Human anti-JC virus serum reacts with native but not denatured JC virus major capsid protein VP1

The immunoreactivity of human anti-JC virus (JCV) serum against the major capsid protein VP1 of JCV was analyzed by Western blot, dot blot, and hemagglutination inhibition (HAI) assays. JCV-positive human serum reacted with native but not denatured JCV major capsid protein VP1, as demonstrated by dot blot and Western blot. Rabbit antiserum raised against native JCV capsid had immunoreactivities similar to those of human anti-JCV serum. These results indicate that the antigenecity of native and denatured JCV VP1 is different. In addition, both JCV-positive human serum and rabbit antiserum raised against native JCV capsid protein inhibited the hemagglutination activity of JCV capsid particles. In contrast, rabbit antiserum raised against denatured JCV VP1 did not inhibit hemagglutination. These findings reveal that denaturation may alter the antigenic epitopes of JCV VP1. Therefore, keeping the JCV capsid protein native appears to be essential for serological or other immunological analyses of the virus.     

Sulfation of L-selectin ligands by an HEV-restricted sulfotransferase regulates lymphocyte homing to lymph nodes

Lymphocytes home to lymph nodes, using L-selectin to bind specific ligands on high endothelial venules (HEV). In vitro studies implicate GlcNAc-6-sulfate as an essential posttranslational modification for ligand activity. Here, we show that genetic deletion of HEC-GlcNAc6ST, a sulfotransferase that is highly restricted to HEV, results in the loss of the binding of recombinant L-selectin to the luminal aspect of HEV, elimination of lymphocyte binding in vitro, and markedly reduced in vivo homing. Reactivity with MECA 79, an adhesion-blocking mAb that stains HEV in lymph nodes and vessels in chronic inflammatory sites, is also lost from the luminal aspects of HEV. These results establish a critical role for HEC-GlcNAc6ST in lymphocyte trafficking and suggest it as an important therapeutic target.     

Activation of striatal dopamine receptors induces pain inhibition in rats

Summary In the rat, elevating dopamine content in corpus striatum with electrical stimulation of substantia nigra or direct administration of apomorphine (50–200g) into the lateral cerebral ventricle or apomorphine (2–10g) into the caudate-putamen complex decreased pain sensitivity (as shown by an increase in the latency to hind-paw lick in the hot plate test). Furthermore, the decreased pain sensitivity after the central administration of apomorphine was antagonized by pretreatment with haloperidol (a dopamine antagonist). On the other hand, lowering dopamine content in corpus striatum with electrolytic destruction of substantia nigra and 6-hydroxydopamine lesions to the substantia nigra, as well as direct injection of haloperidol into the lateral cerebral ventricle or caudate-putamen complex increased pain sensitivity. The data indicate that activation of striatal dopamine receptors in rat brain induces pain inhibition.     

Effects of adenosine 3′, 5′-cyclic monophosphate on thermoregulation in both rats and rabbits

Summary The effects of intraventricular administration of dibutyryl adenosine 3, 5-cyclic monophosphate (db cyclic AMP) on the thermoregulatory responses of unanesthetized rats and rabbits to different ambient temperatures (T_a) were assessed. Administration of db cyclic AMP (10–60 mM) produced dose-dependent hypothermia in both rats and rabbits at T_a 2–22 °C. The hypothermia in response to db cyclic AMP was due to decreased metabolic heat production and cutaneous vasodilatation. There was no change in respiratory evaporative heat loss. In contrast, in the heat (30–32 °C), db cyclic AMP administration produced dose-dependent hyperthermia in these animals. The hyperthermia was due to increased metabolism (due to muscular shivering) and decreased heat losses. The reduction in heat losses was shown by a decrease in both cutaneous circulation and respiratory evaporative heat loss. The data demonstrate that the thermoregulatory responses induced by central administration of db cyclic AMP are T_a-dependent.     

Translation and validation of Taiwan Chinese version of the self-regulation questionnaire for gynecologic cancer survivors

ObjectiveTo culturally adapt the self-regulation questionnaire to the Taiwan Chinese version (TC-SRQ) and to evaluate its psychometric properties for gynecologic cancer survivors.Materials and methodsA cross-sectional study was employed with a purposive sample of 287 gynecologic cancer survivors. The TC-SRQ was adapted from a Germany version through back-translation to ensure its quality. For construct validity, confirmatory factor analysis (CFA) was used to assess the TC-SRQ measurement model with fit indexes including the χ² test, the root mean square error of approximation (RMSEA), and the normed fit index (NFI), the comparative fit index (CFI), and non-normed fit indices (NNFI). For concurrent validity, the Taiwanese version of the European Organization for Research and Treatment of Cancer's 30-item core quality of life (EORTC QLQ-C30) questionnaire was used as a criterion measure for quality of life (QOL). Reliability was evaluated by internal consistency and test-retest reliability.ResultsFor a modified measurement model of TC-SRQ, the model fit (χ² = 311.23, P = .0; RMSEA = .088; NFI = .97, CFI = .98, NNFI = .97) was acceptable. The evidence of construct validity of TC-SRQ scale was confirmed by the model estimates. TC-SRQ correlated positively with the global QOL, physical, cognitive, emotional, and social functioning domains, and negatively with fatigue and pain domains of EORTC QLQ-C30. For known groups validity, TC-SRQ was correlated with groups attributed by age, family support, health status, and sleep quality. A Cronbach's α of .91 indicated good internal consistency; the test-retest reliability was .82.ConclusionsTC-SRQ is a valid and reliable instrument for assessing self-regulation in gynecologic cancer survivors.     

Characteristics of bacteremia between community-acquired and nosocomial Klebsiella pneumoniae infection: risk factor for mortality and the impact of capsular serotypes as a herald for community-acquired infection

BACKGROUND: Although several epidemiological surveys of Klebsiella clinical isolates have been performed, few studies have correlated the clinical isolate with disease. OBJECTIVE: To compare the clinical and bacteriological characteristics of Klebsiella pneumoniae bacteremia acquired as community or nosocomial infections. METHODS: We prospectively enrolled 158 consecutively hospitalized patients with K pneumoniae bacteremia. Clinical data were reviewed. Antimicrobial susceptibility testing and capsular serotyping were performed. We used the chi(2) test, the Fisher exact test, or the t test for statistic analysis. RESULTS: Underlying diabetes mellitus was more common in community-acquired than in nosocomial infection (46/94 [49%] vs. 8/64 [12%]; P<.001). On the other hand, neoplastic disease (34/64 [53%] vs. 13/94 [14%]; P<.001) and antibiotic resistance (P<.01) were more frequent in patients with nosocomial compared with community-acquired infections. Klebsiella pneumoniae liver abscesses, which were all community acquired, accounted for the source of 22 (23%) of 94 community-acquired K pneumoniae infections. No attributable source of infection was found for 37 (58%) of the 64 nosocomial infections vs. 15 (16%) of the 94 community-acquired infections. Only 58 isolates (36.7%) could be serotyped; of these, capsular serotypes K1, K2, and K28 accounted for 37 (23.4%), 8 (5.1%), and 6 (3.8%), respectively, of all strains. However, typeable isolates were significantly more common among community-acquired than nosocomial isolates (42/94 [45%] vs. 16/64 [25%]; P =.01), especially for serotype K1 (28/94 [30%] vs. 9/64 [14%]; P =.02). Significant risk factors for mortality included nosocomial infection, lung infection, thrombocytopenia, leukopenia, ceftazidime resistance, inappropriate antimicrobial therapy, and septic shock. CONCLUSIONS: Significant differences were identified between community-acquired and nosocomial K pneumoniae bacteremia. Ceftazidime resistance in nosocomial K pneumoniae bacteremia carried a high risk for mortality, and serotype K1 in K pneumoniae was more prevalent in community-acquired infection, suggesting more virulence.