Sequential changes of esophageal motility after endoscopic injection sclerotherapy or variceal ligation for esophageal variceal bleeding: a scintigraphic study

OBJECTIVE: Endoscopic injection sclerotherapy and variceal ligation are two popular endoscopic methods used to treat esophageal variceal hemorrhage. These two methods have not been compared with regard to esophageal dysfunction after treatment. This is a prospective investigation of esophageal dysmotility after endoscopic injection sclerotherapy and variceal ligation. METHODS: Sequential changes of esophageal motility after endoscopic injection sclerotherapy (n = 25) and variceal ligation (n = 25) were investigated in 50 cirrhotic patients with recent variceal bleeding. Another 22 cirrhotics without esophageal varices were included as controls. Radionuclide esophageal transit tests were performed before initial endoscopic treatment, and 1 and 3 months after variceal eradication. RESULTS: The baseline esophageal transit time was longer in both the sclerotherapy (n = 25, 7.8 +/- 1.4 s) and ligation groups (n = 25, 8.2 +/- 1.8 s) than in controls (n = 22, 6.7 +/- 0.7 s, p < 0.005). The transit time was longer in patients with large varices than in those with small varices (8.3 +/- 1.7 vs. 7.2 +/- 0.7 s, p < 0.05). In the sclerotherapy group, the transit time was prolonged 1 month after variceal eradication, compared with its pretreatment state (n = 20, 7.6 +/- 1.5 vs. 10.0 +/- 2.2 s, p < 0.0001) but was shortened at 3 months compared with 1 month after variceal eradication (n = 12, 10.7 +/- 1.5 vs. 8.6 +/- 2.2 s, p < 0.05). Multiple regression analysis showed that the number of treatment sessions required to eradicate varices was the only significant factor associated with prolonged transit time (p < 0.05). In the ligation group, the transit time changed little at 1 month or 3 months after variceal eradication. CONCLUSIONS: Impairment of esophageal motility can be significant with endoscopic injection sclerotherapy but is reversible. However, endoscopic variceal ligation exerts no significant impact on esophageal motility.     

Ileal penetration by a Multiload-Cu 375 intrauterine contraceptive device. A case report with review of the literature

A case of a 28-year-old gravida 3 para 2 woman with an ileal penetration by an intrauterine device (IUD) is reported. Four weeks following insertion of a Multiload-Cu 375, the woman underwent laparotomy due to persistent vague abdominal pain and translocation of the IUD. The device had perforated the fundal uterine wall and the two flexible side arms and the copper-bearing rod had completely eroded into the wall of the ileum with only the strings protruding outside the small bowel mesentery. Resection of an ileal segment with end-to-end anastomosis was performed. The woman made an uneventful recovery. It appears that a translocated Multiload-Cu 375 IUD body can penetrate and be entirely embedded within the bowel wall as early as 4 weeks following translocation. This report documents the shortest interval between insertion and proven bowel injury by an IUD.     

Current directions in research on understanding and preventing intoxicated aggression

The present paper describes promising research directions that emerged from a recent international conference on intoxication and aggression and from the scientific literature generally. In this overview, intoxicated aggression is seen as arising from an interactional process involving multiple contributing factors or causes. This model helps to define research directions that can further understanding and prevention. First, the societal/cultural framing of intoxication and aggression exerts a powerful influence on drinking behaviour and needs to be better understood. Another important area for research is the moderating role on alcohol-related aggression of personal factors such as predisposition to aggression and individual differences in expectations about alcohol and aggression. Research on the role of basic pharmacological effects of alcohol in increasing the likelihood of aggressive behaviour is also a critical aspect of understanding intoxicated aggression. Drinking contexts and environments play a considerable role in the relationship between intoxication and aggressive behaviour and need to be better understood. Another critical direction for future research is the study of intoxicated aggression as a process involving the interaction of the person, the situation and the effects of alcohol in natural and experimental settings. Finally, the paper highlights promising directions for research on interventions to prevent intoxicated aggression and violence.     

Astrocytes containing amyloid beta-protein (Abeta)-positive granules are associated with Abeta40-positive diffuse plaques in the aged human brain

Amyloid beta-protein (Abeta) is the major component of senile plaques that emerge in the cortex during aging and appear most abundantly in Alzheimer's disease. In the course of our immunocytochemical study on a large number of autopsy cases, we noticed, in many aged nondemented cases, the presence of unique diffuse plaques in the cortex distinct from ordinary diffuse plaques by immunocytochemistry. The former were amorphous, very faintly Abeta-immunoreactive plaques resembling diffuse plaques, but they stained for Abeta40 and were associated with small cells containing Abeta-positive granules. A panel of amino- and carboxyl-terminal-specific Abeta antibodies showed that such Abeta40-positive diffuse plaques and cell-associated granules were composed exclusively of amino-terminally deleted Abeta terminating at Abeta40, -42, and -43. Double immunostaining also showed that those Abeta-immunoreactive granules are located in astrocytes and not in microglia or neurons. Immunoelectron microscopy revealed that nonfibrillar Abeta immunoreactivity was located within lipofuscin-like granules in somewhat swollen astrocytes. These findings raise the possibility that astrocytes take up Abeta and attempt to degrade it in lysosomes in the aged brain.     

A simplified system for generating recombinant adenoviruses

Recombinant adenoviruses provide a versatile system for gene expression studies and therapeutic applications. We report herein a strategy that simplifies the generation and production of such viruses. A recombinant adenoviral plasmid is generated with a minimum of enzymatic manipulations, using homologous recombination in bacteria rather than in eukaryotic cells. After transfections of such plasmids into a mammalian packaging cell line, viral production is conveniently followed with the aid of green fluorescent protein, encoded by a gene incorporated into the viral backbone. Homogeneous viruses can be obtained from this procedure without plaque purification. This system should expedite the process of generating and testing recombinant adenoviruses for a variety of purposes.     

Medroxyprogesterone acetate antagonizes inhibitory effects of conjugated equine estrogens on coronary artery atherosclerosis

Although estrogen replacement therapy is associated with reduced risk of coronary heart disease and reduced extent of coronary artery atherosclerosis, the effects of combined (estrogen plus progestin) hormone-replacement therapy are uncertain. Some observational data indicate that users of combined hormone replacement consisting of continuously administered oral conjugated equine estrogens (CEE) and oral sequentially administered (7 to 14 days per month) medroxyprogesterone acetate (MPA) experience a reduction in risk similar to that of users of CEE alone. However, the effects of combined, continuously administered CEE plus MPA (a prescribing pattern that has gained favor) on the risk of coronary heart disease or atherosclerosis are not known. We studied the effects of CEE (monkey equivalent of 0.625 mg/d) and MPA (monkey equivalent of 2.5 mg/d), administered separately or in combination, on the extent of coronary artery atherosclerosis (average plaque size) in surgically postmenopausal cynomolgus monkeys fed atherogenic diets and treated with these hormones for 30 months. Treatment with CEE alone resulted in atherosclerosis extent that was reduced 72% relative to untreated (estrogen-deficient) controls (P < .004). Atherosclerosis extent in animals treated with CEE plus MPA or MPA alone did not differ from that of untreated controls. Although treatment had marked effects on plasma lipoprotein patterns, statistical adjustment for variation in plasma lipoproteins did not alter the between-group relationships in atherosclerotic plaque size, suggesting that these factors do not explain substantially the atheroprotective effect of estrogen or the MPA-associated antagonism. Although the mechanism(s) remains unclear, we conclude that oral CEE inhibits the initiation and progression of coronary artery atherosclerosis and that continuously administered oral MPA antagonizes this atheroprotective effect.