[Analysis of the short-and medium-term curative effect of TIPS approach combined with AngioJet thrombus aspiration technology treatment in acute portal vein thrombosis].

Objective: To evaluate the short- and medium-term clinical efficacy of TIPS approach combined with AngioJet thrombus aspiration technology treatment in acute portal vein thrombosis. Methods: 63 cases with acute portal vein thrombosis treated in our center from May 2017 to July 2019 were studied retrospectively, including 49 males and 14 females, aged 35-61 (46 ± 5) years. TIPS approach (with/without) combined with Angiojet thrombus aspiration and gastroesophageal varices embolization was performed simultaneously according to the patient's condition. Regular follow-up for 3-33 (22 ± 3) months after surgery was used to observe the curative effect. Results: The technical success rate was 100%. Portal vein and superior mesenteric vein blood flow were returned to normal after the operation. Two cases of biliary tract injury were untreated. Simultaneously, two cases of intrahepatic arteriovenous fistula were treated with superselective arterial embolization. During the follow-up period, 47 cases (74.61%) had complete portal vein recanalization, 13 cases (20.63%) had partial recanalization, 3 cases (4.76%) had complete portal cavernoma, 7 cases (11.11%) had symptomatic hepatic encephalopathy, 1 case had received artificial liver treatment (1.59%), 1 case had peptic ulcer (11.11%), 6 cases (9.52%) had lost to follow-up, and there was no portal hypertension-related bleeding or death. Conclusion: TIPS approach combined with AngioJet thrombus aspiration technology is safe, effective and feasible in the treatment of acute portal vein thrombosis, and the short- and medium-term clinical effects are satisfactory.

Targeting histone-acetyltransferase Tat-interactive protein 60 inhibits intestinal allergy.

BACKGROUND: The overproduction of IgE plays a critical role in the pathogenesis of allergy; the mechanism is unclear. Histone-acetyltransferase (HAT) activities are required in gene transcription of a large number of molecules in the immune system of the body. OBJECTIVES: This study tests a hypothesis that HAT Tat-interactive protein 60 (Tip60) plays an important role in the initiation of IgE-mediated allergy. METHODS: The effects of Tip60 on regulating IgE expression were assessed with B cells. An intestinal allergy mouse model was developed to assess the role of Tip60 in the induction of IgE-mediated allergic inflammation. RESULTS: High levels of Tip60 were observed in the peripheral B cells of patients with FA. Tat-interactive protein 60 (Tip60) was required in the expression of IgE and IgG1 in B cells by inducing the chromatin remolding at the gene locus, in which histone acetylation, signal transducer and activator of transcription 6 (STAT6), and nuclear factor-κB at the locus of Iε promoter were markedly increased. Blocking Tip60 significantly attenuated the allergic inflammation in the mouse intestinal mucosa. CONCLUSIONS: Tat-interactive protein 60 (Tip60) plays an important role in the induction of IgE in B cells. Blocking Tip60 inhibits the allergic inflammation in the intestine, suggesting Tip60 inhibitor may be a potential anti-allergy drug.

Long-term effects: Galectin-1 and specific immunotherapy for allergic responses in the intestine.

BACKGROUND AND AIMS: Mast cell activation interferes with the effects of allergen-specific immunotherapy (SIT). Galectin-1 (Gal-1) is capable of regulating immune cells' functions. This study tests the hypothesis that administration of Gal-1 promotes and prolongs the efficacy of SIT via suppressing mast cell activation. METHODS: An intestinal allergy mouse model was developed. The coadministration of SIT and Gal-1 on suppression of the allergic responses, prevention of mast cell activation, and generation of antigen-specific regulatory T cells (Treg) in the intestine was observed in sensitized mice. RESULTS: The coadministration of Gal-1 and SIT markedly suppressed the allergic responses in the mouse intestine vs the use of either SIT alone or Gal-1 alone. The Gal-1 binds to the IgE/FcɛRI complexes on the surface of mast cells to prevent mast cell activation during SIT. Gal-1 promoted the SIT-generated allergen-specific Tregs in the intestine of sensitized mice. Coadministration of Gal-1 and SIT significantly enhanced the efficacy of immunotherapy in suppressing allergic responses in the intestine, which lasted for at least for 12 months. CONCLUSIONS: Long-term effects of specific immunotherapy on intestinal allergy can be achieved with Gal-1/SIT therapy by inhibiting mast cell activation and facilitating Treg development.

Vitamin D regulates immunoglobulin mucin domain molecule-4 expression in dendritic cells.

BACKGROUND: Dendritic cell (DC)-derived immunoglobulin domain molecule (TIM)4 plays a critical role in the initiation of T helper (Th)2 polarization. Vitamin D (VitD) involves the regulation of a number of immune responses. OBJECTIVES: This study tests a hypothesis that VitD regulates TIM4 expression in DCs. METHODS: Peripheral blood samples were collected from patients with allergic rhinitis (AR) and healthy subjects. DCs were isolated from the samples and analyzed for the expression of TIM4. RESULTS: We observed that the levels of calcitriol, the active form of VitD3, in the sera of AR patients were lower than that in healthy subjects. The peripheral DC expressed higher levels of TIM4 and lower levels of VDR. A negative correlation was identified between the data of serum calcitriol and TIM4 in DCs. Exposure DCs to calcitriol in the culture increased the expression of VDR. We also found that VDR bound to the TIM4 promoter locus in DCs to repress the TIM4 gene transcription and expression. CONCLUSIONS AND CLINICAL RELEVANCE: VitD deficiency may contribute to the pathogenesis of AR by increasing the TIM4 expression. The results suggest that to regulate the serum calcitriol levels and the expression of VDR in DCs may be necessary to be taken into account in the treatment of AR.

Vitamin D contributes to mast cell stabilization.

BACKGROUND AND AIMS: Mast cells are the major effector cells in allergic disorders and many other informatory disorders. The mechanism of mast cell stabilization is not fully understood. Cumulative reports indicate that vitamin D (VitD) contributes to the homeostasis in the body. This study tests a hypothesis that VitD is required in the maintenance of the stability of mast cells. METHODS: The stability of mast cell lines, HMC1 cells, RBL-2H3 cells, p815 cells, and mouse bone marrow-derived mast cells (BMMC) was tested in the presence or absence of VitD3. RESULTS: Mast cells activated automatically in a VitD-deficient environment. Exposure to calcitriol in the culture increased the expression of VitD receptor (VDR) in mast cells. VDR formed complexes with Lyn in mast cells to inhibit the binding of Lyn to the ß chain of FcεRI and MyD88, which decreased the phosphorylation of Syk, decreased the levels of MAPK and NF-κB. VDR bound to the promoter of TNF-α to decrease the acetylation of histone H3/H4, RNA polymerase II and OCT1 (a transcription factor of TNF-α) at the promoter locus and repressed the expression of TNF-α in mast cells. CONCLUSIONS: The data demonstrate that VitD is required to maintain the stability of mast cells. The deficiency of VitD results in mast cell activation.

Modeling material-degradation-induced elastic property of tissue engineering scaffolds.

The mechanical properties of tissue engineering scaffolds play a critical role in the success of repairing damaged tissues/organs. Determining the mechanical properties has proven to be a challenging task as these properties are not constant but depend upon time as the scaffold degrades. In this study, the modeling of the time-dependent mechanical properties of a scaffold is performed based on the concept of finite element model updating. This modeling approach contains three steps: (1) development of a finite element model for the effective mechanical properties of the scaffold, (2) parametrizing the finite element model by selecting parameters associated with the scaffold microstructure and/or material properties, which vary with scaffold degradation, and (3) identifying selected parameters as functions of time based on measurements from the tests on the scaffold mechanical properties as they degrade. To validate the developed model, scaffolds were made from the biocompatible polymer polycaprolactone (PCL) mixed with hydroxylapatite (HA) nanoparticles and their mechanical properties were examined in terms of the Young modulus. Based on the bulk degradation exhibited by the PCL/HA scaffold, the molecular weight was selected for model updating. With the identified molecular weight, the finite element model developed was effective for predicting the time-dependent mechanical properties of PCL/HA scaffolds during degradation.

Filamin is required for ring canal assembly and actin organization during Drosophila oogenesis.

The remodeling of the actin cytoskeleton is essential for cell migration, cell division, and cell morphogenesis. Actin-binding proteins play a pivotal role in reorganizing the actin cytoskeleton in response to signals exchanged between cells. In consequence, actin-binding proteins are increasingly a focus of investigations into effectors of cell signaling and the coordination of cellular behaviors within developmental processes. One of the first actin-binding proteins identified was filamin, or actin-binding protein 280 (ABP280). Filamin is required for cell migration (Cunningham et al. 1992), and mutations in human alpha-filamin (FLN1; Fox et al. 1998) are responsible for impaired migration of cerebral neurons and give rise to periventricular heterotopia, a disorder that leads to epilepsy and vascular disorders, as well as embryonic lethality. We report the identification and characterization of a mutation in Drosophila filamin, the homologue of human alpha-filamin. During oogenesis, filamin is concentrated in the ring canal structures that fortify arrested cleavage furrows and establish cytoplasmic bridges between cells of the germline. The major structural features common to other filamins are conserved in Drosophila filamin. Mutations in Drosophila filamin disrupt actin filament organization and compromise membrane integrity during oocyte development, resulting in female sterility. The genetic and molecular characterization of Drosophila filamin provides the first genetic model system for the analysis of filamin function and regulation during development.

Bench test of phase measurement on dispersion interferometer for EAST.

In recent years, different traditional interferometers have been the necessary diagnostic of electronic density measurement on fusion devices. Until now, two main problems always influence the density measurement: the mechanical vibration and fringe jump in the calculation. The dispersion interferometer (DI) with a long-wavelength infrared wavelength is a good choice because mechanical vibrations can be canceled and the fringe jump can be inhibited. This paper describes the bench test of phase measurement using a wedge instead of plasma on the DI. The results show good agreement with the theoretical calculations. In the background measurement, this DI without a vibration isolation system has good performance, and the drift of the baseline is less than 2 × 1017 m-2 in 3 s and less than 5 × 1017 m-2 in 400 s. Plasma data will be obtained during the next campaign on EAST (Experimental and Advanced Superconducting Tokamak).

Evidence for cooperative interactions between the two motor domains of cytoplasmic dynein.

Cytoplasmic dynein is a force-transducing ATPase that powers the movement of cellular cargoes along microtubules. Two identical heavy chain polypeptides (> 500 kDa) of the cytoplasmic dynein complex contain motor domains that possess the ATPase and microtubule-binding activities required for force production [1]. It is of great interest to determine whether both heavy chains (DHCs) in the dynein complex are required for progression of the mechanochemical cycle and motility, as observed for other dimeric motors. We have used transgenic constructs to investigate cooperative interactions between the two motor domains of the Drosophila cytoplasmic dynein complex. We show that 138 kDa and 180 kDa amino-terminal fragments of DHC can assemble with full-length DHC to form heterodimeric complexes containing only a single motor domain. The single-headed dynein complexes can bind and hydrolyze ATP, yet do not show the ATP-induced detachment from microtubules that is characteristic of wild-type homodimeric dynein. These results suggest that cooperative interactions between the monomeric units of the dimer are required for efficient ATP-induced detachment of dynein and unidirectional movement along the microtubule.

Cortical contusion induces trans-hemispheric reorganization of blood flow maps.

Cerebral blood flow (CBF), a surrogate of neural activity in the identification of brain regions involved in specific functions, has been used in this report to trace the compensatory enhancement of activity in non-traumatized areas of the brain following a focal lesion. We have previously shown activation of CBF in the cortex contralateral to a focal contusion, 24 h after the event. The present report extends the characterization of this trans-hemispheric cortical blood flow activation by studying its time course and regional distribution from 4 days to 4 weeks post-trauma. Adult male Sprague-Dawley rats received a cortical impact through a 6.3 mm craniotomy under halothane anesthesia. CBF was measured with the quantitative autoradiographic (14)C-Iodoantipyrine technique, in conscious animals, 4 days, 2 weeks and 4 weeks post-trauma. CBF was severely decreased at the site of impact where necrosis developed later, and it remained depressed in the surrounding areas throughout the observation period. Trans-hemispheric CBF enhancement was maximal at 4 days and it returned to control levels 28 days post-trauma. This phenomenon was present in all cortical regions symmetrical to the impact zone, but also in auditory, visual, entorhinal and insular cortex. These results suggest that the participation of the contralateral cortex in the recovery from unilateral brain trauma is not limited to the regions homologous to those that received the impact. The time course of CBF changes was found to be consistent with the recovery of motor function in this model.

The C-terminal module of Chi1 from Aeromonas caviae CB101 has a function in substrate binding and hydrolysis.

The chitinase gene chi1 of Aeromonas caviae CB101 encodes an 865-amino-acid protein (with signal peptide) composed of four domains named from the N-terminal as an all-beta-sheet domain ChiN, a triosephosphate isomerase (TIM) catalytic domain, a function-unknown A region, and a putative chitin-binding domain (ChBD) composed of two repeated sequences. The N-terminal 563-amino-acid segment of Chi1 (Chi1DeltaADeltaChBD) shares 74% identity with ChiA of Serratia marcescens. By the homology modeling method, the three-dimensional (3D) structure of Chi1DeltaADeltaChBD was constructed. It fit the structure of ChiA very well. To understand fully the function of the C-terminal module of Chi1 (from 564 to 865 amino acids), two different C-terminal truncates, Chi1DeltaChBD and Chi1DeltaADeltaChBD, were constructed, based on polymerase chain reaction (PCR). Comparison studies of the substrate binding, hydrolysis capacity, and specificity among Chi1 and its two truncates showed that the C-terminal putative ChBD contributed to the insoluble substrate-protein binding and hydrolysis; the A region did not have any function in the insoluble substrate-protein binding, but it did have a role in the chitin hydrolysis: Deletion of the A region caused the enzyme to lose 30-40% of its activity toward amorphous colloidal chitin and soluble chitin, and around 50% toward p-nitrophenyl (pNP)-chitobiose pNP-chitotriose, and its activity toward low-molecular-weight chitooligomers (GlcNAc)3-6 also dropped, as shown by analysis of its digestion processes. This is the first clear demonstration that a domain or segment without a function in insoluble substrate-chitinase binding has a role in the digestion of a broad range of chitin substrates, including low-molecular-weight chitin oligomers. The reaction mode of Chi1 is also described and discussed.

Cholinergic modulation of cerebral cortical blood flow changes induced by trauma.

These experiments tested the role of cholinergic mechanisms in the changes of cerebral cortical blood flow (CBF) induced by brain trauma. CBF was measured with Iodo-14C-antipyrine autoradiography, in 128 cerebral cortex regions of both hemispheres, distributed in eight coronal slices. The effects of a 6.3-mm diameter craniotomy over the left motor-sensory cortex with no weight drop, and of trauma (drop weight of 20 g from 30 cm height on left motor-sensory cortex through a 6.3 mm circular craniotomy) on CBF were studied at 2 and 24 h after the interventions. A group of control animals that received no intervention was also set up. Animals were treated with the cholinesterase inhibitor physostigmine salicylate (3.3 microg/kg/min i.v. infusion started 60 min before CBF measurements), the cholinergic blocker scopolamine hydrobromide (1 mg/kg i.v. pulse, 18 min before CBF measurements), or with the drugs vehicle (saline). A focus of decreased CBF at the site of impact was observed 2 h after trauma, extending caudally as far as the occipital cortex. CBF on the contralateral cerebral cortex was also decreased. Both phenomena reversed partially at 24 h. This spontaneous recovery of CBF was blocked by scopolamine. Physostigmine reversed the decrease in CBF of the traumatized cortex, partially around the contused area and completely in more distant regions. The cerebral cortex contralateral to the trauma showed significantly higher CBF 24 h after trauma when compared to intact controls or craniotomy that peaked at the area symmetrical to the center of trauma. This phenomenon was also enhanced by physostigmine and completely blocked by scopolamine. These results suggest a prominent role of cholinergic mechanisms in the vascular adjustments that accompany cerebral trauma.

Cerebral cortical blood flow maps are reorganized in MAOB-deficient mice.

Cerebral cortical blood flow (CBF) was measured autoradiographically in conscious mice without the monoamine oxidase B (MAOB) gene (KO, n=11) and the corresponding wild-type animals (WILD, n=11). Subgroups of animals of each genotype received a continuous intravenous infusion over 30 min of phenylethylamine (PEA), an endogenous substrate of MAOB, (8 nmol g-1 min-1 in normal saline at a volume rate of 0.11 microl g-1 min-1) or saline at the same volume rate. Maps of relative CBF distribution showed predominance of midline motor and sensory area CBF in KO mice over WILD mice that received saline. PEA enhanced CBF in lateral frontal and piriform cortex in both KO and WILD mice. These changes may reflect a differential activation due to chronic and acute PEA elevations on motor and olfactory function, as well as on the anxiogenic effects of this amine. In addition to its effects on regional CBF distribution, PEA decreased CBF globally in KO mice (range -31% to -41% decrease from control levels) with a lesser effect in WILD mice. It is concluded that MAOB may normally regulate CBF distribution and its response to blood PEA.

Changes in bone mineral density at the proximal tibia after total knee arthroplasty: a 2-year follow-up of 28 knees using dual energy X-ray absorptiometry.

The change in bone mineral density at the proximal tibia during 2 years after total knee arthroplasty was studied in 28 knees (28 patients: 10 men and 18 women; median age: 71 years) with dual energy x-ray absorptiometry. Bone mineral density was measured at the proximal tibia at nine regions of interest below the tibial component within 1 week after the operation (baseline); measurements were repeated at 3, 6, 12, and 24 months. All but one knee was malaligned before the operation, and all but three were corrected to within the normal range of alignment after it. The mean bone mineral density of all nine regions of interest at the proximal tibia temporarily decreased by 13% (p = 0.001) during the initial 3 months, probably due to a general metabolic reaction of the skeleton to the operative trauma combined with the effect of the postoperative immobilization, and then the initial level was regained for as long as 2 years. The overall changes in mean bone mineral density to 2 years were insignificant (p > 0.05); however, a great variation (43.9% decrease to 98.0% increase) was observed on an individual basis. This change over time was significantly associated (R2 = 0.36, p = 0.002) with the level of the baseline bone mineral density, which in turn was partly related (R2 = 0.24, p = 0.009) to the amount of malalignment of the knee before the operation. Knees with high baseline levels (n = 14: 11 with varus and three with valgus alignment) displayed a decrease of 10.0 +/- 14.0% (mean +/- SD, p > 0.05) for as long as 2 years, whereas those with low baseline levels (n = 14: seven with varus and six with valgus alignment and one neutrally aligned) had an increase of 19.1 +/- 38.2% (p = 0.038). In both groups, the mean bone mineral density converged to a level of 0.75-0.95 g/cm2 at 2 years.

Mapping of cortical metabolic activation in soman-induced convulsions in rats.

The metabolic activation of the cerebral cortex during convulsions induced by the organophosphorus cholinesterase inhibitor soman was studied in detail. Soman was given at a dose equivalent to 0.9 LD50 (100 microgram/kg SC after pretreatment with 26 microgram/kg pyridostigmine, IM, to decrease lethality) to examine separately the metabolic effects of severe acetylcholinesterase inhibition, present always with this dose, and convulsions, present only in some of the animals. Cerebral glucose utilization (CGU) values of cortex divided by CGU of brain stem (nCGU) were calculated for 96 locations in nine coronal slices. Animals injected with pyridostigmine-soman and that developed convulsions (n = 7) showed statistically significant increases of nCGU with regard to animals injected with saline (n = 5) in 33 locations, 27 of which were in a single cluster, with the piriform cortex at its center. Perirhinal cortex, and insular cortex also showed significantly higher nCGU in convulsing rats. Other foci of elevated nCGU were found in frontal and parietal locations. In animals injected with pyridostigmine-soman and that did not develop convulsions (n = 5) in spite of severe cholinesterase inhibition, a single location (piriform cortex) showed significantly higher nCGU than controls. Neuropathology evaluation showed a significant decrease in viable cells only in animals that developed convulsions. This effect correlated with enhanced nCGU. It is concluded that the presence of convulsions, and not exposure to pyridostigmine-soman, determined the pattern of nCGU cortical activation, which correlated closely with the structural changes.

Cholinesterase inhibition improves blood flow in the ischemic cerebral cortex.

The ability of central cholinesterase inhibition to improve cerebral blood flow in the ischemic brain was tested in Sprague-Dawley rats with tandem occlusion of left middle cerebral and common carotid arteries. Cerebral blood flow was measured with lodo- 14C-antipyrine autoradiography in 170 regions of cerebral cortex. The regional distribution of blood flow was characterized in normal animals by cerebral blood flow maxima in the temporal regions. After 2 h ischemia, minimum cerebral blood flow values were found in the lateral frontal and parietal areas on the left hemisphere, and a new maximum was found in the right hemisphere in an area approximately symmetrical to the ischemic focus. Heptyl-physostigmine (eptastigmine), a carbamate cholinesterase inhibitor with prolonged time of action improved cerebral blood flow in most regions, with the exception of the ischemic core. The drug also enhanced the ischemia-induced rostral shift of cerebral blood flow maxima in the right hemisphere. The effects of eptastigmine were more marked 24 h after ischemia. Discriminant analysis showed that data from only 22 regions was sufficient to achieve 100% accuracy in classifying all cases into the various experimental conditions. The redistribution of cerebral blood flow to the sensorimotor area of the right hemisphere of animals with cerebral ischemia, a phenomenon possibly related to recovery of function, was also enhanced by eptastigmine.

Mapping of cerebral metabolic activation in three models of cholinergic convulsions.

Glucose utilization of four cerebral cortex and 35 subcortical regions (CGU) was analyzed in three models of cholinergic seizures induced by the following compounds: 1) soman (pinacolylmethylphosphonofluoridate) an organophosphorus cholinesterase inhibitor, 100 microg/kg SC after pretreatment with pyridostigmine 26 microg/kg IM (n = 6); 2) physostigmine, a carbamate cholinesterase inhibitor, 1.31 mg/kg infused IV over 75 min (n = 6); and 3) pilocarpine, a direct cholinergic agonist, 30 mg/kg SC (n = 6). Physostigmine and pilocarpine were preceded by 3 mmol/kg LiCl IP 20 hrs earlier. Animals injected with saline SC (n = 6) were used as controls. Step-wise discriminant analysis successfully classified 100% of the cases into the four experimental groups with data from only six regions. Pyridostigmine-soman induced the most widespread and greatest increases in CGU. More restricted and lower levels of activation were observed with Li-pilocarpine while Li-physostigmine induced significant increases in CGU only in globus pallidus, entopeduncular nucleus, and substantia nigra. These three regions, which are functionally related, were also activated in the other two models of cholinergic convulsions and may represent the initial step in cholinergic activation of the CNS. Li-pilocarpine failed to activate most of the brainstem and the superior colliculus. All cortical regions were activated by Li-pilocarpine and pyridostigmine-soman, while they were inhibited by Li-physostigmine. This phenomenon may be due in part to the lack of activation with physostigmine of the basal forebrain nuclei (lateral septum, medial septum, vertical and horizontal limbs of the diagonal band, and substantia innominata) resulting in a decreased drive of cortical metabolism.

[Anatomical observation and experimental studies on changes in structure and volume of intravertebral canal during backward extension of neck].

The authors dissected cervical vertebral specimens from 10 cadavers. Changes in structures of intravertebral canal were observed during extension-flexion movement. By pouring wax into vertebral canal, changes of the sagittal diameter and the cross-section area were measured during backward extension of the neck. It was found that the morphology and position of fibrous annuli, subflavous ligaments, the spinal canal and the dura mater were all changed. These changes can affect the volume of the vertebral canal, and can press the spinal cord when they are severe.

Effects of high temperature and noise on erythrocyte membrane ATPase activity in pilots during flight.

Objective. To determine the effect of heat and noise on erythrocyte membrane ATPase activities in pilots during flying. Method. Twenty-four pilots performing bombing for 3 h (45-53 degrees C, 122-97 dB in the cabin) served as the subjects. 21 ground personnel served as control (27 degrees C in the room). Blood samples were taken from both groups before flying (6:00 a.m.), and immediately (12:00 a.m.) and 8 h (8:00 p.m.) after flying. Na(+)-K+ ATPase, and Ca2(+)-Mg2+ ATPase activities in erythrocyte membrane were determined with colorimetry. Result. The Na(+)-K+ ATPase activity in erythrocyte membrane at 6:00 a.m. in pilots was higher than that in control group at the same time (P<0.01). The Ca2(+)-Mg2+ ATPase activities in erythrocyte membrane at 12:00 a.m. and 8:00 p.m. in pilots were significantly higher, compared with those in control group at the same time (P<0.01). Conclusion. The ATPase values obtained in our study were all within normal range, and the daytime variation of both groups are the same. Exposure of human body to heat and noise for long time may be harmful, the higher ATPase activity is, the more catabolism of ATP will be. ATP exhaustion will lead to Ca2+ overload in erythrocyte thus stiffen the red cell membrane.

[Effects of heat and noise environments on lipid peroxidation erythrocyte membrane in pilots].

OBJECTIVE: To investigate the effects of heat and noise environments on lipid peroxidation of erythrocyte membrane in pilots. METHOD: Twenty-four pilots and twenty-one ground personnel (control group) served as the subjects. The pilots performed flying in heat and noise environments. Glutathione peroxidase (GSHpx) and malondialdehyde [correction of malondiadehyde] (MDA) levels in erythrocyte membrane were determined before flying (6:00 a.m.), immediately after flying (12:00 a.m.) and 8 hours after flying (8:00 p.m.) respectively with a spectrophotometer. RESULT: Immediately after flying, GSHpx activity in pilot's erythrocyte membrane decreased significantly as compared with that in control group. Immediately after flying and 8 h after flying, MDA contents in pilots increased significantly as compared with that of control group. CONCLUSION: Heat and noise environments might induce increase of lipid peroxidation reaction and decrease of antioxidant ability.