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BackgroundNon-motor symptoms (NMS) are compulsory clinical features for the clinical diagnosis of multiple system atrophy (MSA), some of which precede motor symptoms onset. To date, few studies have systematically investigated NMS in MSA and the timing of presenting NMS as the disease progresses. Clinically, MSA is difficult to be differentiated from Parkinson's disease (PD) and progressive supranuclear palsy (PSP), and the differences in NMS between MSA and PD/PSP remain unclear. The aim of this study was to compare the burden of NMS between MSA and PD/PSP and to delineate the timing of NMS presentation relative to the onset of motor symptoms in MSA.MethodsA total of 61, 87, and 30 patients with MSA, PD, and PSP, respectively, were enrolled in this study. NMS was systematically assessed in all patients using the NMS scale (NMSS), and the onset of NMS relative to the onset of motor symptoms in MSA was investigated.ResultsMSA group had higher total NMSS scores (82.15 ± 46.10) than the PD (36.14 ± 30.78) and PSP (50.30 ± 55.05) groups (p < 0.001 overall). The number distribution pattern of the NMS was significantly different among the three parkinsonian disorders (p < 0.001 overall). In total, 85.2% of patients with MSA had more than 10 NMS, which was significantly higher than PD (28.7%) and PSP (33.3%). The frequency and scores of many NMSS subdomains and symptoms were higher in MSA than in PD and PSP (all p < 0.05). Multivariate logistic regression analysis revealed that patients with fainting, lack of motivation, swallowing, and loss of sexual interest could be attributed to MSA rather than PD or PSP, while patients with loss of concentration and forgetfulness were characteristic features of PD or PSP rather than MSA. REM-sleep behavior disorder (RBD), constipation, problems having sex, and loss of sexual interest preceded the motor symptoms onset of MSA by 2.81 ± 4.51, 1.54 ± 6.32, 1.35 ± 4.70, and 0.45 ± 3.61 years, respectively.ConclusionThe NMS spectrum in MSA differs from that of PD and PSP. Patients with MSA have a higher NMS burden than patients with PD or PSP. RBD, constipation, problems having sex, and loss of sexual interest may become early diagnostic clinical markers of MSA.

Objective To investigate the clinical phenotype and genotype manifestations of autosomal recessive hereditary spastic ataxia 2 (SPAX2), to help physicians recognize this disease. Methods and Results A 35-year-old male patient presented with postural tremors, ataxia, hyperreflexia and then got worse progressively. Sanger sequencing found a homozygous missense mutation in the exon 13 c.1089T > G (p.Ile363Met) of KIF1C gene. It came from his parents respectively and was consistent with the autosomal recessive genetic law. The patient was clearly diagnosed as SPAX2, and his family was diagnosed as SPAX2 pedigree. Conclusions KIF1C-related SPAX2 may be considered as a candidate diagnosis for adolescent patients with postural tremor, ataxia and hyperreflexia. DOI: 10.3969/j.issn.1672-6731.2019.06.008

Objective To summarize phenotype, treatment principles and prognosis of 4 patients from 2 pedigrees with late-onset methylmalonic aciduria (MMA) and homocystinuria cobalamin C (cblC) type, so as to explore the pathophysiological mechanism of this disease. Methods and Results Exome sequencing was applied to rapidly diagnose 2 pedigrees of late-onset MMA and homocystinuria cblC type. The MMACHC gene mutations of the sisters in pedigree 1 were exon 4 c.482G > A (p.Arg161Gln) and c.615C > A (p.Tyr205X). Their parents carried the gene mutation respectively. The proband presented intelligence deterioration, spastic motor dysfunction of lower limbs and epilepsy. The younger sister presented axonal peripheral neuropathy and optic nerve atrophy, while the mental retardation was mild. For the brother and sister in pedigree 2, c.440_441del (p.Gly147fs) and c.482G > A (p.Arg161Gln) in exon 4 of MMACHC gene were identified which came from their parents respectively. The proband presented mental retardation and behavior disorder, weakness of lower limbs with pyramidal sign, and myelinated and axonal mixed peripheral neuropathy. His younger sister had similar symptoms and suffered earlier. After treated by vitamin B12, folic acid and levocarnitine for 6 months, all patients showed intelligence improved and seizures controlled, while still suffered from different degrees of dyskinesia of lower limbs. Conclusions The clinical symptoms of late-onset MMA and homocystinuria cblC type are complex and variable. Cerebral cortex, pyramidal system, extrapyramidal system and peripheral nerve could be widely involved. Target region gene capture combined with next-generation sequencing technology can be used to diagnose the disease rapidly, and early diagnosis and treatment are crucial to improve the prognosis. DOI: 10.3969/j.issn.1672-6731.2019.06.007

Objective To estimate the accuracy and stability of capillary electrophoresis fragment analysis and clone sequencing in detecting dynamic mutations of spinocerebellar ataxia (SCA). Methods Capillary electrophoresis fragment analysis and clone sequencing were used in detecting trinucleotide repeated sequence of 14 SCA patients (3 cases of SCA2, 2 cases of SCA7, 7 cases of SCA8 and 2 cases of SCA17). Results Capillary electrophoresis fragment analysis of 3 SCA2 cases showed the expanded cytosine-adenine-guanine (CAG) repeats were 31, 30 and 32, and the copy numbers of 3 clone sequencing for 3 colonies in each case were 37/40/40, 37/38/39 and 38/39/40 respectively. Capillary electrophoresis fragment analysis of 2 SCA7 cases showed the expanded CAG repeats were 57 and 34, and the copy numbers of repeats were 69, 74, 75 in 3 colonies of one case, and was 45 in the other case. For the 7 SCA8 cases with the expanded cytosine-thymine-adenine (CTA)/cytosine-thymine-guanine (CTG) repeats of 99, 111, 104, 92, 89, 104 and 75, the results of clone sequencing were 97, 116, 104, 90, 90, 102 and 76 respectively. For 2 SCA17 cases with the short/expanded CAG repeats of 37/50 and 36/45, the results of clone sequencing were 51/50/52 and 45/44 for 3 and 2 colonies. Conclusions Although the higher mobility of polymerase chain reaction (PCR) products containing dynamic mutation in the capillary electrophoresis fragment analysis might cause the deviation for analysis of copy numbers, the deviation was predictable and the results were repeatable. The clone sequencing results showed obvious instability, especially for SCA2 and SCA7 genes, which might owing to their simple CAG repeats. Consequently, clone sequencing is not suited for detection of dynamic mutation, not to mention the quantitative criteria of dynamic mutation sequencing. DOI: 10.3969/j.issn.1672-6731.2018.03.008

Objective To investigate the clinical features and dynamic mutation of 10 cases with juvenile-onset Huntington's disease (HD). Methods The cytosine-adenine-guanine (CAG) repeats of IT15 gene were detected by polymerase chain reaction (PCR) and capillary electrophoresis in 272 individuals of 159 pedigrees with preliminary diagnosis of HD. The correlation between clinical features and expanded CAG repeats in the IT15 gene of 10 cases with juvenile-onset HD were studied carefully. Results Among 211 individuals carried expanded CAG repeats, 10 cases onset before 20 years of age. The predominant clinical manifestations were involuntary movement and cognitive impairment. The average age of onset was (12.50 ± 4.55) years, and the average CAG repeat number of IT15 gene was 63.70 ± 14.83. Pearson correlation analysis showed that the age of onset was significantly and negatively correlated with the CAG repeat number (r = - 0.865, P = 0.001). Conclusions 1) The juvenile?onset case of HD presented with different clinical features compared with adult - onset cases. The most common presentation is cognitive decline. 2) Analysis of CAG repeats of IT15 gene is necessary for the diagnosis of juvenile-onset case of HD with no family history. 3) The variability in age of onset is not completely explained by the effects of expanded CAG repeats of IT15 gene, which is more prominently for the juvenile?onset cases, therefore, it is suggested that other factors may modulate the age of onset. DOI: 10.3969/j.issn.1672-6731.2017.08.008

Objective To make the diagnosis for a patient presented with head tremor and cerebellar atrophy by integrating clinical features and accessory examination with genetic testing and to explore the interpretation of genetic testing results. Methods A 30-year-old male patient's medical information, clinical pheontype, family history and accessory examinations were collected. The next?generation sequencing (NGS) of exons in 3994 causative genes of Mendelian inheritance diseases and the family tree verification were carried out. China Human Phenotype Ontology (CHPO), Phenomizer, Ensembl and Online Mendelian Inheritance in Man (OMIM) database were used to interpret the genetic test results. Results The patient carried heterozygous mutation of spinocerebellar ataxia type 19 (SCA19) related KCND3 gene c.1057A > G (p. Ser353Gly), but his parents did not carry this mutation. The patient also carried heterozygous mutation of parkinsonism type 20 (PARK20) related SYNJ1 gene c.4436C > T (p.Thr1479Ile) which was also seen in his mother. Phenotypic similarity analysis showed the patient's phenotype was correspond with the phenotype of SCA19, and the variation locus of KCND3 gene c.1057A > G was highly conservative with homologous gene in different species. Conclusions By means of the integration of clinical phenotype with the result of genetic test, KCND3 gene c.1057A > G (p.Ser353Gly) carried in the patient is the pathogenic mutation. DOI: 10.3969/j.issn.1672-6731.2017.07.007

Objective In the present experiment we investigate the behavior of 4-month-old transgenic APP/PS-1/tau mice model with Alzheimer's disease (3 × Tg-AD mice) to evaluate their abilities of spatial learning and memory. We observe the changes of synaptic plasticity and soluble amyloid-β protein 42 (Aβ42) expression in the CA1 region of hippocampus to explore the mechanism of early cognitive impairment of 3 × Tg-AD mice. Methods Ten 4-month-old male 3 × Tg-AD mice and matched ten 129/C57BL/6 hybrid wild type (WT) mice were enrolled. The open field test and Morris water maze test were conducted to observe emotion disorder and ability of spatial learning and memory. Field excitatory postsynaptic potential (fEPSP) and theta burst stimulation (TBS)-induced long-term potentiation (LTP) were recorded in CA1 region of hippocampus. The expression changes of soluble Aβ42 in hippocampus were measured by enzyme-linked immunosorbent assay (ELISA). Results The open field test showed that there was no significant differences between 3 × Tg-AD group and control group, which indicated that there was no obvious anxiety tendency in 4-month-old 3 × Tg-AD mice. Compared with control group, 3 × Tg-AD group mice had significantly longer escape latency from the 3rd to 5th day (P = 0.001, 0.003, 0.001) and lower percentage of time through the platform area (P = 0.000). LTP induced by TBS in CA1 region of hippocampus of 3 × Tg-AD group decreased significantly (P < 0.01, for all) compared with that of control group. In contrast to control group, the expression of soluble Aβ42 in the hippocampus of 3 × Tg-AD mice group increased significantly (P = 0.000). Conclusions The expression of soluble Aβ42 in the hippocampus of 4-month-old 3 × Tg-AD mice increased significantly, which impaired synaptic plasticity in CA1 region of hippocampus and led to a significant decline in spatial learning and memory ability. DOI: 10.3969/j.issn.1672-6731.2015.05.012

DOI: 10.3969/j.issn.1672-6731.2016.08.013

Spinocerebellar ataxia type 1 (SCA1) is a kind of autosomal dominant genetic neurodegenerative disorder. To date, the pathogenesis of SCA1 remains unclear. Studies in numerous SCA1 experimental models, including transgenic mice, transgenic drosophila and induced pluripotent stem cells, have shown that phosphorylation of S776 in mutant ataxin-1, molecular chaperones, ubiquitin-proteasome system and down-regulation of several components of RAS-MAPK-MSK1 pathway may involve in the pathogenesis of SCA1. In this review, the clinical and pathological features of SCA1, and the latest advances of pathogenesis, model systems and therapeutic exploration will be briefly summarized. doi: 10.3969/j.issn.1672-6731.2014.05.017

Background 131I-metaiodobenzylguanidine (131I-MIBG) can be intaked by cardiac sympathetic postganglionic fibre, thus becomes the imaging agent to evaluate cardiac sympathetic nerve function. The aim of this study is to investigate the autonomic nerve dysfunction of patients with multiple system atrophy (MSA) by using cardiac 131I-MIBG scintigraphy. Methods Clinical data of 12 MSA patients conforming to the "secord consensus statement on the diagnosis of MSA" was analyzed by Unified Multiple System Atrophy Rating Scale (UMSARS). 131I-MIBG scintigraphy was performed in 12 MSA patients and 7 age-matched controls. Planar images of the chest were obtained 15 min, 4 h and 24 h after the intravenous injection of 3 mCi 13131I-MIBG. Cardiac 131I-MIBG uptake was quantified by comparing region of interest (ROI) over heart/mediastinum (H/M) ratio. Results Cardiac 131131I-MIBG uptake ratio in MSA group was significantly less than that in control group in 15 min (1.90 ± 0.41 vs 2.38 ± 0.32, P = 0.017) and 4 h (1.96 ± 0.63 vs 2.60 ± 0.55, P = 0.039). There were significant difference (P < 0.05) between MSA group and control group. Conclusions Cardiac 131I-MIBG uptake ratio in MSA group was less than that in control group. This finding suggests cardiac sympathetic degeneration may occur in MSA patients. doi: 10.3969/j.issn.1672-6731.2014.03.018

Background Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant genetic disease characterized by cerebellar ataxia, ophthalmoplegia, slow saccade, hyporeflexia, action tremor, cognitive decline and peripheral neuropathy. The brain MRI shows obvious atrophy of cerebellum and brainstem, indicating typical change of olivopontocerebellar atrophy. SCA2 is caused by an expanded cytosine-adenine-guanine (CAG) trinucleotide repeat in the encoding region of ATXN2. The normal CAG repeats range from 13 to 31, and ataxic phenotype occurs when the repeats are more than 34. This study focused on the clinical and imaging features of 5 SCA2 families confirmed by genetic testing. The correlation between phenotype and genotype was analyzed. Methods The pathological CAG triplet repeat expansions of SCA1-3, 6, 7, 17 and dentatorubral-pallidoluysian atrophy (DRPLA) genes were analyzed in the probands of 708 autosomal dominant SCA families and 119 sporadic SCA cases. The CAG repeat of ATXN2 gene was amplified by polymerase chain reaction (PCR) and agarose gel electrophoresis. Fragment analysis based on CEQ8000 sequencer were applied to analyze expanded alleles. Results Expanded CAG repeats of ATXN2 gene were detected in 45 probands of SCA2 families. Most of the patients manifested with the typical clinical features of SCA2 such as cerebellar ataxia, ophthalmoplegia, slow saccade and hyporeflexia. Some of them also associated with action tremor. The brain MRI showed obvious atrophy of cerebellum and brainstem. The correlation between clinical features and CAG repeat of ATXN2 gene wasstudied carefully in 5 families. Conclusion Genetic analysis provides the basis for the diagnosis of SCA2. Clinical and neuroimaging features are very helpful in the diagnosis and differential diagnosis of this disease. For the identification of cases carrying intermediate allele, it is important to combine clinical, imaging features with dynamic mutation analysis in the affected cases within the family.

The diagnosis and discrimination of movement disorders is very difficult in clinical medicine. We usually make a diagnosis according to symptoms and physical examination when the disease develops to a certain stage, but with few objective criteria. Pathological result can provide a definite diagnosis. Recently, a new examination named transcranial sonography (TCS) has been used in the diagnosis of Parkinson's disease (PD) in Europe. It is also helpful in the diagnosis of other movement disorders and neurodegenerative diseases. The advantages of TCS include non⁃invasion, making a diagnosis at the early stage of disease, convenience and short testing time. We give a review about TCS in four parts: the historical development of TCS, the principle of TCS in diagnosing movement disorders, the applications of TCS in movement disorders and the advantages and disadvantages of TCS. DOI：10.3969/j.issn.1672⁃6731.2012.05.021

Background Huntington's disease (HD) is an autosomal dominant hereditary progressive neurodegenerative disorder with a distinct phenotype characterized by chorea, dementia, cognitive and affective impairment. There are selective neural cell loss and atrophy in the caudate and putamen. Dr. George Huntington firstly described the disease accurately and insightfully, which led to a widespread recognition of the inherited chorea that now bears his name. Huntington disease gene (IT15) locus on chromosome 4p16.3, and encompasses 67 exons with a trinucleotide repeat (CAG) in the first exon. The CAG repeat length is highly polymorphic in the population and expanded on at least one chromosome of individuals with HD. Clinically, patient with HD are often onset in adulthood. Juvenile⁃onset HD is relatively rare. Adult⁃onset HD patients usually have a CAG expansion from 40 to 55 whereas those with juvenile ⁃ onset greater than 60 which are often inherited from the father. We investigated the clinical features of a juvenile⁃onset case with Huntington disease and dynamic mutation of his family. Methods The CAG repeats of IT15 gene were detected using polymerase chain reaction and capillary electrophoresis in 115 individuals with preliminary diagnosis as Huntington disease. The repeat numbers of some samples carried expanded or intermediate alleles were verified by the pMD18⁃T vector clone sequencing. Results Fragment analysis showed that one juvenile ⁃ onset case presenting with cognitive dysfunction and hypokinesis carried 15/68 CAG repeats of IT15. His father carried 17/37 and mother carried 15/17. Conclusion 1) The juvenile ⁃onset case of HD presented with different clinical features compared with adult⁃onset cases. The typical signs of adult⁃onset cases include progressive chorea, rigidity and dementia. The most common sign of juvenile⁃onset Huntington disease is cognitive decline. 2) The dynamic mutation of IT15 gene expansion of the CAG repeats in the intergenerational transmission may lead to anticipation, which is a phenomenon characterized by increasing severity and earlier onset in successive generations. The abnormal allele of the patient inherited from his father and substantially expanded between generations, which indicates the CAG repeats is more unstable in the paternal inheritance. DOI：10.3969/j.issn.1672⁃6731.2012.03.011

Multiple system atrophy (MSA) is a sporadic and rapidly progressive neurodegenerative disorder characterised clinically by any combination of autonomic, cerebellar ataxia, parkinsonian, and pyramidal signs. Over the past 10 years, substantial progress has been achieved to establish MSA as an α⁃ synucleinopathy along with other neurodegenerative diseases. Although the diagnosis of this disorder is largely based on clinical expertise, some investigations have been proposed to assist in early differential diagnosis, especially neuroimaging examination, which have resulted in revised diagnostic criteria. The UMSARS is a reliable and valid scale for semiquantitative clinical assessments of MSA patients. An outline of the rationale for managing symptomatic deterioration in MSA is provided including novel neuroprotective therapeutic approaches, together with the treatment of traditional Chinese medicine. DOI：10.3969/j.issn.1672⁃6731.2012.03.006

Objective To investigate the clinical and genetic features of dentatorubral ⁃ pallidoluysian atrophy (DRPLA). Methods The trinucleotide repeats of spinocerebellar ataxia (SCA) disease genes were detected by polymerase chain reaction (PCR) initially in 388 SCA cases which included 234 cases with autosomal dominant inheritance and 154 sporadic cases. Fragment analysis with laser ⁃ induced fluorescence in capillary electrophoresis was performed for the samples with 2 bands detected by agarose gel electrophoresis (AGE). The repeat numbers of the positive or suspicious samples were verified by the pUC18⁃T vector cloning and sequencing. Results Based on the 2 methods, the cytosine⁃adenine⁃ guanine (CAG) repeat expansion of DRPLA gene was detected in one female case with mild ataxia and suspected seizure. The repeat numbers of the 2 alleles were 14 and 54 by fragment analysis, and 15 and 58 by cloning sequencing. The 2 members of her family had a history of seizure, but no obvious ataxia. The CAG repeat numbers of the other 19 cases without abnormal expansions ranged from 7 to 20, of which 9 was common. Conclusion The patient's atypical manifestations suggests that clinical variation may exist in DRPLA. Only one case of DRPLA is found in 388 SCA cases, indicating that DRPLA may be a relatively rare subtype of SCA in Chinese population. The secondary structure of DNA owing to the highly repetitive sequences will induce DNA polymerase sliding during the amplification, which will reduce the fidelity in DNA replication. This problem exists in both fragment analysis and cloning sequencing. For the latter method, the instability also appears in the process of cloning. Therefore, the repeat numbers need to be mutually verified by the 2 methods. DOI：10.3969/j.issn.1672-6731.2010.06.012

Introduction: The population of Taiwan has a long history of ethno-cultural evolution. The Taiwanese population was isolated from other large populations such as the European, Han Chinese, and Japanese population. The Taiwan Biobank (TWB) project has built a nationwide database, particularly for personal whole-genome sequence (WGS) to facilitate basic and clinical collaboration nationally and internationally, making it one of the most valuable public datasets of the East Asian population. Objectives: This study provides comprehensive medical genomic findings from TWB WGS data, for better characterization of disease susceptibility and the choice of ideal treatment regimens in Taiwanese population. Methods: We reanalyzed 1496 WGS using a PrecisionFDA Truth challenge winner method Sentieon DNAscope. Single nucleotide variants (SNV) and small insertions/deletions (INDEL) were benchmarked. We also analyzed pharmacogenomic (PGx) drug-associated alleles, and copy number variants (CNV). Multiple practicing clinicians reviewed and curated the clinically significant variants. Variant annotations can be browsed at TaiwanGenomes (https://genomes.tw). Results: We found that each participant had an average of 6,870.7 globally novel variants and 75.3% (831/1103) of the participants harbored at least one PharmGKB-selected high evidence level human leukocyte antigen (HLA) risk allele. 54 PharmGKB-reported high-level instances of evidence of Cytochrome P450 variant-drug pairs, with a population frequency of over 13.2%. We also identified 23 variants in the ACMG secondary finding V3 gene list from 25 participants, suggesting that 1.67% (25/1496) of the population is harboring at least one medical actionable variant. Our carrier status analyses suggest that one in 25 couples (3.94%) would risk having offspring with at least one pathogenic variant, which is in line with rates found in Japan and Singapore. For pathogenic CNV, we detected 6.88% and 2.02% carrier rates for alpha thalassemia and spinal muscular atrophy, respectively. Conclusion: Our study highlights the overall medical insights of a complete Taiwanese genomic profile.

There is an increasing demand for simple and efficient sample delivery technology to match the rapid development of serial crystallography and its wide application in analyzing the structural dynamics of biological macromolecules. Here, a microfluidic rotating-target device is presented, capable of three-degrees-of-freedom motion, including two rotational degrees of freedom and one translational degree of freedom, for sample delivery. Lysozyme crystals were used as a test model with this device to collect serial synchrotron crystallography data and the device was found to be convenient and useful. This device enables in situ diffraction from crystals in a microfluidic channel without the need for crystal harvesting. The circular motion ensures that the delivery speed can be adjusted over a wide range, showing its good compatibility with different light sources. Moreover, the three-degrees-of-freedom motion guarantees the full utilization of crystals. Hence, sample consumption is greatly reduced, and only 0.1 mg of protein is consumed in collecting a complete dataset.

The biological effects of magnetic fields (MFs) have been a controversial issue. Fortunately, in recent years, there has been increasing evidence that MFs do affect biological systems. However, the physical mechanism remains unclear. Here, we show that MFs (16 T) reduce apoptosis in cell lines by inhibiting liquid–liquid phase separation (LLPS) of Tau-441, suggesting that the MF effect on LLPS may be one of the mechanisms for understanding the “mysterious” magnetobiological effects. The LLPS of Tau-441 occurred in the cytoplasm after induction with arsenite. The phase-separated droplets of Tau-441 recruited hexokinase (HK), resulting in a decrease in the amount of free HK in the cytoplasm. In cells, HK and Bax compete to bind to the voltage-dependent anion channel (VDAC I) on the mitochondrial membrane. A decrease in the number of free HK molecules increased the chance of Bax binding to VDAC I, leading to increased Bax-mediated apoptosis. In the presence of a static MF, LLPS was marked inhibited and HK recruitment was reduced, resulting in an increased probability of HK binding to VDAC I and a decreased probability of Bax binding to VDAC I, thus reducing Bax-mediated apoptosis. Our findings revealed a new physical mechanism for understanding magnetobiological effects from the perspective of LLPS. In addition, these results show the potential applications of physical environments, such as MFs in this study, in the treatment of LLPS-related diseases.

The contact angle, as a vital measured parameter of wettability of material surface, has long been in dispute whether it is affected by gravity. Herein, we measured the advancing and receding contact angles on extremely low contact angle hysteresis surfaces under different gravities (1-8G) and found that both of them decrease with the increase of the gravity. The underlying mechanism is revealed to be the contact angle hysteresis and the deformation of the liquid-vapor interface away from the solid surface caused by gradient distribution of the hydrostatic pressure. The real contact angle is not affected by gravity and cannot measured by an optical method. The measured apparent contact angles are angles of inclination of the liquid-vapor interface away from the solid surface. Furthermore, a new equation is proposed based on the balance of forces acting on the three-phase contact region, which quantitatively reveals the relation of the apparent contact angle with the interfacial tensions and gravity. This finding can provide new horizons for solving the debate on whether gravity affects the contact angle and may be useful for the accurate measurement of the contact angle and the development of a new contact angle measurement system.