[Seroepidemiological investigation of hepatitis C virus in Zhejiang Province: a hospital-based study].

Objective: To study serum HCV antibody (anti-HCV) with geographic distribution characteristics in Zhejiang Province. Methods: A stratified random cluster sampling method was used. Serum samples of the surveyed population were collected from selected hospitals, anti-HCV antibodies were examined, then hepatitis C infection rates among different genders, regions and age groups were analyzed. The anti-HCV rate was compared using the χ (2) test. Results: The average anti-HCV positive rate in Zhejiang Province was 0.24% [95% confidence interval (CI): 0.16% ~ 0.32%]. The antibody positive rate in the plain area was 0.32% (95% CI: 0.19% ~ 0.45%), which was significantly higher than the coastal islands 0.05%(95% CI: 0.00% ~ 0.12%, χ (2) = 7.638, P < 0.05). There was no significant difference between plain area and hilly area 0.22% (95% CI: 0.03% - 0.41%). There was no statistically significant difference in anti-HCV positive rates between males and females (χ (2) = 2.238, P = 0.135). The highest positive rate of anti-HCV (0.93%) was in the population aged 56-60 years and the lowest in the population aged less than 20 years. Anti-HCV positive rate of all age groups in 2017 was lower than that of 2006 seroepidemiological study of hepatitis C. Conclusion: Zhejiang Province is a region with low anti-HCV positive rate and the disease prevalence further reduced than 10 years ago. The positive rate of anti-HCV in plain areas is higher than islands. Middle-aged and elderly people are the age group with high prevalence, and the anti-HCV positive rate in people under 20 years old is exceptionally low. Gender differences in anti-HCV positive rate have little effect.

Dopamine involved in the nociceptive modulation in the parafascicular nucleus of morphine-dependent rat.

Dopamine regulates pain perception in some areas of the central nervous system. Previously, we have confirmed that dopamine potentiated the electric activities of the evoked discharges of pain-excited neurons (PENs) and inhibited those of pain-inhibited neurons (PINs) in the parafascicular nucleus (Pfn) of normal rats. The mechanism of action of dopamine on pain-related neurons in the Pfn of morphine-dependent rat is still unknown. The present study aimed to determine the effects of dopamine and its receptor antagonist droperidol on the pain-evoked responses of the PEN and PIN in the Pfn of morphine-dependent rats, and to compare the effects between the morphine-dependent rat and the normal rat. The trains of electric impulses applied to the sciatic nerve were used as noxious stimulation. The discharges of PEN or PIN in the Pfn were recorded by using a glass microelectrode. The results showed that intra-Pfn microinjection of dopamine decreased the frequency of noxious stimulation-induced discharges of PEN and increased the frequency of PIN. The intra-Pfn administration of droperidol produced an opposite effect. These results demonstrated that dopamine is involved in nociceptive modulation in the morphine-dependent rat, the responses to noxious stimulation between normal rat and morphine-dependent rat are completely opposite. The effect of dopamine is through the dopamine D(2) receptor of PENs and PINs in Pfn. The results suggest that the dopamine system of the Pfn may become a therapeutic target for analgesia and the treatment of morphine dependence.

L-364,718 potentiates electroacupuncture analgesia through cck-a receptor of pain-related neurons in the nucleus parafascicularis.

Electroacupuncture (EA) has been successfully used to alleviate pain produced by various noxious stimulus. Cholecystokinin-8 (CCK-8) is a neuropeptide involved in the mediation of pain. We have previously shown that CCK-8 could antagonize the analgesic effects of EA on pain-excited neurons (PENs) and pain-inhibited neurons (PINs) in the nucleus parafascicularis (nPf). However, its mechanism of action is not clear. In the present study, we applied behavioral and neuroelectrophysiological methods to determine whether the mechanisms of CCK-8 antagonism to EA analgesia are mediated through the CCK-A receptors of PENs and PINs in the nPf of rats. We found that focusing radiant heat on the tail of rats caused a simultaneous increase in the evoked discharge of PENs or a decrease in the evoked discharge of PINs in the nPf and the tail-flick reflex. This showed that radiant heat could induce pain. EA stimulation at the bilateral ST 36 acupoints in rats for 15 min resulted in an inhibition of the electrical activity of PEN, potentiation of the electrical activity of PIN, and prolongation in tail-flick latency (TFL), i.e. EA stimulation produced an analgesic effect. The analgesic effect of EA was antagonized when CCK-8 was injected into the intracerebral ventricle of rats. The antagonistic effect of CCK-8 on EA analgesia was reversed by an injection of CCK-A receptor antagonist L-364,718 (100 ng/µl) into the nPf of rats. Our results suggest that the pain-related neurons in the nPf have an important role in mediating EA analgesia. L-364,718 potentiates EA analgesia through the CCK-A receptor of PENs and PINs in the nPf.

The effect of acetylcholine on pain-related electric activities in the hippocampal CA3 of rats.

Acetylcholine (ACh) regulates pain perception in the central nervous system. However, the mechanism of action of ACh on pain-related neurons in the hippocampal CA3 is not clear. The present study aimed to determine the effect of ACh, muscarinic ACh receptors (mAChRs) agonist pilocarpine and mAChRs antagonist atropine on the pain-evoked responses of pain-excited neuron (PEN) and pain-inhibited neuron (PIN) in the hippocampal CA3 of normal rats. The trains of electric impulses applied to the sciatic nerve were used as noxious stimulation. The electric activities of PEN or PIN in the hippocampal CA3 were recorded by using a glass microelectrode. Our results showed that, in the hippocampal CA3, the intra-CA3 microinjection of ACh (2 µg/1 µl) or pilocarpine (2 µg/1 µl) decreased the discharge frequency and prolonged firing latency of PEN, and increased the discharge frequency and shortened firing inhibitory duration (ID) of PIN, i.e. exhibiting the analgesic effect of ACh or pilocarpine. The intra-CA3 administration of atropine (0.5 µg/1 µl) produced an opposite effect. On the basis of the above-mentioned findings, we can deduce that ACh and mAChRs in the hippocampal CA3 are involved in the modulation of nociceptive response by regulating the electric activities of PEN and PIN.

The effect of dopamine on pain-related neurons in the parafascicular nucleus of rats.

Dopamine (DA) regulates pain perception in the central nervous system (CNS). However, the mechanism of the action of DA in pain-related neurons of the parafascicular nucleus (Pf) is not clear. The present study aimed to determine the effect of DA and its receptor antagonist, droperidol on the pain-evoked responses of the pain-excited neurons (PEN) and pain-inhibited neurons (PIN) in the Pf of rats and to analyze the mechanisms underlying this effect. The trains of electric impulses applied to the sciatic nerve were used as noxious stimulation. The discharges of PEN and PIN in the Pf were recorded by using a glass microelectrode. The results showed that, in the Pf, intra-Pf microinjection of DA (5 microg/0.5 microl) increased the frequency of noxious stimulation-induced discharges of the PEN and decreased the frequency of those of the PIN, while the intra-Pf administration of droperidol (0.15 microg/0.5 microl) produced an opposite effect. On the basis of the above-mentioned findings, we could conclude that DA and its receptors in the Pf are involved in the modulation of the nociceptive response by regulating the discharges of PEN and PIN.

Effects of DCK knockdown on proliferation, apoptosis and tumorigenicity in vivo of cervical cancer HeLa cells.

The present study explored the effect that deoxycytidine kinase (DCK) knockdown had on proliferation, apoptosis and tumorigenicity in vivo of cervical cancer HeLa cells. Human cervical cancer HeLa cells that had received no prior treatment were selected from the HeLa group. The HeLa-negative control (NC) group consisted of cells that had undergone an empty vector treatment, and finally the HeLa-short hairpin RNA (shRNA) group included cells that were treated by means of shRNA-DCK expression. DCK expressions were evaluated by quantitative real-time polymerase chain reaction in addition to western blotting assays. Cell proliferation was estimated using the Cell Counting Kit-8 (CCK-8) assay and cell cycle progression. Cell apoptosis was determined by flow cytometry. BALB/c nude mice (n=24) were selected to establish transplanted tumor models, with gross tumor volume measured every 3 days. The results in vitro were as follows: compared with the HeLa group, the HeLa-shRNA group exhibited downregulation of DCK expression and inhibition of cell proliferation at 48, 72 and 96 h. Additionally, more cells in the HeLa-shRNA group were arrested in G0/G1 stage and less in S and G2/M stages, as well as in promotion of cell apoptosis. In vivo results are as follows: when comparing the HeLa and HeLa-NC groups, the gross tumor volume of the transplanted tumor in nude mice in the HeLa-shRNA group was found to have decreased in 13, 16, 19 and 22 days. Based on these findings, our study suggests that DCK knockdown facilitates apoptosis while inhibiting proliferation and tumorigenicity in vivo of cervical cancer HeLa cells.

[Comparison of two multi-drug chemotherapy regimens based on mitoxantrone and epirubicin in 44 patients with non-Hodgkin's lymphoma].

From June 1987 to June 1989, a comparative study was carried out in 44 NON = Hodgkin's lymphoma patients to-evaluate the effect and side effects of two multi-drug chemotherapy regimens: Group A (cyclophosphamide, mitoxantrone, vincristine, prednisone) and Group B (cyclophosphamide, epirubicin, vincristine, prednisone). The response rate was 86% in Group A (22 patients) and was 82% in Group B (22 patients). By the end of August, 1989, 12 patients in Group A were still alive with a median survival of 16 (5-24) months while 18 patients in Group B were living with a median survival of 15 (4-24) months. The side effects were tolerable in both groups. From the authors' data, mitoxantrone is considered as effective as epirubicin for Non-Hodgkin's lymphoma.

[Phase II clinical trial on mitoxantrone].

Mitoxantrone prepared by Shanghai Institute of Pharmaceutical Industry is reported. 154 patients with various advanced cancers confirmed by pathology were treated by mitoxantrone with a dose of 14 mg/M2, i. v., once every 3 or 4 weeks from Feb. 1985 to Feb. 1987. There were 96 males and 58 females. The ages ranged from 16 to 76 years with an mean age of 48 +/- 15. Objective response rates were 21% in breast cancer, 36% in non-Hodgkin's lymphoma, 56% in acute lymphocytic leukemia, 14% in acute nonlymphocytic leukemia, 31% in gastric cancer and 5% in primary hepatic cancer. The side effects were leukopenia and gastro-intestinal disturbances. No marked cardiac toxicity was observed.