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Effects of total fasting in obese women. I. Response of the thyroid.

The values of serum T4, T3, T4/T3, RT3U, FT4I, PBI, ATR, TSH, 132I uptake and antibodies against thyreoglobulin were estimated in non-obese, healthy women and in obese women with a stabile body weight on total fasting of 14 days. Obesity with no dietary restriction compared with normal controls was accompanied by a tendency to higher serum levels of T4 and T3 and prolonged ATR. Other indicators of thyroid function remained unchanged. Total fasting led to a decrease of serum T3 and to an increase of FT4I and RT3U. The remaining tests were unchanged. These results are conform with a decreased transformation of T4 into T3 in the periphery. The participation of the hypothalamus and hypophysis to adaptation of the thyroid to fasting was discussed.

Fasting↗

Quadriceps mediated changes in soleus motoneuron excitability.

In an effort to investigate the interactions of the quadriceps and soleus muscles, the isometric force-time curve of the Achilles tendon-tap reflex (ATR) was measured in 10 college age subjects. The tendon-jerk was conditioned with a tap to the ipsilateral or contralateral patellar tendon, or by an electrocutaneous (3x perception) stimulus applied to the belly of the quadriceps. The conditioning stimulus preceded the test ATR by 25, 40, 55, 70, 85, 100, 115, 130 or 145 ms. The results indicated that the ipsilateral conditioning tendon-tap produced a wave of short-latency facilitation (40 ms) and long-latency inhibition (85-130 ms) to the triceps surae muscles. The ipsilateral cutaneous conditioning, however, did not alter reflex excitability. A contralateral conditioning to the patellar tendon again produced short-latency (50-70 ms) facilitation, whereas the electrocutaneous stimulus did not alter motoneuron excitability. Moreover, a barrage of electrocutaneous impulses to either the ipsilateral or contralateral quadriceps (1 minute/60 pps) did not significantly alter motoneuron excitability of the soleus muscle. These results indicate that motoneuron excitability changes are observed in the soleus muscle with mechanical conditioning but not with electrocutaneous conditioning. Several neurophysiological mechanisms are proposed to mediate these changes.

Achilles Tendon↗

Edrophonium is better than neostigmine to antagonize residual vecuronium induced neuromuscular block.

Edrophonium (EDR) has the advantages of a quick onset of action and reduced cholinergic effects compared to neostigmine (NST) when they are used to antagonize neuromuscular block (NMB). There are few studies about antagonism of very weak residual NMB. Therefore we compared hemodynamic stability, train-of-four (TOF) characteristics and reversal time (time from administration of antagonists to train-of-four-ratio (TR) at least 0.70) of EDR 0.5 mg kg-1 + atropine (ATR) 0.007 mg kg-1 to NST 0.04 mg kg-1 + glycopyrrolate (GLY) 0.008 mg kg-1 when they were used to antagonize a residual vecuronium (VEC)-induced NMB (T1 25-75%). The NMB was monitored in 64 patients using the evoked electromyogram of the hypothenar muscle of the hand. An adequate antagonism was defined as a TR of 0.70 or higher. Heart rate was significantly higher in NST+GLY group 2 min after administration of the antagonists in comparison with the EDR+ATR group. The advantages of EDR (higher T1, TR and percentage of patients with an adequate recovery) were obvious during the first 5 min of reversal time. Therefore we conclude, that under the conditions described in the present study, EDR antagonizes residual VEC induced NMB faster than NST.

Adult↗

Cholinergic-opioid interactions at brainstem respiratory chemosensitive areas in cats.

Central respiratory chemosensitivity has been ascribed to CO2-sensitive neurons located on the ventral brainstem surface. The effects of cholinergic mechanisms on CO2-sensitive neuronal activity recorded extracellularly at the brainstem respiratory chemosensitive area at the caudal ventral medullary surface (cVMS) were investigated in cats (n = 14) anesthetized with chloralose-urethane. The neurons increased their firing rate from 10.4 +/- 1.6 Hz to 33.9 +/- 5.2 Hz when the mock cerebrospinal fluid (mCSF) superfusing buffer solution was changed from pH 7.4 (control) to pH 7.0 (acidic). Atropine (ATR) applied topically to the cVMS depressed the H(+)-ion-induced increase in neuronal frequency from 32.8 +/- 4.8 Hz to 13.4 +/- 2.2 Hz. ATR also depressed the inspired-CO2-induced increase in neuronal activity from 33.2 +/- 8.3 Hz to 18.9 +/- 4.9 Hz, suggesting the possibility of a muscarinic cholinergic involvement in cVMS neuronal responses to changes in PCO2 and mCSF-pH. Acetylcholine (ACh) increased the activity of cVMS CO2-sensitive neurons by 237.5% +/- 34.9%, and naloxone applied topically to the cVMS augmented the ACh responsiveness to 338.6% +/- 52.7%. Physostigmine (PHY) increased neuronal activity by 254.3% +/- 42.9%, and this increase was augmented to 435.4% +/- 61.2% by naloxone. Although responses of the CO2-sensitive neurons to PHY were biphasic, the depressant phase failed to appear whenever the cVMS was pretreated with naloxone. Naloxone also augmented the responsiveness of cVMS neurons to increased H+ ion superfusion. These findings suggest that the endogenous opiates may be involved in the central regulation of respiration by interaction with CO2-sensitive cholinergic structures at the cVMS.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

X-linked alpha-thalassemia/mental retardation syndrome. Linkage analysis in a new family further supports localization in proximal Xq.

Linkage analysis was performed in a three generation family with three males affected by the recently delineated X-linked form of alpha-thalassemia/mental retardation syndrome (ATR-X). Results are in agreement with the linkage study reported by Gibbons et al in 1992 and further confirm that the ATR-X gene is located in proximal Xq. Positive LOD scores were obtained for several markers situated in the pericentromeric region. A maximum LOD score of 2.09 at a recombination fraction of 0 was obtained for DXS453 located at the boundary q12-q13.1. The nearest flanking loci demonstrating recombination with the disease locus were AR at Xq11.2-q12 on the centromeric side and DXS72 at Xq21.1 on the telomeric side. Consequently the authors were able to reduce the previously defined candidate region for the gene location. Their results are compatible with a distal boundary at Xq21.1 instead of q21.31.

Chromosome Mapping↗

[Acute promyelocytic leukemia. The therapeutic advances].

Acute promyelocytic leukemia (APL) is a rare subtype of acute myelogenous leukemia. It is frequently associated with a life-threatening hemorrhagic diathesis, often aggravated by induction cytotoxic chemotherapy. Patients with APL have bone marrow infiltration by abnormal promyelocytes, usually with prominent cytoplasmic granulation. These patients have a unique cytogenetic abnormality, a balanced reciprocal translocation between the long arms of chromosomes 15 and 17. The nuclear retinoic acid receptor alpha gene, on chromosome 17, is translocated to the PML gene region, on chromosome 15, resulting in the synthesis of two fusion messenger ribonucleic acids, PML/RAR-alpha and RAR-alpha/PML, easily detected by the reverse transcriptase polymerase chain reaction. This assay is extremely useful in the diagnosis and detection of minimal residual disease in APL patients. All trans-retinoic acid (ATR) differentiates the malignant cell clone and corrects the coagulopathy associated with this disease. The most important adverse effect is a respiratory distress syndrome, treatable with steroids, if detected at its onset. ATR yields durable remissions in patients with APL, after consolidation with cytotoxic chemotherapy.

Adolescent↗

Influence of quadriceps conditioning on soleus motoneuron excitability in young and old adults.

In an effort to investigate neuromuscular changes with age, the isometric force-time curve of the Achilles tendon-tap reflex (ATR) was measured in 10 college age (M = 20.9 yr) and 10 healthy active old subjects (M = 74.3 yr). In an effort to investigate spinal interneuronal pathways, the tendon-jerk was also conditioned with a tap to the ipsilateral or contralateral patellar tendon. The conditioning stimulus preceded the ATR by 25, 40, 55, 70, 85, 100, 115, 130, or 145 ms. Three trials were elicited at each conditioning interval plus three unilateral trials, for 30 trials per experimental session. Results indicated that the force production of the unilateral Achilles tendon-tap reflex was significantly reduced and the half-relaxation times were significantly lengthened in the old subjects. Moreover, ipsilateral conditioning produced short-latency facilitation and long-latency inhibition to the triceps surae in young subjects, whereas the same conditioning produced only a delayed long-latency inhibition in the old subjects. Similarly, the contralateral conditioning produced short-latency facilitation in the young subjects, with no changes observed in the old subjects. It is concluded that unilateral Achilles tendon-tap responses are different for the two groups, and that the reflex recovery profiles for the two groups are different. Several neurophysiological mechanisms are proposed to contribute to these differences.

Achilles Tendon↗

The Schizosaccharomyces pombe rad3 checkpoint gene.

The rad3 gene of Schizosaccharomyces pombe is required for checkpoint pathways that respond to DNA damage and replication blocks. We report the complete rad3 gene sequence and show that rad3 is the homologue of Saccharomyces cerevisiae ESR1 (MEC1/SAD3) and Drosophila melanogaster mei-41 checkpoint genes. This establishes Rad3/Mec1 as the only conserved protein which is required for all the DNA structure checkpoints in both yeast model systems. Rad3 is an inessential member of the 'lipid kinase' subclass of kinases which includes the ATM protein defective in ataxia telangiectasia patients. Mutational analysis indicates that the kinase domain is required for Rad3 function, and immunoprecipitation of overexpressed Rad3 demonstrates an associated protein kinase activity. The previous observation that rad3 mutations can be rescued by a truncated clone lacking the kinase domain may be due to intragenic complementation. Consistent with this, biochemical data suggest that Rad3 exists in a complex containing multiple copies of Rad3. We have identified a novel human gene (ATR) whose product is closely related to Rad3/Esr1p/Mei-41. ATR can functionally complement esr1-1 radiation sensitivity in S. cerevisiae. Together, the structural conservation and functional complementation suggest strongly that the mechanisms underlying the DNA structure checkpoints are conserved throughout evolution.

Adenosine Triphosphatases↗

Inhibition of phosphoinositide 3-kinase related kinases by the radiosensitizing agent wortmannin.

Members of the phosphatidylinositol-3 kinase related kinase (PIKK) family function in both cell cycle progression and DNA damage-induced cell cycle checkpoints. The fungal metabolite, wortmannin, is an effective radiosensitizer that irreversibly inhibits certain members of the PIKK family. Based on their roles in DNA damage responses, several PIKKs, DNA-dependent protein kinase (DNA-PK), ataxia telangiectasia mutated (ATM) and the ataxia- and Rad3-related protein (ATR), are potential targets for the radiosensitizing effect of wortmannin. In this report, we demonstrate that wortmannin is a relatively potent inhibitor of DNA-PK (IC50, 16 nM) and ATM (IC50, 150 nM) activities, whereas ATR activity is significantly less sensitive to this drug (IC50, 1.8 microM). In intact A549 lung adenocarcinoma cells, wortmannin inhibited both DNA-PK and ATM at concentrations that correlated closely with those required for radiosensitization. Furthermore, pretreatment of A549 cells with wortmannin resulted in radioresistant DNA synthesis, a characteristic abnormality of ATM-deficient cells. These results identify wortmannin as an inhibitor of ATM activity and suggest that ATM and DNA-PK are relevant targets for the radiosensitizing effect of this drug in cancer cells.

Adenocarcinoma↗

Effects of M1 and M2 receptor agonists and blockers on dog respiration.

AIM: To study the effects of M1 and M2 receptor agonists and blockers on dog respiration. METHODS: Using thoracic respiratory transducer and RM-86 multipurpose polygraph to determine respiratory rate (RR), tidal volume (TV), and minute ventilation volume (MVV), and DH-100G blood gas analysis instrument to analyze pO2, pCO2 and pH. RESULTS: Pilocarpine (Pil, an M1-R subtype agonist) 0.5, 1, and 2 mg.kg-1 iv caused increases in RR, MVV, and pO2, and a decrease in pCO2. The excitatory effects of Pil were antagonized by pretreatment with pirenzepine (Pir, 3 mg.kg-1, iv) and scopolamine (Sco, 2 mg.kg-1, iv). The iv injections of a novel M2-R subtype agonist, 6 beta-acetoxy nortropane (6 beta-AN) 2, 5, and 20 micrograms.kg-1 caused decreases in RR, MVV, and pO2 and an increase of pCO2. The actions of 6 beta-AN were antagonized by iv pretreatment with AF-DX116 ¿11-2 [[2-[(diethylamino)methyl]-1-piperidinyl] acetyl]-5, 11-dihydro-6H[2,3-b][1,4]benzodiazepine-6-one, 0.5 mg.kg-1¿ and atropine (Atr, 2 mg.kg-1). Similar results were obtained when smaller doses of Pil (0.2, 0.4, and 0.8 mg.kg-1) and 6 beta-AN (0.25, 0.5, and 1 microgram.kg-1) were injected into the vertebral artery. Pir and Sco also antagonized the excitatory effects of Pil, and AF-DX116 and Atr antagonized the inhibitory effects of 6 beta-AN on respiration. CONCLUSION: Stimulating M1-R of the respiratory center caused excitation of the respiration while stimulating the M2-R subtype caused inhibition of the respiration.

Animals↗

The effect of strain state on the biostability of a poly(etherurethane urea) elastomer.

The effect of deformation state on degradation of a PEUU without added stabilizers was examined in an oxidative environment that simulates the in vivo biodegradation of the polymer. Polymer tubes were stressed uniaxially and biaxially over glass mandrels and treated in 20% hydrogen peroxide/0.1 M cobalt chloride solution for 12 days at 37 degrees C. The amount of degradation was determined from the ATR-FTIR peak height of the amorphous aliphatic ether absorbance at 1110 cm-1. If a uniaxial stress was applied, degradation was inhibited and the amount of surface ether remaining after treatment increased linearly with strain. If the stress was biaxial, the amount of degradation was not reduced unless the strain was greater than 200%. Decreased degradation correlated with the amount of soft-segment orientation. The decreased degradation rate was attributed to compaction of the polyether phase by orientation, which resulted in lower permeability to oxidative agents, particularly oxygen. Macroscopic damage was confined to a thin peeling surface layer if the stress was uniaxial. In comparison, biaxially stressed PEUU ruptured.

Biocompatible Materials↗

In vivo biocompatibility and biostability of modified polyurethanes.

Modified segmented polyurethanes were examined for biostability and biocompatibility using an in vivo cage implant system for time intervals of 1, 2, 3, 5, and 10 weeks. Two types of materials were used: polyether polyurethanes and polycarbonate polyurethanes. Two unmodified polyether polyurethanes (PEUU A' and SPU-PRM), one PDMS endcapped polyether polyurethane (SPU-S), and two polycarbonate polyurethanes (SPU-PCU and SPU-C) were investigated in this study. Techniques used to characterize untreated materials were dynamic water contact angle, stress-strain analysis, and gel permeation chromatography. Cellular response was measured by exudate analysis and by macrophage and foreign body giant cell (FBGC) densities. Material characterization, postimplantation, was done by attenuated total reflectance-Fourier transform infrared spectroscopy (ATR-FTIR) in order to quantify biodegradation and scanning electron microscopy (SEM) to qualitatively describe the cellular response and biodegradation. The exudate analysis showed that the acute and chronic inflammatory responses for all materials were similar. Lower FBGC densities and cell coverage on SPU-S were attributed to the hydrophobic surface provided by the PDMS endgroups. The polycarbonate polyurethanes did not show any significant differences in cell coverage or FBGC densities even though the macrophage densities were slightly lower compared to polyether polyurethanes. By 10 weeks, biodegradation in the case of PEUU A' and SPU-PRM was extensive as compared to SPU-S because the PDMS endcaps of SPU-S provided a shield against the oxygen radicals secreted by macrophages and FBGCs and lowered the rate of biodegradation. In the case of polycarbonate polyurethanes, the oxidative stability of the carbonate linkage lowered the rate of biodegradation tremendously as compared to the polyether polyurethanes (including SPU-S). The minor amount of biodegradation seen in polycarbonate polyurethanes at 10 weeks was attributed to hydrolysis of the carbonate linkage.

Animals↗

Heterobifunctional membranes by plasma induced graft polymerization as an artificial organ for penetration keratoprosthesis.

Highly biocompatible polymer membrane was developed for an artificial cornea in this surface modification study. Heterobifunctional silicone rubber membranes (hetero-SR) were prepared by grafting different functional polymers on each side of a silicone rubber membrane (SR). A novel type of bifunctional membrane was developed with the upper-side favoring cell attachment and growth, and the lower-side suppressing cell adhesion. The preparation of heterobifunctional membranes, characterization of polymer membrane surface properties such as ATR-FTIR and ESCA and contact angle, and biological analysis (in vitro and in vivo studies) were investigated in this work. Based on the biological analysis, the heterobifunctional membrane displays promising potential for use as an artificial cornea.

Adsorption↗

Prevention of calcification of glutaraldehyde-crosslinked porcine aortic cusps by ethanol preincubation: mechanistic studies of protein structure and water-biomaterial relationships.

Clinical usage of bioprosthetic heart valves (BPHVs) fabricated from glutaraldehyde-pretreated porcine aortic valves is restricted due to calcification-related failure. We previously reported a highly efficacious ethanol pretreatment of BPHVs for the prevention of cuspal calcification. The aim of the present study is to extend our understanding of the material changes brought about by ethanol and the relationship of these material effects to the ethanol pretreatment anticalcification mechanism. Glutaraldehyde-crosslinked porcine aortic valve cusps (control and ethanol-pretreated) were studied for the effects of ethanol on tissue water content and for spin-lattice relaxation times (T1) using solid state proton NMR. Cusp samples were studied for protein conformational changes due to ethanol by ATR-FTIR spectroscopy. The changes in cuspal tissue-cholesterol (in vitro) interactions also were studied. Cusp material stability was assessed in terms of residual glutaraldehyde content and collagenase degradation. Water content of the cusp samples was decreased significantly due to ethanol pretreatment. The cuspal collagen conformational changes (per infrared spectroscopy) brought about by ethanol pretreatment were persistent even after rat subdermal implantation of cusp samples for 7 days. In vitro cholesterol uptake by cusps was greatly reduced as a result of ethanol pretreatment. Ethanol pretreatment of cusps also resulted in increased resistance to collagenase digestion. Cuspal glutaraldehyde content was not changed by ethanol pretreatment. We conclude that ethanol pretreatment of bioprosthetic heart valve cusps causes multi-component effects on the tissue/material and macromolecular characteristics, which partly may explain the ethanol-pretreatment anticalcification mechanism.

Animals↗

Inhibition of aortic wall calcification in bioprosthetic heart valves by ethanol pretreatment: biochemical and biophysical mechanisms.

The effectiveness of ethanol pretreatment on preventing calcification of glutaraldehyde-fixed porcine aortic bioprosthetic heart valve (BPHV) cusps was previously demonstrated, and the mechanism of action of ethanol was attributed in part to both lipid removal and a specific collagen conformational change. In the present work, the effect of ethanol pretreatment on BPHV aortic wall calcification was investigated using both rat subdermal and sheep circulatory implants. Ethanol pretreatment significantly inhibited calcification of BPHV aortic wall, but with less than complete inhibition. The maximum inhibition of calcification of BPHV aortic wall was achieved using an 80% ethanol pretreatment; calcium levels were 71.80+/-8.45 microg/mg with 80% ethanol pretreatment compared to the control calcium level of 129.90+/-7.24 microg/mg (p = 0.001). Increasing the duration of ethanol exposure did not significantly improve the inhibitory effect of ethanol on aortic wall calcification. In the sheep circulatory implants, ethanol pretreatment partly prevented BPHV aortic wall calcification with a calcium level of 28.02+/-4.42 microg/mg compared to the control calcium level of 56.35+/-6.14 microg/mg (p = 0.004). Infrared spectroscopy (ATR-FTIR) studies of ethanol-pretreated BPHV aortic wall (vs. control) demonstrated a significant change in protein structure due to ethanol pretreatment. The water content of the aortic wall tissue and the spin-lattice relaxation times (T1) as assessed by proton nuclear magnetic resonance spectroscopy did not change significantly owing to ethanol pretreatment. The optimum condition of 80% ethanol pretreatment almost completely extracted both phospholipids and cholesterol from the aortic wall; despite this, significant calcification occurred. In conclusion, these results clearly demonstrate that ethanol pretreatment is significantly but only partially effective for inhibition of calcification of BPHV aortic wall and this effect may be due in part to lipid extraction and protein structure changes caused by ethanol. It is hypothesized that ethanol pretreatment may be of benefit for preventing bioprosthetic aortic wall calcification only in synergistic combination with another agent.

Animals↗

Synergistic effects of oxidative environments and mechanical stress on in vitro stability of polyetherurethanes and polycarbonateurethanes.

The in vitro structural stability of polyetherurethanes (PEUs) and polycarbonateurethanes (PCUs and PCUUs) was examined under strong oxidative conditions (0.5N HNO3, pH 0.3; and NaClO, 4% Cl2 available, pH approximately 13) and in the presence of a constant strain state. Solvent-cast dog-bone shaped specimens were strained at 100% uniaxial elongation over extension devices and completely immersed in the oxidative solutions at 50 degrees C for 15 days. Unstrained polyurethane (PU) samples were treated in the same way for comparison. The modification of the PU molecular structure was determined by DSC, GPC, ATR-FTIR, static contact angle, and surface roughness analyses. The incubation in nitric acid and sodium hypochlorite brought about a greater degradation of samples tested under the applied strain with the exception of PEU treated with nitric acid. PEU was the most affected material, showing bulk deterioration in NaClO and significant modifications in nitric acid, with the appearance of new IR bands, which were assigned to oxidation products. A higher phase separation between soft and hard domains occurred in PCUs upon incubation in nitric acid, the treatment with NaClO gave rise to new bands in the IR spectra, denoting the presence of oxidation products at the surface. The surface roughness greatly increased in strained PCUs with SEM evidence of deep cracks and holes or ragged and stretched fractures perpendicular to the direction of stress. PCUU underwent complex chemical modifications with a marked decrease of N-H and urea IR absorptions and showed a lower degradation than PEU and PCUs under mechanical constraint. From these results, sodium hypochlorite appears to be able to create an ESC-like degradation for PUs that are resistant to other aggressive chemical environments.

Microscopy, Electron, Scanning↗

Plasma-based sterilization: effect on surface and bulk properties and hydrolytic stability of reprocessed polyurethane electrophysiology catheters.

Plasma-based sterilization is a promising alternative to ethylene oxide (EO) for reprocessing of electrophysiology catheters. To assess its safety in terms of material damage, modifications of surface and bulk properties as well as hydrolytic stability of sterilized catheters were evaluated. Polyurethane (PU) single-use electrophysiology catheters were subjected to one, five, and ten sterilization cycles by Sterrad-100S and Plazlyte, as well as by pure EO for comparison. Surface analysis techniques (ATR-FTIR, XPS, DCA) showed oxidation limited to the near-surface layer induced by both plasma-based sterilizers, whereas EO induced slight but deeper alkylation. Using bulk analysis techniques (RP-HPLC, SEC), oligomer alteration was observed after all three sterilization techniques, without modification of molecular weights. Hydrolytic stability of catheters was slightly changed by plasma-based sterilization, with a small increase in released oligomers. Finally, although Plazlyte and Sterrad are both plasma-based techniques, they induced different impacts on catheters, such as the degradation of an additive with Sterrad, and a clear difference in coloration with Plazlyte.

Catheterization↗

The relationship between leachability of polymerization initiator and degree of conversion of visible light-cured resin.

Recently, polymerization-initiator-induced radicals have been identified as a biohazard as well as residual monomers. The present investigation was conducted to clarify the leaching behavior of the polymerization initiator and to measure the relationship between the leached amount of polymerization initiator and the degree of conversion of visible light (VL)-cured resin. Moreover, determining a suitable ratio of polymerization initiator to the base monomer according to the above relationship was carried out. The base monomer (UDMA/TEGDMA) was activated with varying concentrations of polymerization initiator (CQ/DMPT, CQ/DMAEMA) from 0.3-0.9 wt%, respectively, which were exposed to light for 40 s. Gas chromatograph mass spectrometry (GCMS) was carried out to evaluate the leached amount of polymerization initiator. The degree of conversion (DC) of the cured sample was estimated using attenuated total reflectance-Fourier transform infrared (ATR-FTIR) spectroscopy. As the result, it was recognized that the leachability of the polymerization initiator (CQ, DMPT, and DMAEMA) depended on the degree of conversion of the VL-cured resin. Therefore, the optimal concentration of polymerization initiator can be determined from the relation between the degree of conversion and the leached amount of polymerization initiator, which is about 0.6 wt% for CQ/DMPT (1:1 in weight) and 0.5 wt% for CQ/DMAEMA (1:1 in weight) relative to the UDMA/TEGDMA (1:1 in weight) monomer.

Dental Cements↗