ObjectiveTo explore the clinical efficacy and mechanism of Bupi Qingfei prescription （BPQF） in treating stable bronchiectasis in the patients with syndromes of lung-spleen Qi deficiency and phlegm-heat accumulation in the lungs. MethodsA randomized， double-blind， placebo-controlled trial was conducted. Patients were randomized into BPQF and placebo control （PC） groups. On the basis of conventional Western medicine treatment， the BPQF granules and placebo were respectively administered at 10 g each time， twice a day， for a course of 24 weeks. The TCM symptom scores， Quality of Life Questionnaire for Bronchiectasis （QOL-B） scores， lung function indicators， T lymphocyte subsets， level of inflammatory factors in the sputum， level of neutrophil elastase （NE） in the sputum， and occurrence of adverse reactions were observed before and after treatment in the two groups. ResultsA total of 64 patients completed the study， encompassing 32 in the BPQF group and 32 in the PC group. After treatment， the BPQF group showed decreased TCM symptom scores （P<0.01）， increased QOL-B scores （P<0.01）， and declined levels of tumor necrosis factor （TNF）-α and NE （P<0.05， P<0.01）. The PC group showed decreased TCM symptom （except spleen deficiency） scores （P<0.01）， increased the QOL-B health cognition and respiratory symptom domain scores （P<0.05， P<0.01）， and a declined TNF-α level （P<0.01）. Moreover， the BPQF group had lower TCM symptom （except chest tightness） scores （P<0.05， P<0.01）， higher QOL-B （except treatment burden） scores （P<0.05， P<0.01）， and lower levels of interleukin-6 and TNF-α （P<0.05） than the PC group. Neither group showed serious adverse reactions during the treatment process. ConclusionBPQF can ameliorate the clinical symptoms of stable bronchiectasis patients who have lung-spleen Qi deficiency or phlegm-heat accumulation in the lungs by regulating the immune balance and inhibiting airway inflammatory responses.

The pathogenesis of recurrent acute exacerbations of bronchiectasis is considered to be "yang floating and yin weakness". Yin weakness refers to the depletion of the water and fire of true yin in the lower jiao （焦）， which is the root of the disease. Yang floating refers to the ministerial fire floating upward and scorching the lung metal due to the failure of true yin to nourish and constrain yang， which is the manifestation of acute exacerbations. Yin weakness and yang floating interact with each other， forming a vicious cycle of "yin depletion leading to fire floating， and floating fire in turn injuring yin"， which leads to recurrent， prolonged， and refractory acute exacerbations of bronchiectasis. Based on the pathogenesis of yang floating and yin weakness， therapeutic formulas are proposed. Yinhuo Decoction （引火汤） can be used to nourish true yin and anchor floating fire， while a combination of Qianyang Pill （潜阳丹） and Fengsui Pill （封髓丹） is applied to warm the kidneys， subdue yang， and secure true fire， and Quanzhen Yiqi Decoction （全真一气汤） is utilized to drastically supplement the primal origin and rescue both yin and yang simultaneously.

Recent studies have identified a missense mutation in the β1-receptor (ADRB1-A187V) that exerts a pronounced impact on human sleep, with a noted decrease in protein abundance in vivo. The administration of β-blockers is frequently associated with sleep disturbances in clinical settings. In this study, we assessed the influence of various β-blockers on sleep within mouse models. Our findings indicated that β-blockers could induce varying degrees of arousal, sleep disruption, and a decrease in REMS (rapid eye movement sleep). We examined the dose-dependent effects of metoprolol and nebivolol on both sleep and cardiac functionality in both wild-type and Adrb1-A187V mutant mice. Our data suggested that, in contrast to cardiac effects, higher doses of metoprolol are required to have noted impact on sleep. No genotype effect was observed with metoprolol in terms of sleep or cardiac function. In contrast, the mutant mice demonstrated increased sensitivity to nebivolol, which exacerbated sleep fragmentation and impeded the onset of REMS. This study is expected to provide some reference for minimizing the occurrence of sleep disorders and reducing the adverse reactions of drugs to the greatest extent.

Amyotrophic lateral sclerosis (ALS) is an irreversible, fatal neurodegenerative disorder whose incidence is positively correlated with the aging population. ALS is characterized by the progressive loss of motor neurons, leading to muscle weakness, atrophy, and ultimately respiratory failure. The pathogenesis of ALS involves multiple factors, including genetic and environmental influences, with genetic factors playing a particularly significant role. To date, several causative genes have been identified in ALS, such as the Cu/Zn superoxide dismutase 1 (Cu/Zn SOD1, also known as SOD1) gene, transactive response DNA-binding protein 43 (TDP-43) gene, fused in sarcoma (FUS) gene, and chromosome open reading frame 72 (C9orf72). Mutations in these genes have been found not only in familial ALS but also in sporadic ALS. Based on the identified ALS risk genes, various ALS animal models have been established through multiple approaches, including transgenic models, gene knockout/knock-in models, and adeno-associated virus-mediated overexpression models. These models simulate some typical pathological features of human ALS, such as motor neuron loss, ubiquitinated inclusions, and neuromuscular junction degeneration. However, these models still have limitations: (1) single-gene mutation models are insufficient to fully replicate the complex multi-factorial pathogenesis of sporadic ALS; (2) significant differences in microenvironmental regulation mechanisms and the rate of neurodegeneration between model organisms and humans may affect the accurate reproduction of disease phenotypes and the reliable evaluation of drug efficacy. To better understand the pathogenesis of ALS and promote the development of effective therapies, constructing and optimizing ALS animal models is crucial. This review aims to summarize commonly used ALS gene mutation mouse models, analyze their phenotypes and pathological characteristics, including transgenic mouse models, gene knockout/knock-in mouse models, and adeno-associated virus-mediated overexpression mouse models, and further discuss their specific applications in ALS pathogenesis research and drug development by comparing the advantages and limitations of each model.

Amyotrophic lateral sclerosis (ALS) is an irreversible, fatal neurodegenerative disorder whose incidence is positively correlated with the aging population. ALS is characterized by the progressive loss of motor neurons, leading to muscle weakness, atrophy, and ultimately respiratory failure. The pathogenesis of ALS involves multiple factors, including genetic and environmental influences, with genetic factors playing a particularly significant role. To date, several causative genes have been identified in ALS, such as the Cu/Zn superoxide dismutase 1 (Cu/Zn SOD1, also known as SOD1) gene, transactive response DNA-binding protein 43 (TDP-43) gene, fused in sarcoma (FUS) gene, and chromosome open reading frame 72 (C9orf72). Mutations in these genes have been found not only in familial ALS but also in sporadic ALS. Based on the identified ALS risk genes, various ALS animal models have been established through multiple approaches, including transgenic models, gene knockout/knock-in models, and adeno-associated virus-mediated overexpression models. These models simulate some typical pathological features of human ALS, such as motor neuron loss, ubiquitinated inclusions, and neuromuscular junction degeneration. However, these models still have limitations: (1) single-gene mutation models are insufficient to fully replicate the complex multi-factorial pathogenesis of sporadic ALS; (2) significant differences in microenvironmental regulation mechanisms and the rate of neurodegeneration between model organisms and humans may affect the accurate reproduction of disease phenotypes and the reliable evaluation of drug efficacy. To better understand the pathogenesis of ALS and promote the development of effective therapies, constructing and optimizing ALS animal models is crucial. This review aims to summarize commonly used ALS gene mutation mouse models, analyze their phenotypes and pathological characteristics, including transgenic mouse models, gene knockout/knock-in mouse models, and adeno-associated virus-mediated overexpression mouse models, and further discuss their specific applications in ALS pathogenesis research and drug development by comparing the advantages and limitations of each model.

Objective To observe the effects of restricted and high-fat diets on behavioral changes of wild-type(Adrb1+/+)and transgenic mice carrying Adrb1-A187V mutation(Adrb1+/m)with short sleep durations.Methods Adrb1+/+and Adrb1+/m C57BL/6 mice were randomized into normal chow group(25 Adrb1+/+and 26 Adrb1+/m mice for behavioral monitoring),odor retention fasting group(17 Adrb1+/+and 19 Adrb1+/m mice for behavioral monitoring;6 Adrb1+/+mice and 6 Adrb1+/m mice for EEG/EMG monitoring),absolute fasting group(6 Adrb1+/+and 4-5 Adrb1+/m mice for behavioral monitoring;6 Adrb1+/+and 6 Adrb1+/m mice for EEG/EMG monitoring),and high-fat diet group(6 Adrb1+/+and 7 Adrb1+/m mice for behavioral monitoring;6 Adrb1+/+and 6 Adrb1+/m mice for EEG/EMG monitoring).Electrodes for EEG and muscle activity monitoring were implanted on the skulls of the mice.After 24 h of odor retention fasting,absolute fasting,or high-fat feeding,the mice were observed for behavioral changes adapted to diet changes.Results In odor retention fasting experiment,Adrb1+/m mice exhibited more stable fluctuations of activities with mildly reduced movement and prolonged sleep duration,indicating enhanced starvation resistance.In absolute fasting experiment,Adrb1+/m mice showed significantly increased nighttime water intake,improved rhythmicity in water intake(frequent intakes in small amounts),and increased duration of non-rapid eye movement sleep(NREM).In the high-fat diet experiment,Adrb1+/m mice showed higher levels of activity with increased instances of nighttime rearing,longer movement distances,and increased rapid eye movement sleep during daytime.Conclusion Adrb1+/m mice can quickly respond to environmental changes and under restricted dietary conditions,they can conserve energy by increasing sleep to maintain energy homeostasis but show higher levels of activity under high-fat dietary conditions.

Objective To observe the effects of restricted and high-fat diets on behavioral changes of wild-type(Adrb1+/+)and transgenic mice carrying Adrb1-A187V mutation(Adrb1+/m)with short sleep durations.Methods Adrb1+/+and Adrb1+/m C57BL/6 mice were randomized into normal chow group(25 Adrb1+/+and 26 Adrb1+/m mice for behavioral monitoring),odor retention fasting group(17 Adrb1+/+and 19 Adrb1+/m mice for behavioral monitoring;6 Adrb1+/+mice and 6 Adrb1+/m mice for EEG/EMG monitoring),absolute fasting group(6 Adrb1+/+and 4-5 Adrb1+/m mice for behavioral monitoring;6 Adrb1+/+and 6 Adrb1+/m mice for EEG/EMG monitoring),and high-fat diet group(6 Adrb1+/+and 7 Adrb1+/m mice for behavioral monitoring;6 Adrb1+/+and 6 Adrb1+/m mice for EEG/EMG monitoring).Electrodes for EEG and muscle activity monitoring were implanted on the skulls of the mice.After 24 h of odor retention fasting,absolute fasting,or high-fat feeding,the mice were observed for behavioral changes adapted to diet changes.Results In odor retention fasting experiment,Adrb1+/m mice exhibited more stable fluctuations of activities with mildly reduced movement and prolonged sleep duration,indicating enhanced starvation resistance.In absolute fasting experiment,Adrb1+/m mice showed significantly increased nighttime water intake,improved rhythmicity in water intake(frequent intakes in small amounts),and increased duration of non-rapid eye movement sleep(NREM).In the high-fat diet experiment,Adrb1+/m mice showed higher levels of activity with increased instances of nighttime rearing,longer movement distances,and increased rapid eye movement sleep during daytime.Conclusion Adrb1+/m mice can quickly respond to environmental changes and under restricted dietary conditions,they can conserve energy by increasing sleep to maintain energy homeostasis but show higher levels of activity under high-fat dietary conditions.

Bronchiectasis is a refractory chronic airway disease characterized by chronic cough and phlegm production. Airway mucus hypersecretion is one of the important causative factors for acute exacerbation of bronchiectasis. Thus， reducing airway mucus secretion during the stable phase of bronchiectasis is the key to the treatment. Phlegm-dispelling therapy is commonly used in modern medicine， which， however， fails to radically reduce mucus secretion. At the moment， it is difficult and urgent to find an intervention that can improve the quality of life of patients and reduce the recurrence of disease during the stable phase of bronchiectasis. Chinese medicine shows remarkable efficacy in reducing airway mucus secretion. Nonetheless， there is a lack of research on the airway mucus hypersecretion of bronchiectasis， and no registered research outcome is available. Traditional Chinese medicine boasts a lot of experience in the treatment of phlegm. It combines clearing and tonifying methods and identifies Yin and Yang and internal organs， thus being advantageous in the treatment of airway mucus hypersecretion of bronchiectasis. Therefore， it is an important topic to improve the effectiveness of Chinese medicine on airway mucus hypersecretion of bronchiectasis by focusing on the "generation"， "transformation" and "excretion" of phlegm.

With the rapid development in cataract operation,characteristics and types of intraocular lens have been improving and altering all along in over fifty years.The correct selection for intraocular lens is significant for cataract patient to get better vision after operation.Description of characteristics and selection of the intraocular lens are summarized.