PubMed Health⌕ Search

Biomedical subjects

C Sweet

Publications and source records attributed to C Sweet.

89 records · Page 5Linked to original sources
PubMed1977

Regulation of cellvibriocin activity.

Attempts were made to enhance the production of cellvibriocin, the bacteriocin produced by Cellvibrio sp. NCIB 9916, by a study of cultural conditions in agar (solid) media. In such media cellvibriocin was unstable: within 24 h all activity disappeared at 45 degrees C, 70% at 37 degrees C and more than 50% within 5 days at 5 degrees C. The temperature at which the producer strain was grown was critical, 25 degrees C being optimal. Cellvibriocin activity was markedly affected by the composition of the medium. Small amounts of metallic salts (Cu2+, Mn2+, Sr2+, Zn2+) and carboxylic acids of the citric acid cycle, especially citrate and tartrate, promoted its activity. Protease inhibitors, p-chloromercuribenzoic acid, N-ethyl maleimide and iodoacetate, enhanced cellvibriocin activity whereas a promoter of protease activity, casein hydrolysate, decreased activity.

Acids↗
PubMed1977

The pregnant ferret as a model for studying the congenital effects of influenza virus infection in utero: infection of foetal tissues in organ culture and in vivo.

Organ cultures of ferret foetal tissues showed a similar pattern of susceptibility to influenza virus to that already observed for human foetal tissues (Rosztoczy et al., 1975); respiratory, alimentary and urogenital tissues supported the replication of influenza virus but nervous and lymphopoietic tissues (those which, in man, are associated with foetal or postnatal abnormalities) were insusceptible. In contrast to corresponding human tissues, ferret foetal placenta and amnion readily supported viral replication although both human and ferret umbilical cord were susceptible. In limited experiments, neither the membranes nor the susceptible foetal tissues became infected after intranasal inoculation of pregnant ferrets of various gestational ages. However, after intracardial inoculation of pregnant ferrets with high titre virus (ca 10(9) EBID50) virus was isolated from both foetal membranes and foetuses. The membranes became infected at early, middle and late gestation, but virus appeared to cross the placental barrier to infect foetal tissues only in late gestation. At this stage virus could be isolated not only from those foetal tissues (respiratory, alimentary and urogenital) susceptible in organ culture, but also in small amounts from tissues which were insusceptible in organ culture (heart, lymphopoietic and nervous tissue). Virus was also isolated from foetal membranes and foetuses of late gestation ferrets following intracardial inoculation with a one hundred-fold lower dose of virus which, unlike the higher dose, did not induce a maternal febrile response. The pregnant ferret appears to be a suitable model for investigating the effects on development of foetal infection with influenza virus but it may have disadvantages with regard to the nature and strength of the placental barrier.

Animals↗
PubMed1976

The behaviour in ferrets of two closely related clones of influenza virus of differing virulence for man.

Clones 7a and 64d of the recombinant influenza virus A/PR/8/34-A/England/939/69(H3N2) which are of different virulence for man as judged by clinical score (7a more virulent than 64d) showed similar differences in ferrets. With intranasal inoculation the approximate 50% minimal infectious doses of both clones were similar (between 10(0) and 10(2) EID(50)) as were their titres in nasal washes 24 h after inoculation and the histologically evident damage they caused in the nasal turbinates. However, clone 7a persisted in the nasal washes more than 64d and produced a more prolonged pyrexia. Furthermore, 7a consistently produced a lung infection which was produced only occasionally by 64d and then to a lesser extent than 7a. In contrast to nasal mucosa, histological damage in the lung was slight with both strains. Differences in replication of 7a and 64d in organ cultures of nasal turbinates appeared only after 24 h incubation. They were not sufficiently large to explain the markedly superior ability of 7a to persist in the nasal tract in vivo. This persistence, which coincides with the production of pyrexia, may be due to a greater ability of 7a to resist induced systemic host defences. Spasmodic isolations of infective virus of both clones were made from extra-respiratory tissues such as liver, spleen and kidney.

Animals↗
PubMed1975

Replication of influenza virus in organ cultures of human and simian urogenital tissues and human foetal tissues.

A survey of human adult tissues in organ cultures showed that influenza viruses (A/Moscow/1019/65 (h2n2) or a recombinant virus virulent for man (PR/8-A/England/939/69 Clone 7a(H3N2)) could infect uterus, bladder and conjunctiva but not oesophagus under the conditions employed; simian bladder and uterus were also susceptible. These results were similar to those already described for corresponding ferret tissues. Organ cultures of human foetal nasal mucosa, trachea, oesophagus, small and large intestine, and bladder consistently supported replication over 4 days or more with high virus yields. Lung, conjunctiva and umbilical cord were less consistently susceptible and gave lower yields. Placenta and kidney cultures allowed replication of virus in one of 8 and one of 4 experiments respectively, the yields being low and of short duration. Organ cultures of neural tissue (meninges and brain), lymphopoietic tissue (spleen, liver and thymus) and amnion did not support significant viral replication. The results are discussed in relation to possible infection of the foetus in utero with influenza virus.

Animals↗
PubMedDate not supplied

Lessons for human influenza from pathogenicity studies with ferrets.

In research on influenza, little attention has been given to factors that determine the patterns of infection in human adults or infants and the severity of disease. Ferret influenza has been used to elucidate the following facets of pathogenicity that bear on these questions about human disease: the differential infectivity of virus strains for the upper respiratory tract (URT); the reasons for less severe infection of the lower respiratory tract (LRT) than of the URT; why pneumonia is rare; and why strains differ in the production of LRT infection. The origin of fever has been defined; viruses have been shown to differ in fever-producing components. Poor spread of virus from the respiratory tract to other susceptible tissues and rarity of fetal infection have been explained. Death in neonatal ferrets due to influenza with either a syndrome akin to cot death or viral pneumonia have been elucidated, and protection of the young by immunized mothers has been demonstrated.

Animals↗