mixture containing appropriately increased amounts of these trace metals has now been evaluated by means of metabolic balance studies carried out on children with phenylketonuria. This new mixture was shown to be satisfactory for zinc, copper, and iron, but minor changes have been recommended for manganese.     

Inducible nitric oxide synthase mediates gut ischemia/reperfusion-induced ileus only after severe insults

Inducible nitric oxide synthase (NOS 2) is thought to play a role in gut motility disorders that occur under proinflammatory conditions. Clinically, ileus occurs after sepsis and shock-induced gut ischemia/reperfusion (I/R). The purpose of this study was to determine if NOS 2 mediates impaired intestinal transit in well-established models of both moderate and severe gut ischemia/reperfusion. At laparotomy, Sprague-Dawley rats had duodenal catheters placed. Small intestinal transit was determined by quantitating the percentage tracer (FITC-dextran) in 10 equal segments of intestine 30 min after catheter injection [expressed as the mean geometric center (MGC) of distribution]. Transit was assessed at 6 and 24 h after gut ischemia [45 or 75 min of superior mesenteric artery occlusion (SMAO) with sham laparotomy as control]. In a separate set of experiments, N(6)-(iminoethyl)-L-lysine (L-NIL), a selective NOS 2 antagonist, was administered 1 h prior to laparotomy and transit was determined after 6 h as described above. Ileal NOS 2 expression was assessed by Western immunoblot and quantitative "real-time" RT-PCR. We observed that both 45 and 75 min of SMAO decreased intestinal transit at 6 h of reperfusion compared to sham. Ileal NOS 2 mRNA and protein were increased after 75, but not 45, min of SMAO. In addition, L-NIL improved transit after 75, but not 45, min of SMAO. We conclude that (1) NOS 2 is upregulated in the gut only after more severe ischemic insults, and (2) ileus is mediated, at least in part, by NOS 2 under these conditions.     

Induction of oxidative stress in the tissues of rats after chronic exposure to TCDD, 2,3,4,7,8-pentachlorodibenzofuran,and 3,3',4,4',5-pentachlorobiphenyl

The abilities of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 3,3',4,4',5-pentachlorobiphenyl (PCB126), and mixtures of these xenobiotics (toxic equivalents, TEQs) to induce oxidative stress in hepatic and brain tissues of rats have been investigated after chronic (30 wk) exposure to these congeners. TCDD, PeCDF, PCB126, and TEQs were administered daily to groups of rats at doses that corresponded to their toxic equivalency factors (TEFs), and the biomarkers of oxidative stress, including the production of superoxide anion, lipid peroxidation, and DNA single-strand breaks (SSBs), were determined in hepatic and brain tissues at the end of the exposure period. The three chemicals caused similar dose-dependent increases in the production of superoxide anion, lipid peroxidation, and DNA SSBs, which plateaued at certain dose ranges, followed by secondary increases at the higher dose levels. Similar effects were also produced by the TEQs; however, the dose-dependent increases in the biomarkers of oxidative stress were continuous and never achieved plateau levels. Except for PCB126, where statistical analyses revealed greater productions of superoxide anion and lipid peroxidation in brain tissues as compared with hepatic tissues, no significant differences were revealed between the two tissues in response to the other xenobiotics or the TEQs. Nonsignificant differences were also revealed when comparing the effects induced by the TEQs with those induced by the individual chemicals.     

Acute respiratory distress syndrome complicating Plasmodium vivax malaria

Malaria is one of the most common infectious diseases in the world, and severe respiratory complications have been described mainly in association with Plasmodium falciparum. We describe a case of acute respiratory distress syndrome complicating infection with P. vivax in the setting of relatively low parasitemia in a 47-yr-old woman after a brief trip to Papua New Guinea. A review of the literature shows that pulmonary complications of P. vivax are rare but occur more frequently than generally acknowledged. Pathogenic mechanisms of these complications are discussed.     

Juvenile aponeurotic fibroma. A case report with a review of the literature

Juvenile aponeurotic fibroma is a rare benign tumour which occurs mainly in young patients under 20 years of age and especially during childhood. Clinical presentation is a unique, hard and painless tumour of the palm or sole. The treatment commonly accepted for this locally recurrent tumour is complete excision with function preservation. In this paper, we report on a case of juvenile aponeurotic fibroma of the thenar area with a thickening of the first metacarpal bone shaft. Bone involvement in juvenile aponeurotic fibroma is a very rare condition. We only found one report of a comparable case in literature.     

INDUCTION OF OXIDATIVE STRESS IN THE TISSUES OF RATS AFTER CHRONIC EXPOSURE TO TCDD, 2,3,4,7,8-PENTACHLORODIBENZOFURAN,AND 3,3',4,4',5-PENTACHLOROBIPHENYL

The abilities of 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD), 2,3,4,7,8-pentachlorodibenzofuran (PeCDF), 3,3',4,4',5-pentachlorobiphenyl (PCB126), and mixtures of these xenobiotics (toxic equivalents, TEQs) to induce oxidative stress in hepatic and brain tissues of rats have been investigated after chronic (30 wk) exposure to these congeners. TCDD, PeCDF, PCB126, and TEQs were administered daily to groups of rats at doses that corresponded to their toxic equivalency factors (TEFs), and the biomarkers of oxidative stress, including the production of superoxide anion, lipid peroxidation, and DNA single-strand breaks (SSBs), were determined in hepatic and brain tissues at the end of the exposure period. The three chemicals caused similar dose-dependent increases in the production of superoxide anion, lipid peroxidation, and DNA SSBs, which plateaued at certain dose ranges, followed by secondary increases at the higher dose levels. Similar effects were also produced by the TEQs; however, the dose-dependent increases in the biomarkers of oxidative stress were continuous and never achieved plateau levels. Except for PCB126, where statistical analyses revealed greater productions of superoxide anion and lipid peroxidation in brain tissues as compared with hepatic tissues, no significant differences were revealed between the two tissues in response to the other xenobiotics or the TEQs. Nonsignificant differences were also revealed when comparing the effects induced by the TEQs with those induced by the individual chemicals.     

Right ventricular dysfunction in chronic lung disease

Right ventricular (RV) dysfunction arises in chronic lung disease when chronic hypoxemia and disruption of pulmonary vascular beds increase ventricular afterload. RV dysfunction is defined by hypertrophy with preserved myocardial contractility and cardiac output. RV hypertrophy seems to be a common complication of chronic and advanced lung disease. RV failure is rare, except during acute exacerbations of chronic lung disease or when multiple comorbidities are present. Treatment is targeted at correcting hypoxia and improving pulmonary gas exchange and mechanics. There are no data supporting the use of pulmonary hypertension-specific therapies for patients with RV dysfunction secondary to chronic lung disease.     

Pulmonary arterial hypertension in connective tissue diseases

Pulmonary arterial hypertension (PAH) may complicate diverse connective tissue diseases (CTDs). Approximately 10% of patients with systemic sclerosis develop PAH, the prevalence being much lower in other CTDs. However, PAH is an important contributor to morbidity and mortality in all forms of CTD. Despite similarities in presentation, hemodynamic perturbations, and pathogenesis, patients with CTD-associated PAH (CTD-PAH) usually have a poorer response to PAH-specific medications and poorer prognosis than patients with idiopathic PAH (IPAH). Select patients with CTD-PAH may be candidates for lung transplantation, but results are less favorable than for IPAH because of comorbidities and complications specifically associated with CTD.