髁突形态与覆深度关系的研究

目的　探讨髁突形态与不同覆深度的关系。方法　选择正常者、开畸形患者、覆正常的错畸形患者和深覆畸形患者各 5 0人 ,均为 18至 2 6岁成人。应用曲面断层片研究左右两侧的髁突形态 ,分别测量并计算上部髁突高度 /升支高度比 (UCH/RH)和髁突高度 /宽度比 (TCH/CW )。将髁突形态分为四种类型 :直立型 (类A) ,前倾型 (类B) ,后倾型 (类C)和尖型 (类D)。结果　开组的上部髁突高度相对升支高度明显小于其他各组 (P <0 0 0 1)。正常组的髁突形态比较粗壮 ,高度宽度比明显小于其他各组 (P <0 0 0 1)。类A和类B属于正常髁突形态 ,占正常组的 99%。类C和类D属于异常髁突形态 ,且在开组中的比例明显高于正常覆组或深覆组。另外 ,只有开组中显示上部髁突高度两侧不对称 (P <0 0 5 )。结论　开组髁突形态与其他各组相比明显不同。     

Visual-ocular motor activity in the macaque pregeniculate complex

The anatomical connections of the pregeniculate complex (PrGC) with components of the visual-ocular motor system suggested its contribution to ocular motor behavior. Subsequent studies reported saccade-related activity in the primate PrGC. To determine its contribution, we characterized pregeniculate units (n = 128) in alert macaques during ocular motor tasks and visual stimulation. We found that 36/109 saccade-related units exhibited postsaccadic bursts or pauses in tonic discharge for saccades of any amplitude or direction. In contrast to previous results, 46/109 responses preceded or coincided with the saccade, while 47/109 responses were directionally tuned. Pregeniculate units were modulated not only in association with saccades (109/128) but also with smooth eye movements and visual motion (20/128) or eye position (23/128). Multiple ocular motor signals were recorded from 19% of the units, indicating signal convergence on individual neurons. Visual responses were demonstrated in 51% of PrGC units: visual field illumination modulated the resting discharge of 33 units; the responses of 37 saccade-related units and all 23 position-dependent units were modulated by visual stimulation. Early saccadic activity in the PrGC suggests that it contributes more to gaze than postsaccadic modulation of visual or ocular motor activity. The patterns of saccadic responses and the modulation of PrGC activity in association with a variety of visual-ocular motor behaviors suggest its potential role as a relay between the parietal cortex and elements of the brain stem ocular motor pathways, such as the superior colliculus and pretectal nucleus of the optic tract.     

Genetic analysis of males from intracytoplasmic sperm injection couples

A total of 392 men referred for intracytoplasmic sperm injection (ICSI) participated in genetic analysis. The control group consisted of 100 normal fertile males. Chromosome and DNA analyses were performed to investigate the frequency of Y-chromosome microdeletions and CFTR mutations (the controls underwent DNA analysis only). An abnormal karyotype was found in 4.6% of all males, but the frequency among men with azoospermia was higher, at 11.7%. Y-chromosome microdeletions were found only among men with azoospermia (6.5%) and men with extreme oligospermia (2%). Compound heterozygosity for CFTR mutations was found in men with azoospermia (3.9%) and congenital bilateral absence of vas deferens (CBAVD) only. We conclude that all couples referred for ICSI should be offered chromosome analysis. DNA analysis for Y-chromosome microdeletions should be reserved for men with azoospermia or extreme oligospermia (<1 x 106 spermatozoa). Analysis for CFTR mutations should be limited to those with obstructive azoospermia or those with a family history of cystic fibrosis.     

Left ventricular dysfunction in Klinefelter syndrome is associated to insulin resistance, abdominal adiposity and hypogonadism

Objective Epidemiological data suggest there is an increased risk of dying from heart disease among patients with Klinefelter syndrome (KS). Due to high prevalence of hypogonadism and metabolic syndrome, we speculated that patients with KS may have subclinical changes in the left ventricular function. Therefore, the aim was to assess left ventricular long axis function by tissue Doppler echocardiography in patients with KS and relate these findings to the metabolic status and testosterone levels. Design Cross-sectional study. Out-patient clinic. Patients We investigated 25 unselected patients with KS, recruited from endocrine and fertility clinics. Twenty-five age-matched males served as controls. Measurements Left ventricular systolic long axis function (velocities and strain rate) assessed by tissue Doppler echocardiography related to free testosterone, fasting values of plasma glucose, insulin, homeostasis model assessment (HOMA)-index, cholesterol and triglycerides in addition to dual energy X-ray absorptiometry (DEXA) scan derived assessment of truncal body fat. Results The long axis function was significantly reduced in patients with KS (peak systolic velocities 4·4 ± 1·3 vs. 5·3 ± 1·0 cm/s, P < 0·01 and strain rate –1·3 ± 0·3 vs.–1·6 ± 0·3 s⁻¹, P < 0·01). However, the ventricular dysfunction was mainly attributed KS patients with metabolic syndrome. The peak systolic velocities were significantly correlated to truncal body fat (r = –0·72, P < 0·01) and free testosterone (r = 0·63, P < 0·01), but uncorrelated to plasma glucose, insulin and HOMA-index. Conclusion Systolic long axis function is decreased in patients with KS and metabolic syndrome. The decrease in myocardial systolic function was significantly related to truncal body fat and hypogonadism, but not correlated to insulin sensitivity.     

Erythropoietin production in a primary culture of human renal carcinoma cells maintained in nude mice

The present studies report erythropoietin (Ep) production in primary cultures of a human renal carcinoma from a patient with erythrocytosis that has been serially transplanted to BALB/c nude mice. The levels of erythropoietin in the culture media were estimated using the exhypoxic polycythemic mouse assay (EHPCMA), fetal mouse liver erythroid colony- forming technique (FMLC), and a radioimmunoassay (RIA). The spent culture media of the exponentially growing cells contained less than 10 mU/ml of Ep measured by RIA. However, after the cells became confluent, Ep levels (RIA) in the spent media showed a marked increase to approximately 300 mU/ml. Ep levels estimated using the FMLC and EHPCMA were approximately 2/3 and 1/10, respectively, of those measured by RIA. Rabbit antiserum to highly purified human urinary Ep (70,400 U/mg protein) was utilized for immunocytochemical (peroxidase-antiperoxidase method) localization of Ep in the cultured cells. Very few of the cells in exponential growth exhibited Ep-like immunoreactivity, whereas intense Ep-like immunoreactivity was observed in the cytoplasm of the cells maintained in culture for a prolonged period after reaching confluency. The most intense staining was observed in some of the cells forming domes. The domes developed after the cells reached confluency, and their numbers increased with increasing time in confluent culture, in parallel with the increase in Ep levels in the spent media. This primary cell culture system of a renal cell carcinoma maintained in nude mice, which produces immunologically and biologically active Ep, may provide a useful model for studies of the mechanism of Ep production.     

Amyloid-independent functional neural correlates of episodic memory in amnestic mild cognitive impairment

Purpose

Although amnestic mild cognitive impairment (aMCI) could have various biological characteristics, little attention has been given to the nature of episodic memory decline in aMCI with pathophysiologies other than Alzheimer’s disease (AD), i.e., aMCI with low beta-amyloid (Aβ) burden. This study aimed to identify the functional neural basis of episodic memory impairment in aMCI with Aβ burden negative (aMCI-Aβ?) and to compare these results with aMCI with Aβ burden positive (aMCI-Aβ+).

Methods

Individuals with aMCI (n?=?498) were selected from the Alzheimer’s Disease Neuroimaging Initiative database. Based on the mean florbetapir standard uptake value ratio, participants were classified as aMCI-Aβ? or aMCI-Aβ+. Correlations between memory scores and regional cerebral glucose metabolism (rCMglc) were analyzed separately for the two subgroups using a multiple regression model.

Results

For aMCI-Aβ?, significant positive correlations between memory and rCMglc were found in the bilateral claustrum, right thalamus, left anterior cingulate cortex, left insula, and right posterior cingulate. For aMCI-Aβ+, significant positive correlations between memory and rCMglc were found in the temporoparietal areas. These correlation patterns remained unchanged when clinical severity was added as a covariate

Conclusion

Our findings indicate that memory impairment in aMCI-Aβ? is related to multimodal integrative processing and the attentional control system, whereas memory impairment in aMCI-Aβ+?is related to the typical brain memory systems and AD signature. These results suggest that although the two subgroups are clinically in the same category as aMCI, the memory impairment process depends on completely different functional brain regions according to their Aβ burden level.

     

Two pathways of exocytosis of cytoplasmic granule contents and target cell killing by cytokine-induced CD3+ CD56+ killer cells

Cytokine-induced killer (CIK) cells are non-major histocompatibility complex-restricted cytotoxic cells generated by incubation of peripheral blood lymphocytes with anti-CD3 monoclonal antibody (MoAb), interleukin-2 (IL-2), IL-1, and interferon-gamma. Cells with the greatest effector function in CIK cultures coexpress CD3 and CD56 surface molecules. CIK cell cytotoxicity can be blocked by MoAbs directed against the cell surface protein leukocyte function associated antigen-1 but not by anti-CD3 MoAbs. CIK cells undergo release of cytoplasmic cytotoxic granule contents to the extracellular space upon stimulation with anti-CD3 MoAbs or susceptible target cells. Maximal granule release was observed from the CD3+ CD56+ subset of effector cells. The cytoplasmic granule contents are lytic to target cells. Treatment of the effector cells with a cell-permeable analog of cyclic adenosine monophosphate (cAMP) inhibited anti-CD3 MoAb and target cell- induced degranulation and cytotoxicity of CIK cells. The immunosuppressive drugs cyclosporin (CsA) and FK506 inhibited anti-CD3- mediated degranulation, but did not affect cytotoxicity of CIK cells against tumor target cells. In addition, degranulation induced by target cells was unaffected by CsA and FK506. Our results indicate that two mechanisms of cytoplasmic granule release are operative in the CD3+ CD56+ killer cells; however, cytotoxicity proceeds through a cAMP- sensitive, CsA- and FK506-insensitive pathway triggered by yet-to-be- identified target cell surface molecules.