0.05).Conclusions The serum concentrations of cortisol,GH,IGF-Ⅰ and IGFBP3 in children suffered from asthma have no obvious change before and after 24 months long-term inhaled corticosteroids.The height changes before and after therapy have no significant difference between observation group and control group with same age and gender.

Objective To determine the prevalence,trends and risk factors of drug-resistant tuberculosis (TB) in Ningbo during 2007-2010,and to explore the efficient control strategy of drugresistant TB.Methods A cross-sectional study of regional anti-TB drug resistance was conducted in Ningbo.The registered and culture-positive TB patients were enrolled and drug sensitivity test was performed.The demographic and clinical information were collected from the national TB report system.Logistic regression model was used to determine the risk factors of drug resistance.Results Of 1613 enrolled TB patients,39.3％-48.3％ were resistant to any first-line anti-TB drug and 14.0％-19.9％ were multidrug resistant (MDR)-TB.The proportion of new cases resistant to any first-line anti-TB drug was 35.4 ％-42.1％ and MDR TB was 9.8％- 12.2 ％,which were both significantly lower than those of retreated patients (69.5％-72.7％ and 33.9％ - 54.5％,respectively).The multivariate Logistic regression model showed that anti-TB treatment history and migration were significantly associated with any drug resistance (OR=3.298,95 ％ CI 2.391 4.550and OR=0.771,95 ％CI 0.608 - 0.978,respectively) ; while age,treatment history and migration were also significantly associated with MDR-TB.Conclusions Drug-resistant TB prevalence showed a decrease trend in Ningbo,while the resistant rates in both new cases and retreated cases still remain at high levels. Improved case management,including directly observed treatment short-course and appropriate treatment regimens specifically for drug-resistant TB,should be developed to prevent further transmission and development of drug-resistant TB in this setting.

Adolescent ; Adult ; Child ; Child, Preschool ; Diagnostic Errors ; statistics & numerical data ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Ulnar Nerve ; injuries ; Ulnar Neuropathies ; diagnosis

Objective To study the effects of different glucocorticasteroid(GCS) inhalation regimens for remissive children with asthma. Methods Three hundred and twenty - three patients with moderate asthma were enrolled on a 12 - week randomized parallel group remissive treatment after a 4 - week baseline treatment. During the baseline treatment terbutaline sulfate 250 ?g tid a day and bud esonide 200 ?g twice a day were given, and oral bronchodilators were used if necessary. The remissive treatment were composed of budesomde inhabit ion 100 ?g once a day (group A), 100 ?g twice a day(group B) and 200 ?g once a day(group 0). Patients subsequently returned to the clinic for 3 additional clinic visits (4,8 and 12 weeks) or telephone visits . On every clinic visit, the daytime and nocturnal time seventy score were recorded and spirometry was conducted in patients who were capable of performing the maneuver. Results Ultimately, 323 children were enrolled on the baseline treatment and 281 (87%) children achieved clinical remission. The rate of compliance decreased gradually during the remissive treatment, but in group B(P

OBJECTIVEAnimal studies have demonstrated a lipid-modulating effect of yun-cai tea. However, little is known about the lipid-lowering effect in humans.The aim of this study was to evaluate the lipid lowering effects and safety of yun-cai tea in patients with elevated lipid levels in a human clinical trial.

METHODSThis was a 12-week, randomly assigned, parallel-group, double-blind, and placebo-controlled pilot clinical study. Sixty primary hyperlipidemia patients were included and randomly assigned to the yun-cai tea group (30 patients) and the placebo group (30 patients), for 8 weeks of treatment and 4 weeks of follow-up. The primary endpoint was changes in plasma low-density lipoprotein-cholesterol (LDL-C) at 8 weeks. The secondary endpoints included total cholesterol (TC) and triglycerides (TG).

RESULTSOur results revealed no statistically signifificant differences in LDL-C and TC between the two groups. Despite the lack of a statistically signifificant difference in the level of TG between the two groups, a declining trend was noted. A signifificant reduction of TG was observed in the yun-cai tea group at week 8, compared to baseline (P=0.048). The incidence of stomach discomfort, gastroesophageal reflfl ux, diarrhea, and constipation was slightly higher in the yun-cai tea group. No other signifificant adverse events were found.

CONCLUSIONIt is unlikely that yun-cai tea used had a blood lipid reduction effect. Further larger scale clinical trials with a longer duration and larger dose are necessary.

Adult ; Double-Blind Method ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Herbal Medicine ; Humans ; Hyperlipidemias ; drug therapy ; Hypolipidemic Agents ; therapeutic use ; Male ; Middle Aged ; Placebos

This study was purposed to investigate the effect of different compositions and concentrations of lyophilizing protectants on recovery of RBCs and hemoglobin (Hb) after rehydration of lyophilized RBCs. The RBC lyophilizing protectants composed of a series concentrations of PVP, trehalose and different osmotic protectants were applied for protecting lyophilizing process of RBCs, the recovery of RBCs and Hb after rehydration of lyophilized RBCs was detected. The results showed that there were significant differences in loss ratio of RBCs between protectants composed of different compositions and concentrations (p<0.05 or p<0.01). The loss ratio of RBCs in protectant containing 30% PVP40, 150 mmol/L trehalose and 2% BSA was minimum (0.02%), the loss ratio of RBCs in protectant containing 6% PVP 360, 100 mmol/L trehalose and 2% BSA was maximum (0.27%). The difference of effect between 150 and 50 mmol/L trehalose was statistically significant (p<0.01). The recovery rates of RBCs and Hb in protectants contained PVP40 of different concentrations were different after rehydration of lyophilized RBCs. The protectant containing 15% PVP40, 150 mmol/L trehalose and 2% BSA showed optimal protective efficacy for lyophilized RBCs, the recovery rates of RBCs and Hb were 61.29+/-4.11% and 62.49+/-5.91% respectively, which were statistically different from other protectants (p<0.01). The protectants containing glycerol displayed best efficiency in lyophilization too, the recovery rates of RBCs and Hb were 65.97+/-4.52% and 67.24+/-5.94%, respectively. It is concluded that the protectants composed of 0.8 mol/L glycerol, 15% PVP40, 150 mmol/L trehalose and 2% BSA (pH 7.3 ) may be used as the protectant lyophilizing human RBCs in future study.
Blood Preservation ; methods ; Cryoprotective Agents ; administration & dosage ; analysis ; Erythrocytes ; Freeze Drying ; methods ; Humans ; Trehalose ; administration & dosage ; analysis

Objectives: . Our study aimed to explore the role of the potassium channel KCNK1 in head and neck squamous cell carcinoma, focusing on its impact on tumor growth, invasion, and metastasis. We also investigated the therapeutic potential of quinidine, a known KCNK1 inhibitor, in both in vitro cell lines and a zebrafish patient-derived xenograft (PDX) model. Methods: . We established primary cell cultures from head and neck cancer tissues and employed the FaDu cell line for in vitro studies, modulating KCNK1 expression through overexpression and knockdown techniques. We evaluated cell migration, invasion, and proliferation. Additionally, we developed a zebrafish PDX model to assess the impact of quinidine on tumor growth and metastasis in vivo. RNA sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted to elucidate the molecular mechanisms underlying the role of KCNK1 in cancer progression. Results: . Overexpression of KCNK1 in FaDu cells resulted in enhanced cell migration and invasion, whereas its knockdown diminished these processes. In the zebrafish PDX model, quinidine markedly inhibited tumor growth and metastasis, demonstrating a significant reduction in tumor volume and micrometastasis rates compared to the control groups. The molecular analyses indicated that KCNK1 plays a role in critical signaling pathways associated with tumor growth, such as the Ras and MAPK pathways. Conclusion . Our findings highlight the critical role of KCNK1 in promoting tumor growth and metastasis in head and neck cancer. The inhibitory effect of quinidine on tumor progression in the zebrafish PDX model highlights the therapeutic potential of targeting KCNK1. These results suggest that KCNK1 could serve as a valuable therapeutic target for head and neck cancer, warranting further investigation into treatments that target KCNK1.

Objectives: . Our study aimed to explore the role of the potassium channel KCNK1 in head and neck squamous cell carcinoma, focusing on its impact on tumor growth, invasion, and metastasis. We also investigated the therapeutic potential of quinidine, a known KCNK1 inhibitor, in both in vitro cell lines and a zebrafish patient-derived xenograft (PDX) model. Methods: . We established primary cell cultures from head and neck cancer tissues and employed the FaDu cell line for in vitro studies, modulating KCNK1 expression through overexpression and knockdown techniques. We evaluated cell migration, invasion, and proliferation. Additionally, we developed a zebrafish PDX model to assess the impact of quinidine on tumor growth and metastasis in vivo. RNA sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted to elucidate the molecular mechanisms underlying the role of KCNK1 in cancer progression. Results: . Overexpression of KCNK1 in FaDu cells resulted in enhanced cell migration and invasion, whereas its knockdown diminished these processes. In the zebrafish PDX model, quinidine markedly inhibited tumor growth and metastasis, demonstrating a significant reduction in tumor volume and micrometastasis rates compared to the control groups. The molecular analyses indicated that KCNK1 plays a role in critical signaling pathways associated with tumor growth, such as the Ras and MAPK pathways. Conclusion . Our findings highlight the critical role of KCNK1 in promoting tumor growth and metastasis in head and neck cancer. The inhibitory effect of quinidine on tumor progression in the zebrafish PDX model highlights the therapeutic potential of targeting KCNK1. These results suggest that KCNK1 could serve as a valuable therapeutic target for head and neck cancer, warranting further investigation into treatments that target KCNK1.

Objectives: . Our study aimed to explore the role of the potassium channel KCNK1 in head and neck squamous cell carcinoma, focusing on its impact on tumor growth, invasion, and metastasis. We also investigated the therapeutic potential of quinidine, a known KCNK1 inhibitor, in both in vitro cell lines and a zebrafish patient-derived xenograft (PDX) model. Methods: . We established primary cell cultures from head and neck cancer tissues and employed the FaDu cell line for in vitro studies, modulating KCNK1 expression through overexpression and knockdown techniques. We evaluated cell migration, invasion, and proliferation. Additionally, we developed a zebrafish PDX model to assess the impact of quinidine on tumor growth and metastasis in vivo. RNA sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted to elucidate the molecular mechanisms underlying the role of KCNK1 in cancer progression. Results: . Overexpression of KCNK1 in FaDu cells resulted in enhanced cell migration and invasion, whereas its knockdown diminished these processes. In the zebrafish PDX model, quinidine markedly inhibited tumor growth and metastasis, demonstrating a significant reduction in tumor volume and micrometastasis rates compared to the control groups. The molecular analyses indicated that KCNK1 plays a role in critical signaling pathways associated with tumor growth, such as the Ras and MAPK pathways. Conclusion . Our findings highlight the critical role of KCNK1 in promoting tumor growth and metastasis in head and neck cancer. The inhibitory effect of quinidine on tumor progression in the zebrafish PDX model highlights the therapeutic potential of targeting KCNK1. These results suggest that KCNK1 could serve as a valuable therapeutic target for head and neck cancer, warranting further investigation into treatments that target KCNK1.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.