Miracle-dz/UniFAR-FTUs huggingface dataset:
The changing face of pleural empyemas in children: epidemiology and management.

OBJECTIVE Empyema remains a significant cause of morbidity in children. This study evaluates the changes that have affected the outcome in children with pleural empyema, including the emergence of resistant organisms, the introduction of the pneumococcal conjugate vaccine, and earlier treatment with video-assisted thoracoscopy (VATS). METHODS A retrospective chart review was performed on all patients who were discharged with a diagnosis of empyema and community-acquired pneumonia over a 10-year period (1993-2002) at Texas Children's Hospital in Houston, Texas. Data collected included demographic information, clinical presentation, radiographic studies, laboratory data including culture results, and hospital course. RESULTS A total of 230 charts were available for review. The mean age of the patients was 4.0 +/- 3.6 years. Of the pleural fluid cultures performed, 32% (69 of 219) were positive. An additional 27 patients had a cause identified by blood culture. The first penicillin-nonsusceptible Streptococcus pneumoniae was identified in 1995, and the first methicillin-resistant Staphylococcus aureus was identified in 1998. After the universal use of the pneumococcal conjugate vaccine, 3 major changes have occurred (1999-2000 vs 2001-2002): 1) the number of patients admitted with empyema (per 10 000 admissions) has decreased from 23 to 12.6; 2) the prevalence of S pneumoniae has decreased from 66% (29 of 44) to 27% (4 of 15); and 3) S aureus has become the most common pathogen isolated (18% vs 60%), with 78% of those being methicillin resistant. The use of early VATS (<48 hours after admission) versus late VATS (>48 hours after admission) significantly decreased the length of hospitalization (11.49 +/- 6.56 days vs 15.18 +/- 8.62 days). CONCLUSIONS The microbiologic cause of empyema has changed with an increasing incidence of S aureus, particularly methicillin-resistant S aureus. The use of VATS for initial therapy of empyema results in decreased duration of fever and length of hospitalization.
Cytosolic and mitochondrial Ca2+ signals in patch clamped mammalian ventricular myocytes

1 Ventricular myocytes isolated from ferret or cat were loaded with the acetoxymethyl ester form of indo‐1 (indo‐1 AM) such that ∼75 % of cellular indo‐1 was mitochondrial. The intramitochondrial indo‐1 concentration was 0.5‐2 mm. 2 Myocytes were also voltage clamped (membrane capacitance, Cm= 100 pF) and a typical wash‐out time constant of cytosolic indo‐1 by a patch pipette was found to be ∼300 s. Depolarizations to +110 mV produced graded and progressive cellular Ca2+ load via Na+‐Ca2+ exchange. 3 During these relatively slow Ca2+ transients, cell contraction (ΔL) paralleled fluorescence ratio signals (R) such that ΔL could be used as a bioassay of cytosolic [Ca2+] ([Ca2+]c), where [Ca2+]CL is the inferred signal which is delayed by ∼200 ms from true [Ca2+]c. 4 In myocytes without Mn2+ quench, the kinetics of the total cellular indo‐1 signal, ΔR (including cytosolic and mitochondrial components), match ΔL during stimulations at low basal [Ca2+]i. However, after progressive Ca2+ loading, ΔR kinetics deviate from ΔL dramatically. The deviation can be completely blocked by a potent mitochondrial Ca2+ uniport blocker, Ru360. 5 When cytosolic indo‐1 is quenched by Mn2+, initial moderate stimulation triggers contractions (ΔL), but no change in indo‐1 signal, indicating both the absence of cytosolic Ca2+‐sensitive indo‐1 and unchanged mitochondrial [Ca2+] (Δ[Ca2+]m). Subsequent stronger stimulation evoked larger ΔL and also ΔR. The threshold [Ca2+]c for mitochondrial Ca2+ uptake was 300‐500 nM, similar to that without Mn2+ quench. 6 At high Ca2+ loads where Δ[Ca2+]m is detected, the time course of [Ca2+]m was different from that of [Ca2+]c. Peak [Ca2+]m after stimulation has an ∼1 s latency with respect to [Ca2+]c, and [Ca2+]m decline is extremely slow. 7 Upon a Ca2+ influx which increased [Ca2+]c by 0.4 μm and [Ca2+]m by 0.2 μm, total mitochondrial Ca2+ uptake was ∼13 μmol (l mitochondria)−1. 8 With Mn2+ quench of cytosolic indo‐1, there was no mitochondrial uptake of Mn2+ until the point at which mitochondrial Ca2+ uptake became apparent. However, after mitochondrial Ca2+ uptake starts, mitochondria continually take up Mn2+ even during relaxation, when [Ca2+]c is low. 9 It is concluded that mitochondria in intact myocytes do not take up detectable amounts of Ca2+ during individual contractions, unless resting [Ca2+]c exceeds 300‐500 nM. At high cell Ca2+ loads and [Ca2+]c, mitochondrial Ca2+ transients occur during the twitch, but with much slower kinetics than those of [Ca2+]c.
Electronic cochlea: CAR-FAC model on FPGA

In the mammalian auditory pathway, the cochlea is the first stage of processing where the incoming sound signal is mapped into various frequency channels. This multi-channel output contains subtle spectrotemporal features essential in sound source identification and segregation. These features have a large dynamic range. They have a large gain and sharp tuning at low sound levels, and a low gain and broad tuning at high sound levels. These properties are inherent in the Cascade of Asymmetric Resonators with Fast-Acting Compression (CAR-FAC) model of the cochlea. The CAR segment of the model simulates the basilar membrane's response to sound while the FAC segment simulates hair cells and sub-cortical responses resulting in a neural activity pattern necessary for sound perception analysis. We have previously implemented the CAR model on an FPGA, and in this paper, we implement the complete CAR-FAC model with 100 sections on an FPGA for a sample rate of 32 kHz. The FAC part includes outer and inner hair cell algorithms incorporating nonlinearity as well as an automatic gain control for modulating basilar membrane output with respect to input sound levels. We have implemented our design using time-multiplexing approach, where hardware resources of one cochlea section are reused for all the 100 sections of the model.
Role of rubrerythrin in the oxidative stress response of Porphyromonas gingivalis

Rubrerythrins are non‐haem iron proteins that have been implicated in oxidative stress protection in anaerobic bacteria and archaea. However, up to now, this role has not been confirmed directly by inactivation of a rubrerythrin gene. Here we report generation of an rbr− mutant of Porphyromonas gingivalis, an obligately anaerobic gingival pathogenic bacterium. Characterization of the rbr− strain clearly showed that P. gingivalis produces a rubrerythrin‐like protein that is absent in the rbr− strain, and that the P. gingivalis rbr− strain is more dioxygen‐ and hydrogen peroxide‐sensitive than the wild type. The latter conclusion is based on two independent results, namely, deeper no‐growth zones upon diffusion of the oxidants through soft agar culture tubes and growth impairment of liquid cultures exposed to the oxidants. A same‐site rbr+ revertant showed increased hydrogen peroxide and dioxygen resistance relative to the rbr− strain. Transcription of the P. gingivalis rubrerythrin gene is induced above its constitutive anaerobic level in response to dioxygen or hydrogen peroxide exposures. Purified rubrerythrins from other organisms have been shown to catalyse reduction of hydrogen peroxide, while showing relatively sluggish reaction with dioxygen and little or no catalase or superoxide dismutase activities. Porphyromonas gingivalis contains a superoxide dismutase but lacks catalase and haem peroxidases. We therefore suggest that rubrerythrin provides oxidative stress protection via catalytic reduction of intracellular hydrogen peroxide.
Absorption, disposition, and metabolism of [14C]didanosine in the beagle dog.

The absorption, disposition, and metabolism of didanosine were investigated in three adult male beagle dogs that received a single iv and po solution dose of 200 mg (ca. 20 mg/kg) of [14C]didanosine. The dog model was "humanized" by predosing with pentagastrin (6 micrograms/kg). The po dose was in buffer, as administered in man. The iv and po sessions were separated by 1 week. Plasma, urine, and feces were collected and assayed for total radioactivity; plasma and urine samples were also analyzed for intact didanosine using validated HPLC/UV assays. Metabolic profiles of [14C]didanosine were obtained in plasma and urine. After iv dose, 87% and 0.5% of the administered radioactivity were recovered in urine and feces within 6 days, respectively; the corresponding recoveries were 84% and 2.1% after po dose. Oral absorption of didanosine was rapid and complete; but due to first pass metabolism, the absolute bioavailability of didanosine was 44%. Mean renal clearance of didanosine (110 ml/min) accounted for about 43% of the total body clearance. The mean steady state volume of distribution of didanosine was 9.6 liters. The mean terminal half-life of didanosine was 0.8 hr after iv or po administration. Five putative metabolites, M1 (allantoin), M2, M3 (uric acid), M4 (hypoxanthine), and M5 (xanthine) of didanosine were observed in plasma and/or urine. The sum of the five metabolites plus unchanged drug accounted for virtually all of the radioactivity in plasma and urine. Allantoin represented the major metabolite in both plasma and urine. The extent of metabolism and the proportion of dose excreted as unchanged didanosine were markedly route dependent. (ABSTRACT TRUNCATED AT 250 WORDS)
Regulation of Fracture Repair by Growth Factors

Summary Fractured bones heal by a cascade of cellular events in which mesenchymal cells respond to unknown regulators by proliferating, differentiating, and synthesizing extracellular matrix. Current concepts suggest that growth factors may regulate different steps in this cascade (10). Recent studies suggest regulatory roles for PDGF, aFGF, bFGF, and TGF-β in the initiation and the development of the fracture callus. Fracture healing begins immediately following injury, when growth factors, including TGF-β1 and PDGF, are released into the fracture hematoma by platelets and inflammatory cells. TGF-β1 and FGF are synthesized by osteoblasts and chondrocytes throughout the healing process. TGF-β and PDGF appear to have an influence on the initiation of fracture repair and the formation of cartilage and intramembranous bone in the initiation of callus formation. Acidic FGF is synthesized by chondrocytes, chondrocyte precursors, and macrophages. It appears to stimulate the proliferation of immature chondrocytes or precursors, and indirectly regulates chondrocyte maturation and the expression of the cartilage matrix. Presumably, growth factors in the callus at later times regulate additional steps in repair of the bone after fracture. These studies suggest that growth factors are central regulators of cellular proliferation, differentiation, and extracellular matrix synthesis during fracture repair. Abnormal growth factor expression has been implicated as causing impaired or abnormal healing in other tissues, suggesting that altered growth factor expression also may be responsible for abnormal or delayed fracture repair. As a complete understanding of fracture-healing regulation evolves, we expect new insights into the etiology of abnormal or delayed fracture healing, and possibly new therapies for these difficult clinical problems.
Substrate-Induced Ubiquitylation and Endocytosis of Yeast Amino Acid Permeases

ABSTRACT Many plasma membrane transporters are downregulated by ubiquitylation, endocytosis, and delivery to the lysosome in response to various stimuli. We report here that two amino acid transporters of Saccharomyces cerevisiae, the general amino acid permease (Gap1) and the arginine-specific permease (Can1), undergo ubiquitin-dependent downregulation in response to their substrates and that this downregulation is not due to intracellular accumulation of the transported amino acids but to transport catalysis itself. Following an approach based on permease structural modeling, mutagenesis, and kinetic parameter analysis, we obtained evidence that substrate-induced endocytosis requires transition of the permease to a conformational state preceding substrate release into the cell. Furthermore, this transient conformation must be stable enough, and thus sufficiently populated, for the permease to undergo efficient downregulation. Additional observations, including the constitutive downregulation of two active Gap1 mutants altered in cytosolic regions, support the model that the substrate-induced conformational transition inducing endocytosis involves remodeling of cytosolic regions of the permeases, thereby promoting their recognition by arrestin-like adaptors of the Rsp5 ubiquitin ligase. Similar mechanisms might control many other plasma membrane transporters according to the external concentrations of their substrates.
Outcome following decompressive craniectomy for malignant swelling due to severe head injury.

OBJECT The aim of this study was to assess outcome following decompressive craniectomy for malignant brain swelling due to closed traumatic brain injury (TBI). METHODS During a 48-month period (March 2000-March 2004), 50 of 967 consecutive patients with closed TBI experienced diffuse brain swelling and underwent decompressive craniectomy, without removal of clots or contusion, to control intracranial pressure (ICP) or to reverse dangerous brain shifts. Diffuse injury was demonstrated in 44 patients, an evacuated mass lesion in four in whom decompressive craniectomy had been performed as a separate procedure, and a nonevacuated mass lesion in two. Decompressive craniectomy was performed urgently in 10 patients before ICP monitoring; in 40 patients the procedure was performed after ICP had become unresponsive to conventional medical management as outlined in the American Association of Neurological Surgeons guidelines. Survivors were followed up for at least 3 months posttreatment to determine their Glasgow Outcome Scale (GOS) score. Decompressive craniectomy lowered ICP to less than 20 mm Hg in 85% of patients. In the 40 patients who had undergone ICP monitoring before decompression, ICP decreased from a mean of 23.9 to 14.4 mm Hg (p < 0.001). Fourteen of 50 patients died, and 16 either remained in a vegetative state (seven patients) or were severely disabled (nine patients). Twenty patients had a good outcome (GOS Score 4-5). Among 30-day survivors, good outcome occurred in 17, 67, and 67% of patients with postresuscitation Glasgow Coma Scale scores of 3 to 5, 6 to 8, and 9 to 15, respectively (p < 0.05). Outcome was unaffected by abnormal pupillary response to light, timing of decompressive craniectomy, brain shift as demonstrated on computerized tomography scanning, and patient age, possibly because of the small number of patients in each of the subsets. Complications included hydrocephalus (five patients), hemorrhagic swelling ipsilateral to the craniectomy site (eight patients), and subdural hygroma (25 patients). CONCLUSIONS Decompressive craniectomy was associated with a better-than-expected functional outcome in patients with medically uncontrollable ICP and/or brain herniation, compared with outcomes in other control cohorts reported on in the literature.
Vers un modèle formel pour le raisonnement à partir des contextes

A control center utilizing individual control units that hang from a unit shelf in a control center section. A tongue on the top of each control unit mates with the groove of the unit shelf to provide quick and easy alignment for electrical connections between the control unit and the vertical bus bar. The unit shelf and door are designed to be secured simultaneously to the cabinet.
Two Waves of Platelet Secretion Induced by Thromboxane A2 Receptor and a Critical Role for Phosphoinositide 3-Kinases*

Thromboxane A2 (TXA2)-mediated platelet secretion and aggregation are important in thrombosis. Here, we present a novel finding that the stable TXA2 analogue, U46619, induces two waves of platelet secretion, each of which precedes a distinct wave of platelet aggregation. ADP released from platelets during the first wave of secretion played a major role in augmenting the first wave of platelet aggregation. The second wave of platelet secretion and aggregation required the first wave of both ADP secretion and aggregation and were blocked by either the integrin inhibitor RGDS or a P2Y12 receptor antagonist, indicating a requirement for both the integrin outside-in signal and ADP-activated Gi pathway. U46619 stimulated phosphoinositide 3-kinase (PI3K)-dependent phosphorylation of Akt, which was augmented by ADP but did not require integrin outside-in signaling. Platelets from PI3Kγ knock-out mice or PI3K inhibitor-treated platelets showed an impaired second wave of platelet secretion and aggregation. However, the second wave of platelet aggregation was restored by addition of exogenous ADP to PI3Kγ deficient or PI3K inhibitor-treated platelets. Thus, our data indicate that PI3K, together with the integrin outside-in signaling, play a central role in inducing the second wave of platelet secretion, which leads to the second wave of irreversible platelet aggregation.
The Effects of Double-Epilayer Structure on Threshold Voltage of Ultralow Voltage Trench Power MOSFET Devices

The effect of double-epilayer structure on threshold voltage (V <sub>th</sub>) has been investigated for p-channel low-voltage (V<sub>ds </sub>) trench power MOSFET devices. By fabricating the device in an intrinsic epilayer grown on the top of a highly doped epilayer, the sensitivity of V<sub>th</sub> to the epidoping concentration has been significantly reduced. This reduction is attributed to the fact that in the double-epilayer structure, the compensation effect of epidoping concentration (N<sub>A</sub>) is minimized. The V<sub>th</sub> variation (sigma<sub>Vth</sub> standard deviation) shows a strong dependence on the intrinsic epilayer thickness (t, in micrometers) as: sigma<sub>Vth </sub> = 2.4 times 10<sup>5-7.1</sup>, while the device-specific on-resistance (sp-R<sub>dson</sub>) is linearly proportional to the intrinsic layer thickness. This intrinsic epilayer can thus be utilized to minimize the boron up-diffusion from both the first epilayer and the substrate and further reduces V<sub>th</sub> variation. For the p-channel device with a V<sub>ds</sub> of 12 V, a 50% lower sigma<sub>Vth</sub> has been achieved while maintaining at least the same sp-R<sub>dson</sub> with the optimized double-epilayer structure which consists of a 4-mum-thick intrinsic layer and a 2.6-mum-thick first doped epilayer (at 4 times 10<sup>17</sup> cm<sup>-3</sup> or 0.07 Omegamiddotcm). Compared to the single epilayer, the double-epilayer structure also leads to 14% higher device output saturation current and shows the body junction much closer to ideal characteristics (abrupt). This structure enables further reductions of both power consumption and V<sub>th</sub> for ultralow voltage power MOSFET
Venture Capital in Transition Economies: The Case of Hungary

This paper examines the Hungarian venture capital industry, one of the most well-developed in the emerging economies of Central and Eastern Europe. Using a combination of secondary data, mail questionnaires, and face-to-face Interviews, the paper identifies areas of both similarity and difference with experience in developed capitalist economies. The need for venture capitalists to obtain control is found to be much stronger in Hungary than in the US. The relative importance of DCF and price/earnings ratio methods of valuation are reversed when Hungary and western experience are compared. There was evidence that Hungarian domestic venture capitalists engage in less detailed monitoring than either venture capitalists elsewhere or foreign-based venture capitalists operating in Hungary.
An Ultra-Wide Range Bi-Directional Transceiver With Adaptive Power Control Using Background Replica VCO Gain Calibration

A transceiver with adaptive power control using a process and frequency monitor (PFM) is proposed. The PFM employs gain calibration with a replica voltage-controlled oscillator (VCO) and operates in the background. A five-bit digital code detected by the VCO gain calibration is applied to an adaptive-amplitude driver, an adaptive-bandwidth receiver, and an adaptive-bandwidth phase-locked loop. A test chip was fabricated in a 110-nm CMOS process and achieved adaptive power control over a wide frequency range (0.05 to 3.4 Gb/s). At data rate of 100 Mb/s, the measured power consumption attained with adaptive power control was 75% lower than that attained with a conventional architecture without adaptive power control.
Approach to Check the Consistency between the UML2.0 Dynamic Diagrams

Nowadays, UML is applied to modeling in the analysis and design of software system widely. However, because of the complexity of the software system, in the UML model, the inevitable will introduce different chart especially inconsistencies between the dynamic view. This paper proposes a method to verify UML2.0 model consistency of state diagram and sequence diagram. First, XYZ/E can express the mechanism of state conversion and formal semantics, so it can characterize State Diagram directly. Second, XYZ/E and Promela are similar in many aspects, an algorithm transforms the XYZ/E code into Promela is proposed. Rules are designed which describe how to use the LTL to express the interaction fragments in UML2.0 Sequence diagram are given in the paper. Finally using the model checking tool Spin, to examine the Promela described system specifications, to test whether the system meets the LTL formulas, to achieve the goal of detection model consistency.
Hepatic cholesterol crystals and crown-like structures distinguish NASH from simple steatosis[S]

We sought to determine whether hepatic cholesterol crystals are present in patients or mice with nonalcoholic fatty liver disease/nonalcoholic steatohepatitis (NASH), and whether their presence or distribution correlates with the presence of NASH as compared with simple steatosis. We identified, by filipin staining, free cholesterol within hepatocyte lipid droplets in patients with NASH and in C57BL/6J mice that developed NASH following a high-fat high-cholesterol diet. Under polarized light these lipid droplets exhibited strong birefringence suggesting that some of the cholesterol was present in the form of crystals. Activated Kupffer cells aggregated around dead hepatocytes that included strongly birefringent cholesterol crystals, forming “crown-like structures” similar to those recently described in inflamed visceral adipose tissue. These Kupffer cells appeared to process the lipid of dead hepatocytes turning it into activated lipid-laden “foam cells” with numerous small cholesterol-containing droplets. In contrast, hepatocyte lipid droplets in patients and mice with simple steatosis did not exhibit cholesterol crystals and their Kupffer cells did not form crown-like structures or transform into foam cells. Our results suggest that cholesterol crystallization within hepatocyte lipid droplets and aggregation and activation of Kupffer cells in crown-like structures around such droplets represent an important, novel mechanism for progression of simple steatosis to NASH.