A sieving method for collecting the metacercariae of trematode parasites from freshwater fish.

This study describes a sieving method for the collection of metacercariae from frozen (-20 degrees C) freshwater fish. Digested fish tissue is filtered through a series of sieves; the crude filtrate is then centrifuged. Centrifugation produces a sediment from which metacercariae can be removed. Half of the metracercariae that were obtained from the fish meat that had been frozen for 10 days (-20 degrees C) were dead; the other half were alive and some larvae were moving slowly.

Analysis of the 1991-2000 influenza epidemic in Guangdong Province, China.

Influenza surveillance networks in Guangdong were established to investigate the epidemiological characteristics of influenza and influenza epidemics. Influenza activity peaked annually from March to July in Guangdong in 1991-2000; influenza H3N2 predominated in the epidemic (7 years of 10); the outbreak of influenza in 1996 was the remarkable result of antigenic drift of H3N2 strain. Ten isolates of H9N2 strains were discovered from human subjects in 1998 and 1999: chicken strains isolated after the Hong Kong fowl influenza outbreak. It was found that there was just one influenza activity season per annum in Guangdong and that the influenza H3N2 subtype still predominates in Guangdong. Further research into the pathogenicity of influenza H9N2 in humans warranted.

Neuronal and endothelial nitric oxide synthase gene knockout mice

Targeted disruption of the neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS) genes has led to knockout mice that lack these isoforms. These animal models have been useful to study the roles of nitric oxide (NO) in physiologic processes. nNOS knockout mice have enlarged stomachs and defects in the inhibitory junction potential involved in gastrointestinal motility. eNOS knockout mice are hypertensive and lack endothelium-derived relaxing factor activity. When these animals are subjected to models of focal ischemia, the nNOS mutant mice develop smaller infarcts, consistent with a role for nNOS in neurotoxicity following cerebral ischemia. In contrast, eNOS mutant mice develop larger infarcts, and show a more pronounced hemodynamic effect of vascular occlusion. The knockout mice also show that nNOS and eNOS isoforms differentially modulate the release of neurotransmitters in various regions of the brain. eNOS knockout mice respond to vessel injury with greater neointimal proliferation, confirming that reduced NO levels seen in endothelial dysfunction change the vessel response to injury. Furthermore, eNOS mutant mice still show a protective effect of female gender, indicating that the mechanism of this protection cannot be limited to upregulation of eNOS expression. The eNOS mutant mice also prove that eNOS modulates the cardiac contractile response to ß-adrenergic agonists and baseline diastolic relaxation. Atrial natriuretic peptide, upregulated in the hearts of eNOS mutant mice, normalizes cGMP levels and restores normal diastolic relaxation.