[Detection of Pneumocystis carinii DNA in clinical samples from children with respiratory diseases].

Method of Pneumocystis carinii DNA detection in clinical samples (sputum) is presented. Primers to one fragment of 16S rRNA gene were used for detection of DNA. Isolation and amplification of DNA were performed in presence of internal DNA control. Analytical sensitivity of method was 200 copies of DNA per 1 ml. Analytical and diagnostic specificities were 100% and 95% accordingly. Sputum from 176 children with frequent respiratory infections were sampled before start of antibacterial therapy and studied simultaneously by the polymerase-chain reaction (PCR) and immunofluorescent assay (IFA). Results of PCR and IFA coincided in 167 (94.89%) children. From them, P.carinii was detected in sputum in 5 (2.85%) children. All children with positive results were treated with antibiotics. Repeated tests of sputum 8 days after start of treatment were all negative. PCR could be recommended as part of complex of clinical diagnostics and control of treatment.

[Detection of Pneumocystis carinii DNA in air and washes from medical equipment in hospitals].

Results of study of rooms' air and washes from medical equipment by PCR assay to detect Pneumocystis carinii DNA are presented. PCR assay sensivity was 200 copies/ml. Method of taking of air samples by MC-2 sample-taking device was modified for P. carinii detection. Sensivity of the method was 10 copies/m3. 27 air samples and 105 washes from medical equipment were studied and P. carinii DNA was not detected. It has been shown during the study that DNA of pneumocysts remains intact at room temperature during 12 days including 2-hour ultraviolet (UV) radiation treatment. After processing of studied surfaces with 0.1% solution of chloramine with subsequent UV radiation treatment during 30 minutes results of PCR assay were negative.

[The analysis of brainstem acoustic evoked potentials in diphtheritic polyneuropathy].

The possibility of central and peripheral impairment of the acoustic analyser was studied in 18 patients with severe diphtheritic polyneuropathy (DP) using brainstem acoustic evoked potentials (BAEPs). The acoustic nerve impairment was found in 27.8%, the central abnormalities--in 44.4%. All the patients with CNS impairment suffered from chronic alcoholism. The data obtained have been compared to those of 26 patients with chronic alcoholism. In this group, peripheral polyneuropathy was confirmed in 76.9% cases; BAEPs revealed isolated involvement of the peripheral part of the acoustic nerve in 7.7% and CNS impairment was found in 84.6% patients. The results of the study suggest that diphtheritic toxin is not implicated in CNS lesions. Central changes found in the BAEPs analysis were related to chronic alcohol intake and did not aggravate diphtheria course.

[Interaction between the human and simian adenoviruses in human cells: complementation, transcapsidation and formation of defective adeno-adeno hybrids]. / Vzaimodeistvie adenovirusov cheloveka i obez'iany v kletkakh cheloveka: komplementatsiia, transkapsidatsiia i obrazovanie defektnykh adeno-adenogibridov.

It was for the first time that complementation between the human and simian adenoviruses in human cells as well as the ability of the human adenovirus Ad2 (HADv2) genome to transform completely into the simian adenovirus SA7(C8) (SADv15) capsid (transcapsidation) was demonstrated. A defective adeno-adeno hybrid (recombinant) between the above viruses is described; the recombinant has the SA7(C8) capsid and Ad2 genome with a 10% insertion of SA7(C8) in the central region. Defective hybrid virions are able to replicate both in human and simian cells by using the SA7(C8) virus as helper. The hybrid virions help the above virus to replicate in human cells: they form a mutually complementing virion pair.

[Clinical and neurophysiological aspects of epilepsy with photosensitivity]. / Kliniko-neirofiziologicheskie aspekty épilepsii s fotosensitivnost'iu.

Using mapping EEG with dipole source location, transcranial magnetic stimulation (TMS), and visual evoked potential (VEP), clinico-neurophysiological analysis of photosensitivity was carried out in 7 patients with different types of epilepsy. In all the patients, an increase of visual response amplitude in VEP assessment and location of photogenic and eye-closing spike activity was observed in parietal and occipital areas that suggested a significant role of the striate and para striate cortex, along with primary projection cortex, in photosensitivity. Although motor cortex excitability by TMS causes hypersynchronization of the background activity and increase of slow wave discharge on the EEG after TMS. TMS is supposed to cause an activation of antiepileptic system.

[Hybrids of human and monkey adenoviruses (adeno-adeno hybrids) that can reproduce in monkey cells: biological and molecular genetic peculiarities]. / Gibridy adenovirusov cheloveka i obez'iany (adeno-adeno gibridy), sposobnye razmnozhat'sia v kletkakh obez'iany: biologicheskie imolekuliarno-geneticheskie osobennosti.

A highly oncogenic monkey adenovirus SA7(C8) facilitates the reproduction of human adenovirus type 2 (Ad2) in monkey cells. Upon mixed infection of monkey cells with both viruses, these viruses recombine producing defective adeno-adeno hybrids Ad2C8 serologically identical to Ad2 and capable of assisting Ad2 to reproduce in monkey cells. Ad2C8 and Ad2 form an intercomplementary pair inseparable in monkey cells. Unlike oncogenic SA7(C8), Ad2C8 is a nononcogenic virus for hamsters but is able to induce tumor antigens of this virus (T and TSTA). Molecular genetic analysis of 68 clones of adeno-adeno hybrids revealed that the left part of their genome consists of Ad2 DNA, and the right part contains no less than 40% of the viral SA7(C8) genome where E2A, E3, and E4 genes are located. Apparently, the products of these genes contribute to the composition of adenoviral tumor antigens, while the E4 gene is involved in complementation of monkey and human adenoviruses and makes a contribution to host range determination of these viruses.

TGFbeta-induced growth inhibition involves cell cycle inhibitor p21 and pRb independent from p15 expression.

It is generally assumed that TGFbeta induces cell cycle arrest through the cooperative action of cell cycle inhibitors p15, p27 and p21. Here, we found that several pancreatic carcinoma cell lines exert TGFbeta-induced negative growth control in spite of the loss of p15 and p16 expression. In these cell lines, TGFbeta-induced growth control correlates with the upregulation of the p21 protein and active pRb expression. Conversely, cells without p21 and/or pRb expression are resistant to TGFbeta -induced growth inhibition. Moreover, overexpression of p21 in the p21-deficient cell line Panc Tu1 leads to growth arrest. Thus, TGFbeta-induced growth control correlates with p21 expression and pRb status independent of p15 and/or p16 expression.

Frequent codeletion of p16/MTS1 and p15/MTS2 and genetic alterations in p16/MTS1 in pancreatic tumors.

BACKGROUND & AIMS: Cell-cycle inhibitor and tumor-suppressor gene p16/MTS1 was found to be altered in a variety of human tumors. To directly investigate genetic alterations and expression of p16/MTS1 and p15/MTS2, this study surveyed pancreatic tumors. METHODS: Cell-cycle inhibitors were analyzed for genetic alterations and expression by polymerase chain reaction, DNA sequencing, reverse-transcription polymerase chain reaction, and Western blotting. RESULTS: The analysis of pancreatic adenocarcinoma (19 cell lines and 3 xenografts) for p16/MTS1 and p15/MTS2 revealed homozygous deletions in 10 of 22 cases (46%) (7 cell lines and 3 xenografts) involving both genes. We show in these 7 cell lines as well as in 3 additional cases (10 of 19[53%]) loss of p16/MTS1 transcripts and in 2 further cases (12 of 19 [63%]) mutations leading to the loss of p16 protein. The frequency of mutations in p16/MTS1 was 56% (5 of 9). In contrast to p16/MTS1, p15/MTS2 transcripts were obtained in all cases exhibiting the p15/MTS2 gene (54%). Loss of expression was not observed for p27 and p18. CONCLUSIONS: These results support that loss of p16 function could be involved in pancreatic cancer and may explain at least in part the aggressive behavior of this tumor type.

[Treatment of the croup syndrome in children with acute respiratory viral infection]. / Opyt lecheniia bol'nykh s sindromom krupa pri ostrykh respiratornykh virusnykh infektsiiakh u detei.

This paper reviews the results of treatment of 234 children, aged 2 months to 8 years, with the croup syndrome. The patients underwent a combined treatment with steam, oxygen and drugs in a chamber, which had certain advantages over the traditional method. It worked faster, caused no deterioration of the health status, and reduced substantially the scope of intensive care medicine measures. The method is simple, easy to use and cheap. It can therefore be recommended for a wide application in croup therapy.