We detected varicella-zoster virus (VZV) DNA sequences in bullous lesions and skin biopsies obtained from healed skin lesions in 16 patients with herpes zoster using polymerase chain reaction. A 385 bp VZV DNA fragment was found in all the bullous lesions and in two of six biopsies from the skin lesions healed within two months. No VZV DNA was found in the skin lesions two months after healing in 10 cases of herpes zoster. VZV DNA may be detected at the sites of resolved herpes zoster lesions within short duration.

Objective To clone rat neuroglobulin (NGB) gene and construct its eukaryotic expression vector. Methods The total RNA was extracted from Wistar rat brain and the full length cDNA encoding NGB was obtained by RT-PCR. After the sequence was confirmed by sequencing and BLAST, it was inserted in the eukaryotic expression vector pCDNA3.1 (+), then the sequence and reading frame were confirmed by two restriction endonucleases and sequencing. Results The NGB gene was cloned with four bases mutated and its eukaryotic expression vector was constructed. Conclusion NGB expressed in Wistar rat brain. NGB gene was successfully cloned and inserted in eukaryotic expression vector.

Objective To observe the protective effect of recombinant plasmid pCDNA3.1(+)/Ngb during focal cerebral ischemia in rat brain.Methods Fifty-four male Wistar rats were randomly divided into three groups:normal saline(NS)control group,plasmid control group,and recombinant neuroglobulin group.NS,plasmid pCDNA3.1(+)and recombinant plasmid pCDNA3.1(+)/Ngb were respectively injected into two sites of the rat cerebra1 cortex 24 hours before induction of neocortical focal ischemia by occlusion of the right middle cerebral artery for 24 hours.The condition of local ischemic damage,expression of bcl-2 and the apoptosis in neural cells were confirmed by staining with 2% 2.3.5-triphenyltetrazolium chloride,in-site cell apoptosis detection,indirect immunofluorescent staining and Western blotting,respectively.Results The extent of cerebral infarction tissue and the apoptosis cells in the pCDNA3.1(+)/Ngb group were significantly reduced than those in other control groups(P

Twelve specimens of genital warts were excised from 12 patients and divided into three parts. One part was untreated, the second and the third part were treated with CO_2 laser and microwave respectively. HPV DNA was amplified and detected in 100% of untreated specimens (HPV16 and HPV11 in six patients each), in 83% and 50% of specimens treated with CO_2 laser and microwave respectively. There was a significant difference in the detection rates between untreated and microwave treated specimens (X~2=4.18, P

The great majority of human diseases are directly or i nd irectly associated with genes. Gene mapping and genetic analysis for human compl ex polygenic disorders has become a hot-spot and the neck of the bottle in the medical genetics research recently. The approach to genome-wide search has pla yed an important role in the respect.

Deseription was given of the effect of electric acupuncture of Neiguan point on the flexion reflex potential (FRP) of the hindlimbs and the dorsal root potential (DRP). On the intact and awake rats, the graded train stimulation (three pulses, 5ms interval, 0.5ms duration) was given to the sural nerve (a pure cutancous n(?), the C-FRP and C-DRP with their proper amplitudes (70～80% maximum) were obtained on the hamstring nerve (a group of nerves innervating the hindlimb flexors) and L5 dorsal root respectively. Then the electric acupuncture with low freqency and low intensity (4Hz, 1～3V)and low freqency and high intensity ( 4Hz, 20～40V), lasting 5 minutes, was given to the ipsilateral Neiguan point. After acupuncture, the amplitudes of both C-FRP and C-DRP decreased without change of their latebcues. The former one declined heavier and recovered slower than the latter one did. The A-FRP and A-DRP were not affected. Te result of the experiment suggests that the ipsilatcral Neiguan point cletric acupuncture can induce hindlimb's analgesia, the presynaptic inhibition might be involved in the mechanism of such analgesia.

On the intact and awake rat, the flexion reflex potential (FRP)and dorsal root potential (DRP) induced by stimulation of the cutaneous nerve with graded intensity stimulations to the sural nerve (a pure cutaneous nerve) were observed, there appeared A-FRP and C-FRP one after the other on the hamstring nerve (a group of nerves innervating the hindlimb flexors), and A-DRP and C-DRP on the L_5 dorsal root at the same time. The threshold and the latencices of A-FRP and A-DRP had no differences, and had significant positive correlations. The amplitudes of A-FRP and A-DRP increased simultaneously with the increase of the stimulating intensity in certain range. The threshold and latency of C-FRP are larger than those of C-DRP. The threshold and the latency of the C-FRP and C-DRP showed significant positive correlation. The amplitudes of C-FRP and C-DRP increased simultaniously with the increase of the stimulating intensity in certain range. The train stimuli (three pulses, 5ms interval, 0. 5ms duration) induced larger FRP and DRP than those induced by single stimulus. Thus, FRP and DRP both have the property of temporal summation.

Objective To investigate the inhibitory effects of traditional Chinese medicine (TCM) on hypermelanosis and provide experimental evidence for treating skin pigmentary disorders. Methods Five TCMs with strong inhibitory effects on tyrosinase activity were tested. The changes of the number and morphology of melanocytes induced by UVB were observed in the experimental hypermelanosis model (brownish guinea pig). Results Decreased melanocytes and melanin granules were found with the treatment of Poria cocos, Polyporus umbellatus, Cornus officinalis Sieb. et Zucc., Atractylodes macrocephala Koidz., Astoagalus complanatus R. Br. ex Bge. Conclusion There are inhibitory effects on hypermelanosis induced by UVB with the treatment of Poria cocs, Polyporus umbellatus, Cornus officinalis Sieb.et Zucc., Atractylodes macrocephala Koidz., Astoagalus complanatus R. Br.ex Bge.

Objectives To observe the effects of arsenic trioxide (As2O3) on the cell cycle, differentiation and proliferation of cultured mouse melanoma Cloudman S91 cells. Methods The cell viability was measured by MTT reduction assay. The morphological changes of the cells were examined by Wright-Giemsa staining. Clone forming was carried out to test the proliferation ability. Apoptosis rate and cell cycle of S91 cells were measured by flow cytometry. Results As2O3 in the concentrations of 0.031~0.25 ?mol/L promoted cell growth markedly and blocked the transformation of cells from G0 to G1. As2O3 in the concentrations of 0.5~8.0 ?mol/L inhibited the cell growth and induced apoptosis markedly. Conclusions As2O3 has marked effects on mouse melanoma S91 cells, which include inducing apoptosis and promoting differentiation and proliferation. These effects are dose- and time-dependent.

Objective To identify the gene mutations and mu tating patterns in a pedigree with X-linked anhidrotic ectodermal dysplasia(EDA)so as to provide a basis for gene diagn osis and genetic counselling of this disorder.Methods Polymerase chain reaction-single s trand conformation polymorphism(PCR-SSCP)analysis and DNA sequencing of amplified prod ucts were performed to screen mutati ons and mutating patterns of EDA1gen e,responsible for EDA pathogenesis,i n a X-linked EDA family of Han people.Results Abnormal single strand bands were found in the amplified fra gments as well of exon 1of EDAgene in t he patients as well as their mothers,the carriers.The DNAsequencing of ampl ified products revealed a point muta tion at nucleotide 404(C→Gtransversion)in the proband compared with that of t he normal controls,which resulted i n the transversion of histidine with glutamine at codon 54in the ectodysplasin-A(H54Q).Meanwhile there were heterozyous double peaks of nucleotide Cand Gat the same position in his mother.Conclusion A missense mutation(404C→G)in exon 1of EDA1gene has been determined in the pedigree with X-linked EDA,which is probably one of the molecular bases of EDA pathogenesis.