Burdens and Psychological Health of Family Caregivers of People with Schizophrenia in Two Chinese Metropolitan Cities: Hong Kong and Guangzhou

Family members charged with the care of those suffering from schizophrenia experience considerable stress due to their multiple responsibilities. Research regarding the burdens of caregiving is scant in Hong Kong and China. The present study quantified the association of the duties of caregivers with mental health symptoms in two Asian cities having distinct health care systems (i.e., Hong Kong and Guangzhou, China). Thirty nine caregivers in Hong Kong and 70 caregivers in Guangzhou were recruited from nongovernmental mental health organizations. They were assessed using the Chinese version of the Involvement Evaluation Questionnaire and the General Health Questionnaire. While the Guangzhou family caregivers had a significantly higher burden than the Hong Kong sample, there was no significant difference in the psychological health status of family caregivers in the two cities. Result of correlational analyses, however, revealed high associations between burden of care variables and the psychological health of the caregivers. Findings for the present study have implications regarding the physical and mental health needs of those caring for seriously disturbed relatives.     

Homocysteine and asymmetric dimethylarginine (ADMA): biochemically linked but differently related to vascular disease in chronic kidney disease.

Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is formed by methylation of arginine residues in proteins and released after proteolysis. In this reaction, S-adenosylmethionine is methyldonor and S-adenosylhomocysteine the demethylated product. ADMA and homocysteine are thus biochemically linked. Both plasma homocysteine and ADMA concentrations are increased in patients with renal dysfunction, probably as a result of an impairment in their metabolic, but not urinary, clearance. Hyperhomocysteinemia has been associated with an increased risk of cardiovascular disease in end-stage renal disease, especially in patients without malnutrition and inflammation. Also, plasma ADMA levels have been associated with cardiovascular disease in renal failure patients. Both homocysteine and ADMA are thought to mediate their adverse vascular effects by impairing endothelial, nitric oxide-dependent function resulting in decreased vasodilatation, increased smooth muscle cell proliferation, platelet dysfunction and increased monocyte adhesion. At the same time, it has been shown that the correlation between plasma ADMA and homocysteine is weak and that, in renal patients, the association of plasma ADMA carotid intima-media thickness, cardiovascular events and overall mortality is independent of homocysteine. This indicates that the negative vascular effects of ADMA and homocysteine have a different etiology. Treatment with folic acid substantially lowers homocysteine, but not ADMA concentration. So far, homocysteine-lowering therapy has not been very successful in decreasing cardiovascular disease. In patients with renal failure, ADMA reduction may be an interesting new goal in the prevention of cardiovascular disease.     

One-stop routing for surgical interventions: a cost-analysis of endoscopic groin repair

Surgical Endoscopy - Single-visit (SV) totally extraperitoneal (TEP) inguinal hernia repair is an efficient service without impairment of safety or complication rate. Data on the economic impact of...     

Positive classic antineutrophil cytoplasmic antibody (C‐ANCA) titer at switch to azathioprine therapy associated with relapse in proteinase 3–related vasculitis

Objective

To analyze disease‐free survival in patients with antineutrophil cytoplasmic antibody (ANCA)–associated small‐vessel vasculitis (AAV) treated with cyclophosphamide only or switched to azathioprine after 3 months of full remission while taking cyclophosphamide.

Methods

We analyzed disease‐free survival in all consecutive patients diagnosed with AAV between 1990 and 2000 at our center. Patients were treated with cyclophosphamide only (1990–1996) or switched to azathioprine after 3 months of remission while taking cyclophosphamide (1997–2000). All patients received at least 12 months of followup.

Results

Of the total 128 patients, 53 (41%) relapsed. Forty‐four of the 128 patients (34%) had been switched to azathioprine therapy. Disease‐free survival at 2 and 4 years was 76% and 65% in the cyclophosphamide group compared with 76% and 51% in the azathioprine group. In patients with proteinase 3 (PR3) classic ANCA (C‐ANCA)–associated vasculitis who were switched to azathioprine (n = 33), a positive C‐ANCA titer at the moment of treatment switch (n = 13) was significantly associated with relapse (RR 2.6, 95% confidence interval 1.1–8.0; P = 0.04). In patients with a negative ANCA titer at the time of switch to azathioprine, disease‐free survival at 2 and 4 years was 80% and 62%, which was identical to that for patients treated with cyclophosphamide only. In patients who were ANCA‐positive at the time of treatment switch, disease‐free survival at 2 and 4 years was only 58% and 17%.

Conclusion

Switching cyclophosphamide to azathioprine after induction of remission in patients with PR3‐ANCA‐associated vasculitis who are still ANCA‐positive at the time of treatment switch is associated with a high risk of relapse.

     

Identification of amino acids in herpes simplex virus DNA polymerase involved in substrate and drug recognition.

Herpes simplex virus (HSV) encodes a DNA polymerase that is similar in several respects to the replicative mammalian DNA polymerase alpha. Recently, these and other DNA polymerases have been shown to share several regions of protein sequence similarity. Despite these similarities, antiviral drugs that mimic natural polymerase substrates specifically inhibit herpesvirus DNA polymerases. To study amino acids involved in substrate and drug recognition, we have characterized and mapped altered drug sensitivity markers of nine HSV pol mutants and sequenced the relevant portions of these mutants. The mutations were found to occur within four relatively small regions. One such region, which we designate region A, has sequence similarity only to DNA polymerases that are sensitive to certain antiviral drugs. The other three regions contain sequences that are similar among various DNA polymerases. The multiple mutations occurring within two of these regions make it likely that the regions interact directly with drugs and substrates. Our results lead us to favor a model in which protein folding allows interactions among the four regions to form the substrate and drug binding sites.