Who's Afraid of Matte Blanco: An Introduction for People with No Mathematical Background

SUMMARY Analysts and therapists have daily to cope with a difficulty, the fact that many of their patients' most important feelings are felt as infinite. For example that boundless despair so often apparent in a depressive patient is a felt infinity. This infinity often masks other unconscious infinities, such as those of boundless guilt, grandiosity or omniscience. It is thus an important aspect of Matte Blanco's work that it draws attention to the whole subject of infinite outcomes. The examination of such outcomes is aided in this paper by illustrations of some useful ways of picturing infinity.
Matte Blanco's work also contains a suggestion as to a major source of these infinities and, in discussing this, this paper will enable an analyst or therapist to look for this source of a particular patient's pathological infinities.
The paper concludes by suggesting some extensions to Matte Blanco's work and some possible auras for future work.     

Dissipative structure and the mind-body problem

A theory explaining the link between mind and body is presented which depends upon viewing personal awareness as a figure against the ground of infinity. It is proposed that a tendency toward dissipation, in tension with an opposite tendency toward structural integrity, determines both the 'illumination' and specificity of awareness. Mind, as an aspect of the awareness bubble, is envisioned as influencing the body via a regressive discrepancy in relation to the current organization of the body mass - a conclusion derived from the fact that the origin of the tension between structure and its dissipation extends regressively back to the time when self was infinite or boundless, i.e., non-existent. This regressive discrepancy drives behavior in an expectable and therefore visible direction [corrected]. The entire thesis rests upon viewing reality as fundamentally personal, such that the linkage between a sensory field and neural activity can be explained on the basis of a simple gap between structure and its dissipation. The significance of this viewpoint for understanding the brain is briefly discussed.     

Isochromosome (12p) and peritriploidy in a highly malignant extrarenal rhabdoid tumor

We describe a case of acute myeloblastic leukemia, French-American-British subclassification of M0 (AML-M0), with an unusual chromosomal abnormality. The diagnosis of AML-M0 was made morphologically, cytochemically, and immunophenotypically. At the time of diagnosis, cytogenetic studies were performed, revealing a translocation involving chromosomes 1 and 14--specifically t(1;14)(p13;q32). The patient responded to high-dose ARA-C. In our survey of the literature, we were unable to find a reported case of AML-M0 with this chromosomal translocation.     

Testing the utility of the newest vital sign (NVS) health literacy assessment tool in older African-American patients

Objective

To evaluate utility of the newest vital sign (NVS) which can be completed in 3 min compared to the short version test of functional literacy in adults (S-TOFHLA) that takes 7 min for health literacy in the older African American patients.

Methods

We enrolled 62 older (age > 65 years) African American patients and administered the NVS and the S-TOFHLA. A score of less than 4 for the NVS and less than 16 for the S-TOFHLA was indicative of limited health literacy.

Results

Mean age of our patients was 73.2 + 7.9 years with an average education level of twelfth grade. Using S-TOFHLA 51% of the subjects were deemed to be sufficiently literate, with a score of 23.0 + 8.6 compared to 56% on the NVS with a score of 3.0 + 1.9. The average time for completing the NVS was 11 min in our patient population.

Conclusion

Based on our data, while health literacy level can be assessed with the NVS its practicality as a quick screening tool in the elderly population appears limited.

Practice implications

Knowing the level of patient's health literacy may help physicians deliver health information in the format that patients can understand.     

Spinal substance P and neurokinin-1 increase with high repetition reaching

Musculoskeletal injury and inflammation is associated with performance of repetitive and forceful tasks. In this study, we examined the effects of performing a voluntary, highly repetitive, negligible force (HRNF) reaching task on spinal cord neurochemicals involved in nociception. To our knowledge, no other laboratories are examining spinal cord nociceptive neurochemicals in response to repetitive motion-induced injury and inflammation. The purpose of this study was to extend our earlier findings related to central neurotransmitters from a low demand task to a higher demand task. Specifically, this study determined immunoreactivity of a peptidergic pro-nociceptive transmitter (substance P) and one of its receptors, neurokinin-1 (NK-1) receptor, in spinal cord dorsal horns in rats performing a HRNF reaching task for 6–10 weeks. The relationship of these spinal cord changes with the number of TNFα immunopositive cells in flexor forelimb muscles and with previously observed forearm grip strength changes from these same rats were examined. Performance of the HRNF task resulted in significantly increased substance P and NK-1 receptor immunoreactivity in the superficial lamina of spinal cord dorsal horns at 6 and 10 weeks compared to trained controls (p < 0.01). The increased substance P and NK-1 receptor immmunoreactivity were positively correlated with declines in forearm grip strength, an assay of movement-related hyperalgesia (r = 0.70, p < 0.01 and r = 0.64, p < 0.05, respectively). The increased substance P and NK-1 receptor immmunoreactivity were also positively correlated with increased TNF immunopositive cells in forelimb flexor muscles (r = 0.85, p < 0.001 and r = 0.88, p < 0.001, respectively). Thus, our highly repetitive task leads to increased spinal cord pro-nociceptive neurochemicals that are most likely directed by forelimb muscle inflammation and pain.     

Effect of sertindole on QTc interval in patients with schizophrenia

Sertindole has been marketed and offered daily clinical practice only for 9 months in our country, so no data has been its QTc prolongation potential. In the present study, we performed a clinical trial to investigate the effects of sertindole on QTc in patients with schizophrenia. The study comprised 21 patients with schizophrenia. Sertindole was administered in the following dosing regime: treatment was initiated with 4 mg/day sertindole. From day 3 to day 6, the dose was increased to 8 mg/day, and up to day 9, it was raised to 12 mg/day. The protocol allowed up to dose of 20 mg/day according to effectiveness and tolerability. QTc values were determined at beginning, months 3 and 6. In addition, Positive and Negative Syndrome Scale (PANSS) were scored concomitantly. At the beginning of 6-month period, the mean QTc interval of patients was 391.7 ± 19.2 ms. At the end of this period, it was 402.8 ± 23.8 ms. Although the mean QTc interval changing was significant throughout 6-month period, of the patients, at any evaluation point, only 1 female (451 ms) and 1 male (433 ms) had borderline prolongation at month 3 for both, without any exceeding the dangerous limits. In summary, our results suggest that sertindole is tolerable and despite dose-related QT prolongation, sertindole had not the proarrhythmic profile. Future studies with larger sample evaluating the effects of treatment are required.     

LRRK2 variant associated with Alzheimer's disease

Overlapping neurodegenerative pathologies (including Alzheimer's disease, AD) have been described in Parkinson's disease (PD) patients with leucine-rich repeat kinase-2 (LRRK2) mutations. We analyzed a LRRK2 PD (R1628P) risk variant in a group of 885 subjects comprising of AD and controls. The frequency of the R1628P allele was higher in AD compared to controls (3.5% vs. 1.6%, OR 2.3, 95 CI 1.2-4.4, p = 0.018). In vitro, the mean percentage of apoptosis and cell death observed for the R1628P transfected human cell lines was higher compared to wild type 21.8 ± 1.9, vs. 17.1 ± 1.3, p < 0.05, 30.2 ± 2.2 vs. 25.7 ± 1.3, p < 0.05). The LRRK2 R1628P variant increases the risk of AD in our population and our in vitro findings suggest that it is a functional variant and predisposes to apoptosis.     

基于脉搏波传导时间的连续血压监测系统

为了实现无创连续血压测量,提出了一种基于脉搏波传导时间(pulse transit time,PTT)的连续血压测量方案。通过同步采集心电(electrocardiogram,ECG)信号与光电脉搏波(photoplethysmograph,PPG)信号,以ECG的R波峰值点作为PTT的开始点,PPG信号的最大值点作为PTT的结束点,得到PTT,与水银血压计测得舒张压(diastolic blood pressure,DBP)与收缩压(systolic blood pressure,SBP)进行回归分析,得到了DBP和SBP的数学模型。利用该方法对41名身体健康的青年人进行实验,利用本方案得到的SBP与水银血压计的相关系数为0.82,其差值的平均数与标准偏差为0.15±2.05 mm Hg;得到的DBP与水银血压计的相关系数为0.73,其差值的平均数与标准偏差为0.12±2.16 mm Hg。利用Bland-Altman差值法对本系统血压测量方法与水银血压计测血压方法进行一致性检验,结果显示两种血压测量方法具有很好的一致性。     

Genetic heterogeneity of X-linked mental retardation with fragile X Association of tight linkage to factor IX and incomplete penetrance in males

X-linked mental retardation with fragile X or Martin–Bell Syndrome (MBS) is a frequent cause of mental retardation. So far segregation analysis of MBS in pedigrees ascertained by different, incomplete criteria has produced results, difficult to interpret, which suggest genetic complexity (Sherman et al. 1985). Biochemical and cell biological studies have failed to provide an assay for genetic heterogeneity in MBS and linkage analysis is the only available method. Such analysis, however, is complicated by the incomplete penetrance of the disease in males and the variable penetrance and expression of the defect in heterozygous females. We have used a new approach to test the heterogeneity of recombination between MBS and the coagulation factor IX gene or the anonymous probe 52A in a group of nine families who have sought genetic counselling at Guy's Hospital. We find that both our families alone and our families plus apparently complete samples of pedigrees reported in the literature, separate into two groups: one tightly and one loosely linked to factor IX. In the combined family sample these represent respectively 0·3 and 0·7 of the total and show recombination fractions of 0·0–0·15 and 0·25–0·5. Furthermore, the families with non-penetrant carrier males show tighter linkage to factor IX than the others, thus confirming the suggestion of a systematic difference among MBS families in the recombination between the disease and the factor IX locus. By contrast, no significant differences were found in the recombination between 52A and factor IX in the two groups of MBS families or in these families versus those with Hunter syndrome examined in our laboratory. The causes of the linkage heterogeneity we describe are not known. At least two alternatives can be considered: The existence of two MBS loci or differences in the recombination between a single MBS locus and the factor IX gene. The association between incomplete penetrance and tight, linkage to factor IX as well as the discontinuous variation in recombination fraction we have observed seem to favour the former alternative.     

Facilitating actions of an AMPA receptor potentiator upon extinction of contextually conditioned fear response in stressed mice

Mounting evidence supports the association between a polymorphism in the serotonin transporter gene promoter region (5-HTTLPR) and suicidal behaviour. Recently, a novel variant of the 5-HTTLPR L allele was identified. The previously unknown L_G allele produced similar levels of gene expression to the S allele and might have been misclassified as a “high-expression” allele in previous association studies. In this study, we aimed to compare the genotype distribution of the tri-allelic 5-HTTLPR polymorphism in 168 Chinese patients with schizophrenia, including 60 suicide attempters and 108 non-suicide attempters. In our analysis, which used the L_A dominant model, it was found that the L_A allele carriers were significantly more likely to have attempted suicide (p = 0.035). Further analysis showed this association existed only in male patients (p = 0.012). A similar association between the L_A allele and violent suicide attempt was also found (p = 0.028). In addition, logistic regression confirmed our findings that male L_A allele carriers were at a higher risk of suicide, although the lack of a significant association in females may reflect insufficient power due to small sample size. However, no association was found when we examined the traditional bi-allelic 5-HTTLPR. These findings differ from those reported in Caucasian subjects, where no associations have been reported. Different genetic backgrounds may give rise to different allelic distribution, causing differential effects on the expression of endophenotypes of suicide behaviours. Although the potential influence of multiple comparisons might weaken our findings, our study provides preliminary evidence for a potentially gender-specific role of a “high-expression” 5-HTTLPR polymorphism in susceptibility to suicide in Chinese patients with schizophrenia.     

Impaired exercise capacity, but unaltered mitochondrial respiration in skeletal or cardiac muscle of mice lacking cellular prion protein

The studies of physiological roles for cellular prion protein (PrP(c)) have focused on possible functions of this protein in the CNS, where it is largely expressed. However, the observation that PrP(c) is expressed also in muscle tissue suggests that the physiological role of PrP(c) might not be limited to the central nervous system. In the present study, we investigated possible functions of PrP(c) in muscle using PrP(c) gene (Prnp) null mice (Prnp(0/0)). For this purpose, we submitted Prnp(0/0) animals to different protocols of exercise, and compared their performance to that of their respective wild-type controls. Prnp(0/0) mice showed an exercise-dependent impairment of locomotor activity. In searching for possible mechanisms associated with the impairment observed, we evaluated mitochondrial respiration (MR) in skeletal or cardiac muscle from these mice during resting or after different intensities of exercise. Baseline MR (states 3 and 4), respiratory control ratio (RCR) and mitochondrial membrane potential (DeltaPsi) were evaluated and were not different in skeletal or cardiac muscle tissue of Prnp(0/0) mice when compared with wild-type animals. We concluded that Prnp(0/0) mice show impairment of swimming capacity, perhaps reflecting impairment of muscular activity under more extreme exercise conditions. In spite of the mitochondrial abnormalities reported in Prnp(0/0) mice, our observation seems not to be related to MR. Our results indicate that further investigations should be conducted in order to improve our knowledge about the function of PrP(c) in muscle physiology and its possible role in several different neuromuscular pathologies.     

No association between IL-1RN VNTR and the risk of duodenal ulcer: A meta-analysis

The aim of this study was to perform a meta-analysis to investigate a more authentic association between interleukin-1 RN variable number of tandem repeats (IL-1RN VNTR) and duodenal ulcer (DU). Systematic searches of electronic databases Embase, PubMed and Web of Science were performed. Statistical analyses were conducted using software Stata 11.0. The pooled odds ratios (ORs) with 95% confidence intervals (95%CIs) were applied. Publication bias was tested by Begg’s funnel plot and Egger’s regression test. A total of 16 studies including 2115 cases and 3622 controls were included in our final meta-analysis. There was no evidence of significant association between IL-1RN VNTR and DU (allelic model: OR = 1.04, 95%CI = 0.87–1.26; additive model: OR = 0.85, 95%CI = 0.62–1.16; dominant model: OR = 1.06, 95%CI = 0.92–1.23; and recessive model: OR = 0.83, 95%CI = 0.61–1.12). Significant protective associations were found in additive model (OR = 0.51, 95%CI = 0.31–0.83) and recessive model (OR = 0.45, 95%CI = 0.28–0.73) in Caucasian subgroup. In conclusion, our meta-analysis suggests that there is no evidence of significant association between IL-1RN VNTR and DU with or without Helicobacter pylori infection in overall population, whereas significant association is found by subgroup analyses which showed protective effect of IL-1RN allele 2 against DU risk in Caucasian population.     

Study of thyroid hormone receptor alpha gene polymorphisms on Alzheimer's disease

Because the action of thyroid hormone (T3) is involved in adult cognitive functions, we wanted to assess the association between THRA gene polymorphisms, which encodes the T3 nuclear receptor TRα1, and Alzheimer's disease (AD) risk.We analysed 5 single nucleotide polymorphisms (SNPs) of THRA, covering the known common genetic variability of the gene, in the Lille AD case-control study (710 cases/597 controls). We observed that subjects bearing the rs939348 TT genotype had a tendency to have a higher risk of developing AD (adjusted OR [95%CI] = 1.71 [0.99-2.95] p = 0.06). We extended our finding to three other independent AD case-control studies and observed similar trends. When combining the 4 studies (1749 cases/1339 controls), we observed an overall significant higher risk of AD in TT subjects (adjusted OR [95%CI] = 1.42 [1.03-1.96], p = 0.03) compared with C allele bearers. However, when combining our data with the available data coming from 2 American genome wide association studies on AD, we observed a weak and not significant association (OR = 1.19 [0.97-1.45], p = 0.10).The relationship between the genetic variability of the THRA gene and AD risk remains uncertain but cannot be entirely excluded.     

Lack of association between the functional c-kit rs6554199 polymorphism and achalasia in a Spanish population

A functional polymorphism (rs6554199) located in the c-kit gene was associated with achalasia in a Turkish cohort. Our aim was to replicate this result in a large cohort of Spanish patients and controls. A case-control study was performed with 282 Spanish white unrelated patients and 687 healthy controls. All were genotyped for SNP rs6554199 using a TaqMan Assay. No association was found in our study (T allele frequency in patients and controls: 47.3% vs. 49.4%; OR = 0.92, p = 0.41). The finding that the T allele of the c-kit rs6554199 polymorphism could be associated with achalasia as reported in a Turkish population could not be replicated in a Spanish cohort. Although ethnic differences might explain these data, the sample size that compromised the statistical power in the Turkish cohort and is higher in our study, led us to suggest that the reported association seems to be a false positive.     

Eigenspace Template Matching for Detection of Lacunar Infarcts on MR Images

Detection of lacunar infarcts is important because their presence indicates an increased risk of severe cerebral infarction. However, accurate identification is often hindered by the difficulty in distinguishing between lacunar infarcts and enlarged Virchow-Robin spaces. Therefore, we developed a computer-aided detection (CAD) scheme for the detection of lacunar infarcts. Although our previous CAD method indicated a sensitivity of 96.8 % with 0.71 false positives (FPs) per slice, further reduction of FPs remained an issue for the clinical application. Thus, the purpose of this study is to improve our CAD scheme by using template matching in the eigenspace. Conventional template matching is useful for the reduction of FPs, but it has the following two pitfalls: (1) It needs to maintain a large number of templates to improve the detection performance, and (2) calculation of the cross-correlation coefficient with these templates is time consuming. To solve these problems, we used template matching in the lower dimension space made by a principal component analysis. Our database comprised 1,143 T₁- and T₂-weighted images obtained from 132 patients. The proposed method was evaluated by using twofold cross-validation. By using this method, 34.1 % of FPs was eliminated compared with our previous method. The final performance indicated that the sensitivity of the detection of lacunar infarcts was 96.8 % with 0.47 FPs per slice. Therefore, the modified CAD scheme could improve FP rate without a significant reduction in the true positive rate.     

Effect of chronic activation of 5-HT3 receptors on 5-HT3, 5-HT(1A) and 5-HT(2A) receptors functional activity and expression of key genes of the brain serotonin system

The dopamine D3 receptor gene (DRD3) is considered being one of the candidate genes contributing to the development of tardive dyskinesia (TD). In a recent meta-analysis with mixed ethnicities, only a barely positive association was found between the functional DRD3 Ser9Gly polymorphism and TD in patients with schizophrenia (OR = 1.17; 95% CI: 1.01-1.37; p = 0.041). To further evaluate the controversial association between the polymorphism and TD using only Japanese subjects, we tested the association in a case-control design. We also conducted a meta-analysis including 8 studies with 3 East Asian populations (Japanese, Chinese, and Korean). In our Japanese case-control sample (43 with TD/157 without TD), we found no association between the DRD3 Ser9Gly polymorphism in schizophrenia and TD (genotype: p = 0.92; allele: p = 1.00). Furthermore, no significant difference in the mean AIMS score among the three genotypic groups was observed in our sample. The meta-analysis comprising 1291 East Asian subjects also showed no association between the polymorphism and TD; the Mantel-Haenszel pooled OR for TD among carriers of the DRD3 Ser9Gly of the eight Asian studies was 0.94 (95% CI: 0.78-1.12). Overall, our results suggest that the DRD3 Ser9Gly polymorphism may not confer susceptibility to TD in East Asian populations. Given that the Ser9Gly variant may play a putative role in the DRD3 function, further studies on the DRD3 are warranted.     

Autoantibodies against the H1(0) subtype of histone H1

The specificity of antinuclear autoantibodies in a patient with a sensory neuropathy associated with cancer has been analyzed. The autoantibodies recognize the histone H1(0) as shown by its dissociation from DNA, perchloric solubility, electrophoretic mobility in SDS or urea/acid polyacrylamide gels, and by the capacity of purified H1(0) to block the reactivity of these autoantibodies. Almost no reactivity was observed with other subtypes of H1. To our knowledge, this is the first autoantibody described with such specific reactivity for the H1(0) subtype.     

Variation in the CTLA4/CD28 gene region confers an increased risk of coeliac disease

Susceptibility to coeliac disease involves HLA and non-HLA-linked genes. The CTLA4/CD28 gene region encodes immune regulatory T-cell surface molecules and is a strong candidate as a susceptibility locus. We evaluated CTLA4/CD28 in coeliac disease by genetic linkage and association and combined our findings with published studies through a meta-analysis. 116 multiplex families were genotyped across CTLA4/CD28 using eight markers. The contribution of CTLA4/CD28 to coeliac disease was assessed by non-parametric linkage and association analyses. Seven studies were identified that had evaluated the relationship between CTLA4/CD28 and coeliac disease and a pooled analysis of data undertaken. In our study there was evidence for a relationship between variation in the CTLA4/CD28 region and coeliac disease by linkage and association analyses. However, the findings did not attain formal statistical significance ( p = 0·004 and 0·039, respectively). Pooling findings with published results showed significant evidence for linkage (504 families) and association (940 families): p values, 0·0001 and 0·0014 at D2S2214, respectively, and 0·0008 and 0·0006 at D2S116, respectively. These findings suggest that variation in the CD28/CTLA4 gene region is a determinant of coeliac disease susceptibility. Dissecting the sequence variation underlying this relationship will depend on further analyses utilising denser sets of markers.     

No association between IL-1β −31 C/T polymorphism and the risk of duodenal ulcer: A meta-analysis of 3793 subjects

The aim of this study was to perform a meta-analysis to investigate a more authentic association between IL-1β −31 C/T polymorphism and duodenal ulcer (DU). Systematic searches of electronic databases Embase, PubMed and Web of Science were performed. Study selection, data abstraction and study quality evaluation were independently conducted in duplicate. Statistical analyses were conducted using software Stata 11.0. The pooled odds ratios (ORs) with 95% confidence intervals (95%CIs) were applied. Publication bias was tested by Begg’s funnel plot and Egger’s regression test. A total of 12 studies including 1151 cases and 2642 controls were included in our final meta-analysis. There was no evidence of significant association between IL-1β −31 C/T polymorphism and DU (allelic model: OR = 0.96, 95%CI = 0.86–1.07; additive model: OR = 0.85, 95%CI = 0.67–1.07; dominant model: OR = 0.95, 95%CI = 0.81–1.13; and recessive model: OR = 0.95, 95%CI = 0.79–1.15). Significant association was found in additive model for PB subgroup (OR = 0.65, 95%CI = 0.44–0.96) and recessive model for non-Asian subgroup (OR = 0.72, 95%CI = 0.52–0.99). In conclusion, our meta-analysis suggested that there was no evidence of significant association between IL-1β −31 C/T polymorphism and DU with or without Helicobacter pylori infection in overall population, whereas significant association was found by subgroup analyses which showed protective effect of C/C genotype against DU risk.     

Chronic myelogenous leukemia in sickle cell/beta 0-thalassemia

Sickle cell/beta (0)-thalassemia (S/β(0)-thal) is a compound heterozygous state for βS and β(0) thalassemia. There are rare reported cases of patients with sickle cell disease who developed hematological neoplasms including myeloid and lymphoid conditions; however, to the best of our knowledge, chronic myelogenous leukemia (CML) occurring in S/β(0) -thal has been reported in one case and this is the second such report.