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Notes: Abstract Primary infections with herpes simplex virus type 2 (HSV-2) suppress the antibody response to secondary HSV-1 and -2 infections in the BALB/c mouse. In contrast, a challenge by the i.p. route using a vaccinia virus-HSV-1 glycoprotein B (VV gB1) recombinant induces a significant enhancement of the antibod response. This booster reaction is also observed if a challenge with a formalin-inactivated HSV-1 vaccine is performed. Although no or low humoral and vaginal antibodies are detectable after a single i.p. infection with the VV gB1 recombinant or the HSV-1 vaccine, protection against vaginal challenge with HSV-2 is induced. This points to the important role of cellular immunity for vaginal infections.

Notes: Zusammenfassung Das in der pädiatrischen Literatur wenig bekannte Rothmund-Syndrom wird dadurch gekennzeichnet, daß sich im zweiten Lebenshalbjahr poikilodermieartige Hautveränderungen entwickeln und im späteren Kleinkindesalter beiderseitige Katarakte auftreten. Häufig kommen in verschieden starker Ausprägung Störungen der inneren Sekretion, Minderwuchs, Hypotrichose hinzu. Andererseits kann das Hauptsymptom der Kataraktentwicklung auch in einzelnen Fällen fehlen. Die Ätiologie des Syndroms ist noch unklar. Ein größerer Teil der bisher bekannt gewordenen Patienten entstammt Ehen nahe blutsverwandter Eltern. Die Schwierigkeiten der differentialdiagnostischen Abgrenzung gegen ähnliche und möglicherweise auch pathogenetisch verwandte Krankheitsbilder wird ausführlich behandelt. Schilderung zweier Geschwister, die insofern Besonderheiten bieten, als bei ihnen noch Störungen der enchondralen Ossifikation bestehen, deren möglicher Zusammenhang mit dem Syndrom diskutiert wird.

Notes: Macrophages play a central role in establishing a specific immune response by acting as professional antigen presenting cells (APC) for T cells leading to a vigorous immune response. In order to analyze if Herpes simplex Virus (HSV) type 1 infection might affect the macrophage APC-function, monocyte-derived human macrophages were infected with HSV-1 strain F in vitro. Cocultures with allogeneic T cells revealed a strongly impaired stimulatory capacity of HSV-infected macrophages compared to uninfected controls which was not owing to a productive viral infection in macrophages. An increased expression of Fas ligand (FasL/CD95L) was detected in HSV-infected macrophages by FACS analysis. Although the majority of the macrophages expressed high levels of Fas (CD95/Apo-1), the HSV-induced upregulation of FasL did not result in an increased autocrine apoptosis of macrophages which might be related to endogenous expression of the apoptosis inhibitor FLICE inhibitory protein (FLIP). However, substantial apoptosis occurred in peripheral T cells as well as Fas-sensitive Jurkat T cells when cocultured with HSV-infected macrophages. These findings suggest that the paracrine killing of activated T cells by FasL expressing APC might be a novel strategy of immune evasion by HSV.

Notes: Abstract The technique of differential γγ-angular correlation measurements has been applied to an investigation of the hyperfine interactions in the 1274 keV level of204Pbm. Using liquid sources we derived from the interaction with an external magnetic field of 35,2 kgauss for the g-factor g=+0.055±0.003 in agreement with earlier measurements. The investigation of the quadrupole interaction with the statistically oriented electric field gradient of204Pbm embedded in the lattice of metallic Thallium gave for the electric interaction frequency in the definition ofSteffen andFrauenfelder ω01=(2.23±0.15) MHz. We observed an additional frequency of ω02=(6.91±0.15) MHz. This second frequency is probably caused by crystal imperfections. It vanished when the metal sources were annealed after the cyclotron irradiation. Finally we investigated the perturbation of the γγ-angular correlation of the 912– 375 keV cascade by a combined interaction of the dipole moment of the intermediate 1274 keV state with an external magnetic field and its quadrupole moment with an statistically oriented static electric field gradient. We found good agreement with the theory ofAlder et al. 2.

Notes: Abstract. It has long been established that cancer cells exhibit altered local dielectric properties compared with normal cells. Consequently, different electrical conductivity and capacitance are measurable in malignant vs normal tissues. In this study we evaluated the reliability of electrical impedance scanning (EIS), a new technology, for the classification of suspicious lesions: differentiating benign from malignant, and as a primary means of detection of breast cancer. Fifty-two women with 58 sonographically and/or mammographically suspicious findings were examined using electrical impedance scanning. Two different examination modes of TransScan TS2000 (Siemens, Erlangen, Germany), the standard-resolution mode for a routine overview examination, and the targeted high-resolution mode for a local examination of the suspicious lesion were used. All patients were additionally imaged by MR mammography (MRM) and underwent core-biopsy and/or surgical treatment after the EIS examination. With respect to the histopathological findings (29 malignant and 29 benign lesions) 27 of 29 (93.1 %) malignant lesions were correctly identified using the high-resolution mode of EIS, whereas 19 of 29 (65.5 %) benign lesions were correctly identified as benign (10 of 29 benign lesions showed as false-positive findings). Negative and positive predictive values of 90.5 and 73.0 % were observed, respectively. Using the standard-resolution mode 22 of 29 malignancies were correctly detected (sensitivity 75.9 %), whereas 22 of 29 were correctly identified as benign (specificity 72.4 %). Electrical impedance scanning appears to be a promising new technology providing a relatively high sensitivity for the verification of suspicious mammographic and/or sonographic lesions especially using the high-resolution mode for local examinations. Artifacts, such as signals from superficial skin lesions, poor contact, and air bubbles, are currently a limitation.

Notes: Summary After vaginal infections of mice with neuroinvasive strains of herpes simplex virus type 1 and 2 (HSV-1, HSV-2) virus replicates in the epithelium of the vagina, in the paravaginal ganglia, in the spinal cord and finally in the brain and in the adrenal glands. However, viral antigens could be demonstrated only in the medulla of the adrenal glands but not in the cortex, as assessed by immunohistochemistry (IHC). HSV could not be isolated from liver, spleen, uterus, and ovaries. This contrasts to the intraperitoneal (i.p) route of infection with replication in different visceral organs including the adrenal gland's cortex.

Notes: Summary One of the causes of genital tract infections in humans are herpes simplex virus types 1 and 2 (HSV-1, HSV-2). Although primary and recurrent infections can be clinically apparent and in part very serious, many infections are asymptomatic and result only in temporary genital shedding of virus (recurrences). During our investigations of vaginitis, strain IES of HSV-1 produced an asymptomatic infection. Replication in the murine vaginal (vag.) epithelium as well as antibody formation after vag. infection was comparable to those of survivors after infection with highly virulent strains. Titration of liver, spleen, ovaries, adrenal glands, spinal cord, or brain after vag. IES infection revealed no virus, whereas after i.p. infection virus could be demonstrated in many organs examined. Histological examination with a DNA probe (in situ hybridisation), HSV antibodies (immunohistochemistry), and haematoxylin and eosin (HE) staining showed only small focal HSV lesions of the vaginal epithelium in early stages of the infection, never exceeding to the subepithelial tissue. Severe infiltrations and ulcerations after infection with highly virulent strains (17syn+, ER−) could never be demonstrated after IES vag. infection. Identical replication rates of both groups of HSV despite much greater areas of epithelial necrosis with the virulent strains may be explained by the large number of virus inactivating granulocytes induced by the virulent strains, thus inactivating the hypothetical higher virus load.

Notes: Summary A scoring system for herpes simplex virus (HSV) induced vaginitis/vulvitis in Balb/c mice was delineated from vaginal infections. Four degrees of vaginitis/vulvitis could be distinguished after infection with suitable strains of HSV despite nearly identical replication rates. The time course of replication, inflammation and pathohistology was compared further. Grade 0 was defined by lack of symptoms despite presence of strong replication, which was detectable at days 3–6. Focal necrotic lesions of the epithelial layer were present containing HSV-specific antigens. DNA could be detected by hybridization only in the outer zone of these areas. At day 6 these zones began to be re-epithelialized. In the vaginal lumen abundant detached epithelial cells and granulocytes were already present by day 2. Grade 1 was macroscopically characterized by a slight inflammation commencing on days 5–6. Replication and antigens in the epithelium were found on days 2–6. HSV-antigens were only detected above the basal membrane, and some infiltration with granulocytes and lymphocytes was observed below the basal membrane at day 4. Grade 2 showed strong redness and inflammation as well as hyperemia. Cellular infiltrates were present in the large antigen containing epithelial lesions and below the basal membrane. From day 4 on, neurons were HSV-antigen and DNA positive and macrophages in the stroma contained antigen. The vulva was also shown to be involved. Grade 3 exhibited prolonged severe hyperemia, and destruction of the epithelium and the stroma with necrosis and infiltration, especially of the vulva. This grading system was shown to depend on certain unknown genetic properties of HSV-strains. Neither thymidine-kinase activity, replication in macrophages, fusion activity of strains nor presence or absence of the Hpa I P-fragment were shown to be of importance for severity of vaginitis/vulvitis. Vaginitis/vulvitis was shown to be an all or none response to HSV independent of the rate of replication. The set of virus genes responsible for neuroinvasiveness after vaginal or i.p. inoculation was found to be different. The time course of replication (mainly days 3–6) and inflammation (days 5–10) indicates that inflammation seems to be a secondary immunological phenomenon induced later by the replication phase of HSV. Our system could be useful for separately testing drugs with antiviral and anti-inflammatory properties.