The population distribution pattern in Xinjiang autonomous region.
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Biomedical subjects
Publications and source records attributed to X Yuan.
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Soft tissue defects of the hand have been repaired with free pudendo-femoral skin flaps in 13 patients. The results are quite satisfactory in all cases. The flaps are thin with little fat to interfere with post-operative appearance. The donor sites are well-hidden and can be primarily closed with no functional disturbances. Hence the ideal donor site for soft tissue defects of the hand.
24 cases (25 thumbs) of thumb reconstruction and 14 cases (10 fingers) of finger reconstruction by second toe transplantation, 11 cases of thumb reconstruction by the big toe-nail flap, and 1 case of "hand" reconstruction by both second toes are presented. 48 cases (52 fingers and thumbs) are successful. Functions and aesthetic results are satisfactory.
In-frame stop codons were introduced into the coding region of human immunodeficiency virus type 1 (HIV-1) transmembrane protein (gp41). Truncation of 147 amino acids from the carboxyl terminus of gp41 (TM709) significantly decreased the stability and cell surface expression of the viral Env proteins, while truncation of 104 amino acids (TM752) did not. Truncation of 43 or more amino acids from the carboxyl terminus of gp41 generated mutant viruses which were noninfectious in several human CD4+ T lymphoid cell lines and fresh peripheral blood mononuclear cells. Analysis of the noninfectious mutant virions revealed significantly reduced incorporation of the Env proteins compared with the wild-type virions. Comparable amounts of Env proteins were detected on the surfaces of wild-type- and TM752-transfected cells, suggesting that the structures of gp41 required for efficient incorporation of Env proteins were disrupted in mutant TM752. Truncation of the last 12 amino acids (TM844) from the carboxyl terminus of gp41 did not significantly affect the assembly and release of virions or the incorporation of Env proteins into mature virions. However, the TM844 virus had dramatically decreased infectivity compared with the wild-type virus. This suggests that the cytoplasmic domain of gp41 also plays a role in other steps of virus replication.
The matrix domain of human immunodeficiency virus type 1 Gag polyprotein was studied for its role in virus assembly. Deletion and substitution mutations caused a dramatic reduction in virus production. Mutant Gag polyproteins were myristoylated and had a high affinity for membrane association. Immunofluorescence staining revealed a large accumulation of mutant Gag precursors in the cytoplasm, while wild-type Gag proteins were primarily associated with the cell surface membrane. These results suggest a defect in intracellular transport of the mutant Gag precursors. Thus, in addition to myristoylation, the N-terminal region of the matrix domain is involved in determining Gag protein transport to the plasma membrane. Wild-type Gag polyproteins interacted with and efficiently packaged mutant Gag into virions. This finding is consistent with the hypothesis that intermolecular interaction of Gag polyproteins might occur in the cytoplasm prior to being transported to the assembly site on the plasma membrane.
To determine the influence of electrical hypoglossal (HG) nerve stimulation on upper airway airflow mechanics, we analyzed pressure-flow relationships obtained during bilateral supramaximal HG nerve stimulation over a range of frequencies from 0 to 100 Hz in the isolated feline upper airway. Inspiratory airflow (VI), hypopharyngeal pressure (Php), and pharyngeal pressure (Pph) immediately upstream from the flow-limiting site (FLS) were recorded while Php was rapidly lowered to achieve inspiratory flow limitation in the isolated upper airway. Pressure-flow relationships were analyzed to determine the maximum in VI (VImax) and the mechanical determinants of VImax, the upper airway critical pressure (Pcrit) and the nasal resistance (RN) upstream to the FLS. In groups of decerebrate spinally anesthetized (n = 6) and unanesthetized (n = 6) cats, graded increases in VImax (p < 0.05) and decreases in Pcrit (p < 0.001) were observed as the stimulation frequency of the intact HG nerves was increased. In the cats with and without spinal anesthesia, VImax increased by 139 and 201%, and Pcrit decreased by 159 and 280%, respectively. RN was also correlated with stimulation frequency in the cats without spinal anesthesia (p = 0.01) and increased in four of six cats with spinal anesthesia. In an additional six decerebrate cats, significant increases in VImax (p < 0.001) and decreases in Pcrit (p = 0.01) were elicited by stimulating the distal cut HG nerve ends (50 Hz), whereas no changes were noted in these parameters when the proximal ends were stimulated. The findings suggest that HG stimulation increases VImax by decreasing Pcrit, which indicates a decrease in upper airway collapsibility at the FLS.(ABSTRACT TRUNCATED AT 250 WORDS)
The nucleus accumbens septi (NAcc) is a key brain region in the rewarding effects of addictive drugs such as opiates and ethanol. We recently showed that opiate peptides reduced both excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) in NAcc neurons of a slice preparation, with naloxone (Nal) reversal (Yuan et al., 1992). To test other addictive drugs, we used intracellular recording in this rat NAcc slice preparation to investigate ethanol actions on NAcc neuronal properties. Ethanol 22 to 66 mM had little reproducible effect on membrane potential or input slope resistance, but reduced the amplitude of EPSPs evoked by stimulation of the peri-tubercle region ventral to NAcc. Ethanol 22, 44 and 66 mM all significantly decreased the EPSPs evoked by half-maximal stimulation to 80, 60 and 68% of control, respectively. Superfusion of 11 mM ethanol had no effect. To confirm a direct ethanol action on EPSPs, we tested 44 mM ethanol in the presence of 30 microM bicuculline to block IPSPs. In these cells ethanol still decreased EPSP size, suggesting GABAAergic IPSPs are not involved in this effect. The glutamate receptor blocker 6-cyano-7-nitroquinoxaline-2,3-dione abolished the EPSPs evoked at resting membrane potentials. As ethanol actions mimic those of opiates in reducing EPSPs without effect on resting membrane potentials in the NAcc, we applied the opiate antagonist Nal together with ethanol. Nal 1 to 2 microM significantly reversed ethanol (44 mM) reduction of EPSP amplitude. Thus, our data suggest that a major effect of intoxicating concentrations of ethanol in NAcc is to reduce glutamatergic synaptic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)
Several group-I introns have been shown to specifically invade intron-minus alleles of the genes that contain them. This type of intron mobility is referred to as 'intron homing', and depends on restriction endonucleases (ENases) encoded by the mobile introns. The ENase cleaves the intron-minus allele near the site of intron insertion, thereby initiating gene conversion. The 23S (LSU) rRNA-encoding gene (LSU) of the chloroplast genome of Chlamydomonas reinhardtii contains a self-splicing group-I intron (CrLSU) that has a free-standing open reading frame (ORF) of 163 codons. Translation of CrLSU intron RNA in cell-free systems produces a polypeptide of approx. 18 kDa, the size expected for correct translation of the ORF. The in vitro-synthesized 18-kDa protein cleaves plasmid DNA that contains a portion of LSU where the intron normally resides, but lacking the intron itself. Cleavage by the intron-encoded enzyme (I-CreI) occurs 5 bp and 1 bp 3' to the intron insertion site (in the 3'-exon) in the top (/) and bottom (,) strands, respectively, resulting in 4-nt single-stranded overhangs with 3'-OH termini. We also show that the recognition sequence of I-CreI spans the cleavage site and is 24 bp in length (5'-CAAAACGTC,GTGA/GACAGTTTGGT).
Accumulating evidence suggests that the matrix (MA) protein of retroviruses plays a key role in virus assembly by directing the intracellular transport and membrane association of the Gag polyprotein. In this report, we show that the MA protein of human immunodeficiency virus type 1 is also critical for the incorporation of viral Env proteins into mature virions. Several deletions introduced in the MA domain (p17) of human immunodeficiency virus type 1 Gag polyprotein did not greatly affect the synthesis and processing of the Gag polyprotein or the formation of virions. Analysis of the viral proteins revealed normal levels of Gag and Pol proteins in these mutant virions, but the Env proteins, gp120 and gp41, were hardly detectable in the mutant virions. Our data suggest that an interaction between the viral Env protein and the MA domain of the Gag polyprotein is required for the selective incorporation of Env proteins during virus assembly. Such an interaction appears to be very sensitive to conformational changes in the MA domain, as five small deletions in two separate regions of p17 equally inhibited viral Env protein incorporation. Mutant viruses were not infectious in T cells. When mutant and wild-type DNAs were cotransfected into T cells, the replication of wild-type virus was also hindered. These results suggest that the incorporation of viral Env protein is a critical step for replication of retroviruses and can be a target for the design of antiviral strategies.
Cytogenetic studies were carried out on peripheral lymphocytes of 30 members from two typical familial polyposis coli (FPC) families. It was found that, under low folic acid culture conditions, the chromosome aberration rate of FPC family members (10%) was much higher than that of the control group (2.3%). No significant difference in SCE was found between the two groups. We suggest that the chromosome aberration rate under certain conditions may be used as a parameter for the early detection of FPC in certain FPC families. The analysis of fragile sites sensitive to low folic acid in FPC family members revealed that besides the significant increase of 3p14, which is frequently seen in tumor patients, other unique sites (1p22, 1p32 and 6q21) were also present in most of the FPC patients. Fragile sites 1p22, 1p32 and 6q21 are located near certain well known oncogene loci; thus, they may have something to do with the pathogenesis of FPC. The actual relationship between these fragile sites and FPC remains to be elucidated.
Forty cases of overlap syndrome of progressive systemic sclerosis and polymyositis (OS PSS-PM) are reported in this paper. All of these cases had manifestations of both PSS and PM as well as Raynaud's phenomenon. The sclerodermatous skin changes were diffused over the whole body in most cases. All cases had muscular weakness, elevated skeletal muscle enzyme levels and muscle damage as seen on the electromyogram. Histopathologic changes showed characteristics of myositis. There was noticeable systemic involvement, especially with the digestive and circulatory systems. Serologic examination frequently revealed autoantibodies. The patients responded well to traditional Chinese medicines and corticosteroids.
The vpr gene of human immunodeficiency virus type 1 (HIV-1) is one of the seven accessory genes that are believed to have roles in the virus replication cycle. We report here the detection of a 13 kD vpr protein in sucrose gradient-purified HIV-1. This protein was not detected in cells infected with a virus having a truncated vpr gene that lacks the potential to encode for 26 C-terminal amino acid residues. These findings raise the possibility that virion-associated vpr proteins may be involved in the early life cycle of HIV-1 replication and suggest that the C-terminal region of the vpr gene is essential for its expression.
We studied 40 patients who had clinical features of both typical progressive systemic sclerosis (PSS) and polymyositis (PM). The indurated skin extended over the metacarpophalangeal joints in all patients. The sclerotic changes, diffuse in type, involved the whole body, including the face, neck, extremities and trunk in most cases. All showed Raynaud's phenomenon. All patients had muscle weakness, elevated skeletal muscle enzymes and myogenic disorders in electromyograms, and biopsy of muscles showed myositic changes. The symptoms involved multiple systems, particularly the gastrointestinal and circulatory systems, presenting features of both PSS and PM. Serologic examinations often revealed auto-antibodies in these patients. Treatment with small doses of corticosteroid and traditional chinese medicines usually had good results. We found that either PSS or PM might appear first, or they might appear simultaneously. It is our opinion that as long as we keep alert and carefully observe the features and their development, we can easily diagnose the disease early.
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Clinical analysis of 60 cases of scleredema is reported with emphasis on clinical manifestations, microcirculatory changes, histopathological and ultrastructural observations. It is noted that the prognosis of scleredema may not always be good, and severe cases may lose their working capacity or even die. Attention should be paid to proper treatment of scleredema and long term follow-up is indicated to observe its course, outcome and pattern of evolution.
Of 725 cases of scleroderma, 265 were of systemic type (the sex ratio being 1M:6F) and 460 of circumscribed type (the sex ratio being 1M:9F). The patients were divided into three groups and treated with three different stimulating circulation to end stasis (SCES) prescriptions. Satisfactory therapeutic effects were obtained in all. According to the clinical practice and laboratory findings, although SCES therapy exerted manifold actions on the disease, it not only softened the indurated connective tissues, tonified the body and improved the symptoms, but also improved laboratory indexes as follows: nailfold bed capillary, parameter of the peripheral blood stream in patients, content of urinary 2-ketol, 17-KS, free corten, serum joint-hexose, amino-hexose and histopathology including ultrastructure of the skin. The main effect was the improvement of circulation, especially the microcirculation and regulation of the metabolism of the connective tissues. Great attention should be paid to the drug's function of softening the indurated connected tissues. For further investigation, the authors have stressed three important points: screening of clinical symptoms and signs, examination of blood circulatory disturbances, and examination of pathological changes of the connective tissue. The necessity of developing new criteria for judging the therapeutic effects was emphasized.
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