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Abstract Background Friedel-Crafts acetylation is an important route to aromatic ketones, in research laboratories and in industry. The acetyl derivatives of 3,3′-dimethylbiphenyl (3,3′-dmbp) have applications in the field of liquid crystals and polymers and may be oxidized to the dicarboxylic acids and derivatives that are of interest in cancer treatment. Findings The effect of solvent and temperature on the selectivity of monoacetylation of 3,3’-dmbp by the Perrier addition procedure was studied using stoichiometric amounts of reagents. 4-Ac-3,3′-dmbp was formed almost quantitatively in boiling 1,2-dichloroethane and this is almost twice the yield hitherto reported. Using instead a molar ratio of substrate:AcCl:AlCl3 equal to 1:4:4 or 1:6:6 in boiling 1,2-dichloroethane, acetylation afforded 4,4′- and 4,6′-diacetyl-3,3′-dmbp in a total yield close to 100%. The acetyl derivatives were subsequently converted to the carboxylic acids by hypochlorite oxidation. The relative stabilities of the isomeric products and the corresponding σ-complexes were studied by DFT calculations and the data indicated that mono- and diacetylation followed different mechanisms. Conclusions Friedel-Crafts acetylation of 3,3′-dmbp using the Perrier addition procedure in boiling 1,2-dichloroethane was found to be superior to other recipes. The discrimination against the 6-acetyl derivative during monoacetylation seems to reflect a mechanism including an AcCl:AlCl3 complex or larger agglomerates as the electrophile, whereas the less selective diacetylations of the deactivated 4-Ac-3,3′-dmbp are suggested to include the acetyl cation as the electrophile. The DFT data also showed that complexation of intermediates and products with AlCl3 does not seem to be important in determining the mechanism.

The formation of an inclusion complex between hydroxypropyl-β-cyclodextrin (H-CD) and 4-acetylphenyl-4-(((6-chlorobenzo[d]thiazol-2-yl)-imino)-methyl)-benzoate (L) was investigated by FT-IR, 1 H-NMR, X-ray diffraction (XRD), FT-Raman, scanning electron microscope (SEM) techniques in the solid-state, absorption and emission spectroscopy in the liquid state and the virtual state as molecular docking technique. The binding properties of the inclusion complex (H-CD: L) with cations in deionized water was observed via absorbance and photoluminescence (PL) emission spectroscopy. The fluorescence probe (H-CD: L) inclusion complex (IC) was examined for several heavy metal cations, and identified that the PL emission wavelength of the complex displayed a continuous rise in the fluorescence intensity for Hg 2+ . A linearity range of 1 × 10 -8 - 11 × 10 -8  M and limit of detection value of 2.71 × 10 -10  M was found to be achieved for the detection of Hg 2+ . This outcome proves that the inclusion complex H-CD: L would be a promising material for the development a solid-state fluorescence probe for detecting Hg 2+ . It also shows application in real sample analysis and cell imaging., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Novel sulfa Schiff bases were synthesized and characterized by a reaction between aromatic sulfonamides and aromatic aldehydes or heterocyclic ketones in equimolar ratios. Their cytotoxicity was evaluated by the resazurin assay towards human sensitive CCRF-CEM and multidrug-resistant CEM/ADR5000 leukemia cells. Three of the tested compounds viz., 4-(anthracen-9-ylmethyleneamino)-N-(pyrimidin-2-yl)benzenesulfonamide (4), 4-(anthracen-9- ylmethyleneamino)benzenesulfonamide, (5) and 4-((3-phenylallylidene)amino)benzene-sulfonamide, (6) were cytotoxic (IC50 values: 5.38-19.96 µM). CEM/ADR5000 cells were not cross-resistant to these compounds, indicating activity against otherwise drug-resistant tumors. Compound 6 inhibited P-glycoprotein by increasing doxorubicin accumulation and reducing expression of P-glycoprotein in CEM/ADR5000 cells. A human P-glycoprotein homology model was used for molecular docking studies. Compound 6 and verapamil (a well-known P-glycoprotein inhibitor) docked with similar binding energies to the same binding pocket.

We describe the clinical patterns and case-fatality rate associated with severe Rift Valley fever (RVF) in patients who were admitted to the Gizan regional referral hospital during an outbreak of RVF in Saudi Arabia from September through November 2000. A total of 165 consecutive patients (136 men and 29 women) were prospectively studied; all were identified according to a strict case definition, were confirmed to have RVF by serologic testing, and were treated according to a predetermined protocol. The major clinical characteristics of RVF included a high frequency of hepatocellular failure in 124 patients (75.2%), acute renal failure in 68 patients (41.2%), and hemorrhagic manifestations in 32 patients (19.4%). Sixteen patients had retinitis and 7 patients had meningoencephalitis as late complications in the course of the disease. A total of 56 patients (33.9%) died. Hepatorenal failure, shock, and severe anemia were major factors associated with patient death.

T lymphocytes were recovered from recurrent vesicular and ulcerative herpes simplex virus type 2 (HSV-2) lesions from 4 patients and cloned without exogenous secondary antigenic stimulation. Resultant cultures were screened for antigen-specific proliferative and cytotoxic responses. Of the 39 HSV-specific clones recovered, all were CD3-positive; 38 were CD4-positive and 1 was CD8-positive. Of the T cell clones recovered directly from lesions, 6%-10% had HSV-specific proliferative responses, in contrast to a peripheral blood precursor frequency of HSV-specific CD4 cells of approximately 1/10(3) to 1/10(4) as measured by limiting dilution assays. CD4+ clones studied restricted by HLA-DR, -DP, and -DQ were detected and both type-common and type-specific CD4+ T cell clones were recovered. HSV-specific T cells localize to recurrent human genital HSV-2 lesions and can be obtained directly from early lesions. The ability to isolate HSV-specific T cell clones from lesions allows the study of antigenic specificities and functional properties of tissue-resident antigen-specific T lymphocytes.

CD8+ cytotoxic T lymphocytes (CTL) clones with specificity for herpes simplex virus (HSV) were derived from two donors with genital HSV-2 infection. These CTL clones specifically lysed HSV-infected autologous B lymphoblastoid cells, but not HSV-infected fibroblasts. Exogenous peptide loading sensitized both cell types to lysis by an HSV-specific CTL clone of known specificity. HSV infection rendered fibroblasts refractory to peptide sensitization. HSV infection also rendered fibroblasts and keratinocytes insensitive to lysis by allospecific CD8+ CTL clones. Lysis of B lymphoblastoid cells in this system was only slightly reduced by HSV infection. Reduction of fibroblast allospecific lysis was dose and time dependent and was blocked by acyclovir, indicating the involvement of a late HSV gene product. HSV caused a reduction of fibroblast cell surface HLA class I antigen, at least in part due to reduction of synthesis of heavy chain-beta 2 microglobulin heterodimers. These results suggest that HSV-induced blockade of antigen presentation by cutaneous cells to CD8+ CTL may be a mechanism by which HSV limits or evades the immune response of the host.

Cytomegalovirus (CMV) was detected in 56 of 275 specimens (20%); 50 of 56 (89%) were detected by conventional culture, and 37 (66%) were detected by rapid assay at 72 h with a commercial monoclonal antibody and a pooled monoclonal antibody. Although the two antibodies were equally sensitive at 72 h, the pooled antibody gave a brighter, more easily detected signal. Other viruses were isolated from 9 specimens (3.3%) by conventional culture. Use of rapid assays alone fails to detect slow-growing CMV and non-CMV viral pathogens.

Detailed antigenic analysis using a panel of monoclonal antibodies was carried out on the haemagglutinin antigen of 53 influenza B viruses isolated from an epidemic in a single school. Thirteen distinguishable antigenic groupings of influenza B viruses could be detected but 26 of the viruses were in two groups (III and IV) which co-existed during the entire epidemic. Antigenically distinguishable influenza B viruses were isolated from an epidemic in a second nearby school. Influenza B viruses isolated from the two schools could be further distinguished by different electrophoretic mobilities of NS1 polypeptides and of genes 1, 2, 3 and 6, whereas viruses from a single school epidemic were very closely related as regards these biochemical characteristics. The findings are consistent with the hypothesis that the outbreak was initiated by a single individual who excreted antigenic mutants of which predominantly two spread and co-existed during the epidemic, although the additional occurrence of random mutations during the evolution of the epidemic cannot be excluded.