The impact of glucose-insulin-potassium infusion in acute myocardial infarction on infarct size and left ventricular ejection fraction [ISRCTN56720616]

Background

Stopping antipsychotic treatment can interrupt improvement and exacerbate the illness. The reasons for discontinuing treatment during controlled clinical trials were analyzed to explore this phenomenon.

Methods

A post-hoc, pooled analysis was made of 4 randomized, double-blind clinical trials, 24–28 weeks in duration, involving 1627 patients with schizophrenia or a related disorder. Analyses combined all the atypical antipsychotic treatment groups in the studies.

Results

The majority of patients (53%) stopped their treatment at an early stage. Poor psychiatric response along with worsening symptoms was the most frequently given reason for discontinuing the course (36%), which was substantially more common than discontinuation due to poor tolerability of the medication (12%). This phenomenon was corroborated by less improvement in patients who discontinued treatment compared with those who completed, based on the PANSS total scores. Discontinuation due to poor response was, apparently, more predominantly linked to patient perception than to physicians' conclusions alone (80% vs. 20%). Discontinuation due to patient perception of poor response appeared to occur particularly early in the course of treatment. Patients who discontinued due to poor toleration of the medication responded in a more comparable manner with completers.

Conclusion

Discontinuing treatment may lead to exacerbation of symptoms, undermining therapeutic progress. In these studies, poor response to treatment and worsening of underlying psychiatric symptoms, and to a lesser extent, intolerability to medication were the primary contributors to treatment being discontinued. Our findings suggest that adherence may be enhanced by effective symptom control, as objectively measured and as subjectively perceived. Such strategies may improve patients' willingness to undertake long-term therapy and increase the likelihood of a better prognosis.     

A new pyeloureteral drainage catheter

We describe a new pyeloureteral drainage catheter that can be used for both genitourinary tract stenting and drainage, as well as tamponade of bleeding from the renal parenchyma or subcutaneous tissue. Primary indications for the use of this catheter and recommendations on insertion techniques are presented. With the exception of one case of minor kinking of the catheter, we have had no complications or failures with this catheter. While insertion through an unprotected tissue track is somewhat difficult, we have had good success introducing the catheter through a 24-F or larger Teflon working sheath. The catheter has excellent patient retention properties. It can be converted from external to internal drainage or vice versa simply and quickly on the ward.     

European cervical cancer screening：experiences and results

1　ＯｖｅｒｖｉｅｗｏｆｆｅｍａｌｅｍａｌｉｇｎａｎｃｉｅｓｉｎＥｕｒｏｐｅＣａｎｃｅｒｉｎｃｉｄｅｎｃｅａｎｄｍｏｒｔａｌｉｔｙｅｓｔｉｍａｔｅｓｆｏｒ 1995ｗｅｒｅｒｅｐｏｒｔｅｄｒｅｃｅｎｔｌｙｆｏｒ 38ｃｏｕｎｔｒｉｅｓｉｎＥｕｒｏｐｅ[1] .Ｔｈｅｒｅｗｅｒｅｅｓｔｉｍａｔｅｄ 2 .6ｍｉｌｌｉｏｎｎｅｗｃａｓｅｓｏｆｃａｎｃｅｒｉｎＥｕｒｏｐｅｉｎ 1995 ,ｒｅｐｒｅｓｅｎｔｉｎｇｏｖｅｒｏｎｅ ｑｕａｒｔｅｒｏｆｔｈｅｗｏｒｌｄｂｕｒｄｅｎｏｆｃａｎｃｅｒｗｈｉｌｅＥｕｒｏｐｅ’ｓｉｎｈａｂｉ…     

Effects of furazolidone, PCB77, PCB126, Aroclor 1248, paraquat and p,p'-DDE on transketolase activity in embryonal chicken brain

The effect of in ovo exposure to PCBs, DDE and paraquat on transketolase activity was measured in 19-day-old chicken embryos. Furazolidone was used as a positive control for decreased activity of the enzyme. The potency of contaminants to interact with transketolase was also tested in an in vitro system, using control brain 7000xg supernatants containing the enzyme. No effects were found on transketolase activity after in ovo or in vitro exposure to PCB126, Aroclor, DDE or paraquat. PCB77 decreased transketolase activity in vitro, but only at concentrations that, extrapolated to in ovo exposure, would be lethal to the embryo. Furazolidone decreased transketolase activity both in ovo and in vitro. For this contaminant, thiamine residues were analysed in the yolk sacs, but no differences were found between exposed and non-exposed eggs. Transketolase is dependent on thiamine pyrophosphate as a cofactor, and therefore, the decreased enzyme activity could be the result of an interaction between furazolidone and thiamine metabolism. Since thiamine residues were not affected by furazolidone and transketolase inhibition in vitro was similar to the inhibition after in ovo exposure, it was concluded that furazolidone interacted with transketolase on the enzymatic level rather than by a depletion of thiamine.     

Temperature-dependent effects of EDTA on the membrane glycoprotein IIb- IIIa complex and platelet aggregability

In agreement with previous studies, we observed that incubation of washed human platelets with EDTA at 37 degrees C for short periods caused an irreversible loss of their aggregation response to adenosine diphosphate and markedly diminished their capacity to bind fibrinogen. AP-2 is a monoclonal antibody that reacts with a determinant specific to the glycoprotein (GP) IIb-IIIa complex. We now report that in a direct binding assay, the number of sites for AP-2 on platelets incubated with EDTA at 37 degrees C fell to approximately 30% of those present on control platelets. This effect of EDTA was not observed at room temperature. Analysis of the treated platelets by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed normal amounts of GP IIb and GP IIIa. However, studies using crossed immunoelectrophoresis with 125I-AP-2, 125I-Tab (anti-GP IIb), or 125I- AP-3 (anti-GP IIIa) in intermediate gels showed that at 37 degrees C, EDTA was inducing an irreversible change in GP IIb-IIIa complexes. A reduction in size and probable dissociation of the GP IIb-IIIa precipitate was accompanied by the appearance of precipitates having the characteristics of those given by free GP IIb and free GP IIIa and the location of a major new cathodal precipitate, which bound Tab and AP-3 but not AP-2. Membrane modifications associated with the loss of antigenic determinants on GP IIb-IIIa may explain EDTA-induced loss of platelet aggregability at 37 degrees C.