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Competing Interests: All authors have disclosed no conflicts of interest.

The Addenbrooke's Cognitive Examination III is a brief cognitive screening tool that is widely used for the detection and monitoring of dementia. Recent findings suggest that the three variants of primary progressive aphasia can be distinguished based on their distinct profiles on the five subdomain scores of this test. Here, we investigated the utility of the Addenbrooke's Cognitive Examination III to differentiate the primary progressive aphasia variants based on their item-by-item performance profiles on this test. From these results, we created an interactive primary progressive aphasia Addenbrooke's Cognitive Examination III calculator which predicts the variant based on a patient's unique item-by-item profile. Twenty-eight logopenic variant, 25 non-fluent variant and 37 semantic variant primary progressive aphasia patients and 104 healthy controls completed the Addenbrooke's Cognitive Examination III at first clinical presentation. Multinomial regression analyses were conducted to establish performance profiles among groups, and R Shiny from RStudio was used to create the interactive Addenbrooke's Cognitive Examination III diagnostic calculator. To verify its accuracy, probability values of the regression model were derived based on a 5-fold cross-validation of cases. The calculator's accuracy was then verified in an independent sample of 17 logopenic, 19 non-fluent and 13 semantic variant primary progressive aphasia patients and 68 Alzheimer's disease patients who had completed the Addenbrooke's Cognitive Examination III (or an older version of this test: Revised) and had in vivo amyloid-PET imaging and/or brain autopsy pathological confirmation. Cross-validation of cases in the calculator model revealed different rates of sensitivity in classifying variants: semantic = 100%, non-fluent = 80.6% and logopenic = 79.9%; healthy controls were distinguished from primary progressive aphasia patients with 100% sensitivity. Verification of in vivo amyloid and/or autopsy-confirmed patients showed that the calculator correctly classified 10/13 (77%) semantic variant, 3/19 (16%) non-fluent variant and 4/17 (24%) logopenic variant patients. Importantly, for patients who were not classified, diagnostic probability values mostly pointed toward the correct clinical diagnosis. Furthermore, misclassified diagnoses of the primary progressive aphasia cohort were rare (1/49; 2%). Although 22 of the 68 Alzheimer's disease patients (32%) were misclassified with primary progressive aphasia, 19/22 were misclassified with the logopenic variant (i.e. falling within the same neuropathological entity). The Addenbrooke's Cognitive Examination III primary progressive aphasia diagnostic calculator demonstrates sound accuracy in differentiating the variants based on an item-by-item Addenbrooke's Cognitive Examination III profile. This calculator represents a new frontier in using data-driven approaches to differentiate the primary progressive aphasia variants., (© The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain.)

Competing Interests: The authors have no conflicts of interest to disclose.

Competing Interests: The authors have no conflicts of interest to disclose.

Competing Interests: The authors have no conflicts of interest to disclose.

The original version of this article omitted the following from the Acknowledgements: "CAM and AL were supported by the NSF MRSEC program through Columbia in the Center for Precision Assembly of Superstratic and Superatomic Solids (DMR-1420634). Additionally, this research used resources of the National Energy Research Scientific Computing Center, a DOE Office of Science User Facility supported by the Office of Science of the U.S. Department of Energy under 'Contract No. DE-AC02-05CH11231'." This has now been corrected in both the PDF and HTML versions of the article.

In its orthorhombic T d polymorph, MoTe 2 is a type-II Weyl semimetal, where the Weyl fermions emerge at the boundary between electron and hole pockets. Non-saturating magnetoresistance and superconductivity were also observed in T d -MoTe 2 . Understanding the superconductivity in T d -MoTe 2 , which was proposed to be topologically non-trivial, is of eminent interest. Here, we report high-pressure muon-spin rotation experiments probing the temperature-dependent magnetic penetration depth in T d -MoTe 2 . A substantial increase of the superfluid density and a linear scaling with the superconducting critical temperature T c is observed under pressure. Moreover, the superconducting order parameter in T d -MoTe 2 is determined to have 2-gap s-wave symmetry. We also exclude time-reversal symmetry breaking in the superconducting state with zero-field μSR experiments. Considering the strong suppression of T c in MoTe 2 by disorder, we suggest that topologically non-trivial s +- state is more likely to be realized in MoTe 2 than the topologically trivial s ++ state.

We report the successful synthesis and characterization of a new type I-II-V bulk form diluted magnetic semiconductor (DMS) Li(Zn,Mn,Cu)As, in which charge and spin doping are decoupled via (Cu,Zn) and (Mn,Zn) substitution at the same Zn sites. Ferromagnetic transition temperature up to  ∼33 K has been observed with a coercive field  ∼40 Oe for the 12.5% doping level. μSR measurements confirmed that the magnetic volume fraction reaches nearly 100% at 2 K, and the mechanism responsible for the ferromagnetic interaction in this system is the same as other bulk form DMSs.

Bortezomib-based regimens have significant activities in multiple myeloma (MM). In this study, we tested the efficacy of a total therapy with a staged approach where newly diagnosed MM patients received vincristine/adriamycin/dexamethsone (VAD). VAD-sensitive patients (> or =75% paraprotein reduction) received autologous hematopoietic stem cell transplantation (auto-HSCT), whereas less VAD-sensitive patients (<75% paraprotein reduction) received bortezomib/thalidomide/dexamethasone (VTD) for further cytoreduction prior to auto-HSCT. On an intention-to-treat analysis, a progressive increase of complete remission (CR) rates was observed, with cumulative CR rates of 48% after HSCT. Seven patients progressed leading to three fatalities, of which two had central nervous system disease. The 3-year overall survival and event-free survival were 75.1% and 48.3%, respectively. Six patients developed oligoclonal reconstitution with new paraproteins. In the absence of anticoagulant prophylaxis, no patients developed deep vein thrombosis. The staged application of VAD+/-VTD/auto-HSCT resulted in an appreciable response rate and promising survivals. Our approach reduced the use of bortezomib without compromising the ultimate CR rate and is of financial significance for less affluent communities.

Radio frequency identification (RFID) is a powerful automatic remote identification technique that has wide applications. To facilitate RFID deployment, an RFID benchmarking instrument called aGate has been invented to identify the strengths and weaknesses of different RFID technologies in various environments. However, the data acquired by aGate are usually complex time varying multidimensional 3D volumetric data, which are extremely challenging for engineers to analyze. In this paper, we introduce a set of visualization techniques, namely, parallel coordinate plots, orientation plots, a visual history mechanism, and a 3D spatial viewer, to help RFID engineers analyze benchmark data visually and intuitively. With the techniques, we further introduce two workflow procedures (a visual optimization procedure for finding the optimum reader antenna configuration and a visual analysis procedure for comparing the performance and identifying the flaws of RFID devices) for the RFID benchmarking, with focus on the performance analysis of the aGate system. The usefulness and usability of the system are demonstrated in the user evaluation.

Recent advances in mobile technologies have greatly extended traditional communication technologies to mobile devices. At the same time, healthcare environments are by nature "mobile" where doctors and nurses do not have fixed workspaces. Irregular and exceptional events are generated in daily hospital routines, such as operations rescheduling, laboratory/examination results, and adverse drug events. These events may create requests that should be delivered to the appropriate person at the appropriate time. Those requests that are classified as urgent are referred to as alerts. Efficient routing and monitoring of alerts are keys to quality and cost-effective healthcare services. Presently, these are generally handled in an ad hoc manner. In this paper, we propose the use of a healthcare alert management system to handle these alert messages systematically. We develop a model for specifying alerts that are associated with medical tasks and a set of parameters for their routing. We design an alert monitor that matches medical staff and their mobile devices to receive alerts, based on the requirements of these alerts. We also propose a mechanism to handle and reroute, if necessary, an alert message when it has not been acknowledged within a specific deadline.

Intra-abdominal cystic lesions are increasingly recognized in the newborn because of the advent of routine antenatal ultrasonography. As these lesions are often asymptomatic or non-specific in clinical presentation in the newborn, imaging by ultrasonography has an important role in diagnosis. We present a pictorial review of the commonly encountered intra-abdominal cystic lesions in the newborn, with emphasis on ultrasonographic features that can aid differentiation between the various lesions.

Enhanced computed tomography (CT) is frequently performed for possible bowel ischaemia. It has the distinct advantage of possible detection of the causes of ischaemia. Radiologists therefore need to be familiar with the spectrum of diagnostic CT signs. We present the CT imaging findings in surgically proven cases of small bowel ischaemia. In addition to signs pertaining to the underlying aetiological pathology, bowel dilatation, bowel wall thickening, mural gas, occlusion of mesenteric vessels, ascites and infarct of other abdominal organs were observed.

Aim: To report two cases of intense and persistent adrenal enhancement on computed tomography (CT) examinations of the abdomen., Materials and Methods: Two patients presented with septic shock, one due to pyogenic liver abscess and the other strangulated obturator hernia with gangrenous bowel. Both patients were resuscitated with fluid before undergoing unenhanced and enhanced CT., Results: In both patients intravascular volume was not reduced as evident by normal calibre of the aorta and inferior vena cava. One patient had abnormal enhancement pattern in the liver and kidneys, suggesting hypoperfusion. The other patient had normal enhancement pattern of the other abdominal viscera. Both patient subsequently died with multi-organ failure., Conclusion: We propose that adrenal enhancement may be a sign of hyperperfusion in early stage of shock due to the crucial role of the adrenal glands in this clinical situation. This may not persist with further circulatory compromise due to vasoconstriction. If confirmed, its recognition has potential value of identifying a therapeutic window before irreversible shock set in.

Aggrecan, a large cartilage proteoglycan, interacts with hyaluronan (HA), to form aggregates which function to resist compression in joints. The N-terminal region of aggrecan contains two structurally related globular domains, G1 and G2 separated by IGD domain. The G1 domain consists of three subdomains, A, B, and B', structural features characteristic to many other HA-binding proteoglycans. Here, we studied the interaction of aggrecan domains with HA using recombinant proteins expressed in 293 cells, an embryonal kidney cell line. Deglycosylation of the recombinant aggrecan fragment reduced the HA binding activity. We found that both the B and B' subdomains were required for HA binding and that a single module of A, B, or B' was unable to bind HA. The A subdomain increased the HA binding activity of the B-B' region. The G2 domain had no HA binding activity confirming previous reports. Studies of HA-binding properties using a BIAcoreTM biosensor system revealed that the KD of recombinant aggrecan fragment (AgW) consisting of G1, IGD, and G2 was 0.226 microM, whereas the KD of another HA-binding protein, native bovine link protein, is 0.089 microM. In contrast, AgMut11 which lacked subdomain A showed little HA binding activity. AgMut12 consisting of only B-B' had a 3.4-fold lower affinity and AgMut13 containing A-B-B' was 1.5-fold lower than AgW. These results suggest that carbohydrates are essential for high level aggrecan binding to HA and that the A subdomain of aggrecan functions in a cooperative manner with subdomains B and B'.

Primary amyloid light chain (AL) amyloidosis of the heart is a rare cause of congestive heart failure. Approximately 15% of patients with primary AL amyloidosis demonstrate no monoclonal proteins on serum or urine immunoelectrophoresis:(so-called nonsecretory immunoglobulin-derived amyloidosis). The histologic findings of endomyocardial biopsy from these patients may be indistinguishable from those with senile cardiac amyloidosis. However, the AL type may respond favourably to chemotherapy while the latter type does not. The prognosis is also better in the senile cardiac amyloid type. The precise diagnosis in the present case was made by applying immunohistochemical techniques on cardiac tissues.

We describe a family with two cases of adult-onset mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) syndrome. Interestingly, the proband also had non-insulin dependent diabetes mellitus and hyperthyroidism. Endocrinological studies demonstrated a high titer of TSH receptor antibody in the proband and elevated levels in her maternal relatives. Analysis of mitochondrial DNA (mtDNA) showed an A-to-G transition at nucleotide position 3243 in the tRNA (Leu(UUR)) gene (A3243G) in the three generations of the family. Furthermore, a previously described -260 bp tandem duplication in the D-loop region of mtDNA was also found in the proband and her maternal relatives. To our knowledge, such kind of duplication has never before been reported in the MELAS syndrome. The proportions of mtDNA with the -260 bp tandem duplication and A3243G point mutation were 12.5% and 82% in the muscle, respectively, and 1.6% and 35% in the blood cells, respectively, of the proband. We conclude that the hyperthyroidism in this MELAS patient may be related to the tandem duplication in the D-loop of mtDNA. This study further substantiates the importance of searching for additional genetic mutations in mitochondrial encephalomyopathic patients with new clinical phenotypes.

Monoclonal polyreactive antibodies can bind to many structurally dissimilar self and non-self antigens. Neither the precise antigen-binding site on the polyreactive antibody molecule nor the molecular basis of polyreactivity has been elucidated. The present study was initiated to see whether antibody genes encoding the Fab fragment of a human monoclonal polyreactive IgM antibody (MoAb 67) could be efficiently expressed in Escherichia coli, and whether the bacterially expressed Fab fragments possessed biological activity. cDNA encoding the variable domains of the heavy and light chains of MoAb 67 were cloned, amplified by polymerase chain reaction (PCR) and expressed in E. coli. Neither the recombinant heavy nor light chain showed antigen-binding activity. In contrast, the recombinant Fab 67 fragment showed the same antigen-binding reactivity profile as the native IgM antibody. It is concluded that the antigen-binding activity of polyreactive antibodies resides in the Fab fragment, and that both the heavy and light chains are required for activity.

In the carpal tunnel syndrome (CTS), decreased conduction velocity (CV) of the median nerve in the forearm segment has been ascribed to an electrodiagnostic artefact rather than pathophysiological changes. Standard CV of the forearm segment is calculated by subtracting the distal latency, which may not represent an exact assessment of CV in the proximal median nerve. A new technique modified from the method of Stoehr et al. and Pease et al. can exactly measure CV over the forearm. Using this new technique, the forearm nerve action potentials (FNAP) amplitude and forearm nerve conduction velocity (FNCV) proximal to the wrist can be directly determined. Normal subjects and patients with CTS were studied by both the standard and the new FNAP methods. Patients were divided into subgroups according to the severity derived from standard electro-diagnostic findings. By comparing the normal control and patient subgroups, the results show that there was a significant decrease in FNAP amplitudes proportional to severity, but FNCV was reduced to a lesser extent. In addition, the standard forearm median motor CV (MMCV) correlated well with severity, but the reduced MMCV did not correlate with the decreased FNCV. These findings suggest that retrograde degeneration of the median nerve does exist in CTS; however, retrograde degeneration contributes little to the reduced forearm MMCV which substantially results from the block of faster conduction fibres at the wrist. Therefore, technique artefact plays a major role in causing the proximal slowing in the standard electrodiagnosis.

Four patients presented with a distinctive syndrome of "numb, clumsy hand" and tactile agnosia. Myelography and computed tomographic myelography (CTM) of the cervical spine documented major spondylotic compressive lesions mainly between the C3 and C5 levels. The cortical responses of dermatomal somatosensory evoked potentials (DSEPs) revealed progressively prolonged peak latencies and progressively decreased amplitudes of early components from C6 to C8 dermatomal stimulation. In comparison, the C5 and L2 DSEPs were affected to a lesser extent. This finding suggests that high cervical cord compression may produce dysfunction of the dorsal column caudal to the direct compressive sites. In other words, the funiculus cuneatus of C6-8 cord is most affected in high cervical myelopathy. Moreover, the funiculus cuneatus is within the border zone susceptible to an overall reduction in blood flow. We conclude therefore, that ischemia secondary to cord compression is the pathophysiology resulting in this unique syndrome of "numb, clumsy hands" and tactile agnosia.

A recombinant human anti-rabies monoclonal antibody (MAb-57) Fab was prepared by cloning the heavy (Fd)- and light-chain domains into the same bacterial expression vector. To construct the recombinant Fab, mRNA was extracted from MAb-57-producing hybridoma cells, reverse transcribed, and then amplified by polymerase chain reaction (PCR) by using oligonucleotides specific for immunoglobulin heavy- and light-chain DNA sequences. PCR-amplified Fd-chain cDNA was fused, in frame, between a bacterial leader peptide (PelB) at the amino terminus and a 10-amino-acid peptide tag at the carboxy terminus. The PCR-amplified lambda-chain cDNA was also fused to the PelB leader peptide. The immunoglobulin Fab was then expressed as a dicistronic message in bacteria by using the isopropyl-beta-D-thiogalactopyranoside-inducible lactose promotor (lacZ). DNA sequencing was used to define the gamma-chain isotype (immunoglobulin G1) and VH (VHI) chain and VL (V lambda II) chain gene usage. The recombinant Fab (rFab57) specifically bound the rabies virus coat glycoprotein, while the Fd and lambda chains, when expressed individually, did not. The binding specificity of rFab57 was indistinguishable from that of the intact MAb in direct enzyme-linked immunosorbent assays; however, the dissociation constant of rFab57 for rabies virus protein G was approximately 1 log10 U lower than that of complete MAb-57 in competition enzyme-linked immunosorbent assays. A fluorescent-focus inhibition assay showed that bacterially expressed rFab was capable of neutralizing rabies virus strain CVS-11. We conclude that a human Fab expressed in bacteria maintains its specificity and biologic activity.

We determined the oxidative phenotype and metabolic ratio of debrisoquine in 96 Chinese patients with Alzheimer's disease (n = 12), Parkinson's disease (n = 55), and using patients with stroke and cervical spondylosis as controls (n = 29). We did not find any difference in debrisoquine metabolic phenotype among Parkinson's disease, Alzheimer's disease, and control patients as judged by chi-square analysis. In addition, the metabolic ratio of all our patients was less than 12.6. The result suggested that Chinese patients with Parkinson's disease and Alzheimer's disease metabolize debrisoquine at a velocity not different from that of their Western counterparts even though the frequency distribution of debrisoquine metabolism phenotyping in these two populations is quite different.

The levels of circulating IFN in mice infected with Newcastle disease virus (NDV) are regulated by the If-1 locus. In this study we show that in NDV-infected C57BL/6 mice, which carry the If-1h allele and produce high levels of IFN, high levels of both IFN-alpha and -beta mRNA can be detected in the spleen. In contrast, only very low levels of IFN mRNA could be detected in spleens of infected BALB/c mice containing the If-1l allele and producing low levels of IFN or in B6.C-H28c mice that are congenic for the If-1l allele. The relative levels of all individual IFN-alpha 1, alpha 4, and alpha 6 mRNA in spleens of infected BALB/c were lower than in spleens of infected C57BL/6 mice, indicating that the If-1 locus affects the expression of all IFN-alpha subtypes and is not associated with the deletion or inactivation of a specific IFN gene. The relative levels of IFN regulatory factor-1 mRNA in infected mice carrying the If-1l and If-1h loci were comparable, suggesting that the If-1 regulation is not associated with the altered expression of the IFN regulatory factor-1 gene. Quantitative difference in the expression of IFN-alpha and -beta genes was also observed in in vitro-infected peritoneal macrophages isolated from either C57BL/6 or BALB/c mice. A surprise finding was that the If-1 locus also affected the NDV-induced expression of two other cytokine genes, TNF-alpha and IL-6. Priming of the macrophage cultures with murine IFN enhanced the expression of all cytokine genes, and the relative levels of IFN, TNF-alpha, and IL-6 mRNA induced by NDV in macrophages derived from C57BL/6 and BALB/c mice were comparable. We propose that the If-1 locus affects the early stages of a signal transduction pathway which are common to the virus-mediated induction of IFN, TNF-alpha, and IL-6 genes.

A syndrome characterized by severe immunodeficiency and lymphoproliferation develops in susceptible strains of mice infected with a mixture of murine leukemia viruses (MuLVs) designated LP-BM5 MuLV. The etiologic agent in this mixture has been shown to be a replication-defective virus (BM5d) with a 4.8-kb genome that required replication-competent helper viruses, primarily ecotropic (BM5e), for cell-to-cell spread in the host. In the present study, we studied the expression of BM5d and BM5e in tissues of infected mice at various times after inoculation in relation to the expression of cytokine genes that may contribute to the pathogenesis of this disorder. Northern (RNA) analysis of total RNA showed that BM5d was expressed at significant levels in lymphoid tissues within 1 week of infection and that the levels of expression increased with time after inoculation. By 16 weeks postinfection, BM5d was expressed in all tissues examined. Expression of BM5e was relatively more restricted to lymphoid tissues and was detected at lower levels than expression of BM5d at early times after infection, but this virus was expressed in all tissues by 16 weeks. Infection with the virus mixture was associated with constitutive expression of tumor necrosis factor in all tissues examined and of interleukin-1 (IL-1) in lymphoid tissues within 1 week of infection, and at later times with widespread expression of these cytokines and gamma interferon. Also, the levels of interferon regulatory factor 1 mRNA were significantly increased in all infected tissues during the infection. In contrast, expression of IL-3, IL-4, IL-5, and IL-6 was not detectable by Northern analysis of the respective mRNAs in any infected tissue at early or late times postinfection.

Mice infected with LP-BM5 murine leukemia virus (MuLV) develop a syndrome denoted as murine AIDS. Macrophages harvested from the peritoneal cavities of these mice at 4 or 9 wk postinoculation with LP-BM5 MuLV were analyzed by Northern hybridization for the presence of the defective LP-BM5 virus and their ability to synthesize various cytokines upon induction with Newcastle disease virus (NDV) or (LPS). Neither IFN-alpha or IFN-beta was found to be constitutively expressed in LP-BM5-infected macrophages and in NDV induction studies, and the levels of biologically active IFN-alpha and its mRNA were found to be lower in LP-BM5 MuLV-infected macrophages than in the macrophages from uninfected controls. Similarly, after NDV or LPS induction, the levels of TNF mRNA and TNF protein were significantly lower in LP-BM5-infected macrophages than in macrophages from uninfected mice. The LP-BM5 MuLV-infected macrophages constitutively expressed low levels of IL-1 beta, and when induced with LPS, the relative levels of IL-1 beta were significantly higher in infected than in uninfected macrophages. Although no constitutive expression of IL-6 was detected, the levels of IL-6 mRNA induced with NDV were higher in LP-BM5 MuLV-infected macrophages than in controls. Thus, we found alterations in the expression of selected cytokines in macrophages from mice inoculated with LP-BM5 MuLV rather than a general deregulation of all cytokine expression. These results show that macrophages infected with the defective LP-BM5 virus respond differently to NDV- or LPS-stimulation and suggest that aberrant expression of certain cytokine genes may play a role in the immunopathologic condition in mice with murine AIDS.

Cycloheximide and chloramphenicol in combination have a greater effect on yeast cells of Histoplasma capsulatum than on the mycelial phase of this fungus. In contrast, clotrimazole was found to be more effective against mycelia. Miconazole produced a pronounced effect against both phases wheras tolnaftate was only slightly active. Sulfadiazine and griseofulvin were completely inactive against both phases. The differential sensitivities of the 2 phases of H. capsulatum to various antibiotics can be useful in studying the transition of the dimorphic fungus from 1 phase to the other.

We have found that amphotericin B is unstable in two commonly employed fungal culture media. This instability leads to inaccuracies in determining the actual level of susceptibility of slow-growing strains that require prolonged incubation for growth. To help compensate for this problem, we have described two rapid methods of susceptibility testing.

Murine L-929 cells were treated with benzene or a series of benzene metabolites, washed and then interferon-alpha/beta was induced with polyriboinosinic-polyribocytidylic acid. Exposure of the cells to benzene or phenol, a monocyclic metabolite of benzene, did not affect interferon-alpha/beta induction. However, exposure of the cells to p-benzoquinone, hydroquinone or catechol, dihydroxy- and diketo-metabolites of benzene, resulted in a severe inhibition of interferon-alpha/beta production. There was no significant loss of viability of the cell cultures. Additional studies with p-benzoquinone indicated that inhibition of interferon-alpha/beta was reversible and could be abrogated by addition of reduced glutathione to the cell cultures.

The dimorphic fungus Histoplasma capsulatum exists in two phases: a unicellular yeast form at 37 C and a mycelium at 25 C. We have found that these two phases have selective drug susceptibilities. The mycelial form of H. capsulatum was much more susceptible to the polyene antibiotic amphotericin B than the yeast form; in contrast, the yeast form was more susceptible to the antibiotic actinomycin D. The changes in susceptibility occurred early in the transition between the two phases and permitted the transitions to be blocked by sublethal concentrations of the appropriate drugs.

The addition of a simple X--Y sampling circuit to a closed circuit television system (CCTV) permits measurements of a narrow profile of the laser diffraction patterns from single frog muscle fibres at rest. Results confirm that maximum intensity occurs at 2.95-3.00 micron, but a positive linear relationship between the dispersions of sarcomeres and sarcomere lengths from 2.7--3.8 micron is obtained in four isolated single fibres.

Levels of dopamine (DA), 3-methoxy-4-hydroxy-phenylacetic acid (HVA), 5-hydroxy-indoleacetic acid (HIAA), 5-hydroxytryptamine (HT), 5-hydroxytryptophan (HTP), and 3, 4-dihydroxyphenylalanine (DOPA) in cerebrospinal fluids (CSF) of twenty-four Chinese with or without neurological diseases were determined simultaneously. The level of HIAA in the CSF of myelopathy-spondylosis patients and the level of DA in CSF of the myelopathy-tumor patients were higher than that of the control. No difference in levels of monoamines and their metabolites was observed between the control and patients with dementia.

We exposed spleen cells from female Swiss/Webster mice to benzene and benzene metabolites to determine the effects of such exposure on interferon gamma induction by concanavalin A. Exposing the cells to benzene or phenol did not affect interferon gamma production, but exposing them to p-benzoquinone, catechol, or hydroquinone significantly inhibited interferon gamma production. Cell viability, as determined by trypan blue viability staining, was not influenced by the chemical treatment. When interferon gamma production was inhibited, the inhibition was dose dependent. The time of optimum production of interferon gamma after exposure to concanavalin A was not affected by treatment of the cells with p-benzoquinone. These data indicate the importance of dihydroxy and diketo metabolites as immunotoxic derivatives of benzene.