[Research on body composition of soldiers in the graduating class of armed services colleges].

OBJECTIVE: To master the distribution of male and female soldiers' body composition with bioelectrical impedance analysis (BIA) method in order to provide data for building up the standards in comparison with those of ordinary residents. METHODS: A cluster stratified sample of 5968 graduated soldiers among different armed services colleges was measured by BIA. Five percent-95% distributions with in the upper and lower limits were established on basis of the above result. The crosswise comparison was also performed. RESULTS: (1) Five percent-95% reference ranges of people in the graduating class of armed services colleges were body fat percentage (BF%): 10.30%-20.70% (male) and 19.20%-30.10% (female), body mass index (BMI): 19.30-25.70 (male) and 18.00-23.99 (female), lean body mass percentage (LBM%): 79.27%-86.69% (male) and 69.89%-80.69% (female), muscle percentage (M%): 74.24%-83.96% (male) and 65.23%-75.27% (female), bone percentage (B%): 5.01% 5.77% (male) and 4.65%-5.51% (female). (2) Soldiers in the graduating class of armed services colleges have less BF%, more B% and M% than those of ordinary residents in the same age and the same sex. CONCLUSION: (1) Soldiers in the graduating class of armed services colleges have better body composition than that of ordinary residents in the same age and the same sex; (2) Standard of body composition for soldiers in the graduating class of armed services colleges should be different from that of ordinary residents, a new standard should be built up.

[A randomized controlled trial: acclimatization training on the prevention of motion sickness in hot-humid environment].

OBJECTIVE: Incidence and severity of motion sickness (MS) in hot-humid environment are extremely high. We tried to know the effect of two-stage training for reducing incidence and severity of ms. METHODS: Sixty male subjects were divided into experimental group and control group randomly. Subjects in experimental group received: (2) adaptation training including sitting, walking and running in hot lab. After adaptation confirmation based on subjective feeling, rectal temperature, heart rate, blood Pressure, sweat rates and sweat salt concentration, we tested both groups by Coriolis acceleration revolving chair test and recorded Graybiel's score and grading of severity to evaluate whether adaptation training was useful; (2) Anti-dizzy training 3m later of deacclimatization contained revolving chair training for 10 times. Then we did the same test as mentioned above to evaluate effect of anti-dizzy training. RESULST: Graybiel' s score and grading of severity had no difference between two groups through acclimatization training (P > 0.05). While they had difference through anti-dizzy training (P < 0.01). CONCLUSION: Adaptation training seems useless for reducing incidence and severity of MS in hot-humid environment, but anti-dizzy training is useful.

Effect of acclimation training on physiological changes in a randomized controlled trial in hot-humid environment.

OBJECTIVE: This study was aimed to explore the physiological changes and the effect of heat acclimation training via a randomized control trial study. METHODS: Forty healthy male volunteers were chosen and divided into experimental group and control group randomly. Those in experimental group received heat acclimation training including but not limited to meditation, unarmed run, yoga, and stepping in hot lab environment. And then, subjective feeling, rectal temperature, average skin temperature, and sweat electrolytes concentration were detected in order to describe their physiological changes. Before and after the training, both groups received some tests and their 3 000 m run-race time, nervous reaction time and subjective perception scores were recorded to evaluate the effect of acclimation training. RESULTS: (1) There was no difference in 3 000 m between the 2 groups in the same environment. Subjects' 3 000 m race time in experimental group was obviously shortened than that in control group in room temperature environment (t = 2.326, P < 0.05). And subjects' 3 000 m race time in experimental group was obviously shortened than that in control group in hot-humid environment (t = 4.518, P < 0.01). (2) Subjects' reaction time (RT) in experimental group was shortened than that in control group in room temperature environment (Z = 11.258, P < 0.05). And Subjects' RT in experimental group was sharply shortened than that in control group in hot-humid environment (Z = 6.519, P < 0.01). (3) No difference between the experimental and control groups was observed in subjective perception score (SPS) in room temperature environment. But subjects' SPS in experimental group was obviously lowered than that in control group and in hot-humid environment (t = 17.958, P < 0.01).(4) Anal temperature (AT) was lowered during training, while the change of mean skin temperature (MST) was not significant. Sweat sodium concentration (SSC) was lowered during training. SPS continued to decrease and entered plateau on the 13th day after training.(5) After acclimation training, the working capacity of the experimental group in hot-humid environment was over 85% of that in room temperature environment. While subjects' working capacity in control group in hot-humid environment was about 80% of that in room temperature environment. CONCLUSION: Hot-humid environment acclimation training improved the working capacity. After training, subjects' working capacity in hot-humid environment remained over 85% of that in room temperature environment, which was higher than that of those subjects who did not take part in training.

A Rac GTPase-activating protein, MgcRacGAP, is a nuclear localizing signal-containing nuclear chaperone in the activation of STAT transcription factors.

In addition to their pleiotropic functions under physiological conditions, transcription factors STAT3 and STAT5 also have oncogenic activities, but how activated STATs are transported to the nucleus has not been fully understood. Here we show that an MgcRacGAP mutant lacking its nuclear localizing signal (NLS) blocks nuclear translocation of p-STATs both in vitro and in vivo. Unlike wild-type MgcRacGAP, this mutant did not promote complex formation of phosphorylated STATs (p-STATs) with importin alpha in the presence of GTP-bound Rac1, suggesting that MgcRacGAP functions as an NLS-containing nuclear chaperone. We also demonstrate that mutants of STATs lacking the MgcRacGAP binding site (the strand betab) are hardly tyrosine phosphorylated after cytokine stimulation. Intriguingly, mutants harboring small deletions in the C'-adjacent region (betab-betac loop region) of the strand betab became constitutively active with the enhanced binding to MgcRacGAP. The molecular basis of this phenomenon will be discussed, based on the computer-assisted tertiary structure models of STAT3. Thus, MgcRacGAP functions as both a critical mediator of STAT's tyrosine phosphorylation and an NLS-containing nuclear chaperone of p-STATs.

Rac1 and a GTPase-activating protein, MgcRacGAP, are required for nuclear translocation of STAT transcription factors.

STAT transcription factors are tyrosine phosphorylated upon cytokine stimulation and enter the nucleus to activate target genes. We show that Rac1 and a GTPase-activating protein, MgcRacGAP, bind directly to p-STAT5A and are required to promote its nuclear translocation. Using permeabilized cells, we find that nuclear translocation of purified p-STAT5A is dependent on the addition of GTP-bound Rac1, MgcRacGAP, importin alpha, and importin beta. p-STAT3 also enters the nucleus via this transport machinery, and mutant STATs lacking the MgcRacGAP binding site do not enter the nucleus even after phosphorylation. We conclude that GTP-bound Rac1 and MgcRacGAP function as a nuclear transport chaperone for activated STATs.

[Investigation into "Hor Mongolian Moxibustion"].

Hor, a tribe name, is a general denomination for the nomad lived north to the Great Wall, including Hun (Xiongnu), eastern Tartars (Donghu), and Xianbei, people. Hor Mongolian moxibustion is a therapeutic method discovered by those Hor people. Many types of treatments formed during its coming into being and developments, but the treatment principles came down in one continuous line.

The constitutive centromere component CENP-50 is required for recovery from spindle damage.

We identified CENP-50 as a novel kinetochore component. We found that CENP-50 is a constitutive component of the centromere that colocalizes with CENP-A and CENP-H throughout the cell cycle in vertebrate cells. To determine the precise role of CENP-50, we examined its role in centromere function by generating a loss-of-function mutant in the chicken DT40 cell line. The CENP-50 knockout was not lethal; however, the growth rate of cells with this mutation was slower than that of wild-type cells. We observed that the time for CENP-50-deficient cells to complete mitosis was longer than that for wild-type cells. Centromeric localization of CENP-50 was abolished in both CENP-H- and CENP-I-deficient cells. Coimmunoprecipitation experiments revealed that CENP-50 interacted with the CENP-H/CENP-I complex in chicken DT40 cells. We also observed severe mitotic defects in CENP-50-deficient cells with apparent premature sister chromatid separation when the mitotic checkpoint was activated, indicating that CENP-50 is required for recovery from spindle damage.

A GTPase-activating protein binds STAT3 and is required for IL-6-induced STAT3 activation and for differentiation of a leukemic cell line.

We previously identified a guanosine triphosphatase (GTPase)-activating protein (GAP) male germ cell Rac GAP (MgcRacGAP) that enhanced interleukin-6 (IL-6)-induced macrophage differentiation of murine M1 leukemia cells. Later, MgcRacGAP was found to play crucial roles in cell division. However, how MgcRacGAP enhanced IL-6-induced differentiation remained elusive. Here we show that MgcRacGAP enhances IL-6-induced differentiation through enhancement of signal transducer and activator of transcription-3 (STAT3) activation. MgcRacGAP, Rac, and STAT3 formed a complex in IL-6-stimulated M1 cells, where MgcRacGAP interacted with Rac1 and STAT3 through its cysteine-rich domain and GAP domain. In reporter assays, the wild-type MgcRacGAP enhanced transcriptional activation of STAT3 while a GAP-domain deletion mutant (DeltaGAP) did not significantly enhance it, suggesting that the GAP domain was required for enhancement of STAT3-dependent transcription. Intriguingly, M1 cells expressing DeltaGAP had no effect on the differentiation signal of IL-6, while forced expression of MgcRacGAP rendered M1 cells hyperresponsive to the IL-6-induced differentiation. Moreover, knockdown of MgcRacGAP by RNA interference profoundly suppressed STAT3 activation, implicating MgcRacGAP in the STAT3-dependent transcription. All together, our data not only reveal an important role for MgcRacGAP in STAT3 activation, but also demonstrate that MgcRacGAP regulates IL-6-induced cellular differentiation in which STAT3 plays a pivotal role.

Identification and characterization of a new pair of immunoglobulin-like receptors LMIR1 and 2 derived from murine bone marrow-derived mast cells.

We have identified and characterized two mouse cDNAs in a mouse antigen-stimulated bone marrow-derived mast cell cDNA library, both of which encode type I transmembrane proteins. The genes were closely mapped in the distal region of mouse chromosome 11 and expressed not only in mast cells but also widely in leukocytes. The extracellular domains of their encoded proteins contain a single variable immunoglobulin (Ig) motif sharing about 90% identity with amino acids, showing that they comprise a pair of molecules and belong to the Ig superfamily. We named these molecules leukocyte mono-Ig-like receptor1 and 2 (LMIR1 and 2). The intracellular domain of LMIR1 contains several immunoreceptor tyrosine-based inhibition motifs (ITIMs). When cross-linked, the intracellular domain was tyrosine phosphorylated and capable of recruiting tyrosine phosphatases, SHP-1 and SHP-2 and inositol polyphosphate 5-phosphatase, SHIP. LMIR2, on the other hand, contains a short cytoplasmic tail and a characteristic transmembrane domain carrying two positively charged amino acids associated with three kinds of immunoreceptor tyrosine-based activation motif (ITAM)-bearing molecules, DAP10, DAP12, and FcRgamma. These findings suggest that a new pair of ITIM/ITAM-bearing receptors, LMIR1 and 2, regulate mast cell-mediated inflammatory responses through yet to be defined ligand(s).

Identification of a human cDNA sequence which encodes a novel membrane-associated protein containing a zinc metalloprotease motif.

We report the cloning and characterization of a human cDNA predicted to encode a novel hydrophobic protein containing four transmembrane domains and a zinc metalloprotease motif, HEXXH, between the third and fourth transmembrane domains, and have named the molecule metalloprotease-related protein-1 (MPRP-1). The MPRP-1 gene was localized to chromosome 1-p32.3 by radiation hybrid mapping, and Northern blot analysis revealed expression in many organs, with strong expression in the heart, skeletal muscle, kidney and liver. Immunohistochemical analyisis showed that MPRP-1 was localized in the endoplasmic reticulum (ER), and not in the Golgi compartment. Fragments of DNA encoding a segment homologous to the HEXXH motif of MPRP-1 are widely found in bacteria, yeast, plants, and animals. These results suggest that the MPRP-1 may have highly conserved functions, such as in intracellular proteolytic processing in the ER.

Phosphorylation by aurora B converts MgcRacGAP to a RhoGAP during cytokinesis.

Cell division is finely controlled by various molecules including small G proteins and kinases/phosphatases. Among these, Aurora B, RhoA, and the GAP MgcRacGAP have been implicated in cytokinesis, but their underlying mechanisms of action have remained unclear. Here, we show that MgcRacGAP colocalizes with Aurora B and RhoA, but not Rac1/Cdc42, at the midbody. We also report that Aurora B phosphorylates MgcRacGAP on serine residues and that this modification induces latent GAP activity toward RhoA in vitro. Expression of a kinase-defective mutant of Aurora B disrupts cytokinesis and inhibits phosphorylation of MgcRacGAP at Ser387, but not its localization to the midbody. Overexpression of a phosphorylation-deficient MgcRacGAP-S387A mutant, but not phosphorylation-mimic MgcRacGAP-S387D mutant, arrests cytokinesis at a late stage and induces polyploidy. Together, these findings indicate that during cytokinesis, MgcRacGAP, previously known as a GAP for Rac/Cdc42, is functionally converted to a RhoGAP through phosphorylation by Aurora B.