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42 cases with gastroesophageal varices were prospectively included. The groups were treated with endoscopic band ligation or combined with tissue adhesive. The results showed that the left gastric vein internal diameter, average blood flow velocity and blood flow volume after the treatment of band ligation combined with tissue adhesive were significantly lower than that of the treatment of band ligation alone, and the differences were statistically significant (P < 0.05). Spleen and portal vein internal diameter, blood flow and average velocity, the liver and spleen size, shear wave velocity and liver function grade of the two groups after treatment did not change significantly (P > 0.05). The effective rate of band ligation combined with tissue adhesive in the treatment of esophageal and gastric varices (66.67%, 52.38%) were higher than that of band ligation alone (42.85%, 23.81%) (P > 0.05), and the re-bleeding rate of the latter was higher (9.52% and 19.05%, P > 0.05). Hence, it is suggested that the combined therapy is safe and more effective, and has no apparent effect on liver function and portal hypertension.

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Using acupuncture to treat cerebral hypoperfusion is a hot topic. However, there is a lack of effective tools to clarify the therapeutic effect of acupuncture on cerebral hypoperfusion. Here, we show in a mouse model of cerebral hypoperfusion that photoacoustic tomography (PAT) can noninvasively image cerebral vasculature and track total hemoglobin (HbT) concentration changes in cerebral hypoperfusion with acupuncture stimulation on the YangLingQuan (GB34) point. We measured the changes of HbT concentration and found that the HbT concentration in hypoperfusion regions was clearly lower than that in the control regions when the acupuncture was absent; however, it was significantly increased when the acupuncture was implemented on the GB34 point. We also observed the increase of vessel size and the generation of new vessels in cerebral hypoperfusion during acupuncture. Laser speckle imaging (LSI) was employed to validate some of the PAT findings.

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Viral load reduction facilitates recovery of antiviral T-cell responses. Dynamic alterations in intrahepatic viraemia clearance and immune cell reactivity during the early phase of nucleoside analogue (NA) therapy and the impact of these changes on HBeAg seroconversion are unknown. Fifteen HBeAg-positive chronic hepatitis B (CHB) patients were treated with adefovir dipivoxil. T-cell reactivity to HBV core and surface antigens were tested using ELISPOT assay from baseline to week 48 post-treatment (at 4-week intervals). Before and at week 12 of treatment, paired liver biopsies were analysed for intrahepatic HBV-DNA and cccDNA via real-time fluorescent PCR. In situ detection of CD4(+) , CD8(+) T cells and NK cells was analysed by immunohistochemistry. With viral load reduction, HBV-specific IFN-γ-producing CD4(+) T cells in patients with HBeAg loss were greatly enhanced and reached the highest level at week 12, with further increase observed between week 36 and week 48. After 12 weeks of treatment, total intrahepatic HBV-DNA and cccDNA had significantly decreased; however, there was no difference in the viral loads or extent of reduction between patients with and without HBeAg loss. Paralleling reduction in viral load, intrahepatic CD8(+) T lymphocytes increased in patients with HBeAg loss compared with baseline values. Only one patient without HBeAg loss exhibited similar results. Increased immune cells were observed in certain patients along with reduced hepatic viral loads during the second phase of HBV-DNA decline, which could promote the recovery of antiviral immunity and facilitate HBeAg loss.

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54 consecutive cases of small cell lung cancer (SCLC) were treated with longterm short-interval combined treatment modalities of chemotherapy, radiotherapy (55-65 GY), immunotherapy, traditional Chinese medicine (leaf of Asiatic Ginseng, root of Astragalus membranaceus Bge, etc) and other adjuvants. Chemotherapy consisted of vincristine, cyclophosphamide, methotrexate and carmustine. A complete response of 59.2%, partial response of 38.9% and an overall response of 98.1% were achieved. According to Kaplan-Meier, the survival rates of SCLC with limited disease for 1, 3, 5 and 10 years were 78.1%, 42.6%, 32.1% and 21.4% respectively; while those with extensive disease for 1, 3, and 5 years 90.5%, 13.4% and 13.4%. According to classification of international TNM staging (1988), the survival rates of stage II SCLC for 1, 3, 5 and 10 years were 92.9%, 61.9%, 53.1% and 31.8% respectively; of stage IIIa for 1, 3 and 5 years 80.0%, 30.0% and 20.0%, and of stage IIIb 83.3%, 20.8% and 15.6%. Our combined modalities raised the survival rates considerably; the improved effect was mainly due to the long-term (especially more than 2 years or 10 courses), short-interval, effective and timely combined treatment with chemotherapy, radiotherapy and adjuvants such as traditional Chinese medicine and immunotherapy. By using the above therapeutic strategy, 10 out of 12 SCLC patients including 4 with extensive disease, who were relatives of our hospital staffs, have gained more than 3-17 years of survival. Therefore small cell lung cancer even with extensive disease was a hopeful curable disease.

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We described previously the molecular characterization of a rat alpha 2B-adrenergic receptor and have shown also that the rat genome contains three closely related alpha 2-adrenergic receptor genes. To characterize the ligand-binding properties of these receptor gene products, we expressed the DNAs encoding these receptors individually in COS-1 cells and studied their binding to a wide variety of typical and atypical adrenergic ligands. The receptors displayed high affinity binding to the radioligand [3H] rauwolscine, with equilibrium dissociation constants ranging from 1.4 to 2.8 nM. Kinetic analysis of the binding of [3H]rauwolscine to membranes from transfected cells was in very good agreement with data obtained from saturation analysis. We examined the ability of a number of agents to compete for the binding of [3H]rauwolscine to the alpha 2-adrenergic receptor-transfected membranes. Whereas one of these receptors displayed a pharmacological profile typical of an alpha 2A-adrenergic receptor, the other two receptors showed similar pharmacological properties characteristic of an alpha 2B-adrenergic receptor. The two alpha 2B-like adrenergic receptors differed, however, in the ratios of Ki values for oxymetazoline and prazosin, as well as the Ki ratio of prazosin and yohimbine. In addition, the two alpha 2B-like adrenergic receptors had a 9-fold difference in affinity for chlorpromazine. The pharmacological characterization of the three rat alpha 2-adrenergic receptor gene products is consistent with the known pharmacology of alpha 2-adrenergic receptors, as documented using tissues and cell lines.

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alpha 2-Adrenergic receptors (ARs) are involved in central nervous system (CNS) control of blood pressure. It is now known that there are three human genes that encode subtypes of alpha 2-ARs, but little is known regarding the distribution of these subtypes throughout the CNS. The availability of receptor clones allows the mapping of mRNAs encoding the individual alpha 2-AR subtypes in the CNS. In this communication, we report that there are three, closely related rat alpha 2-AR genes. We have developed subtype-specific hybridization probes from each of these genes and have used these reagents to measure alpha 2-AR subtype mRNA accumulation in extracts of discrete regions of the rat CNS. We found that mRNAs encoding the alpha 2A-AR and alpha 2C-AR subtypes are distributed widely, but unevenly, throughout the rat CNS. The A subtype is prominent in the midbrain, brainstem, spinal cord, pituitary and diencephalon while the C subtype predominates in basal ganglia and cerebellum. The cortex, olfactory bulb and hippocampus contain roughly equal amounts of the alpha 2A- and alpha 2C-AR mRNAs. A third subtype's (alpha 2B-AR) mRNA is far less abundant in brain tissues, and is only found in the diencephalon.

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Alpha 2-adrenergic receptors comprise a heterogeneous population based on pharmacologic and molecular evidence. We have isolated a cDNA clone (pRNG alpha 2) encoding a rat alpha 2-adrenergic receptor. A rat kidney cDNA library was screened with an oligonucleotide complementary to a highly conserved region found in all biogenic amine receptors described to date. The deduced amino acid sequence displays many features of guanyl nucleotide-binding protein-coupled receptors except it does not have a consensus N-linked glycosylation site near the amino terminus. Membranes prepared from COS cells transfected with pRNG alpha 2 DNA display high affinity and saturable binding to [3H]rauwolscine (Kd = 2 nM). Competition curve data analysis shows that RNG alpha 2 protein binds to a variety of adrenergic drugs with the following rank order of potency: yohimbine greater than or equal to chlorpromazine greater than or equal to prazosin greater than or equal to clonidine greater than norepinephrine greater than or equal to oxymetazoline. RNG alpha 2 RNA accumulates in both rat kidney and neonatal rat lung (predominant species is 4000 nucleotides). When a cysteine residue (Cys-169) that is conserved among all members of the seven-transmembrane-region superfamily is changed to phenylalanine, the RNG alpha 2 protein fails to bind [3H]rauwolscine after expression in COS cells. We conclude that pRNG alpha 2 likely represents a cDNA for a rat alpha 2B-adrenergic receptor.

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