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Biomedical subjects

D Jung

Publications and source records attributed to D Jung.

At least 37 records · Page 2Linked to original sources

Human Ku70 interacts with heterochromatin protein 1alpha.

Ku is involved in the metabolism of DNA ends, DNA repair, and the maintenance of telomeres. It consists of a heterodimer of 70- and 80-kDa subunits. Recently we have demonstrated that Ku70 interacted with TRF2, a mammalian telomere-binding protein. Using the same yeast two-hybrid screening system, we now show that Ku70 also interacts with heterochromatin protein 1alpha (HP1alpha), a protein known to be associated with telomeres as well as heterochromatin. HP1 is a suppressor of the position effect variegation in Drosophila and acts as a transcriptional suppressor in mammalian cells. The interaction with Ku70 in the two-hybrid system was confirmed by a glutathione S-transferase pull-down study using bacterial recombinant proteins in vitro. The interaction was also reproduced in vivo in HeLa cells, where endogenous Ku70 coimmunoprecipitated with HP1alpha. This interaction was more effective in acidic pH and weakened considerably as the pH of the reaction buffer was elevated up to 7.5. Ku80 did not interact with HP1alpha directly. The interaction domains of Ku70 and HP1alpha included the Leu-Ser repeat (amino acids 200-385) and the chromo shadow domain, respectively. Ku70 was largely colocalized with transfected HP1alpha but not with a C-terminal deletion mutant, HP1alpha(Delta)C. In contrast to HP1alpha, Ku70 did not repress transcriptional activity of the reporter gene when tethered to DNA after transfection to mammalian cells. The implication of this interaction is discussed.

Antigens, Nuclear↗

Acute effects of 200 ppm 1,1,1-trichloroethane on the human EEG.

OBJECTIVES: Even low concentrations of organic solvents used at work may cause acute effects on the human central nervous system. We investigated the acute effects of 200 ppm 1,1,1-trichloroethane on the human EEG. METHODS: 12 healthy subjects were exposed for 4 hours to 200 ppm and to 20 ppm (control) in an exposure chamber in a cross-over design. EEG was recorded before (reference) and at the end of each exposure with eyes closed and open and during the Color Word Stress test. Spectral power was calculated by Fast Fourier transformation and related to reference values (per cent of baseline). Subjective symptoms and effects of blinding with 20 ppm 1, 1,1-trichloroethane were assessed by questionnaire. RESULTS: Blinding was not effective because of the strong smell of 1,1, 1-trichloroethane. The score for tiredness increased slightly during and after exposure to 200 ppm. In the closed eye condition, the median percentage of spectral power increased at all electrodes of the delta -band, significantly at temporo-occipital leads. In the theta-band, the percentage of the median spectral power was elevated at most of the electrodes but the parietal and some temporal ones. As to the alpha subset1-band, the percentage of the median spectral power was lower at the temporo-parieto-occipital electrodes, yielding significance at T subset4. In the alpha subset2-band, the percentage of the median spectral power was lower at all electrodes, significantly at T subset4 and T subset5. The percentage of the median spectral power of the temporo-parieto-occipital electrodes of the beta subset1 -band was lower during exposure to 200 ppm. There were no clear-cut changes in the beta subset2 -band, in the open eye condition and during the Color Word Stress test. CONCLUSION: The changes in EEG and the increased score for tiredness indicate a slight sedative effect of 200 ppm 1,1,1-trichloroethane.

Adult↗

Changes in cellular proliferation rate of lymphocytes after long-distance flights as a possible risk for patients with HIV-infection.

OBJECTIVES: Several studies showed that long-distance flights can influence cellular immunity. This might be due to a cortisol- and catecholamin- induced change in immunity with an impairment of T-lymphocyte dependent cellular immunity and an enhancement of B-lymphocyte dependent humoral immunity. Similar results can be found in patients with HIV. It is also known that progress of this disease and affection of T-helper-cells by the virus are induced by stimulation of the immune system, a phenomenon that also occurs during long distance flights. Therefore, a possible interaction between long-distance flights and the progression of HIV-infection should be discussed. METHODS: Cell cultures of 22 subjects after long-distance flights with and without rapid time zone shifts and of 16 patients with HIV (stage 2 3) were investigated. Mononuclear blood cells were stimulated with different lectins in culture and proliferation was measured by incorporation of bromodesoxyuridine. Moreover, all cultures were titrated with chromate concentrations between 0 to 700 ng/ml to measure the tolerance of the cells against chromate (VI) in vitro as a marker of the functional efficiency of the cellular part of the immune system. Maximal proliferation rate and tolerance against chromate were compared in both groups. RESULTS: After long distance flights tolerance against chromate decreased significantly during the first 24 h after flight. After 48 h levels were similar to those 1 week after flights. The decrease was similar to the results found in the stage 2 group of HIV-patients, but by far less to the decrease in stage 3 patients. Maximal proliferation rate dropped significantly during the second day after arrival compared to 1-week control values. CONCLUSION: Changes in the cellular immune system in healthy subjects after long-distance flights have been similar to the results of patients with stage 2 of HIV-infection. Mechanisms of changes in both groups are comparable in influencing T-cell-induced immunity. This could point to an additive effect on cellular immunity of HIV-patients by long distance-flights. Rosen neopterin concentrations and increases of apoptotic T-cells in both groups support this assumption. Therefore, further studies are urgently needed to investigate the interactions between HIV-infection and long-distance flights.

Adolescent↗

Interaction of human Ku70 with TRF2.

Ku, a heterodimer of 70- and 80-kDa subunits, plays a general role in the metabolism of DNA ends in eukaryotic cells, including double-strand DNA break repair, V(D)J recombination, and maintenance of telomeres. We have utilized the yeast two-hybrid system to identify Ku70-interacting proteins other than Ku80. Two reactive clones were found to encode the dimerization domain of TRF2, a mammalian telomeric protein that binds to duplex TTAGGG repeats at chromosome ends. This interaction was confirmed using bacterial fusion proteins and co-immunoprecipitations from eukaryotic cells overexpressing TRF2. The transfected TFR2 colocalized with Ku70.

Animals↗

Characterization of the CD30L binding domain on the human CD30 molecule using anti-CD30 antibodies.

CD30 and its counter-receptor CD30 ligand (CD30L) are members of the TNF-receptor/TNFalpha superfamily and function to regulate lymphocyte survival and differentiation. Several monoclonal antibodies (MAbs) have been developed against CD30 and, based on mutual inhibition assays, are grouped into three nonoverlapping serologic clusters. However, the relationship between the epitopes recognized by the antibodies comprising each cluster and the binding domain for CD30L is not known. Using a soluble CD30L/CD8alpha chimeric protein, we assessed the ability of anti-CD30 MAb to inhibit the binding of CD30L to CD30 expressed by the CD30+ Karpas 299 cell line. CD30L binding by CD30 is blocked by MAb that recognize epitopes belonging to cluster Group A (like Ber-H2, Ber-H8, and HRS-4) as well as cluster Group C (like HeFi-1 and M44). Cluster Group B antibodies, including M67 and Ki-1, do not affect CD30L binding to CD30. The pattern of CD30L binding inhibition shows only limited correspondence to the functional capacity of some anti-CD30 MAb to trigger CD30 signaling. Finally, we demonstrate that the anti-CD30L MAb M81 also completely inhibits CD30/CD30L interaction. This information is useful for applying these MAbs in functional studies to further investigate the CD30/CD30L system and for designing assays for soluble CD30L.

Antibodies, Monoclonal↗

Saliva as an alternate for blood to measure concentrations of acetone under exposure to isopropanol.

OBJECTIVES: In occupational medicine, blood concentrations are often measured to judge the internal burden of workers at work-place during exposure to a potentially hazardous substance. However, blood-withdrawals are invasive and can often not be taken at work-place due to hygienic reasons. Sampling of saliva is non-invasive and easy to perform even at workplace. In order to substitute blood analysis, analysis of saliva has to be as specific and sensitive as blood investigations. Therefore acetone-concentrations in blood and in saliva during exposure to isopropanol were compared. METHODS: 18 healthy non-smokers were exposed to 360 ppm isopropanol in an exposure chamber over 4 h. Once an hour during exposure and 30 min after, blood and saliva were sampled. Saliva was collected by a cotton plug over 10 minutes and stored in an airtight closed headspace tube. Concentrations of the metabolite acetone were measured by gas chromatography. - RESULTS: The concentrations of acetone in blood and saliva rose continually during exposure and dropped after exposure-cessation. High correlations between concentrations of acetone in blood and saliva were found for each individual and the entire group (entire group: r = 0.8568, p <0.0001, y = 0.8374x - 0.4404). CONCLUSIONS: Acetone-measurement in saliva is a non-invasive, easily conductable and reliable method for estimating the internal burden of isopropanol-exposure. Further studies for the standardization and validation are necessary to impose a threshold limit value on work-place isopropanol-exposure.

2-Propanol↗

Overexpression of ptc1 inhibits induction of Shh target genes and prevents normal patterning in the neural tube.

Patched (Ptc) is a human tumor suppressor protein and a candidate receptor for Hedgehog (Hh) proteins, which regulate growth and patterning in embryos. Ptc represses expression of Hh target genes such as Gli1 and ptc1 itself. Localized secretion of Hh appears to induce transcription of target genes in specific patterns by binding to Ptc and preventing it from functioning in recipient cells. People who are heterozygous for PTC1 exhibit a range of developmental defects, suggesting that some genes are inappropriately expressed when there is not enough Ptc protein. To test the idea that a balance between Hh and Ptc activities is essential for normal development, we overexpressed Ptc in the neural tube. We find that excess Ptc is sufficient to inhibit expression of Gli1 and ptc1, suggesting that Sonic hedgehog (Shh) cannot signal effectively. This leads to partial dorsalization of the neural tube and a wide spectrum of neural defects, ranging from embryonic lethality to hydrocephaly.

Animals↗

Induction of immunogenicity of a human renal-cell carcinoma cell line by TAP1-gene transfer.

Reduced expression of the major-histocompatibility-complex(MHC)-class-I antigens has been demonstrated in renal-cell carcinoma (RCC), and appeared to be associated with deficiencies in the expression and function of different components of the MHC-class-I-antigen-processing pathway and poor recognition by cytotoxic T-lymphocytes (CTL). In order to investigate the role of peptide transporters for the immunogenic phenotype of RCC, tumor cells were stably transfected with the human TAP1A gene. While the TAP1 transfectants showed heterogeneous TAP1-transgene expression pattern of mRNA and protein, high TAP1 expression and a TAP-controlled increase in MHC-class-I surface expression could be achieved in selected transfectants. IFN-gamma up-regulates the expression of MHC-class-I antigens and TAP1 both in control and in TAP1-transfected RCC cells to a similar level. No additive effect of TAP1 over-expression was observed in TAP1 transfectants. Although no enhanced CTL-mediated lysis was obtained, cytokine release was substantially increased in response to TAP1-transfected RCC cells, but not to control cells. Furthermore, TAP1 transfectants were able to stimulate the proliferation of allogeneic T cells. These studies suggest that abnormalities of MHC-class-I surface expression due to dysfunctional peptide transporters contribute to the immune escape phenotype of RCC cells and that the immune tolerance of RCC could be altered by TAP1-gene transfer.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

The pharmacokinetics and safety profile of oral ganciclovir in combination with trimethoprim in HIV- and CMV-seropositive patients.

AIMS: We investigated the pharmacokinetics and safety profile of oral ganciclovir coadministered with trimethoprim in HIV-and CMV-seropositive patients. METHODS: In an open-label, randomized, 3-way crossover study, 12 adult males received oral ganciclovir 1000 mg every 8h, oral trimethoprim 200 mg once daily, or both drugs concomitantly in a sequence of three 7-day treatment periods. Pharmacokinetic parameters were determined and adverse events recorded for each treatment. RESULTS: The presence of trimethoprim significantly decreased CLr (12.9%, P=0.0068) and increased t1/2 (18.1%, P=0.0378) of ganciclovir. However, these changes are unlikely to be clinically meaningful. There were no statistically significant changes in trimethoprim pharmacokinetic parameters in the presence of ganciclovir, with the exception of a 12.7% increase in Cmin. Ganciclovir was well tolerated when administered alone or in combination with trimethoprin. CONCLUSIONS: There was no clinically significant pharmacokinetic interaction between oral ganciclovir and trimethoprim when coadministered.

Administration, Oral↗

Gene transfer of the Co-stimulatory molecules B7-1 and B7-2 enhances the immunogenicity of human renal cell carcinoma to a different extent.

Stimulation of a specific antitumour immune response with recruitment and induction of T-cell effector functions represents an attractive concept in human cancer therapy. Different cytokines and the B7 co-stimulatory molecules are both able to provide proliferation and activation signals for T cells. In the present study, we first demonstrated the absence of both B7-1 and B7-2 expression in human renal cell carcinoma (RCC) cell lines. The lack of B7 expression was associated with a low or absent proliferative response of allogeneic and autologous T cells upon stimulation with tumour cells. In order to investigate the role of B7-1 and B7-2, the human RCC cell line, MZ1257RC, which expresses normal levels of adhesion molecules and major histocompatibility complex (MHC) class I surface antigens, was transfected with B7-1 and B7-2 expression vectors, respectively. The B7-1- and B7-2-transduced MZ1257RC cells were potent stimulators of allogeneic and autologous T-cell proliferation. B7-2 transfectants were approximately two- to threefold more effective in the induction of primary T-cell activation than B7-1-transduced cells. Interleukin (IL)-12 synergized with the B7/CD28 interaction to enhance allogeneic T-cell proliferation, independently of the B7 molecule transduced. In contrast, IL-2 only co-operatively increased T-cell activation in the presence of B7-2. Our results suggest the following: first, that co-stimulatory molecules are required for efficient T-cell responses directed against RCC; second, that B7-2 appears to be a more potent stimulator of tumour immunity as compared to B7-1; and third, that B7 molecules selectively co-operate with different T-cell stimulatory cytokines. The different activity of B7-1 and B7-2 molecules on the immunogenicity of RCC will have implications for the development and optimization of RCC-specific cancer vaccines.

Antigens, CD↗

Treatment of human immunodeficiency virus 1-infected infants and children with the protease inhibitor nelfinavir mesylate.

An open-label study was conducted of nelfinavir mesylate, given with reverse transcriptase inhibitors to human immunodeficiency virus 1 (HIV-1)-infected infants and children 3 months to 13 years of age. Doses of nelfinavir mesylate of 20-30 mg/kg yielded drug exposures comparable to those seen in adults. The drug was well tolerated; mild diarrhea was the primary toxic effect observed. Seventy-one percent (39) of the 55 evaluable subjects had an initial decrease in plasma HIV-1 RNA, of at least 0.7 log10 copies/mL; suppression of plasma HIV-1 RNA levels to < 400 copies/mL was observed in 15. Children who began taking at least one new reverse transcriptase inhibitor near the time when nelfinavir mesylate was started, and those with a > or = 24% proportion of CD4 lymphocytes, had a greater chance of achieving and maintaining a decline in plasma HIV-1 RNA to < 400 copies/mL. Suppression of viremia was achieved in children as young as 3 months of age.

Adolescent↗

Increased risk of sensory neuropathy in workers with chloracne after exposure to 2,3,7,8-polychlorinated dioxins and furans.

OBJECTIVE: The existence of a peripheral neuropathy after exposure to polychlorinated dioxins (PCDD) is still discussed, as studies concerning dioxin effects on the peripheral nervous system are rare and contradictory. MATERIAL AND METHODS: Clinical and neurophysiological examinations (motor conduction velocity of the peroneal nerve, sensory conduction velocities of the sural and ulnar nerves) were made in 156 dioxin exposed workers (42 with, 114 without cloracne) from one pesticide producing plant. Because of known risk factors for peripheral neuropathy, 7 workers with and 28 without cloracne were excluded from further analysis. RESULTS: Workers with chloracne had a significantly higher exposure against PCDD as documented by back calculated lipid levels. They complained significantly more often of sexual impotence (28.6% compared to 5.8% of workers without chloracne, P<0.001), had significantly more frequent clinical signs of a sensory neuropathy (= abnormal sensory findings plus deep tendon reflex abnormalities) restricted to the legs (17.1% compared to 1.2%, P<0.001), had significantly more frequent > or =2 neurophysiologic abnormalities (34.3% compared to 14.0%, P<0.025), and had significantly lower mean amplitudes of the motor compound muscle potential of the peroneal nerve. CONCLUSION: PCDD has a mild toxic effect on the peripheral nervous system manifesting as mild sensory neuropathy of the legs in a minority of the most severely exposed persons.

Acne Vulgaris↗

Effect of food on high-dose oral ganciclovir disposition in HIV-positive subjects.

The effect of food on the steady-state pharmacokinetics of ganciclovir following high-dose oral ganciclovir in HIV- and CMV-seropositive subjects was investigated in an open-label, randomized, two-treatment crossover study. Over 2 consecutive weeks, subjects received in random order multiple oral doses of ganciclovir 2,000 mg tid for 3 consecutive days either on an "empty stomach " (i.e., at least 1 hour before or 2 hours after a meal or snack) or within 30 minutes of finishing a meal. For the 3 days of dosing each week, the breakfast consisted of a standardized 602 calorie, high-fat (46.5%) meal, while the contents of lunch, dinner, and snacks met American Dietetic Association recommendations (25%-35% fat). Serial blood samples over 24 hours were obtained on day 3 of each regimen over the first dosing interval. When ganciclovir was administered within 30 minutes following the breakfast, there was a mean increase of 110.6% +/- 79.0% and 114.1% +/- 81.7% in Cmax0-5 and AUC0-5, respectively, with a prolongation of mean Tmax from 1.8 to 2.7 hours. Over the total day of dosing, there was a mean increase of 47.6% +/- 12.3% and 97.2% +/- 30.9% in Cmax0-24 and AUC0-24, respectively, and a 36.0% +/- 18.0% decrease in half-life when doses were taken following a meal as compared to when taken on an empty stomach. Since food increases the systemic availability of ganciclovir, it is recommended that patients be instructed to take each dose of ganciclovir with food.

Administration, Oral↗

Single-dose pharmacokinetics of valganciclovir in HIV- and CMV-seropositive subjects.

As a result of the low oral bioavailability of ganciclovir, a prodrug was developed to improve the bioavailability of ganciclovir. This study was designed to investigate the fasting, single-dose pharmacokinetics as well as the absolute and relative bioavailability of a valine ester prodrug of ganciclovir, valganciclovir, as compared to oral and intravenous ganciclovir in asymptomatic HIV+ and CMV+ subjects. In this open-label, randomized, three-period crossover study, 18 subjects received, in random order, single oral doses of valganciclovir 360 mg and ganciclovir 1000 mg and an intravenous infusion of ganciclovir 5 mg/kg over 1 hour. Valganciclovir was rapidly and extensively hydrolyzed to ganciclovir, resulting in significantly greater bioavailability compared to 1000 mg oral ganciclovir (60.9% vs. 5.6%, respectively). Higher peak serum concentrations were reached earlier following valganciclovir (ganciclovir [2.98 +/- 0.77 micrograms/mL at 1.0 +/- 0.3 h]) than following oral ganciclovir (0.47 +/- 0.17 microgram/mL and 2.2 +/- 1.0 h). Mean total ganciclovir AUCs following oral ganciclovir (1000 mg) and 360 mg valganciclovir (3.8 +/- 1.2 and 10.8 +/- 1.9 micrograms-h/mL) were less than that following a standard 5 mg/kg intravenous infusion of ganciclovir (25.1 +/- 3.8 micrograms-h/mL). In summary, valganciclovir is a prodrug with a favorable safety profile with enhanced bioavailability and significantly higher serum concentrations of ganciclovir than following oral administration of ganciclovir itself.

Adult↗

The pharmacokinetics and safety profile of oral ganciclovir combined with zalcitabine or stavudine in asymptomatic HIV- and CMV-seropositive patients.

Two open-label, randomized, multiple-dose, three-way crossover studies were performed to assess the pharmacokinetics and safety of oral ganciclovir 1000 mg q8h in asymptomatic patients seropositive for human immunodeficiency virus and cytomegalovirus. Ganciclovir was administered alone and in combination with zalcitabine 0.75 mg q8h (study 1) or stavudine 40 mg q12h (study 2). In the presence of zalcitabine, the only statistically significant change in the pharmacokinetic parameters of ganciclovir was a 22.2% mean increase in AUC0-8. However, there was no significant change in the renal clearance of ganciclovir when coadministered with zalcitabine, suggesting that the increase in serum ganciclovir concentration cannot be attributed to competition for active renal tubular secretion. No change in zalcitabine pharmacokinetics was observed in combination with ganciclovir. There were no significant changes in the pharmacokinetics of ganciclovir or stavudine when coadministered. Ganciclovir was well tolerated when given alone and in combination with either zalcitabine or stavudine.

Administration, Oral↗

[Time zone shift and the immune system during long-distance flights].

Recurrent infections could be seen in frequent flyers indicating an impaired immune reaction after long-distance flights. The increase of the concentration of neopterin points to an activation of the cellular part of the immune system. In combination with the altered differential blood counts, the changes in the proliferation rate of lymphocytes and the immune phenotyping the increase of neopterin leads to an explanation of the down-regulation of the immune system after flights. The mild hypoxia on board of an aircraft triggers an increase of catecholamines and cortisol in serum. Catecholamines lead to a shift of leukocytes from different compartments to the circulating blood and to an activation of immune cells. Cortisol triggers the differentiation of a subgroup of T-Lymphocytes with a rise in TH2-helper cells and a down-regulation of TH1-cells. The latter ones are, however, essential for an induction of a reaction of the cellular immune system and so the function of the cellular part of the immune system will be reduced. If no infection occurs, the concentration of neopterin in serum will drop to normal.

Aerospace Medicine↗

[Time zone shifts and jet lag after long-distance flights].

Long distance flights with rapid time zone shifts of more than 3 hours lead to a dissociation of the inner circadian clock to the outer pacer. Additionally, the different endogenous circadian rhythms will not longer be synchronized by the endogenous pacer melatonin. This leads to complaints like sleepiness, sleep-disturbances and others. These symptoms are called jet-lag. The subject's performance is disturbed, as well. Different studies showed smaller problems with jet lag when travelling to the west. Since the inner circadian rhythm tends to be 24 up to 26 hours, travelling to the west with a prolongation of the daylight will be tolerated better than flights to the east with a shortening of the day length. Rapid time zone shifts with more than 8 hours to the east lead to individual different ways of resynchronization. Subject either try to adapt to the new time zone by shortening the day (backward adaptation) or they resynchronize forward with a longer duration of adaptation time. Elder subjects with already diminished circadian hormonal rhythm often get more problems concerning symptoms of the jet-lag and in time to recover from the disturbance of the inner clock. No differences can be found between business travelers, tourists and high-performance sportsmen. After flights to the west within 3 to 7 days, most of our inner circadian rhythm will be re-synchronized. After flights to the east, resynchronization can take 5 to 14 days. A symptomatic therapy of jet lag symptoms with a short-acting benzodiazepine like triazolam in a dosage of 12.5 mg or less is well tolerated. A therapy with oral melatonin in a dosage of 0.5 to 5 mg/day given in the evening 1 to 2 hours prior to the desired sleeping-time may be helpful for a group of subjects. Another group of subjects will not have any benefit of a therapy with melatonin, but cannot be defined in advance. A recommendation for a therapy with melatonin to treat jet lag symptoms cannot be given at the moment, since scientific data are still missing. Additionally, the same contaminants, which caused some deaths, as in the related substance tryptophan has been found in some tablets of melatonin.

Aircraft↗

Central neuronal synapse formation on micropatterned surfaces.

Controlling synapse formation is a key to patterning of neurons into functional circuits and networks in vitro. However, the process of synapse formation among neurons grown on artificial surfaces is relatively unstudied. We cultured embryonic hippocampal cells on trimethoxysilylpropyl-diethylenetriamine (DETA) and tridecafluoro-1, 1,2,2-tetrahydrooctyl-1-dimethylchlorosilane (13F), and on patterns composed of DETA lines separated by 13F spaces. For comparison, neurons were concurrently plated on surfaces coated with uniform poly-d-lysine (PDL). Pre- and postsynaptic specializations were identified by immunostaining for synapsin I and microtubule-associated protein-2 (MAP-2). Spontaneous (SPCs) and evoked (EPCs) postsynaptic currents were recorded using dual patch-clamp techniques. We found that DETA promoted synapse formation, whereas evidence for synapse formation on 13F was barely detected. MAP-2+ neuronal soma and rapidly growing dendrites were co-localized with synapsin I puncta faithfully along DETA lines. The expression of synapsin I puncta, and MAP-2+ soma and dendrites correlated well with the appearance of SPCs. Synapsin I, MAP-2 and SPCs emerged together at days 3-4 and increased at day 7, when EPCs appeared. Synaptic signals occurring during 4-7 days in culture were all GABAergic. These results indicate that fully functional synapses are formed on silane surfaces, demonstrating the suitability of patterned silane surfaces for organizing synapse formation in vitro.

Animals↗