Miracle-dz/UniFAR-FTUs huggingface dataset:
A histopathologic and morphometric differentiation of nerves in optic nerve hypoplasia and Leber hereditary optic neuropathy.

OBJECTIVES To characterize and quantitate optic nerve histopathologic and morphometric differences between optic nerve hypoplasia (ONH) as an early and congenital form of intrinsic axonal loss and Leber hereditary optic neuropathy (LHON) as a late and acquired form of intrinsic axonal loss. MATERIALS AND METHODS Optic nerves from 3 sources were examined: a 42-year-old healthy woman (control), a 53-year-old woman with ONH diagnosed postmortem, and a 74-year-old woman with LHON. The optic nerves were processed, embedded, and stained with a 1% solution of paraphenylene diamine. Histopathologic and morphometric analyses were performed via light microscopy and a semiautomatic computer image analysis system. RESULTS The ONH showed severe axonal depletion without degenerated profiles in an inferonasal sector, with only a small superotemporal sector having a near normal appearance. The LHON revealed general axonal depletion centrally, fibrocytic scarring, scattered "degeneration dust," and evidence of minimal inflammation, with residual axons limited to superior and temporal peripheral clusters. Morphometric analysis revealed total fiber populations of 98,000 in the ONH optic nerve and 48,000 in the LHON optic nerve, representing 90% and 95% reductions, respectively, compared with the control optic nerve (1.2 million fibers). CONCLUSIONS Optic nerve hypoplasia and LHON present 2 distinguishable and distinctive patterns of nerve fiber distribution and axonal dropout. The lack of degenerated axons in ONH indicates that any axonal death probably occurred through apoptosis during development. In LHON, degenerated axons and minimal grade of inflammation were obvious, implicating a more "active" pathologic process. This study describes distinctions between these 2 optic neuropathies.
Forming strategic alliances : the role of social compatibility

This thesis investigates how social compatibility between the parties of strategic alliances in the formation phase affects the ability to realize outcomes from the cooperation. This research question has two sources: The first is the general development within business relationships, where traditional market mechanisms, which are based on supply and demand, and organizations, which are based on bureaucratic control mechanisms, increasingly are supplanted with longterm, stable relationships between the market actors. One example is outsourcing where organizations split up and establish long-term relationships as partly independent actors, the other is strategic alliances where autonome actors establish more mutual dependency through long-term cooperation. The result is an increasing number of «quasi-organizations» operating in the intermediate space between market and hierarchy. This raises the question of what role social processes play in business relationships. The other source is the line of theory called contracts theory, specifically the part that adresses relational contracts. According to the reasoning within this line of theory, long-term contracts imply a quasi-interdependence between firms, which, put simply, requires more informal, social mechanisms of governance than the market or a traditional organization. Most commonly, these governance mechanisms are conceptualized as relational norms, or trust. My main question vis-a-vis this line of theory is how such mechanims are established, as they rarelyare the result of some «invisible hand» as in a market, nor unilaterally shaped as in a bureaucratic organization. Underlying the study is the assumption that social governance mechanisms are developed in early phases of a strategic alliance, and that personal interaction plays a major role in this development.
Determinants of capital structure choice: Empirical evidence from Vietnamese listed companies

This paper examines the impact of firm-specific and industry characteristics on capital structure during a sample period spanning from 2007 to 2013. We used panel regression with fixed effects and found strong evidence that capital structure is most affected by firm-specific factors such as tangibility, non-debt tax shields, liquidity, firm size, taxes paid, profitability, Tobin’s Q ratio, and growth assets. In addition, the empirical results indicate that firms operating in different industries have dissimilar capital structures.
Characterization of Memory Profile in Subjects with Amnestic Mild Cognitive Impairment

Different aspects of episodic long-term, short-term and implicit long-term memory were investigated in subjects who strictly fulfilled the criteria for the amnestic form of Mild Cognitive Impairment (a-MCI). Results showed normal short-term memory abilities in these subjects, while each of the episodic long-term memory indices explored showed poorer results in a-MCI subjects with respect to normal controls. Although some episodic memory functions were relatively well preserved, others appeared to have deteriorated to a level comparable to that of mild AD patients. The finding of an extensive impairment of all memory functions depending on hippocampal structures in a population with a high risk of developing dementia is strongly supportive of the hypothesis that a pure amnesic syndrome characterizes the preclinical phase of AD.
Perceptions of Social Support and Eating Disorder Characteristics

Poor social support is a risk factor for the development of eating disorders (Ghaderi, 2003). We designed this study to investigate the relationship between social support and eating disorder symptomatology among a female, nonclinical population. The work is of international interest because disordered eating behavior is common across many nations. The results of this research should help build a better understanding of the links between social support and participants at risk of developing an eating disorder. In this study, family support was not correlated with disordered eating, but satisfaction with social support was.
Non‐invasive detection of bladder cancer via expression‐targeted gene delivery

Because of the time and expense associated with the procedures and possible distress to the patient, cystoscopy or other imaging techniques are typically not used for bladder cancer detection before symptoms become present. Alternatively, commercial assays for urinary tumor markers exist but are marred by low sensitivity and high cost. There is a need for a simple and sensitive means of tumor detection, such as via the analysis of urine.
Human Defensin α-1 Causes Trypanosoma cruzi Membrane Pore Formation and Induces DNA Fragmentation, Which Leads to Trypanosome Destruction

ABSTRACT Human defensins play a fundamental role in the initiation of innate immune responses to some microbial pathogens. Here we show that human defensin α-1 displays a trypanocidal role against Trypanosoma cruzi, the causative agent of Chagas' disease. The toxicity of human defensin α-1 against T. cruzi is mediated by membrane pore formation and the induction of nuclear and mitochondrial DNA fragmentation, leading to trypanosome destruction. Exposure of trypomastigote and amastigote forms of T. cruzi to defensin α-1 significantly reduced parasite viability in a peptide concentration-dependent and saturable manner. The toxicity of defensin α-1 against T. cruzi is blocked by anti-defensin α-1 immunoglobulin G. Electron microscopic analysis of trypomastigotes exposed to defensin α-1 revealed pore formation in the cellular and flagellar membranes, membrane disorganization, and blebbing as well as cytoplasmic vacuolization. Furthermore, human defensin α-1 enters the trypanosome when membrane pores are present and is associated with later intracellular damage. Trypanosome membrane depolarization abolished the toxicity of defensin α-1 against the parasite. Preincubation of trypomastigotes with defensin α-1 followed by exposure to human epithelial cells significantly reduced T. cruzi infection in these cells. Thus, human defensin α-1 is an innate immune molecule that causes severe toxicity to T. cruzi and plays an important role in reducing cellular infection. This is the first report showing that human defensin α-1 causes membrane pore formation in a human parasite, leading to trypanosome destruction.
Di (n-butyl) Phthalate Inhibits Testosterone Synthesis Through a Glucocorticoid-Mediated Pathway in Rats

The present study focused on investigating whether the inhibitory effect of di (n-butyl) phthalate (DBP) on testosterone (T) biosynthesis was mediated by the glucocorticoid (GC) pathway in prepubertal male rats and T production after the exposure to DBP ceased. Prepubertal male rats were administered DBP in corn oil orally at 0, 250, 500, 1000, and 2000 mg/kg daily for 30 days. Serum T and GC were measured by radioimmunoassay and enzyme-linked immunosorbent assay, respectively. The responses, including glucocorticoid receptor (GR), type I 11β-hydroxysteroid dehydrogenase (11β-HSD1), and steroidogenesis acute regulatory protein (StAR) in the testes tissues, were determined by Western blotting and reverse transcriptase PCR. DBP exposure resulted in testicular toxicity, such as seminiferous tubule degeneration and a decrease in the number of spermatogenic cells. T was decreased and GC was increased in a DBP concentration-dependent manner in the exposure group. The expression of GR and 11β-HSD1 was significantly increased, with an associated decrease in expression of StAR. Neither the expression of the GR nor 11β-HSD1 and StAR were statistically significantly different in the postexposure group compared with the control. However, the weight and morphology of the testes did not recover in the postexposure group. These data suggest that DBP inhibits testosterone production through a GC-mediated pathway in prepubertal male rats, and after exposure to DBP ceases, testosterone biosynthesis returns.
Differences in Foot and Forearm Skin Microcirculation in Diabetic Patients With and Without Neuropathy

OBJECTIVE We have compared the hyperemic response to heat and the endothelium-dependent and endothelium-independent vasodilatation between the dorsum of the foot and the forearm in diabetic neuropathic and non-neuropathic patients and healthy control subjects. RESEARCH DESIGN AND METHODS We studied the cutaneous microcirculation in the forearm and foot in 15 diabetic patients with neuropathy, in 14 diabetic patients without neuropathy, and in 15 control subjects matched for age, sex, BMI, and in the case of diabetic patients, for the duration of diabetes. Patients with peripheral vascular disease and/or renal impairment were excluded. The cutaneous microcirculation of the dorsum of the foot and the flexor aspect of the forearm was tested in all subjects. Single-point laser Doppler was employed to measure the maximal hyperemic response to heating of the skin to 44°C and laser Doppler imaging scanner was used to evaluate the response to iontophoresis of 1% acetylcholine chloride (Ach) (endothelium-dependent response) and 1% sodium nitroprusside (NaNP) (endothelium-independent response). RESULTS The transcutaneous oxygen tension was lower in the neuropathic group at both foot and forearm level, while the maximal hyperemic response to heat was similar at the foot and forearm level in all three groups. The endothelium-dependent vasodilation (percent increase over baseline) was lower in the foot compared to the forearm in the neuropathic group (23 ± 4 vs. 55 ± 10 [mean ± SEM] P < 0.01)], the non-neuropathic group (33 ± 6 vs. 88 ± 14; P < 0.01), and the control subjects (43 ± 6 vs. 93 ± 13; P < 0.001). Similar results were observed during the iontophoresis of NaNP (P < 0.05). No differences were found among the three groups when the ratio of the forearm:foot response was calculated for both the endothelium-dependent (neuropathic group, 2.25 ± 0.24; non-neuropathic group, 2.55 ± 0.35; and control subjects, 2.11 ± 0.26; P = NS) and endothelium-independent vasodilation (neuropathic group, 1.54 ± 0.27; non-neuropathic group, 2.08 ± 0.33; and control subjects, 2.77 ± 1.03; P = NS). The vasodilatory response, which is related to the C nociceptive fiber action, was reduced at the foot level during iontophoresis of Ach in the neuropathic group. In contrast, no difference was found during the iontophoresis of NaNP at the foot and forearm level and of Ach at the forearm level among all three groups. CONCLUSIONS In healthy subjects, the endothelial-dependent and endothelial-independent vasodilatation is lower at the foot level when compared to the forearm, and a generalized impairment of the microcirculation in diabetic patients with neuropathy preserves this forearm-foot gradient. These changes may be a contributing factor for the early involvement of the foot with neuropathy when compared to the forearm.
The effect of exposure to high flux density static and pulsed magnetic fields on lymphocyte function

We investigated whether a combination of static electromagnetic field (EMF) at a flux density of 4.75 T together with pulsed EMF at a flux density of 0.7 mT generated by an NMR apparatus (NMRF), could promote movements of Ca2+, cell proliferation, and the eventual production of proinflammatory cytokines in human lymphocytes as well as in Jurkat cells, after exposure to the field for 1 h. The same study was also performed after activation of cells with 5 μg/ml phytohaemagglutinin (PHA) immediately before the exposure period. Our results clearly demonstrate that NMRF exposure increases the [Ca2+]i, without any proliferative, or activating, or proinflammatory effect on both normal and PHA stimulated lymphocytes. Accordingly, the levels of interferon γ, tumor necrosis factor α, interleukin‐1β, interleukin‐2, and interleukin‐6 remained unvaried after exposure. Exposure of Jurkat cells statistically decreased the [Ca2+]i and the proliferation. This is consistent with the low levels of IL‐2 measured in supernatants of these cells after exposure. On the whole our data suggest that static and pulsed NMRF exposure contribute synergistically in the increase of the [Ca2+]i without any activating or proinflammatory effect either in normal or in PHA challenged lymphocytes. In Jurkat cells, by changing the properties of cell membranes, NMRF exposure can influence Ca2+ transport processes and hence Ca2+ homeostasis, causing a marked decrease of proliferation. Bioelectromagnetics 24:373–379, 2003. © 2003 Wiley‐Liss, Inc.
Evaluation of book backpack load during walking

This investigation evaluated accumulated mean and peak impact forces per stride and per metre associated with two book backpack loads and two cadences during single and double support phases of walking. Thirty college participants randomly performed three trials while either walking a self-selected cadence or fixed cadence without (empty pack) or with a load (15% body mass) carried in a bookbag. The fixed cadence (55.5 steps/min) was regulated by a metronome. A computerized Kistler force platform system (phase-locked timing device) recorded (200 Hz) three-dimensional reaction forces, impulses, and time in single and double support phases. A Panasonic video camera AG-450 was set perpendicular to the plane of walking motion to film (60 Hz) the walking pattern from which stride length and selected kinematic data were determined. Repeated measure ANOVA (p < 0.05) determined differences of loads and cadences in walking. Accumulated force was evaluated as impulses per stride and impulses per metre (stress index). When carrying the 15% load, there was a decrease in speed, a decrease in single support time (SST), and an increase in double support time (DST). The impulses per stride significantly increased in DST, and significantly decrease in SST. When impulses were analysed per metre, the stress index signficantly increased in DST, but not during SST. These differences in SST may be important when load stress is applied to the single support leg/foot in any given distance of walking. While stride analysis identifies accumulative forces resulting from varying stride lengths, the stress index provides a standardized measure per metre of the accumulative forces that negate the variances of individual stride lengths, and the index measure can easily represent data for any given distance traversed.
Keratoconus and Allergic Diseases Among Israeli Adolescents Between 2005 and 2013

Purpose: The aim of this study was to evaluate the association between keratoconus (KC) and common allergic conditions, such as asthma, atopic dermatitis, and allergic rhinitis in a large-scale database–based epidemiological study. Methods: We conducted a cross-sectional study to estimate the epidemiologic relationship between KC and allergic diseases. The study population included all Israeli adolescents who underwent medical evaluation by the Israeli Defense Force, between the years 2005 and 2013. The presence of KC was determined by corneal topography read by an ophthalmologist. Results: A statistically significantly increased odds ratio (OR) for the presence of KC was found for asthma [OR: 2.0; 95% confidence interval (CI): 1.6–2.5; P < 0.001], allergic rhinitis (OR: 1.6; 95% CI: 1.3–2.0; P < 0.001), and the combination of allergic conjunctivitis, chronic blepharitis, and vernal keratoconjunctivitis (AC/CB/VKC), for which a particularly strong association was found (OR: 6.0; 95% CI: 4.0–9.2; P < 0.001). No significant association was found between angioedema, urticaria, history of anaphylaxis, allergy to hymenoptera sting or atopic dermatitis, and KC. After stratifying the patients according to the severity of the allergic disease, the association between severe (AC/CB/VKC) and KC was very high (OR: 36.5; 95% CI: 20.4–65.4; P < 0.001). Conclusions: In this study, we demonstrated a substantial association between (AC/CB/VKC), asthma, allergic rhinitis, and KC, with no significant association between other allergic diseases and KC. The severity of the allergic status is without doubt associated with a greater risk of having KC. The mechanism causing this association is still unclear.
Analysis of gene mutations in four cases of dermatofibrosarcoma protuberans

Fusion of the collagen type I α 1 (COL1A1) gene with the platelet‐derived growth factor B‐chain (PDGFB) gene has been described in dermatofibrosarcoma protuberans (DFSP). Various exons of the COL1A1 gene have been shown to be involved in the fusion with exon 2 of the PDGFB gene. We examined the breakpoints of the COL1A1 gene using the tumour specimens from four patients with DFSP. The COL1A1‐PDGFB fusion transcripts were detected from the cultured tumour cells by reverse transcriptase polymerase chain reaction. Sequence analysis revealed that the ends of exons 23, 25, 26 and 36 in the COL1A1 gene were fused with the start of exon 2 in the PDGFB. This study identified three novel COL1A1 breakpoints: exons 23, 26 and 36 of the COL1A1 gene. In one case, the tumour was composed of two areas that differed in cytological atypia, cellularity and mitotic activity, indicating the dedifferentiation of the tumour. In tumour cells from two different areas the same aberrant fusion transcripts were identified. These results suggest that the dedifferentiation of tumour cells has nothing to do with the specific breakpoints of the COL1A1 gene, but depends on other unknown factors.
CEREBROSPINAL FLUID‐RELATED COMPLICATIONS WITH AUTOLOGOUS DURAPLASTY AND ARACHNOID SPARING IN TYPE I CHIARI MALFORMATION

OBJECTIVE Although there is a current consensus that Type I Chiari malformations (CM-I) should be treated only in the setting of symptomatic disease, significant controversy surrounds the most appropriate surgical procedure. Recent enthusiasm for osseous decompression without duraplasty is supported by the purportedly lower morbidity of this approach. Precise rates of morbidity with duraplasty, however, have not been reported. This study is intended to assess the cerebrospinal fluid-related morbidity associated with a patient population treated uniformly with autologous duraplasty for symptomatic CM-I. METHODS A review of one surgeon's practice (MMS) from 1997 to 2007 identified patients treated for symptomatic CM-I with osseous decompression and autologous duraplasty. A retrospective chart review was then performed for these patients with an emphasis on cerebrospinal fluid-related complications. RESULTS Forty patients were treated for CM-I with decompression and autologous duraplasty. Twenty-four patients presented with a preoperative syrinx. The mean age was 13.3 years, and the median age was 12.9 years (range, 3.3–45.8 yr). The mean follow-up period was 11.4 months (range, 1–101 mo). There was no mortality associated with the procedure. Clinical response was observed in 91.8% of patients, with 70.2% experiencing complete symptomatic resolution and 21.6% experiencing partial improvement. Two patients (5.4%) had persistent symptomatic syringomyelia requiring syringosubarachnoid shunting. There was an overall morbidity rate of 2.5% due to one pseudomeningocele treated with a single percutaneous tap. There were no incidences of cerebrospinal fluid leak, meningitis, or postoperative hydrocephalus. CONCLUSION The cerebrospinal fluid-related morbidity associated with autologous duraplasty for CM-I in a uniformly treated population is negligible. These results challenge the current rationale for a less aggressive surgical approach to CM-I.
Long-term persistence of zoster vaccine efficacy.

BACKGROUND The Shingles Prevention Study (SPS) demonstrated zoster vaccine efficacy through 4 years postvaccination. A Short-Term Persistence Substudy (STPS) demonstrated persistence of vaccine efficacy for at least 5 years. A Long-Term Persistence Substudy (LTPS) was undertaken to further assess vaccine efficacy in SPS vaccine recipients followed for up to 11 years postvaccination. Study outcomes were assessed for the entire LTPS period and for each year from 7 to 11 years postvaccination. METHODS Surveillance, case determination, and follow-up were comparable to those in SPS and STPS. Because SPS placebo recipients were offered zoster vaccine before the LTPS began, there were no unvaccinated controls. Instead, SPS and STPS placebo results were used to model reference placebo groups. RESULTS The LTPS enrolled 6867 SPS vaccine recipients. Compared to SPS, estimated vaccine efficacy in LTPS decreased from 61.1% to 37.3% for the herpes zoster (HZ) burden of illness (BOI), from 66.5% to 35.4% for incidence of postherpetic neuralgia, and from 51.3% to 21.1% for incidence of HZ, and declined for all 3 outcome measures from 7 through 11 years postvaccination. Vaccine efficacy for the HZ BOI was significantly greater than zero through year 10 postvaccination, whereas vaccine efficacy for incidence of HZ was significantly greater than zero only through year 8. CONCLUSIONS Estimates of vaccine efficacy decreased over time in the LTPS population compared with modeled control estimates. Statistically significant vaccine efficacy for HZ BOI persisted into year 10 postvaccination, whereas statistically significant vaccine efficacy for incidence of HZ persisted only through year 8.