Objective:This study aimed to reveal the age-related changes in prevalence and symptom characteristics in kidney deficiency syndrome (KDS) with varied health status.Methods:This cross-sectional observational study was conducted in6 hospitals.Investigators queried participants aged 20-79 about their health,including symptoms if any,and completed questionnaires to collect participants responses.Prevalence,severity,and frequency of KDS and other relevant parameters were observed and recorded.Comparative analysis of count-able variables,including prevalence,was performed by frequency analysis and x2 test and ex-pressed as a composite ratio.Comparative analysis of quantitative scores of the severity and frequency of symptoms was performed by the rank-sum test.Regression analysis of the corre-lation of KDS with potential contributing factors was performed by non-conditional binary lo-gistic stepwise regression of numerical variables.Results:Prevalence of KDS in healthy and unhealthy participants correlated with increasing age (P ＜ 0.05).In those with chronic disease,KDS prevalence was comparatively high,but the trend was not obvious.KDS prevalence in participants age 20-39 showed an increasing trend with deteriorating health (P ＜ 0.05).Compared to healthy individuals,KDS prevalence in subhealthy persons and those with chronic disease showed an increasing trend (P ＜ 0.05)in the 40-59 and 60-79 age groups,whereas there was no difference between subhealthy per-sons and those with chronic disease age 40-59 and 60-79.Symptom severity scores of KDS showed an increasing trend with increasing age and deteriorating health status (P ＜ 0.05).Higher symptom frequency scores were also positively correlated with increasing age(P ＜ 0.05),but health status deterioration was not significantly correlated (P ＞ 0.05).Age,health status,lower back pain,shin soreness or heel pain,tinnitus or deafness,hair loss or loose teeth,incomplete bladder emptying or incontinence,and sexual dysfunction or infer-tility were potential factors contributing to KDS (P ＜ 0.05),but age was the only independent variable for which OR ＞1.Moreover,the distribution of typical KDS-related symptoms showed dramatic regularities.Conclusion:Prevalence and symptom characteristics of KDS were found to increase consis-tently with increasing age and deteriorating health status.Kidney deficiency may be an impor-tant mechanism of aging in the subhealthy and chronic disease states.

As a non-invasive approach, sonogenetics is applied to control neuronal activity. The mechanosensitive channel(MSC), which has low threshold of responding to ultrasound, may be the alternative solution. Sonogenetics is the technique that activates the MSC expressed in targeted neurons by low intensity ultrasound, thus achieve the neuromodulation. In this review, we introduce the mechanosensitive channel of large conductance, transient receptor potential, channels of the two-pore-domain potassium family, Piezo and the recent progress on their application in sonogenetics.
Biomechanical Phenomena ; Ion Channels ; metabolism ; Neurons ; Ultrasonic Waves

OBJECTIVE: To investigate the mechanism of congenital paramyotonia caused by human skeletal muscle voltage-gated sodium channel hNav1.4 mutant I1363T. METHODS: The conservation of the mutant site were detecled by using amino acid sequence alignment; the C-terminal mCherry fusion hNav1.4 was constructed, and the expression and distribution of wild type and hNav1.4 mutant I1363T were determined by confocal microscopy; the steady-state activation, fast inactivation and window current of wild type and hNav1.4 mutant I1363T were examined by whole-cell patch clamp. RESULTS: Alignment of the amino acid sequences revealed that Ile1363 is highly conserved in human sodium channels. There was no significant difference in expression level and distribution between wild type and I1363T. Although no significant differences were observed between I1363T mutant and wild type in the activation upon channel gating, the of voltage-dependence of fast inactivation of I1363T mutant[(-59.01±0.26) mV] shifted 9 mV towards depolarization as compared with wild type[(-68.03±0.34) mV], and the slope factor of voltage-dependence curve increased to (5.24±0.23) mV, compared with (4.55±0.21) mV of the wild type. Moreover, I1363T showed the larger window current than that of the wild type. CONCLUSIONS I1363T causes the defect in fast inactivation of hNav1.4, which may increase the excitability of muscle cells and be responsible for myotonia. The increased window current of I1363T may result in an increase of inward Na+ current, could subsequently inactivate the channels and lead to loss of excitability and paralysis.
Gene Expression Profiling ; Humans ; Ion Channel Gating ; genetics ; Muscle, Skeletal ; physiopathology ; Mutation ; NAV1.4 Voltage-Gated Sodium Channel ; genetics ; Sequence Analysis, Protein

Female ; Infant, Newborn ; Humans ; Pregnancy ; Premature Birth ; Retrospective Studies ; Risk Factors ; Cerclage, Cervical ; Cervix Uteri