Trigeminal nuclear complex of the ferret: anatomical and immunohistochemical studies

In order to establish the ferret as an animal model for studies of trigeminal pain, we describe the cytoarchitecture and neurochemistry of the trigeminal nuclear complex in the ferret and compare them to those of the cat and rat. The complex was divided as previously described, but the ferret differed in the extent of the nuclear boundaries. The neuroanatomical istribution of substance P-, calcitonin gene-related peptide-, galanin-, enkephalin-, serotonin-, somatostatin-, neuropeptide Y-, and neurotensin-immunoreactivity was determined throughout the rostrocaudal extent of the complex. In subnucleus caudalis, substance P-, calcitonin gene-related peptide-, enkephalin-, serotonin-, somatostatin-, neuropeptide Y-, and galanin-immunoreactivity was densest in laminae I and II. In subnucleus interpolaris, immunoreactivity for all the above neurochemicals was most dense along the lateral border and the ventral third of the caudal part of the subnucleus. Enkephalin-immunoreactive cell bodies were present in subnucleus caudalis and interpolaris. In subnucleus oralis, labelling for substance P, calcitonin gene-related peptide, galanin, enkephalin, and serotonin was most prominent in the dorsomedial part of the subnucleus. Somatostatin-immunoreactive cell bodies were distributed throughout the spinal nucleus. Labelling of serotonin, substance P, calcitonin gene-related peptide, galanin, enkephalin, and somatostatin was present in the main sensory nucleus. The motor nucleus contained fibers immunoreactive for substance P, enkephalin, serotonin and neuropeptide Y, and cell bodies immunoreactive for calcitonin gene-related peptide. The majority of neurotensin-immunoreactivity was found at the level of subnucleus caudalis, where it was densest in the trigeminal extension of the lateral cervical nucleus. The distribution of peptides in this species throughout the spinal nucleus is consistent with the notion that all the subnuclei may be involved in the processing of nociceptive inputs.     

Rochalimaea henselae, Afipia felis and cat-scratch disease

Several years ago, Rochalimaea henselae has emerged as an agent of bacillary angiomatosis, bacillary peliosis and recurrent septicaemia that generally occur in patients infected with human immunodeficiency virus. An aetiologic role in cat scratch disease is also suspected widely on the basis of a serologic survey. Its slow growth and its culture requirement explain that this pathogen, a gram-negative bacterium, could not be isolated until 1990. Moreover, blood and tissue samples request lysis and crushing for recovering by culture. The clinical, histological, microbiological and pathogenic aspects of these infections are described and discussed.     

A homeotic transformation is generated in the rostral branchial region of the head by disruption of Hoxa-2, which acts as a selector gene

The Hoxa-2 gene was disrupted by homologous recombination. Homozygous mutant mice died at birth. Defects were found in the branchial region of the head, which corresponds to the Hoxa-2 rostral expression domain. While rhombomeric and neural crest cell (NCC) segmentation was not affected, mesenchymal NCC derivatives of the second arch were lacking, and second arch mesenchymal NCC identity was changed to first arch identity, resulting in homeotic transformation of second to first arch skeletal elements. These results reveal the existence of a skeletogenic ground pattern program common to at least the mesenchymal NCC that originated from rhombomeres 2 and 4. The appearance of an atavistic reptilian pterygoquadrate element in Hoxa-2 mutants suggests that this ground pattern is intermediate between reptiles and mammals. The ground pattern program appears to be modified in the mouse first arch by a Hox-independent process, whereas Hoxa-2 acts as a selector gene in the second arch.     

Local expression of tumor necrosis factor alpha and interleukin-2 correlates with protection against corneal scarring after ocular challenge of vaccinated mice with herpes simplex virus type 1

To correlate specific local immune responses with protection from corneal scarring, we examined immune cell infiltrates in the cornea after ocular challenge of vaccinated mice with herpes simplex virus type 1 (HSV-1). This is the first report to examine corneal infiltrates following ocular challenge of a vaccinated mouse rather than following infection of a naive mouse. Mice were vaccinated systemically with vaccines that following ocular challenge with HSV-1 resulted in (i) complete protection against corneal disease (KOS, an avirulent strain of HSV-1); (ii) partial protection, resulting in moderate corneal disease (baculovirus-expressed HSV-1 glycoprotein E [gE]); and (iii) no protection, resulting in severe corneal disease (mock vaccine). Infiltration into the cornea of CD4+ T cells, CD8+ T cells, macrophages, and cells containing various lymphokines was monitored on days 0, 1, 3, 7, and 10 postchallenge by immunocytochemistry of corneal sections. Prior to ocular challenge, no eye disease or corneal infiltrates were detected in any mice. KOS-vaccinated mice developed high HSV-1 neutralizing antibody titers (> 1:640) in serum. After ocular challenge, they were completely protected against death, developed no corneal disease, and had no detectable virus in their tear films at any time examined. In response to the ocular challenge, these mice developed high local levels of infiltrating CD4+ T cells and cells containing interleukin-2 (IL-2), IL-4, IL-6, or tumor necrosis factor alpha (TNF-alpha). In contrast, only low levels of infiltrating CD8+ T cells were found, and gamma interferon (IFN-gamma)-containing cells were not present until day 10. gE-vaccinated mice developed neutralizing antibody titers in serum almost as high as those of the KOS-vaccinated mice (> 1:320). After ocular challenge, they were also completely protected against death. However, the gE-vaccinated mice developed low levels of corneal disease and virus was detected in one-third of their eyes. Compared with KOS-vaccinated mice, the gE-vaccinated mice had a similar pattern of IFN-gamma, but a delay in the appearance of CD4+ T cells, CD8+ T cells, and IL-4-, IL-6-, and TNF-alpha-containing cells. In sharp contrast to those of the KOS-vaccinated mice, no cells containing IL-2 were detected in the eyes of gE-vaccinated mice at any time. Mock-vaccinated mice developed no detectable neutralizing antibody titer and were not protected from lethal HSV-1 challenge.(ABSTRACT TRUNCATED AT 400 WORDS)     

Management of depressed patients by family physicians. Questionnaire study in Hamburg

METHOD: With the aid of a questionnaire specially developed for the purpose, general practitioners were questioned about their management of depressed patients attending their offices. A number of physician-related aspects that might have been the cause of the differences in prevalence and management of the patients, were investigated. RESULTS: Estimations on the part of the physicians that patients with psychological problems accounted for some 20% of their total case load were in agreement with figures obtained from other studies. Those specifically with depression accounted for 8.6%. The practitioners' assessment of their own competence in caring for depressed patients, and their cooperation with other institutions play a key role in the incidence of the diagnosis and the nature of medical treatment--by means of drugs, psychotherapy, referral, yes or no. The results obtained suggest a need to improve the psychiatric training of general practitioners and for closer cooperation with neurologists, psychologists, and hospitals.     

Extended major histocompatibility complex haplotypes in celiac patients in the west of Ireland

The highest reported prevalence of celiac disease (gluten-sensitive enteropathy) is found in the West of Ireland. Recent genetic data have suggested that major histocompatibility complex-linked loci may have a dominant genetic effect for disease susceptibility in this population compared with a recessive effect in other groups. To further understand the role of the MHC in celiac disease in the West of Ireland, we analyzed markers for 22 MHC haplotypes from celiac patients and compared them with 18 nontransmitted haplotypes found in the parents of celiac children, and with reported haplotypes from other populations. An extended MHC haplotype including [HLA-B8, DR3, DQw2, Bf*S, C4A*Q0, and C4B*1] accounted for 50% of celiac haplotypes but only 27% of nontransmitted parental haplotypes. Compared with other reported haplotypes in celiacs, patients from the West of Ireland show a higher prevalence of HLA-A1 as a component of this extended haplotype, suggesting that although the core haplotype is similar between Irish patients and others, the celiac population in the West of Ireland differs at other HLA loci. We did not observe any other common haplotypes among our patients unlike the situation in other populations. These differences may underlie the possible dominant effect of HLA-linked loci and the unusually high prevalence of celiac disease in the Irish population. We also found that the serum levels of complement components C3c, C4, and factor B were significantly lower among celiac patients than nonceliacs. The lower serum level of C4 appears to be related to the presence of deletions and null alleles at the C4A and C4B loci in celiacs.     

Effects of angiotensin I of the American bullfrog Rana catesbeiana on amphibian tissues

1. The effect of bullfrog angiotensin I [Asp1, Val5, Asn9] angiotensin I, (AT I) on short-circuit current (SCC) on isolated toad skin and aorta contractility was examined. 2. AT I increased SCC in toad skin, the effect was partially inhibited by angiotensin-converting enzyme inhibitor (ACEI) teprotide. 3. AT I induced contractile responses in isolated rings of toad aorta. This effect was partially inhibited by captopril and completely blocked by the peptide antagonist [Sar1, Ile8] angiotensin II. 4. Present results indicate that this homologue AT I would act in amphibian tissues by conversion to AT II.