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Expression levels of VEGF and Her-2, levels of T-regulatory (Treg) cells, levels of CD3+ cells, and ratios of Th (CD4+ T cells)/Tr (Treg) cells were compared between stage I, II, III, and IV breast cancer patients (n = 120) prior to chemotherapy and healthy women (n = 30). Cells from peripheral blood were counted by flow cytometry, Her-2 and VEGF expression was detected by pathological examination, and Her-2 was detected by FISH. Breast cancer patients had more Treg cells and a lower ratio of Th/Tr cells than the healthy women. Stage IV breast cancer patients had more Treg cells and a lower ratio of Th/Tr cells than stage I, II, or III breast cancer patients. Patients positive for VEGF had a lower ratio of Th/Tr cells compared with patients negative for VEGF, and those positive for both VEGF and Her-2 also had a lower ratio of Th/Tr cells compared with patients not positive for both VEGF and Her-2. The decreased Th/Tr cells ratio indicates impaired immune function, suggesting that the stage IV breast cancer and the Her-2/VEGF-positive breast cancer patients have lower immune function.

High-grade glioma cells express subunits of the ENaC/Deg superfamily, including members of ASIC subfamily. Our previous work has shown that glioma cells exhibit a basally active cation current, which is not present in low-grade tumor cells or normal astrocytes, and that can be blocked by amiloride. When ASIC2 is present within the channel complex in the plasma membrane, the channel is rendered non-functional because of inherent negative effectors that require ASIC2. We have previously shown that high-grade glioma cells functionally express this current because of the lack of ASIC2 in the plasma membrane. We now hypothesize that ASIC2 trafficking in glioma cells is regulated by a specific chaperone protein, namely Hsc70. Our results demonstrated that Hsc70 co-immunoprecipitates with ASIC2 and that it is overexpressed in glioma cells as compared with normal astrocytes. In contrast, there was no difference in the expression of calnexin, which also co-immunoprecipitates with ASIC2. In addition, glycerol and sodium 4-phenylbutyrate reduced the amount of Hsc70 expressed in glioma cells to levels found in normal astrocytes. Transfection of Hsc70 siRNA inhibited the constitutively activated amiloride-sensitive current, decreased migration, and increased ASIC2 surface expression in glioma cells. These results support an association between Hsc70 and ASIC2 that may underlie the increased retention of ASIC2 in the endoplasmic reticulum of glioma cells. The data also suggest that decreasing Hsc70 expression promotes reversion of a high-grade glioma cell to a more normal astrocytic phenotype.

Gliomas are primary brain tumors with a complex biology characterized by antigenic and genomic heterogeneity and a propensity for invasion into normal brain tissue. High grade glioma cells possess a voltage-independent, amiloride-inhibitable, inward Na+ current. This current does not exist in normal astrocytes or low grade tumor cells. Inhibition of this conductance decreases glioma growth and cell migration making it a potential therapeutic target. Our previous results have shown that the acid-sensing ion channels (ASICs), members of the epithelial Na+ channel (ENaC)/degenerin (DEG) family of ion channels are part of this current pathway. We hypothesized that one member of the ENaC/DEG family, ASIC2, is retained intracellularly and that it is the lack of functional expression of ASIC2 at the cell surface that results in hyperactivity of this conductance in high grade gliomas. In this study we show that the chemical chaperone, glycerol, and the transcriptional regulator, sodium 4-phenylbutyrate, inhibit the constitutively activated inward current and reduce cell growth and migration in glioblastoma multiforme. The results suggest that these compounds induce the movement of ASIC2 to the plasma membrane, and once there, the basally active inward current characteristic of glioma cells is abolished by inherent negative regulatory mechanisms. This in turn compromises the ability of the glioma cell to migrate and proliferate. These results support the hypothesis that the conductance pathway in high grade glioma cells is comprised of ENaC/DEG subunits and that abolishing this channel activity promotes a reversion of a high grade glioma cell to a phenotype resembling that of normal astrocytes.

To evaluate the clinical value of magnetic resonance (MR) diffusion-weighted imaging (DWI) for diagnosing radiation-induced liver injury (RILI) and detecting changes in hepatic pathology at different post-irradiation times.Male New Zealand white rabbits received no irradiation (C0, control group; n = 10) or irradiation of 50 Gy/10F once every other day by virtual three dimensional conformal radiotherapy (3D-CRT) for one day (C1; n = 10), three days (C2; n = 10), two weeks (C3; n = 10), one month (C4; n = 10) or two months (C5; n = 10). One member of all groups were sacrificed for DWI examination and pathologic study on post-irradiation day 1, day 3, week 2, month 1 and month 2. The apparent diffusion coefficient (ADC) values were measured using a range of b values (50, 300, 600, 800 and 1000 s/mm2).Hematoxylin-eosin (H-E) staining showed that livers of rabbits in the C3, C4 and C5 groups had the characteristic features of veno-occlusive disease. DWI examination showed that the irradiated livers of rabbits in C2, C3, C4 and C5 groups had significantly lower ADC values than the livers of the non-irradiated rabbits at b values of 300, 600, 800 and 1000 s/mm2 (P less than 0.05). When the b value was 600 s/mm2, the best negative correlation between ADC values and pathological stage was seen for the irradiated livers (Spearman's rank, r = -0.459, P less than 0.01). The threshold ADC value to distinguish the normal group (C0) from an irradiated group (more than or equal toC1) was 1.955 * 10-3 mm2/s at 600 s/mm2 b value. When the b value was 1000 s/mm2, the threshold ADC value to predict an irradiated group with normal H-E staining (C1) from an irradiated group with abnormal H-E staining (more than or equal toC2) was 1.5250 * 10-3 mm2/s; the ADC threshold value was 1.5150 * 10-3 mm2/s to predict groups C0-2 and groups C3-5.DWI has high sensitivity for detecting RILI at three days after irradiation with proper b values. Use of the ADC value is feasible for estimating the evolutionary process of pathological features of RILI damage. DWI may represent an important clinical tool for detection of early pathological changes in RILI.

A defect-free silicon epitaxial layer was deposited by in-situ electron cyclotron resonance (ECR) hydrogen plasma cleaning at room temperature (25°C) in a multi-chamber chemical vapor deposition (MS-CVD) system with a load lock chamber. ECR hydrogen plasma was used and films were deposited thermally at low temperature (600 °C). Plain-view transmission electron microscopy (TEM), cross-sectional TEM, Rutherford backscattering spectroscopy, secondary ion mass spectrometry and in-situ emission-Fourier transform infrared spectroscopy results were presented to demonstrate the efficiency of room-temperature in-situ wafer cleaning processes. Process variables such as microwave power (and gas pressure), cleaning temperature and d.c. bias were investigated, and a.d.c. bias turned out to play a crucial role in low-temperature in-situ cleaning processes. Also, the effect of the in-situ cleaning temperature on cleaning efficiency was investigated and discussed. The results were shown to help understand the mechanism of the low-temperature wafer cleaning process.

Real-time in situ applications of the emission Fourier transform infrared (E/FT-IR) technique are reported in this paper. For real-time process monitoring, we found that the real-time growth rate measured by the E/FT-IR is responsive to variations of process parameter(s) (i.e., temperature, pressure, and gas composition). For real-time epi-film thickness control, two control algorithms were used: 1) first past the post (FPP) method; and 2) linear forecasting. A closed-loop precise epi-film thickness end-point control is demonstrated. Additionally, by real-time monitoring of the incubation time and growth rate, we are able to obtain qualitative information about the effectiveness of the predeposition wafer cleaning process. Thus, plasma cleaning process optimization time is shortened and postdeposition materials characterization cost is reduced. Using the optimized conditions, we have demonstrated the growth of defect free epitaxial silicon films. >

This paper reports the measurement of epitaxial silicon film thickness using a Fourier transform infrared spectrometer. The implementation and characteristics of emission Fourier transform infrared spectroscopy (E/FT-IR) for film thickness measurement are described. The limitation and robustness of the E/FT-IR technique, and its comparison to conventional FT-IR are reported in detail. Issues such as E/FT-IR's repeatability, reproducibility, the effect of vacuum window material and its coating, and the effect of wafer rotation, are evaluated. We find that good repeatability and reproducibility of the E/FT-IR technique can be achieved. The repeatability of the E/FT-IR technique in terms of standard deviation is 0.01 /spl mu/m, in terms of coefficient of variation is about 0.1% for all wafer temperatures (550/spl deg/C, 610/spl deg/C, and 660/spl deg/C). The window material, window stress, and its coatings do not affect the film thickness measurement as long as sufficient light intensity reaches the FT-IR detector. Additionally, when FT-IR thickness measurements are performed on a rotating wafer (with speeds up to 55 rpm), we find that only a small amount of noise is introduced, and a good measurement repeatability can still be maintained. >

Procedures and results of refractive index measurements using a Fourier transform infrared spectrometer are reported. These measurements were performed on both lightly and heavily doped silicon samples over the midinfrared (2.5–25 μm) spectrum region. A strong dependence of refractive index as a function of substrate dopant concentration was observed. Moreover, it was observed that the refractive index of heavily doped silicon also varies significantly with wavelength. Furthermore, it was also observed that the refractive index of silicon decreases with increasing wafer temperature for long wavelengths. Finally, the effect of refractive index dispersion on epifilm thickness measurement was examined. The results suggest that the spectral dispersion of the refractive index cannot be neglected for epifilm thickness measurements.

An emission Fourier transform infrared (E/FT‐IR) technique for epifilm thickness measurement will be reported. The E/FT‐IR technique takes advantage of the heated wafer as the source of IR radiation. It is a noncontact, nondestructive, real‐time, and in situ epifilm thickness monitoring tool that we demonstrated to be useful for observing real‐time growth rates and incubation times. In addition, this method is especially applicable to precise end point control when critical film thicknesses are required. Moreover, we have identified some limitations to this method, and found the operable temperature ranges. Furthermore, we have demonstrated, for the first time, a closed‐loop feedback control of epitaxial silicon film thickness in a multichamber single‐wafer chemical vapor deposition reactor.

The results of a novel emission Fourier transform infrared (E/FT-IR) spectrometer for in-situ characterization of semiconductor materials is presented. For the experiments, the wafers were heated and the infrared emission profiles from the substrates were collected by a standard FT-IR spectrometer. Differences in the emission spectra from different substrates are explained through correlation to the optical properties of the corresponding substrates. The in-situ infrared emission spectrum of a lightly doped (10-20 /spl Omega//spl middot/cm) silicon wafer at 200/spl deg/C is very similar to its ex-situ transmission spectrum at room temperature, although the spectrum is inverted. This similarity makes possible the analysis of E/FT-IR spectra by using existing spectral libraries. Finally, it is shown that the E/FT-IR technique can be used for noncontact and noninvasive real-time identification and possibly quantification of impurities during silicon oxidation and for real-time epi-film thickness monitoring during silicon epitaxy. >

Cleaning wafer surfaces in situ using gaseous reagents facilitates automated cluster tool processing of microelectronic devices. Moreover, to remain within stringent thermal processing budgets for making ultralarge scale integrated (ULSI) circuit devices, it is desirable to perform these dry cleaning processes at low temperatures. We report here the use of attenuated total reflectance Fourier transform infrared (ATR-FTIR) spectroscopy to study and optimize room-temperature plasma cleaning of native oxide contaminated Si surfaces. By monitoring the vibrational modes of Si-H, H-SiO, O-H, and C-H in real-time, we develop a hybrid process where an upstream microwave discharge and the gas-flow rate are used to control the neutral atom flux while direct exposure to a radio-frequency plasma is used to control the ion energy flux

Low defect-density epitaxial silicon was grown at 550°C, but it became polysilicon or amorphous silicon when the substrate was submitted to bombardment of ECR argon plasma prior to growth. Through carefully characterizing the interface and structure of low temperature epitaxial silicon films using ultrahigh resolution cross-sectional transmission electron microscopy (UHRXTEM), defects were found to have different features in silicon epitaxial layers grown on {100} and {111} silicon substrates. Twinning was more likely to generate in the epitaxial layer grown on the {111} silicon substrate while stacking faults had priority in forming in the epitaxial layer grown on the {100} substrate. The probable causes of different defect formation mechanisms were analyzed and discussed with the help of UHRXTEM lattice images. The atom model of the twin boundary in the epitaxial silicon film was analyzed in detail.

Human acid-sensing ion channel 1b (hASIC1b) is a H+-gated amiloride-sensitive cation channel. We have previously shown that glioma cells exhibit an amiloride-sensitive cation conductance. Amiloride and the ASIC1 blocker psalmotoxin-1 decrease the migration and proliferation of glioma cells. PKC also abolishes the amiloride-sensitive conductance of glioma cells and inhibits hASIC1b open probability in planar lipid bilayers. In addition, hASIC1b's COOH terminus has been shown to interact with protein interacting with C kinase (PICK)1, which targets PKC to the plasma membrane. Therefore, we tested the hypothesis that PKC regulation of hASIC1b at specific PKC consensus sites inhibits hASIC1b function. We mutated three consensus PKC phosphorylation sites (T26, S40, and S499) in hASIC1b to alanine, to prevent phosphorylation, and to glutamic acid or aspartic acid, to mimic phosphorylation. Our data suggest that S40 and S499 are critical sites mediating the modulation of hASIC1b by PKC. We expressed mutant hASIC1b constructs in Xenopus oocytes and measured acid-activated currents by two-electrode voltage clamp. T26A and T26E did not exhibit acid-activated currents. S40A was indistinguishable from wild type (WT), whereas S40E, S499A, and S499D currents were decreased. The PKC activators PMA and phorbol 12,13-dibutyrate inhibited WT hASIC1b and S499A, and PMA had no effect on S40A or on WT hASIC1b in oocytes pretreated with the PKC inhibitor chelerythrine. Chelerythrine inhibited WT hASIC1b and S40A but had no effect on S499A or S40A/S499A. PKC activators or the inhibitor did not affect the surface expression of WT hASIC1b. These data show that the two PKC consensus sites S40 and S499 differentially regulate hASIC1b and mediate the effects of PKC activation or PKC inhibition on hASIC1b. This will result in a deeper understanding of PKC regulation of this channel in glioma cells, information that may help in designing potentially beneficial therapies in their treatment.

To study the morphologic features and clinical significance of atypical small acinar proliferation (ASAP) suspicious but not diagnostic of cancer in prostatic biopsies.The slides of 11 cases of prostatic needle biopsies collected during a two-year period with the diagnosis of ASAP were reviewed. Immunohistochemical study for 34betaE12, p63 and P504S was performed on the archival paraffin sections.All the 11 ASAP cases were characterized by the presence of a few compacted small acini in the prostatic stroma. Six cases had acini of less than three in number. The acini were round or slightly irregular in shape. The nuclei were enlarged, round or irregular, arranged in single layer and focally separated by broad interval. The nucleoli were usually prominent. Cytoplasm was amphophilic or pale and the lumen border was often well-defined. Basophilic mucus was also seen in some of the lumen. Immunohistochemical study for 34betaE12 and p63 was negative, while that for P504S was positive. In 4 of the 11 cases, the acini were more than three in number, round or slightly irregular, but without cytologic atypia. The nuclei were slightly enlarged with small or inconspicuous nucleoli. Immunohistochemical study for 34betaE12 and p63 was negative or at most focally positive. P504S staining was either negative or weakly positive. Second repeat biopsy was carried out in all cases, and 4 of them (36%) showed definite adenocarcinomatous changes. The positive cases were those with fewer acini but definite cytologic atypia in the initial biopsy.ASAP is a morphologic interpretation closely associated with prostatic adenocarcinoma. The histologic features are suspicious of but not diagnostic of cancer, due to insufficient criteria in terms of acinar number, cytologic or architectural abnormalities. The positive rate in subsequent repeat biopsy is higher than that for cases with usual nodular hyperplasia.

To assess the clinical feature, diagnosis and treatment of primary pulmonary cryptococcosis.From 1996 to 2004, 11 patients with primary pulmonary cryptococcosis were surgical treated and confirmed by histologic study. At the same period, 2715 patients with pulmonary abnormalities received surgery. Their clinical data were retrospectively reviewed.Sixty-four percent (7/11) of the patients were symptomatic at the time of diagnosis. All 11 cases were misdiagnosed as lung cancer or inflammatory or tuberculosis by X-ray and CT scan before surgery. Three cases received fluorine-18 fluorodeoxyglucose-positron emission tomography (FDG-PET) scan and their primary pulmonary lesions showed FDG avid. All 11 patients were treated by antibiotics and antituberculosis therapy but no responses appeared. Primary pulmonary cryptococcosis was diagnosed by ultrasound-guided fine needle aspiration biopsy in only 2 cases, but antifungal therapy was not effective. All 11 patients underwent thoracotomy and their pulmonary cryptococcosis were resected. Only 1 patient with multiple nodules received antifungal therapy postoperatively. No recurrence was found in any patients.Primary pulmonary cryptococcosis is non-specific and can be confused with lung cancer, tuberculosis, etc. The pulmonary abnormalities should be resected unless the diagnosis is established. Antifungal therapy is not necessary in patients whose abnormality has been resected thoroughly.

Acid sensing ion channel (ASIC)2 belongs to the amiloride-sensitive Na(+)-channel/ degenerin family. Our previous studies suggested that differential regulation of ASIC2 expression occurs between high-grade glial-derived tumor cells and normal astrocytes. To investigate the mechanisms involved in the regulation of ASIC2 gene expression, the human ASIC2 promoter region (-1551 to +117) was cloned and characterized. The ASIC2 promoter lacked a canonical TATA box, but contained one putative CCAAT box. Nucleotide sequencing of the promoter revealed the presence of a number of transcription factor-binding sites and a 404 bp CpG island upstream the transcription start site. Nested deletion mutants and transfection results showed that the construct between -133 and +117 base pairs conferred basal transcription specific activity. Mutation of Sp1 and CP2 sites in this region resulted in a 70 and 95% decrease in promoter activity, respectively. Gel shift assays demonstrated the existence of specific protein binding to the SP1 and CP2 elements. There was no mutation in the CpG island in six glioma cell lines, but methylation-specific PCR showed methylation in some of glioma cell lines and tumor tissues, and treatment with the methylation inhibitor 5-Aza-2'-deoxycytidine could partially restore ASIC2 expression in cell lines, suggesting that epigenetic mechanisms may contribute to dysregulated ASIC2 expression.

Hybridomas are fused immortal lymphocytes that typically secrete monoclonal antibodies to a known antigen. Hybridomas express two ionic conductances that have properties consistent with epithelial sodium channel (ENaC) and CFTR. Both ion channels are expressed by lymphocytes. Both of these channels are known to play a role in epithelial cell physiology. However, the physiological role of these channels in lymphocytes is unclear. We tested the hypothesis that ENaC plays a role in the process of regulated antibody secretion. We have been able to demonstrate that hybridomas can be provoked to acutely secrete monoclonal antibodies by a variety of agonists. Concurrently, we were able to show that these same agonists activate amiloride-sensitive sodium currents in whole cell clamped hybridomas. Inhibition of ENaC by amiloride inhibited the acute provoked antibody secretion, thereby linking ENaC to the process of acute antibody secretion. Interestingly, the concentration of amiloride necessary to completely inhibit the provoked secretion was approximately an order of magnitude higher than the concentration necessary to inhibit all of the transmembrane current. However, because amiloride is a weak base, the equilibrium concentration necessary to produce partial inhibition was precisely in accord with the Kifor amiloride and ENaC, indicating that the inhibition was intracellular.

The structures of full and empty capsids of CPV were studied by negative staining and electron cryomicroscopy and computer reconstruction techniques. By comparing the structures and biochemical compositions, the CPV was identified as a single-layered capsid with its five structural proteins located on it. This single capsid is arranged according to T=1 icosahedral symmetry with 12 turret-like spikes at its icosahedral vertices. The empty and full CPV show identical capsid but differ inside. The dense and ordered genomic dsRNA is located inside the full CPV. The internal space of the empty CPV has almost no electron density except for 12 electron densities attributed the transcriptional enzyme complexes extending inward from the base part of CPV spikes.

Some members of the epithelial Na+ channel/degenerin (ENaC/DEG) family of ion channels have been detected in mammalian brain. Therefore, we examined the RNA and protein expression of these channels in another part of the central nervous system, the rabbit retina. We next sought to demonstrate physiological evidence for an amiloride-sensitive current in Müller glia, which, on the basis of a previous study, are thought to express α-ENaC (Golestaneh N, de Kozak Y, Klein C, and Mirshahi M. Glia 33: 160–168, 2001). RT-PCR of retinal RNA revealed the presence of α-, β-, γ-, and δ-ENaC as well as acid-sensing ion channel (ASIC)1, ASIC2, ASIC3, and ASIC4. Immunohistochemical localization with antibodies against α-ENaC and β-ENaC showed labeling in Müller cells and neurons, respectively. The presence of α-ENaC, β-ENaC, and ASIC1 was detected by Western blotting. Cultured Müller cells were whole cell patch clamped. These cells exhibited an inward Na+ current that was blocked by amiloride. These data demonstrate for the first time both the expression of a variety of ENaC and ASIC subunits in the rabbit retina as well as distinct cellular expression patterns of specific subunits in neurons and glia.

The mechanosensitivity of the epithelial sodium channel (ENaC) is controversial. Using cell-attached patch-clamp techniques, we found that mechanical stretch stimulated ENaC in A6 distal nephron cells in only three of nine cell-attached patches. However, stretch consistently activated ENaC after apical ATP was scavenged with apical hexokinase plus glucose or after P2receptors in the patch were blocked. The mean open probability ( P o) of ENaC was increased from 0.31 ± 0.04 to 0.61 ± 0.06 ( P < 0.001; n = 9) when patch pipettes contained hexokinase and glucose, or from 0.24 ± 0.05 to 0.55 ± 0.11 ( P < 0.01; n = 7) when patch pipettes contained suramin, respectively. A poorly hydrolyzable ATP analog, ATPγS, in the patch pipettes inhibited ENaC, reducing the P o from 0.41 ± 0.06 to 0.19 ± 0.05 ( P < 0.01; n = 8). Pretreatment of A6 cells with the phospholipase C (PLC) inhibitor U-73122 abolished the effect of ATP on ENaC activity. These data together suggest that ATP, acting through a PLC-dependent purinergic pathway, masks stretch-induced ENaC activation.

Pathophysiological features of both primary aldosteronism and pseudohyperaldosteronism are hyperactive amiloride-sensitive epithelial Na+channels (ENaC) and refractory hypertension. Peripheral blood lymphocytes express ENaC, which functions and is regulated similarly to ENaC expressed by renal principal cells. Thus it was hypothesized that individuals with either of these hypertensive etiologies could be identified by assessment of the function and regulation of peripheral blood lymphocyte ENaC, by whole cell patch clamp. We also tested the hypothesis that specific inhibition of hyperactive ENaC with amiloride could ameliorate the hypertension. To test these hypotheses, we solicited blood samples from normotensive, controlled hypertensive, and refractory hypertensive individuals. Lymphocytes were examined electrophysiologically to determine whether ENaC was hyperactive. All positive findings were from refractory hypertensive individuals. Nine refractory hypertensive patients had amiloride added to their hypertensive therapy. Amiloride normalized the blood pressure of four subjects. These individuals all had hyperactive ENaC. Amiloride had no effect on individuals with normal ENaC. These findings suggest that whole-cell patch clamp of peripheral blood lymphocytes can be used to identify accurately and rapidly hypertensive individuals who will respond to amiloride therapy.

Aldosterone is involved in salt and water homeostasis. The main effect is thought to involve genomic mechanisms. However, the existence of plasma membrane steroid receptors has been postulated. We used whole cell patch clamp to test the hypothesis that epithelial sodium channels (ENaC) expressed by renal collecting duct principal cells can be regulated nongenomically by aldosterone. In freshly isolated principal cells from rabbit, aldosterone (100 nM) rapidly (

Many human immunodeficiency virus (HIV)-infected patients suffer from impaired neurological function and dementia. This facet of the disease has been termed acquired immunodeficiency syndrome (AIDS)-associated dementia complex (ADC). Several cell types, including astrocytes and neurons, are not productively infected by virus but are involved in ADC pathophysiology. Previous studies of rat astrocytes showed that an HIV coat protein (gp120) accelerated astrocyte Na+/H+exchange and that the resultant intracellular alkalinization activated a pH-sensitive K+conductance. The present experiments were conducted to determine whether gp120 affected human astrocytes in the same fashion. It was found that primary human astrocytes express a pH-sensitive K+conductance that was activated on intracellular alkalinization. Also, gp120 treatment of whole cell clamped human astrocytes activated this conductance specifically. Furthermore, gp120 inhibited glutamate uptake by primary human astrocytes. These altered physiological processes could contribute to pathophysiological changes in HIV-infected brains. Because the gp120-induced cell physiological changes were partially inhibited by dimethylamiloride (an inhibitor of Na+/H+exchange), our findings suggest that modification of human astrocyte Na+/H+exchange activity may provide a means of addressing some of the neurological complications of HIV infection.

Real-time epi-film thickness is measured by an Emission Fourier Transform Infrared Spectrometer (E/FT-IR). The E/FT-IR takes advantage of the heated wafer as the source of IR radiation. In our experiments, wafers were cleaned using in-situ ECR hydrogen plasma followed by film growth. The cleaning and deposition processes were monitored in real-time using the E/FT-IR technique. We have demonstrated the application of E/FT-IR for observing real-time growth rates and incubation times. Based on these real-time observations, the predeposition plasma cleaning process and the deposition process can be effectively monitored and controlled in real-time. Application of E/FT-IR in optimizing the predeposition hydrogen plasma cleaning process was demonstrated.

A multichamber single‐wafer chemical vapor deposition reactor has been designed and built for ultrahigh vacuum, low temperature, selective silicon epitaxy. The reactor is equipped with in situ monitors for study and control of both predeposition wafer cleaning and epitaxial growth process. A detailed description of the system and its preliminary performance are reported. An argon or helium plasma excited by electron cyclotron resonance (ECR) has been used for predeposition wafer cleaning. Results of the ECR plasma characterization by a Langmuir probe are presented. Furthermore, structural quality of the wafers subjected to plasma cleaning were evaluated by Rutherford backscattering spectroscopy and scanning electron microscopy. Results showed that a damage free substrate can potentially be achieved at a wafer temperature of 500 °C.

We report a case of papillary carcinoma of the duodenum combined with right renal carcinoma. A 58-year-old man underwent a physical examination that revealed intrahepatic and extrahepatic bile duct dilatation on B ultrasound. Intrahepatic bile duct dilatation could be seen on magnetic resonance imaging (MRI), but the head of the pancreas and distal bile duct showed no tumor signals, which led to a diagnosis of periampullary carcinoma and right renal carcinoma. Considering the trauma of pancreaticoduodenectomy combined with renal resection operation is greater, we carried out the laparoscopic right renal radical resection first, and then a pylorus-preserving pancreaticoduodenectomy was performed. However, postoperative intra-abdominal infections and bleeding occurred; our patient improved after vascular interventional microcoil embolization for the treatment of hemostasis. The second operation for celiac necrotic tissue elimination, jejunal fistulization and peritoneal lavage and drainage was performed 14 days latter. Our patient improved gradually and was discharged on the 58th postoperative day. There has been no tumor recurrence after a follow-up of 26 months.