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There is evidence that indirect airborne transmission of smallpox can occur, but not frequently. For example, over a 10-year period in the Madras Infectious Diseases Hospital, out of more than 130, 000 non-smallpox patients housed in wards only a few feet away from the smallpox wards, only seven cases of smallpox could be presumed to have been acquired in the hospital. The smallpox vaccination status of these 130, 000 patients was also known to be poor. However, two outbreaks of smallpox in Germany, at Monschau and at Meschede, were almost certainly due to airborne transmission. In Meschede, an electrician was admitted to the isolation ward of a large general hospital with a fever suspected to be typhoid. He was confined to his room and three days later developed a rash. Smallpox was confirmed two days later and the patient was transferred to the smallpox hospital. Despite rigorous isolation of the patient due to the suspicion of typhoid fever, and vaccination of all patients and nurses in the general hospital, 19 further cases of smallpox occurred on all three floors of the building where the electrician had been housed. Extensive examinations conducted in the hospital included measurement of air currents. Notably, smoke released in the isolation room where the index patient was housed easily spread to many other areas on the same floor and significantly into many areas on the two floors above the patient's room. Following the investigation, three unusual factors were identified that facilitated this airborne transmission of smallpox: 1 ; the electrician index case ; had an unusual case of smallpox with a densely confluent rash and severe bronchitis and cough facilitating expulsion of infectious aerosol droplets; 2 ; the relative humidity of the hospital was very low, promoting survival of the virus; and 3 ; the hospital design was such that when the building's heat was turned on and it was as it was winter ; strong air currents were generated. A substantive study on indirect transmission through the contaminated clothing and bed linens of smallpox patients concluded that for laundry workers, the greatest risk of infection was among those who sorted the incoming laundry and could thus inhale contaminated dust. Once the bed linens were wet down, they were no longer infectious. Average Transmissibility of Smallpox in the Human Population An important factor in assessment of the risk from an outbreak of smallpox is R0: the average number of secondary cases infected by each primary case of smallpox. Based on the variables described above, this value for smallpox is estimated to be between 3.5 and 6 for populations with negligible herd immunity. This places smallpox at the same level of infectiousness as diphtheria, mumps, polio, and rubella, but far below that of measles, pertussis and influenza. This R0 figure is consistent with the data summarized above and reflects the fact that infection almost always involves prolonged face-to-face contact with an infectious person, and that smallpox spreads very slowly. There generally was an interval of two to three weeks between each generation of cases, and data indicate that even during the winter transmission season, the R0 value rarely exceeded 5. Surveillance and Containment for Controlling Transmission of Smallpox Data from the campaign to eradicate smallpox showed conclusively that the strategy of surveillance and containment also known as ring vaccination ; was remarkably successful at detecting and containing disease transmission from multiple outbreaks of smallpox. During the eradication campaign, it was shown that despite mass vaccination efforts, smallpox cases continued to occur among unvaccinated persons. Surveillance and containment involves surveillance for cases of smallpox, the provision of immunity around each case via vaccination and quarantine, and then the provision of immunity and quarantine around the contacts. This strategy is facilitated by the slow spread of disease from the primary cases to the secondary contacts. Ultimately, the eradication of smallpox was due to the success of the surveillance and containment strategy. Survivability of the Variola Virus A study has been performed by Rao on the ability of the variola virus to survive on various inanimate objects. Significantly, even on heavily contaminated objects, the virus was rapidly inactivated. Virus in scabs has a much longer survival time but such virus is not a source of infection. Smallpox virus survivability is adversely affected by both high heat and high humidity. It has been shown that aerosols of infectious droplets can survive for 60 minutes in low relative humidity and that 60-minute survivability drops somewhat at a high relative humidity. For longer periods, experiments with vaccinia virus indicate that viability of virus within aerosols is greatest at low temperatures 51F to 53F ; and low humidity less than 50% ; . In these conditions, 59% to 66% of virus can survive for 23 hours. However, when the humidity increases to 82%, even at low temperatures, survivability at 23 hours drops to 27%. Significantly, at 71F to 73F and 50% humidity.
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And with an interval between the first and last episode 6 months; and positive response to baseline head-up tilt testing. The diagnosis of vasovagal syncope was based, in addition to a positive tilt test result, on the exclusion of all other possible causes of syncope by means of a systematic work-up. This included, in all patients, careful history and physical examination, full neurological assessment, standard laboratory tests, supine and orthostatic blood pressure measurements, 12-lead surface ECG, bilateral bedside and upright carotid sinus massage, 24-hour Holter recording, and 2-dimensional echocardiography. Other diagnostic investigations, such as exercise stress testing, electrophysiological study, cardiac catheterization, electroencephalogram, Doppler flowmeter analysis of neck vessels, and CT scan or MRI of the brain were performed only when clinically indicated. Exclusion criteria included moderate or severe hypertension not controlled by drugs, recent 6 months ; acute myocardial infarction or angina pectoris, class III or IV NYHA functional class, other common contraindications to the use of -sympathetic agents, concomitant severe chronic disease eg, diabetes mellitus, neurological disease, terminal neoplasia ; , use of drugs that can favor or prevent vasovagal syncope eg, nitrates, beta-blocking agents ; , age 18 years, weight 50 kg, pregnancy, and refusal to participate in the study. All eligible patients were informed as to the nature of the trial and gave their written consent before enrolment.
Adjusted ORs indicated no association between CYP2A6var genotypes and lung cancer OR, 1.19; 95 % CI, 0.562.45 ; . Adjusting with confounding factors age, sex and smoking behavior ; in the study groups balanced the slight difference between the adjusted and crude ORs.
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Above-mentioned pathways to suppress multidrug resistance gene expression. Ongoing research focuses on elucidating the mechanism of action of bexarotene in maintaining genomic integrity to prevent and overcome multidrug resistance. In the present study, we observed that cells that developed acquired drug resistance showed an increased invasiveness and angiogenic potential, whereas cells treated with the combination regimen were chemosensitive and had reduced invasive and angiogenic ability. Coexpression of drug resistance and invasion metastasis has been observed in patient samples 49, 50 ; . Cells that coexpress these properties are due either to selection of more aggressive cells or to increase in the metastatic potential following chemotherapeutic insults 27 ; . It likely that the bexarotene cytotoxic combination interfered with increased survival and tumor progression after drug exposure through maintaining and or increasing genomic integrity. Using cDNA microarray analysis, we have recently identified several bexarotene-regulated genes, many of which were important for drug resistance, metastasis, and angiogenesis.1 We are currently evaluating the functional roles of these genes. Our present findings have important implications for patients with breast cancer as well as other diseases. For example, we have recently reported that the bexarotene paclitaxel combination delayed and overcame paclitaxel resistance in non small cell lung cancer 51 ; . In addition, the results from a recent phase I II clinical trials showed that addition of Targretin capsules to cisplatin vinorelbine.
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Assuming that 0- and 12-h values were identical. The association between blood levels sampled at different times and AUC was estimated by Pearson's correlation coefficient. Pairs of correlation coefficients were compared by an asymptotic Wald-type test. The elimination rate K was estimated by the method of residuals [5] and subsequently analysed by a mixed model with systematic difference between days and random subject levels in the PROC MIXED procedure of the SAS statistical software [6]. Comparison of inter-individual and intra-individual K estimates was performed using an asymptotic Chi square test REML-likelihood, 1 degree of freedom ; . Significance of the estimated systematic difference between days 3 and 14 was tested by approximate F-test based on the REMLlikelihood with Satterthwaite approximation of the denominator number of degrees of freedom [6]. Renal biopsies were taken in all cases of suspected rejection and graded according to the Banff 97 nomenclature [7].
Abbreviation: MR, magnetic resonance. * The findings described for each follow-up image are the changes from the immediately preceding scan. Treatment with mitoxantrone hydrochloride was started in each patient immediately after the pretreatment imaging. The MR images of patient 1 are shown in Figure 3 and taxotere.
Figure 1. Scatterplot showing the significant relation between reduced EDD and reduced response to nitroglycerin NTG ; . In this series of 800 subjects, the statistically significant relation between EDD and the vasodilator response to NTG is observed independently of the effects of vessel size or traditional vascular risk factors see Results.
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To further explore whether the level of CD99 expression is associated with different functional abilities within CD34 cells, we sorted the CD34 CD99low and CD34 CD99high cell populations Figure 1B ; . As shown in Figure 3A-B, the CD34 CD99high subset contains the majority of granulocyte-macrophage colony-forming units CFU-GMs ; and HPP-CFCs, whereas erythroid clonogenic progenitors are mostly present in the CD34 CD99low subset. The frequency of more immature clonogenic progenitors granulocyte, erythrocyte, megakaryocyte, macrophage colony-forming units and targretin.
An analysis of 134 human-therapeutics companies either based in massachusetts or with facilities here ; demonstrates that the farther one goes down the value chain from research, the less likely companies are to locate activity in the state and tenex.
This interaction indicates that the effect of ETD was relevant only among children living in improved conditions of overcrowding OR 3.06 ; , but not among those who lived in worse overcrowding conditions OR 1.44; 95% CI: 0.90, 2.31.
Question as to whether the CsA amplification of the sustained phase to TG exposure arose from an increase of Ca2 entry or a decrease of Ca2 export rate, we measured the Ca2 entry rate by Mn2 binding and quenching of fura-2 fluorescence. The rationale of these experiments was that if CsA stimulated Ca2 influx, then a further increase in Ca2 entry rate was expected. However, a striking result became apparent; as shown in Figure 2, cells stimulated with 5 M TG the presence of 400 nM CsA did not display different Mn2 quenching rate from the those exposed to equimolar amounts of TG in the absence of CsA. It follows that the amplification of the late phase of Ca2 response after CsA application was not due to stimulation of Ca2 influx, but rather to a dampening of Ca2 extrusion mechanisms. Finally, it could be demonstrated that the inhibition of Ca2 extrusion rate by CsA was mediated by the inhibition of PMCA. As shown in Figure 4, the addition of CsA to incubation medium resulted in a significant inhibition of PMCA. Was this effect mediated by the same mechanisms leading to immunosuppression in T cells? When inside the T cell CsA, in fact, binds to cyclophilins A, a member of immunophilins, a and teniposide.
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IFN-, y may induce HLA-DR expression by gingival keratinocytes cell pvresenting during periodontal disease Recent evidence suggesting that early and advanced periodontal lesions are associated with a Th I and a Th2 response, respectively, has been reviewed elsewhere Seymour et al., 1993; Gemmell and Seymour, 1994 ; . As for epidermal keratinocytes, IFNy has been shown to upregulate HLADR expression by oral keratinocytes T cell T cell '\A Mutlu et al., 1991 ; , suggesting that this Figure 2. a ; T-cell receptors TCR ; recognize conventional antigen Ag ; associated with cytokine could play a role in regulating antigen-presenting cells. To gingival keratinocyte interactions with major histocompatibility MHC ; molecules on the surfaces ofantigen and MHC molecule be activated, the TCR must interact favorably with both the T-cells. Several studies show that HLA- MHC restriction ; . b ; Superantigens SAg ; bind TCRs that are not able to recognize the DR expression, minimal or absent in Ag MHC complex and lead to the activation of large numbers of T-cells. healthy tissues, is upregulated in inflamed tissues Walsh et al., 1985; Crawford, 1992; Nunes et al., 1994 ; . The ok ; servation that tion and cytokine release, through molecules such as HLA-DR expression by junctional epithielium during B7 BB-1 and ICAM-1 interacting with CD28 and lymphoinflammation appears less uniform than ICAM- I sugcyte-function-associated antigen LFA ; - 1, respectively gests that HLA-DR may be downregulate d by a lack of Liu and Linsley, 1992 ; . These co-stimulatory signals lead responsiveness of the gingival keratinocyt es to IFN--y, as to T-cell proliferation and cytokine release. reported for psoriasis. Only those juncticDnal epithelial 2 ; Superantigen presentation by "non-professional" cells that are capable of antigen preseritation by coAPCs such as keratinocytes may activate T-cells or expressing ICAM- 1 and HLA-DR may parti cipate actively induce T-cell death in the inflammatory response involving T- cells Walsh et al., 1985 ; Fig. 1 ; . However, a wider distrib, ution of HLASuperantigens are comprised of two groups of potent DR expression by gingival keratinocyt es has been immunomodulatory molecules Scherer et al., 1993 ; : i ; observed in some rapidly progressing les; ions and may soluble exotoxins derived from Gram-positive bacteria, be indicative of a greater inflammatory restponse favoring such as staphylococci and streptococci Marrack and disease progression, as shown in patient : s with Down's Kappler, 1990; Tomai et al., 1991 and ii ; viral superantigens such as those encoded by endogenous mouse syndrome Sohoel et al., 1995 ; . mammary tumor viruses Webb and Gascoigne, 1991 ; . C ; ACTIVATION OF T-CELLS BY KERATINOCYT 'ES Superantigens play an important role in auto-immune disease by activating anergic T-cells which then react 1 ; T-cell activation by "professional" Xantigenwith self-antigens Kotzin et al., 1993 ; , and they are also presenting cells involves co-stimulatorry signals responsible for acute reactions such as toxic-shock synAntigen recognition and subsequent cytokiine production drome and food poisoning Ulrich et al., 1995 ; . by T-cells determine the type of imm une response Interestingly, superantigens may also induce T-cell death against invading pathogens. Conventiona 1 protein antiand or anergy, since administration of the staphylococcal gen recognition by T-cells is mediated by tthe interaction enterotoxin B leads to expansion of T-cell clones folof the variable domains, Vo and VP, of o3 T'-cell receptors lowed by Fas-mediated apoptosis and or anergy TCR ; with peptide determinants and majorr histocompat MacDonald et a!., 1991 ; . ibility complex MHC ; molecules Fig. 2a ; . Cells that are Superantigens interact directly with variable regions present on the TCR a chain in the absence of concomicapable of MHC class II restricted antigerin presentation are collectively termed antigen-presenting cells ABCs ; , tant recognition of MHC molecules by the TCR Herman and include cells of the dendritic lineage B-cells, and et al., 1991; Fleischer, 1992 ; Fig. 2b ; . Thus, although macrophages. These cells express MHC claess II molecules superantigen expression requires binding to intact MHC molecules, the specificity of the activated T-cells is deterconstitutively and are considered to be "professional" APCs, since they have the ability to uptak e and process mined by VP elements, and does not, in most instances, antigen and subsequently to express the p rocessed antirequire MHC specificity, since it does not involve the Tgen associated with MHC class 11 molecule These APCs cell recognition of the peptide binding site Woodland provide co-stimulatory signals leading rto '-cell. proliferaand Blackman, 1993 ; . Strong T-cell activation by superantif and tarka.
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