[Current status of vaccination services for adults in urban and rural areas of nine provinces in China from 2019 to 2021].

Objective: To understand the current situation of vaccination services for adults in China, explore how to establish a stable and efficient vaccination service system for adults, and provide reference for formulating corresponding policies. Methods: The vaccination information systems of nine provinces in China were used to obtain information on urban and rural vaccination of influenza vaccine, 23-valent pneumococcal polysaccharide vaccine (PPV23), and human papillomavirus vaccine (HPV) from 2019 to 2021. The indicator, vaccination rate/full vaccination rate, was used for statistical description. Results: The vaccination rate/full vaccination rate of the three vaccines in eastern China was generally higher than that in central and western China. The vaccination rate/full vaccination rate in urban areas was generally higher than that in rural areas. From 2019 to 2021, the vaccination rates of influenza vaccine among people aged 60 years and above in urban and rural areas were 2.96%, 6.29%, 6.14% and 1.29%, 2.58%, 2.94%, respectively. The vaccination rates of the PPV23 among people aged 60 years and above in urban and rural areas increased year by year, with rates of 0.38%, 1.05%, 1.15% and 0.14%, 0.49%, 0.59%, respectively. From 2019 to 2021, the HPV coverage of female adults aged 27-45 years in urban and rural areas increased year by year, with rates of 0.46%, 0.93%, 1.88% and 0.17%, 0.40%, 1.08%, respectively. Conclusion: The vaccination rates of influenza vaccine,PPV23 vaccine and HPV vaccine for adults in China are relatively low, with higher rates in the eastern region than in the central and western regions, and higher rates in urban areas than in rural areas. It is recommended to formulate corresponding health and economic policies and explore a suitable vaccination service system for adults in China to improve vaccination rates.

[Diagnostic value of endoscopic ultrasonography, fibroscan, acoustic radiation pulse imaging, serological index, and their combination for early stage liver cirrhosis].

Objective: To investigate the diagnostic value of endoscopic ultrasonography (EUS), Fibroscan, acoustic radiation force impulse (ARFI), and aspartate aminotransferase-to-platelet ratio (APRI) and their combination for early stage liver cirrhosis. Methods: Three hundred and twenty-two hospitalized patients who had been diagnosed with chronic viral liver disease from March 2016 to April 2018 were included. According to the clinical diagnosis, patients were divided into chronic hepatitis and the early stage liver cirrhosis group (Child-Pugh A grade). All patients were examined by Fibroscan to detect liver stiffness measurement (LSM), ARFI to detect liver virtual touch tissue quantification (VTQ) value, esophagogastroduodenoscopy and EUS to detect esophagogastric varices, laboratory and imaging examination. The index of EUS, Fibroscan, ARFI, and APRI was analyzed and the regression model was established by binary logistic regression, and the diagnostic efficacy of the above index and regression model for early stage of cirrhosis was evaluated by the area under a receiver operating characteristic curve (AUROCs). Results: An early stage cirrhosis group had significantly higher detection rate with EUS (esophagogastric varices), Fibroscan (LSM), ARFI (VTQ) and APRI than chronic hepatitis group [76.7% vs. 10.7%, 10.4 (7.8, 17.3) vs. 6.1 (5.2, 8.4) kPa, 1.71(1.48, 2.07) m/s vs. 1.25(1.14, 1.43) m/s and 0.65 (0.38, 1.15) vs. 0.38(0.26, 0.62), respectively]. The corresponding chi-square test were 140.86, Z = -9.069, Z = -9.948 and Z = -5.764, respectively and the differences were statistically significant (P < 0.01). The areas under the receiver operating characteristic curve and regression model were 0.830 (0.783 ~ 0.877), 0.793 (0.744 ~ 0.841), 0.821 (0.775 ~ 0.868), 0.686 (0.628 ~ 0.744) and 0.947 (0.925 ~ 0.969) for the diagnosis of early stage cirrhosis, respectively. Among them, the regression model of three indices (EUS, LSM and VTQ) had the largest AUROCs (0.947) and the corresponding sensitivity and specificity were 0.878 and 0.867, respectively. Conclusion: The combination of EUS, LSM and ARFI had a superior diagnostic value for early stage liver cirrhosis, and may improve the diagnosis rate and reduce the misdiagnosis rate.

Clinical efficacy and mechanism of lymphoplasma exchange in the treatment of Guillain-Barre syndrome.

Guillain-Barre syndrome (GBS) is an autoimmune disease of the nervous system and is the most common acute polyneuropathy. Both cellular and humoral immunity are believed to be involved in the pathogenesis of GBS, and various types of activated CD4+ T cells are thought to orchestrate the onset and progression of GBS. Lymphoplasma exchange (LPE) filtering out activated lymphocytes while exchanging plasma has been used for GBS treatment for years. However the treatment is still not yet optimal. In order to assess the efficacy of this treatment, we evaluate the effect of LPE and determine the appropriate frequency of LPE treatments for GBS patients through comparing the neurological deficit scores and the changes in related immunology indicators of GBS patients before and after LPE treatment. Twenty-four patients with GBS who received LPE were evaluated for immunologic indicants before treatment, on the second day, and the fourth day after the treatment. The immunoglobulin complement and CD4+ T lymphocyte subsets were tested by flow cytometry. The patients' Medical Research Council sum scores were increased from 25.7±10.4 up to. 36.7±10.4 (P=0.019) and their Hughes scores decreased from 3.7±0.76 to 3.1±0.73 (P=0.027) at 7 days after LPE. In the peripheral blood from patients received LPE treatment, the levels of immunoglobulin, complement, monocytes and fibrinogen were significantly reduced. The percentages of Th1 and Th17 cells in the CD4+ T lymphocyte subsets were significantly decreased, whereas the Th2 and Treg cells were increased in patients after treatment. The changes in CD4+T lymphocyte subsets were correlated with patient MRC score changes. Our data indicate that LPE is effective in treating GBS patients by directly removing immunoglobulin, complement, monocytes, and fibrinogen as well as regulating lymphocyte subsets in the peripheral blood.

Estrogen deficiency inducing shifted cytokines profile in bone marrow stromal cells inhibits Treg cells function in OVX mice.

The study aims to reveal the effect of estrogen deficiency on Treg cells population in bone marrow in the development of osteoclastogenis with comparing the differences about Treg cells phenotypes and cytokines related with the homeostasis and functions maintenance of Treg cells in bone marrow in OVX mice and health control group. Wide—type C57BL/6 mice were operated OVX to mimic estrogen deficiency in PMO women. Treg cells population and their surface markers expressions were detected by flow cytometry. Cytokines profiles in bone marrow with examined by real—time PCR and ELISA analysis. Signal pathways and key modulators responsible to inflammatory cytokines expressions in bone marrow stromal cells were also detected with using western blotting. Estrogen deficiency in OVX mice decreased Treg cells and their functions, and cytokines profile in bone marrow were found shifted in bone marrow when compared with control group. Consistent to these observations, signal pathways in bone marrow stromal cells were reported altered by estrogen deficiency in our model. Estrogen deficiency effects Treg cells population and their functions in OVX mice with altering cytokines profile in bone marrow stromal cells.

MiR-19b Functions as a Potential Protector in Experimental Autoimmune Encephalomyelitis.

BACKGROUND: MicroRNA-19b (miR-19b) is essential in determining oligodendroglia proliferation. Phosphatase and tensin homologue on chromosome 10 (PTEN) is considered the target of miR-19b and participates in oligodendrocyte differentiation and proliferation. METHODS: Murine EAE was induced by myelin oligodendrocyte glycoprotein (MOG35- 55). For EAE reversal, artificially synthesized agomiR-19b was intravenous injected after immunization. RESULTS: We found that the expression of miR-19b is significantly reduced in an experimental autoimmune encephalomyelitis (EAE) mouse model. This downregulation, which is associated with the neurological scores, can be dramatically ameliorated by agomiR-19b. Our results show that agomiR-19b increases the expression of myelin basic protein (MBP) and cyclic nucleotide phosphodiesterase (CNP), which are regularly utilized as molecular markers of oligodendrocytes. Furthermore, our study also revealed that miR-19b probably affects the expression of PTEN in the EAE model. CONCLUSION: These results indicate that the restoration of miR-19b probably exerts its therapeutic effect by affecting PTEN in the pathogenesis of EAE.

Lentiviral-mediated RNAi targeting caspase-3 inhibits apoptosis induced by serum deprivation in rat endplate chondrocytes in vitro.

Current studies find that degenerated cartilage endplates (CEP) of vertebrae, with fewer diffusion areas, decrease nutrient supply and accelerate intervertebral disc degeneration. Many more apoptotic cells have been identified in degenerated than in normal endplates, and may be responsible for the degenerated grade. Previous findings suggest that inhibition of apoptosis is one possible approach to improve disc regeneration. It is postulated that inhibition of CEP cell apoptosis may be responsible for the regeneration of endplates. Caspase-3, involved in the execution phase of apoptosis, is a candidate for regulating the apoptotic process. In the present study, CEP cells were incubated in 1% fetal bovine serum. Activated caspases were detected to identify the apoptotic pathway, and apoptosis was quantified by flow cytometry. Lentiviral caspase-3 short hairpin RNA (shRNA) was employed to study its protective effects against serum deprivation. Silencing of caspase-3 expression was quantified by reverse transcription-polymerase chain reaction and Western blots, and inhibition of apoptosis was quantified by flow cytometry. Serum deprivation increased apoptosis of rat CEP cells through activation of a caspase cascade. Lentiviral caspase-3 shRNA was successfully transduced into CEP cells, and specifically silenced endogenous caspase-3 expression. Surviving cells were protected by the downregulation of caspase-3 expression and activation. Thus, lentiviral caspase-3 shRNA-mediated RNAi successfully silenced endogenous caspase-3 expression, preventing inappropriate or premature apoptosis.

Lentiviral-mediated RNAi targeting caspase-3 inhibits apoptosis induced by serum deprivation in rat endplate chondrocytes in vitro

Current studies find that degenerated cartilage endplates (CEP) of vertebrae, with fewer diffusion areas, decrease nutrient supply and accelerate intervertebral disc degeneration. Many more apoptotic cells have been identified in degenerated than in normal endplates, and may be responsible for the degenerated grade. Previous findings suggest that inhibition of apoptosis is one possible approach to improve disc regeneration. It is postulated that inhibition of CEP cell apoptosis may be responsible for the regeneration of endplates. Caspase-3, involved in the execution phase of apoptosis, is a candidate for regulating the apoptotic process. In the present study, CEP cells were incubated in 1% fetal bovine serum. Activated caspases were detected to identify the apoptotic pathway, and apoptosis was quantified by flow cytometry. Lentiviral caspase-3 short hairpin RNA (shRNA) was employed to study its protective effects against serum deprivation. Silencing of caspase-3 expression was quantified by reverse transcription-polymerase chain reaction and Western blots, and inhibition of apoptosis was quantified by flow cytometry. Serum deprivation increased apoptosis of rat CEP cells through activation of a caspase cascade. Lentiviral caspase-3 shRNA was successfully transduced into CEP cells, and specifically silenced endogenous caspase-3 expression. Surviving cells were protected by the downregulation of caspase-3 expression and activation. Thus, lentiviral caspase-3 shRNA-mediated RNAi successfully silenced endogenous caspase-3 expression, preventing inappropriate or premature apoptosis.