Family management of schizophrenia: A comparison of behavioral and supportive family treatment

This paper reports a comparison of behavioral and supportive family treatment for family management of schizophrenia. The family project applied two psychoeducational approaches to a highly treatment resistant population of young adults afflicted with chronic mental illness. The study compares and contrasts the effects of behavioral and supportive family management programs on clinical outcomes. Clinical improvements were associated with both family interventions. Discussion is provided on the relevance of this work to the growing body of evidence concerning the efficacy of psychoeducational family intervention for the management of schizophrenia.     

Recurrence of duodenal ulcer and Campylobacter pylori infection after eradication

The role of Campylobacter pylori gastritis in dyspepsia could be clarified more readily if reliable eradication therapy were available. Antibiotic monotherapy and combined therapy with an antibiotic agent plus a bismuth compound have yielded poor long-term results. In this study, bismuth-tetracycline-metronidazole triple therapy has been used to eradicate C. pylori infection in 100 consecutive patients who were suffering from either a duodenal ulcer or non-ulcer dyspepsia. Examination of a follow-up endoscopic biopsy at eight weeks after treatment showed an eradication rate of C. pylori of 94%. Of 64 patients whose biopsy samples were free of C. pylori infection at eight weeks and who were available for reassessment, 60 (94%) patients had samples that remained free of C. pylori infection on examination of a repeat endoscopic biopsy at 12-37 months (mean, 19.3 months). It is concluded that "triple chemotherapy" can achieve long-term eradication of C. pylori infection effectively in the majority of treated patients and that the recurrence of duodenal ulcers thus may be diminished.     

CD8： Adhesion Molecule, Co-Receptor and Immuno-Modulator

CD8 is a cell surface glycoprotein found in cytotoxic T lymphocytes, which are important components in cellular immunity, esp. in the immune response to cancer and chronic infections. There are two forms of CD8, either as an alphaalpha homodimer or alphabeta heterodimer. It acts as an "assistant" or co-receptor in the function of cytotoxic T cells where specific immunity is mediated by interaction of specific T cell receptor (alphabeta TCR) and its ligand peptide major histocompatibility complex (pMHC). CD8 also binds to pMHC but away from the interface of pMHC and TCR contact, thereof no influence on the specificity of this interaction. If the TCR and CD8 bind to the same pMHC at the same time, CD8 is defined as a co-receptor, functioning through its signalling via its cytoplasmic tyrosine phosphorylation pathway; if CD8 binds to pMHC independently of the TCR, it is defined as an adhesion molecule. At present, the co-receptor function theory is dominated in the field. Recent study has also shown that murine CD8 alphaalpha binds to TL antigen, an MHC homologue, therefore acts as an immuno-modulator. In this review, we discuss these current understandings of the three aspects of the CD8 functions and their structural basis.     

Immunosuppressive properties of the Mycoplasma arthritidis T-cell mitogen in vivo: inhibition of proliferative responses to T-cell mitogens.

We have previously shown that Mycoplasma arthritidis produces a soluble T-cell mitogen (MAM) which is active for most mouse strains that express the alpha chain of the I-E molecule (E alpha) encoded within the murine major histocompatibility complex. The lymphocytes from mice injected intravenously with the MAM exhibited a marked decrease in their ability to respond in vitro to MAM, to phytohemagglutinin, or to concanavalin A T-cell mitogens. Suppression could only be induced in MAM-responsive mouse strains and was most marked 1 to 4 days postinjection. Splenic and node cells and, to a lesser extent, thymic cells from MAM-injected mice could inhibit the ability of lymphocytes from normal mice to respond to MAM and lectin mitogens. A minimum of 2.5 x 10(4) viable cells was required for significant transfer of suppression, and no major histocompatibility complex restrictions were seen. Unlike concanavalin A-induced suppressor cells, which consist of a CD4-, CD8+ T-cell subset, suppressor cells induced by MAM were due to a CD4+ CD8- subset. We hypothesize that MAM may play a role in M. arthritidis-mediated disease by both its inflammatory and immunosuppressive properties.     

Toxicity but not arthritogenicity of Mycoplasma arthritidis for mice associates with the haplotype expressed at the major histocompatibility complex.

The use of inbred and congenic mouse strains established that toxicity and death induced by Mycoplasma arthritidis associates with the haplotype expressed at the murine major histocompatibility complex. Mice bearing H-2k and H-2d are susceptible, whereas those bearing H-2b are much more resistant. Mice susceptible to toxicity exhibited massive peritoneal adhesions and a decreased ability to clear organisms from the peripheral circulation. However, the severity of acute arthritis developing over a 3-month period was not statistically related to the haplotype expressed at the major histocompatibility complex. Lymphocyte activation in vitro by a soluble T-cell mitogen is also dependent on a similar haplotype expression.     

The application of linkage analysis to genetic counselling in families with Duchenne or Becker muscular dystrophy.

A total of 278 families of probands with Duchenne or Becker muscular dystrophy has been ascertained and offered genetic counselling. Linkage studies have been performed in these families using polymorphic DNA markers identifying loci linked to Duchenne and Becker muscular dystrophy. The clinical features of the probands are discussed: there was marked intrafamilial resemblance in the severity of the disease. We estimate that a complete study of potential carriers in these families would require analysis of samples from approximately 1400 subjects. The results of linkage studies tended to move women's carrier risk estimates (based on CK and pedigree data) towards the extremes of the risk categories, providing a more definitive risk estimate for 81% of the women who were previously in the middle range of carrier risk probabilities. About 70% of the families had only one affected member. Linkage analysis altered carrier risk estimates in 95% of sisters and aunts of index cases, but only affected estimates of the mother's carrier risks in about 11% of isolated cases. Even where linkage studies were not helpful in elucidating carrier risks, information could usually be obtained for use in prenatal diagnosis if required. We have assessed the attitudes to pregnancy and prenatal diagnosis of women at risk of being carriers of Duchenne or Becker muscular dystrophy and report 17 pregnancies in these women.     

SARS coronavirus induces apoptosis in Vero E6 cells

Severe acute respiratory syndrome (SARS) is an emerging infectious disease. Its etiological agent has been convincingly identified as a new member of family Coronaviridae (SARS-CoV). It causes serious damage to the respiratory system yet the mechanism is not clear. Infection-induced apoptosis or necrosis is suspected but no direct evidence for this yet exists. To date, Vero E6 cells are the only cell line that could be used to replicate the virus with obvious CPE (cytopathic effect) in vitro. It is known for some viruses (including members of family Coronaviridae) that CPE can be caused either by virus-induced apoptosis (active death) or cell necrosis (passive death). In this study, we examined the apoptosis in the SARS-CoV infected Vero E6 cells. Indeed, the results do show that the CPE was induced by apoptosis rather than necrosis, shown by typical DNA fragmentation, through the existence of apoptotic bodies and swollen mitochondria. This observation has some implications for the SARS-CoV pathogenicity: SARS-CoV does induce apoptosis in cell cultures and might have the same effect in vivo, responsible for the severe damage of the respiratory system.     

Presence of immunoglobulin M antibodies around the glomerular capillaries and in the mesangium of normal and passive Heymann nephritis rats

Summary Diffuse distribution of small, faintly staining, beaded deposits of rat immunoglobulin M (IgM) around the glomerular capillary blood vessels, and a more intensely staining larger deposition in the mesangium, were observed on the kidney sections of normal rats. As glomerular-fixed nephritogenic antigens are known to be present on the epithelial aspect of the glomerular basement membrane (GBM), especially at the soles of foot processes and at the slit pores, it was assumed that the IgM antibodies were directed against these antigens. Investigation by immunofluorescent antibody double-staining techniques of rat kidney sections obtained from normal and rabbit anti-FX1A-injected rats stained for the nephritogenic antigen showed that a number of antigenic sites in the glomeruli and in the mesangium shared antibody hits by heterologous rabbit IgG and autologous rat IgM antibodies. Most sites in the glomeruli stained specifically for rat IgM or rabbit IgG, but preferentially for the latter. The intensely fluorescent mesangial deposits stained mainly for rat IgM, indicating that at these sites the antigenic material was virtually saturated, while areas at the entry to the mesangial space also stained for rabbit IgG, indicating that at these locations free nephritogenic epitopes were still available for reaction with the anti-FX1A antibody. Western blot analysis have shown that the rabbit anti-rat FX1A IgG and the rat anti-rat KF3 IgM antibodies are directed against the same renal tubular-derived antigen with a molecular weight of 70,000. These experimental findings collectively demonstrate that the heterologous IgG and autologous IgM antibodies are directed against the same nephritogenic antigen, which is found in the glomeruli, the mesangium and the proximal convoluted tubules. Thus, the IgM autoantibody has a possible physiological role but, in addition, there is evidence of active immunophagocytic events, manifested in a rapid and continuous entrapment and expulsion of macromolecules after their processing by the mesangial cells of normal and passive Heymann nephritis rats.