Progress in evaluation of return to sports after anterior cruciate ligament reconstruction / 中国修复重建外科杂志

OBJECTIVE@#To summarize the evaluation methods of return to sports (RTS) after anterior cruciate ligament reconstruction (ACLR) in recent years, in order to provide reference for clinical practice.@*METHODS@#The literature related to the RTS after ACLR was searched from CNKI, Wanfang, PubMed, and Foreign Medical Information Resources Retrieval Platform (FMRS) databases. The retrieval range was from 2010 to 2023, and 66 papers were finally included for review. The relevant literature was summarized and analyzed from the aspects of RTS time, objective evaluation indicators, and psychological evaluation.@*RESULTS@#RTS is the common desire of patients with ACL injury and doctors, as well as the initial intention of selecting surgery. A reasonable and perfect evaluation method of RTS can not only help patients recover to preoperative exercise level, but also protect patients from re-injury. At present, the main criterion for clinical judgement of RTS is time. It is basically agreed that RTS after 9 months can reduce the re-injury. In addition to time, it is also necessary to test the lower limb muscle strength, jumping, balance, and other aspects of the patient, comprehensively assess the degree of functional recovery and determine the different time of RTS according to the type of exercise. Psychological assessment plays an important role in RTS and has a good clinical predictive effect.@*CONCLUSION@#RTS is one of the research hotspots after ACLR. At present, there are many related evaluation methods, which need to be further optimized by more research to build a comprehensive and standardized evaluation system.

Clinical and genetic analysis of a family with autosomal dominant-familial Mediterranean fever / 中华医学遗传学杂志

OBJECTIVE@#To analyze a pathogenic variant of MEFV gene in a family with autosomal dominant-familial Mediterranean fever (AD-FMF).@*METHODS@#A 5-year-old boy presented with recurrent aseptic meningitis and his major symptoms included recurrent fever with headache and vomiting. His family members including his mother, sister and brother also had recurrent fever. A genetic disease was considered. DNAs were extracted from patient and all his family members' blood samples. Whole exome sequencing was performed to identify putative pathogenic variants that can explain this family's condition and Sanger sequencing was conducted. The impact of detected variants were predicted and validated by bioinformatics.@*RESULTS@#A missense variant c.2229C>G (p.Phe743Leu) in MEFV gene was identified in the proband and his family members including his mother, sister and brother. This variant had not been reported in China previously, but the locus of it had already been reported in Arabic patient with AD-FMF (PS1). This variant was absent in major allele frequency databases (PM2) and had been predicted to be pathogenic based on Mutationtaster, PROVEAN and PolyPhen-2. In addition, the change of amino acid, locating in 743 locus of pyrin protein, encoding by MEFV gene, was found to cause SPRY_PRY_TRIM20 and SPRY_superfamily domain destroyed and finally influenced the fuction of pyrin protein. On the other hand, using UCSF chimera software, we find the variant c.2229C>G (p.Phe743Leu) can induce serious influence to the spatial structure of pyrin protein and loss of protein fuction (PP3). According to the ACMG variant classification guideline, the variant c.2229C>G (p.Phe743Leu) in MEFV gene was classified as likely pathogenic (PS1+PM2+PP3).@*CONCLUSION@#The condition of this AD-FMF family may be attributed to the missense variant c.2229C>G (p.Phe743Leu) in MEFV gene. The recurrent aseptic meningitis was a very rare manifestation in AD-FMF patients and had not been reported in China previously. The clinical and genetic findings of the present study are helpful for the further understanding of AD-FMF.

Correlation between blood urea nitrogen level and Traditional Chinese Medicine syndromes in sepsis patients / 国际中医中药杂志

Objective:To explore the characteristics of Traditional Chinese Medicine (TCM) syndromes in sepsis patients with different blood urea nitrogen (BUN) levels.Methods:From January 2017 to December 2018, 252 sepsis patients, who were admitted in the Department of Intensive Care Unit of the Second Affiliated Hospital of Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine) and met the inclusion criteria, were divided into lower level group (BUN<9.25 mmol/L) and higher level group (BUN≥9.25 mmol/L) according to BUN levels. The baseline data, complications, infection sites and other data were collected. TCM syndromes were judged according to the four diagnostic information of TCM and BUN levels. Variables with P<0.2 in univariate analysis were introduced as candidate variables, and the correlation between TCM syndrome elements and BUN was analyzed by multivariate logistic regression. Results:The comparison of TCM syndromes showed that the proportion of blood stasis syndrome in higher level group was significantly higher than that of the lower level group [74.60% (94/126) vs. 53.17% (67/126), P<0.01)], and the proportion of toxic heat syndrome in the higher level group was significantly lower than that of the lower level group [52.38% (66/126) vs. 65.87% (83/126), P=0.029]. The comparison of TCM deficiency syndromes showed that the proportion of qi deficiency syndrome and yang deficiency syndrome in the higher level group was significantly higher than that of the lower level group [67.46% (85/126) vs. 45.24% (57/126), P<0.01; 11.90% (15/126) vs. 3.97% (5/126), P=0.032, respectively]. Logistic regression analysis showed that the higher blood urea nitrogen level was correlated with the increased incidence of qi deficiency syndrome ( OR=3.425, 95% CI: 1.934-6.068, P<0.01), yang deficiency syndrome ( OR=3.460, 95% CI: 1.160-10.325, P=0.026) and kidney deficiency syndrome ( OR=2.212, 95% CI: 1.173-4.173, P=0.014) in sepsis patients. Conclusion:Sepsis patients with higher blood urea nitrogen level have a higher proportion of blood stasis syndrome, qi deficiency syndrome and yang deficiency syndrome and may be related to the increased incidence of qi deficiency syndrome, yang deficiency syndrome and kidney deficiency syndrome.

Analysis of a child with congenital muscular dystrophy due to a novel variant of the LMNA gene / 中华医学遗传学杂志

OBJECTIVE@#To report on a patient with congenital muscular dystrophy (CMD) due to a missense variant of LMNA gene and explore its pathogenicity.@*METHODS@#The 1-year-and-1-month-old boy has presented with motor development delay and elevation of muscle enzymes for more than half a year. Congenital myopathy was suspected. Following muscle biopsy, HE staining, immunostaining and electron microscopy were conducted to clarify the clinical diagnosis. Meanwhile, DNA was extracted from the child and his parents' peripheral venous blood samples. Trio-whole exome sequencing (trio-WES) was carried out to detect pathogenic variant in the child. Candidate variant was verified by Sanger sequencing and bioinformatic analysis.@*RESULTS@#Both light and electron microscopy showed a large area of necrotic muscle tissues with infiltration of inflammatory cells. Immunohistochemistry revealed a large amount of muscle cells to be diffusely positive for Dysferlin. The patient's motor delays, elevations of muscle enzymes and histopathological results suggested a clinical diagnosis of CMD. A de novo missense c.1072G>A (p.E358K) variant was detected in the LMNA gene by trio-WES. The variant was unreported previously (PS2) and was absent from major allele frequency databases (PM2). It was a loss of function variant and was considered as hotspot variant in the LMNA gene (PM1) as the amino acid (E), located in position 358, was highly conserved, and change of this amino acid was found to cause destruction of the filament domain (AA: 30-386), which may result in serious damage to the intermediate filament protein. Furthermore, c.1072G>A (p. E358K) in LMNA gene was also predicted to be pathogenic based on MutationTaster, PROVEAN and PolyPhen-2 (PP3) analysis. According to the guidelines of the American College of Medical Genetics and Genomics (ACMG), the variant was classified to be likely pathogenic (PS2+PM1+PM2+PP3).@*CONCLUSION@#The child's condition may be attributed to the de novo missense c.1072 G>A (p.E358K) variant of the LMNA gene. Above discovery has expanded the variant spectrum of the LMNA gene.

Identification of a novel missense variant of the KAT6B gene in a child with Say-Barber-Biesecker-Young-Simpson syndrome / 中华医学遗传学杂志

OBJECTIVE@#To explore the genetic basis for a child suspected for Say-Barber-Biesecker-Young-Simpson syndrome.@*METHODS@#Genomic DNA was extracted from peripheral blood samples of the child and her parents. Whole exome sequencing was carried out for the proband. Suspected variants were validated by Sanger sequencing. The impact of the variants was predicted by bioinformatic analysis.@*RESULTS@#The child was found to harbor a de novo missense variant c.2623C>T (p.Asp875Tyr) in exon 13 of the KAT6B gene. The variant was previously unreported, and was not recorded in the major allele frequency database and predicted to be pathogenic based on PolyPhen-2, MutationTaster and PROVEAN analysis. As predicted by UCSF chimera and CASTp software, the variant can severely impact the substrate-binding pocket of histone acetyltransferase, resulting in loss of its enzymatic activity. Based on standards and guidelines by the American College of Medical Genetics and Genomics, the variant was classified to be likely pathogenic (PS2+PM2+PP3).@*CONCLUSION@#The child's condition may be attributed to the de novo missense c.2623C>T (p.Asp875Tyr) variant of the KAT6B gene.

Identification of a novel frameshift variant in the SRCAP gene of a child with Floating-Harbor syndrome / 中华医学遗传学杂志

OBJECTIVE@#To explore the molecular basis for a child featuring with Floating-Harbor syndrome.@*METHODS@#The 2-year-and-8-month-old child presented with retarded growth and language development. Genomic DNA was extracted from peripheral blood samples from the child and his parents with informed consent and subjected to whole exome sequencing. Suspected variants were verified by Sanger sequencing. Pathogenecity of the variants were predicted by using bioinformatic tools.@*RESULTS@#The child was found to carry a de novo frameshift variant c.7273dupA (p. Thr2425Asnfs*18) in the SRCAP gene. The variant was unreported previously and predicted to be pathogenic by MutationTaster. Analysis using HomoloGene system and MEGA software indicated position 2425 of the SRCAP protein to be highly conserved. Substitution of amino acid (Thr) at this position may cause destruction of three AT-hook domains (Amino acid 2857-2869, 2936-2948 and 3004-3016) and serious damage to the function of SRCAP protein.@*CONCLUSION@#The patient's condition may be attributed to the de novo frameshift variant c.7273dupA (p. Thr2425Asnfs*18) of the SRCAP gene. Above finding can facilitate diagnosis of Floating-Harbor syndrome among Chinese population.

Identification of a novel missense NIPBL variant in a juvenile with severe type of Cornelia de Lange syndrome / 中华医学遗传学杂志

OBJECTIVE@#To detect pathogenic variant in a juvenile with severe type Cornelia de Lange syndrome (CdLS).@*METHODS@#A 12-year-old female presented with comprehensive developmental retardation and deformity of lower limbs. Genomic DNA was extracted from peripheral blood sample of the patient. Whole exome sequencing was performed to identify pathogenic variants. Putative variant was verified by Sanger sequencing. The impact of variants was predicted and validated by bioinformatic analysis.@*RESULTS@#A de novo missense variant, c.1507A>G (p. Lys503Glu), was found in the NIPBL gene of the proband. The variant was unreported previously and predicted to be pathogenic by PolyPhen-2, MutationTaster and SIFT. Using HomoloGene system, the 503 loci in the NIPBL protein are highly conserved. The change of amino acid (Glu), locating in 503 locus, was found to cause the Neuromodulin_N superfamily domain destroyed, resulting in severe damage to the function of NIPBL protein.@*CONCLUSION@#The de novo missense variant c.1507A>G (p. Lys503Glu) of the NIPBL gene probably underlies the disease in this patient.

Identification of a novel de novo variant of CSNK2A1 gene in a boy with Okur-Chung neurodevelopmental syndrome / 中华医学遗传学杂志

OBJECTIVE@#To analyze pathogenic variant of CSNK2A1 gene in a boy with Okur-Chung neurodevelopmental syndrome (OCNS).@*METHODS@#The 8-year-old boy presented with growth retardation, intellectual disability and spells of breath holding. With genomic DNA extracted from peripheral blood samples of the patient and his parents, whole exome sequencing was carried out. Putative pathogenic variants were verified with Sanger sequencing. The nature and impact of detected variants were predicted through bioinformatic analysis.@*RESULTS@#A novel de novo missense variant c.149A>G (p.Tyr50Cys) of the CSNK2A1 gene was identified, which was unreported previously. The variant was predicted to be pathogenic by PolyPhen-2, Mutation Taster and SIFT software. Based on a HomoloGene system, 50 loci within the CK2alpha protein are highly conserved. The change of amino acid (Cys) at position 50 has destroyed the ATP binding loop domain, causing serious damage to its function. As predicted by a Swiss PDB viewer, the variant can significantly alter the spatial structure of CK2alpha, resulting in loss of protein function.@*CONCLUSION@#The patient's condition may be attributed to the novel de novo missense variant c.149A>G (p.Tyr50Cys) of the CSNK2A1 gene.

Identification of a novel nonsense IQSEC2 variant in a child with X-linked intellectual disability / 中华医学遗传学杂志

OBJECTIVE@#To explore the genetic basis for a child featuring X-linked intellectual disability.@*METHODS@#The 1-year-and-6-month-old child presented with growth retardation, intellectual disability and bilateral alternating squint. With DNA extracted from the child and his parents' peripheral venous blood samples, whole exome sequencing was carried out to identify potential variants that can explain his condition. Suspected variants were validated by Sanger sequencing. The impact of variants was predicted by bioinformatic tools.@*RESULTS@#The child was found to harbor a de novo nonsense c.3163C>T (p.Arg1055*) variant of the IQSEC2 gene. The variant, unreported previously, was predicted to be pathogenic based on MutationTaster, PROVEAN and SIFT. Analysis using a HomoloGene system suggested Arg1055 in IQSEC2 residues to be highly conserved evolutionarily, and that replacement of Arg1055 may cause destroy of the PH domain (AA 951-1085) and serious damage to the function of IQSEC2 protein. Analysis with UCSF chimera software suggested that the c.3163C>T (p.Arg1055*) variant can induce serious damages to the secondary structures of IQSEC2 protein, causing loss of its function.@*CONCLUSION@#The patient's condition may be attributed to the de novo nonsense variant c.3163C>T (p.Arg1055*) of the IQSEC2 gene.

Analysis of ARSA gene variant in an infant with late infantile metachromatic leukodystrophy / 中华医学遗传学杂志

Objective@#To detect pathogenic variant of ARSA gene in an infant with late infantile metachromatic leukodystrophy (MLD).@*Methods@#The male proband had an onset of walking dysfunction and seizure at 28 months. Arylsulfatase A activity of his peripheral blood leucocytes was 26.9 nmol/mg.17h, and cranial MRI showed wild symmetrical demyelination. With genomic DNA extracted from his peripheral blood sample, all coding exons and splicing sites of the ARSA gene were subjected to Sanger sequencing. PubMed Protein BLAST system was employed to analyze cross-species conservation of the mutant amino acid. Ucsf chimera software was used to analyze the impact of candidate variants on the secondary structure of the protein product. Impact of potential variants was also analyzed with software including PolyPhen-2, Mutation Taster, SIFT and PROVEAN. Whole-exome sequencing was carried out to identify additional variants which may explain the patient’s condition.@*Results@#The proband was found to harbor compound heterozygous variants of the ARSA gene [c.467G>A (p.Gly156Asp) and c. 960G>A (p.Trp320*)], neither of which was reported previously. As predicted by Ucsf chimera software, the c. 960G>A (p.Trp320*) variant may demolish important secondary structures including α-helix, β-strand and coil of the ARSA protein, causing serious damage to its structure and loss of function. The c. 467G>A (p.Gly156Asp) variant was predicted to be "probably damaging" by PolyPhen-2, Mutation Taster and SIFT software.@*Conclusion@#The patient’s condition may be attributed to the compound heterozygous c. 467G>A (p.Gly156Asp) and c. 960G>A (p.Trp320*) variants of the ARSA gene. Above results have facilitated genetic counseling and prenatal diagnosis for this family.

Analysis of ARSA gene variant in an infant with late infantile metachromatic leukodystrophy / 中华医学遗传学杂志

OBJECTIVE@#To detect pathogenic variant of ARSA gene in an infant with late infantile metachromatic leukodystrophy (MLD).@*METHODS@#The male proband had an onset of walking dysfunction and seizure at 28 months. Arylsulfatase A activity of his peripheral blood leucocytes was 26.9 nmol/mg.17h, and cranial MRI showed wild symmetrical demyelination. With genomic DNA extracted from his peripheral blood sample, all coding exons and splicing sites of the ARSA gene were subjected to Sanger sequencing. PubMed Protein BLAST system was employed to analyze cross-species conservation of the mutant amino acid. Ucsf chimera software was used to analyze the impact of candidate variants on the secondary structure of the protein product. Impact of potential variants was also analyzed with software including PolyPhen-2, Mutation Taster, SIFT and PROVEAN. Whole-exome sequencing was carried out to identify additional variants which may explain the patient's condition.@*RESULTS@#The proband was found to harbor compound heterozygous variants of the ARSA gene [c.467G>A (p.Gly156Asp) and c.960G>A (p.Trp320*)], neither of which was reported previously. As predicted by Ucsf chimera software, the c.960G>A (p.Trp320*) variant may demolish important secondary structures including α-helix, β-strand and coil of the ARSA protein, causing serious damage to its structure and loss of function. The c.467G>A (p.Gly156Asp) variant was predicted to be "probably damaging" by PolyPhen-2, Mutation Taster and SIFT software.@*CONCLUSION@#The patient's condition may be attributed to the compound heterozygous c.467G>A (p.Gly156Asp) and c.960G>A (p.Trp320*) variants of the ARSA gene. Above results have facilitated genetic counseling and prenatal diagnosis for this family.

Analysis of HEXB gene mutations in an infant with Sandhoff disease / 中华医学遗传学杂志

Objective@#To detect potential mutations of HEXB gene in an infant with Sandhoff disease (SD).@*Methods@#Genomic DNA was extracted from peripheral blood sample of the infant. All coding exons (exons 1 to 14) and splicing sites of the HEXB gene were subjected to PCR amplification and direct sequencing.PubMed Protein BLAST system was employed to analyze cross-species conservation of the mutant amino acid. PubMed BLAST CD-search was performed to identify functional domains destroyed by thecandidate mutations. Impact of the mutations was analyzed with software including PolyPhen-2, Mutation Taster and SIFT. Whole-exome sequencing was carried out to identify additional mutations.@*Results@#The infant was found to carry compound heterozygous mutations c. 1652G>A(p.Cys551Tyr) and c. 1389C>G (p.Tyr463*) of the HEXB gene. The c. 1389C>G (p.Tyr463*) mutation may lead to destruction of two functional domains in β subunit of the Hex protein. The c. 1652G>A(p.Cys551Tyr)mutation, unreported previously, was predicted to be probably damaging by Bioinformatic analysis.@*Conclusion@#Compound heterozygous mutations c. 1652G>A(p.Cys551Tyr) and c. 1389C>G (p.Tyr463*) in the HEXB gene probably underlie the disease in this patient.

Analysis of HEXB gene mutations in an infant with Sandhoff disease / 中华医学遗传学杂志

OBJECTIVE@#To detect potential mutations of HEXB gene in an infant with Sandhoff disease (SD).@*METHODS@#Genomic DNA was extracted from peripheral blood sample of the infant. All coding exons (exons 1 to 14) and splicing sites of the HEXB gene were subjected to PCR amplification and direct sequencing.PubMed Protein BLAST system was employed to analyze cross-species conservation of the mutant amino acid. PubMed BLAST CD-search was performed to identify functional domains destroyed by thecandidate mutations. Impact of the mutations was analyzed with software including PolyPhen-2, Mutation Taster and SIFT. Whole-exome sequencing was carried out to identify additional mutations.@*RESULTS@#The infant was found to carry compound heterozygous mutations c.1652G>A(p.Cys551Tyr) and c.1389C>G (p.Tyr463*) of the HEXB gene. The c.1389C>G (p.Tyr463*) mutation may lead to destruction of two functional domains in β subunit of the Hex protein. The c.1652G>A(p.Cys551Tyr) mutation, unreported previously,was predicted to be probably damaging by Bioinformatic analysis.@*CONCLUSION@#Compound heterozygous mutations c.1652G>A(p.Cys551Tyr) and c.1389C>G (p.Tyr463*) in the HEXB gene probably underlie the disease in this patient.

Quantitative Assessment of Upper Urinary Tract Pump Function After Unilateral Lower Urinary Tract Obstruction Using 640-slice Dynamic Volumetric CT / 中国医学影像学杂志

Purpose To investigate the value of quantitative evaluation of upper urinary tract pump function after unilateral lower urinary tract obstruction using 640-slice dynamic volumetric CT. Materials and Methods Twenty-six healthy subjects (control group), thirty cases of acute upper urinary tract obstruction caused by unilateral ureteral calculi and thirty cases of chronic upper urinary tract obstruction were selected, all receiving dynamic volume scan of 640-slice dynamic volumetric CT during renal excretion. The value of contrast agent volume, volumetric difference, time difference correspondent to the difference, volumetric change rate, and flow rate in ureteropelvic and partial upper ureter were calculated and analyzed. Results Volumetric change rate of obstruction side of upper urinary tract in acute obstruction group was higher than that of contralateral upper urinary tract. Volumetric average value, volumetric difference and flow rate were increased with time difference value decreased, the difference of which were all statistically significant (P<0.001). Volumetric change rate, volumetric difference and flow rate of obstruction side of upper urinary tract in acute obstruction group was lower compared with those of contralateral upper urinary tract, while volumetric average value and time difference raised, the difference was statistically significant (P<0.001). The difference of five pump function values among acute obstruction group, obstruction side of chronic obstruction group and control group were statistically significant (P<0.001). Conclusion 640-slice dynamic volumetric CT can be used to quantitatively evaluate changes of urinary tract pump function in physiological and obstructive status.

The multivariate analysis of CA125 and inflammation indicators in gynecological diseases / 国际检验医学杂志

Objective To investigate whether there is a correlation between carbohydrate antigen125(CA125) and inflammation indicators in gynecological diseases ,analyze the possible mechanism of the disease .Methods Retrospectively analyze the regression and correlation between CA125 and routine blood classification indicators in 4 291 patients from department of reproductive health and gynaecology .Stepwise multiple regression model was used to analyze the common disease from department of gynaecology in‐cluding pelvic infection ,endometriosis ,uterine fibroids .Results The analysis of 4 291 cases showed that there was a correlation be‐tween CA125 and leukocyte count ,neutrophil‐to‐lymphocyte ratio (NLR) .The correlation coefficient was 0 .170 .For diseases of different types ,in patients with pelvic inflammation and endometrial ectopic there were correlations between CA125 and NLR .The correlation coefficient were 0 .290 and 0 .342 respectively .Conclusion There might be a correlation between CA125 and the inflam‐mation indicators .It should be carefully to diagnose cancer related diseases ,especially when inflammatory factors and CA125 in‐creased at the same time .

The pregnancy outcomes of selective reduction of triplet pregnancy by assisted reproductive technology / 实用医学杂志

Objective To study the outcomes of selective reduction of triplet pregnancy by assisted reproductive technology. Methods The clinical data of 31 women who succeeded in conception by vitro fertilization-embryo transfer in the third affiliated hospital of Guangzhou Medical University were retrospectively investigated to analyze and compare the rates of abortion from triplet pregnancy, twin pregnancy and single pregnancy after selective reduction of triplet pregnancy, the incidence of pregnant complications, outcomes of perinatal period. Results There were no significant differences between triplet pregnancy and the twin and single pregnancy after selective reduction of triplet pregnancy in terms of pregnancy and parity time, fetal disease, premature rupture of membrane, severe eclampsism, gestational diabetes and postpartum hemorrhage (P>0.05). There were significant differences in gestational weeks, birth weight, rate of premature birth, rate of neonatal transfer to NICU and neonatal RDS: The gestational time in the triplet group longer than the groups of twin pregnancy and single pregnancy after selective reduction of triplet pregnancy (P<0.05). (37.3 ± 1.9) vs. (35.2 ± 0.9), (32.6 ± 2.3), respectively), the rate of premature birth dropped (100%vs. 100%, 33.3%, respectively), the body weight was increased (1 707 ± 360.4)g vs. (2 066.1 ± 307.5)g, (2 712.5 ± 514.1)g, respectively and the neonatal complication rate was reduced (P<0.05). Conclusion The selective reduction of multiple pregnancy may decrease the risk of premature birth and reduce the rate of lower body weight of neonates, improving the pregnancy outcomes, but the higher rate of abortion at the early or middle course of pregnancy after selective reduction is worth our attention.

Correlation between environmental factors and liposoluble and hydrophilic constituents of Polygalae Radix / 中国中药杂志

<p><b>OBJECTIVE</b>To analyze the correlation between environmental factors and the lipophilic and hydrophilic constituents of Polygalae Radix.</p><p><b>METHOD</b>The contents of lipophilic constituent were determined by GC-MS and hydrophilic constituents by HPLC. Geographical factors were collected by on-site inspection and climate factors by the local meteorological data. The relationship between the content of the lipophilic and hydrophilic constituents and the factors were analyzed by SPSS 18.0.</p><p><b>RESULT</b>There was linear relationship between the content of lipophilic constituent and climate factors such as average temperature of July, average temperature of January. There was also linear relationship between hydrophilic constituents and climate factors such as annual average temperature, latitude, annual average rainfall.</p><p><b>CONCLUSION</b>The main climate factors that affect liposoluble constituent content were average temperature of July, average temperature of January, and the main climate factors that affect hydrophilic constituent content were annual average temperature, latitude, annual average rainfall. The study would contribute to the quality evaluation and suitability of origin of Polygalae Radix.</p>