Oral nanoliposome in postoperative home care of patients with myelitis.

Acute myelitis (AM) mainly presents with paralysis, and sensory and autonomic dysfunction, which affects the daily life and quality of life (QoL) of patients. Reasonable selection of treatment and nursing can promote the recovery of patients. It was to explore the effect of oral nanoliposomes combined with home care on the rehabilitation of patients. A total of 100 AM patients who received surgical treatment were enrolled. According to the treatment and nursing methods, they were grouped into a control (oral administration of nanoliposomes plus routine nursing, n=50) and an observation group (oral administration of nanoliposomes plus home care, n=50). Differences between patients' neurological recovery, lower limb muscle strength, activities of daily living, QoL, and satisfaction with quality of care were assessed. As against control, the time of muscle strength to level 2, urination recovery time, walking time, and sensory recovery time was shorter, and the degree of lower limb muscle strength recovery was higher, the Barthel and Newcastle Satisfaction with Nursing Scale (NSNS) scores of daily living ability increased, and the QoL EuroQol-5 dimensions (EQ-5D) score decreased in the observation group (P<0.05). Oral administration of nanoliposome plus home care can promote the recovery of lower limb muscle strength, improve daily living ability and QoL, and improve nursing satisfaction in patients with AM surgery.

[Fine Needle Aspiration Cytology of Hyalinizing Trabecular Tumor of the Thyroid].

Objective To investigate the fine needle aspiration cytology and differential diagnosis of hyalinizing trabecular tumor (HTT) of the thyroid.Methods The fine needle aspiration smears of four HTT cases with histopathological controls were analyzed,which were then combined with the histopathological changes and immunophenotypes for diagnosis.The key points of cytological diagnosis and the differential diagnosis of HTT were then summarized.Results The fine needle aspiration cytology showed that the tumor cells were scattered,presenting as partially cohesive clusters or clusters with trabecular manifestations.The tumor cells were polygonal or spindle,with medium or rich cytoplasm.The nuclei were oval or short spindle,with fine granular chromatin,visible small nucleoli,common nuclear grooves and nuclear pseudoinclusions,and irregular outline,which demonstrated the nucleus characteristics of papillary thyroid carcinoma.The interstitium showed transparent basement membrane-like material deposition,loose tumor cell clusters,trabecular or syncytial structure,radially distributed tumor cells around the hyaline-like material,rich eosinophilic or dichromophile cytoplasm,elongated nuclei,no papillary structure or fibrovascular axis,and no psammoma bodies.Histopathology showed tumor cells arranged in beam and organoid,transparent basement membrane-like material deposition between trabecular beams,and polygonal or spindle cells containing fine granular eosinophilic cytoplasm and round or oval nuclei with common nuclear grooves and nuclear pseudoinclusions.Conclusion Combining the ultrasound results with the arrangement,interstitial components,and cytological characteristics of tumor cells,we suggest that Ki-67(MIB-1)staining can be employed to assist diagnosis and improve the diagnostic accuracy of HTT or intraoperative freezing can be adopted for further diagnosis.

SOX9 dependent FOXA1 expression promotes tumorigenesis in lung carcinoma.

The malignant proliferation is one of the major characteristic for tumor cells, however the mechanism of lung cancer cells uncontrollable proliferation is still confusing. This study investigated the mechanism of up-regulated FOXA1 in lung cancer and its tumorigenic function in lung cancer. FOXA1 showed an increasing expression pattern with the pathological progression in lung cancer, and SOX9 expression pattern is positively correlated with FOXA1. Furthermore, combined up-regulated FOXA1 and SOX9 usually resulted in a poor survival prognosis of patients with lung cancer. In addition, SOX9 was identified as a transcription factor of FOXA1 in lung cancer and involved in affecting the expression of FOXA1 targeted genes-Bcl2, CDKN1B, RPRM and NKX2. What's more, SOX9 can rescue the declining tumorigenic ability of lung cancer cells caused by FOXA1 silenced. This study indicates that SOX9 dependent FOXA1 expression promotes tumorigenic ability of lung cancer cells.

Gender Disparity in the Relationship between Prevalence of Thyroid Nodules and Metabolic Syndrome Components: The SHDC-CDPC Community-Based Study.

The study is aimed to investigate the pathogenesis underlying the increased prevalence of thyroid nodule (TN) in different levels of metabolic syndrome (MetS) components and analyze the relationships between TN and MetS components. A total of 6,798 subjects, including 2201 patients with TN, were enrolled in this study. Anthropometric, biochemical, thyroid ultrasonographic, and other metabolic parameters were all measured. There was obviously sexual difference in the prevalence of TN (males 26.0%, females 38.5%, resp.). The prevalence of TN in hyperuricemia (45.7% versus 37.4%, P = 0.001), NAFLD (41.2% versus 36.4%, P < 0.05), and MetS (41.4% versus 35.4%, P < 0.001) groups was significantly increased only in females. Insulin resistance [OR = 1.31 (1.15, 1.49)], MetS [OR = 1.18 (1.03, 1.35)], and diabetes [OR = 1.25 (1.06, 1.48)] were all independent risk factors for TN in total subjects, whereas, after stratified analysis of gender, MetS [OR = 1.29, (1.09, 1.53)] and diabetes [OR = 1.47, (1.17, 1.84)] are still strongly and independently associated with the higher risks of TN in female subjects, but not in males. Our results suggest that the components of MetS might associate with the higher risks of TN in women than in men, but further cohort study of this gender disparity in the association between TN and MetS is required.

Epithelial-mesenchymal transition in keloid tissues and TGF-ß1-induced hair follicle outer root sheath keratinocytes.

Keloid is a skin fibrotic disease with the characteristics of recurrence and invasion, its pathogenesis still remains unrevealed. The epithelial-mesenchymal transition (EMT) is critical for wound healing, fibrosis, recurrence, and invasion of cancer. We sought to investigate the EMT in keloid and the mechanism through which the EMT regulates keloid formation. In keloid tissues, the expressions of EMT-associated markers and transforming growth factor (TGF)-ß1/Smad3 signaling were examined by immunohistochemistry. In the keloid epidermis and dermal tissue, the expressions of genes related to the regulation of skin homeostasis, fibroblast growth factor receptor 2 (FGFR2) and p63, were analyzed using quantitative real-time polymerase chain reaction. The results showed that accompanying the loss of the epithelial marker E-cadherin and the gain of the mesenchymal markers fibroblast-specific protein 1 (FSP1) and vimentin in epithelial cells from epidermis and skin appendages, and in endothelial cells from dermal microvessels, enhanced TGF-ß1 expression and Smad3 phosphorylation were noted in keloid tissues. Moreover, alternative splicing of the FGFR2 gene switched the predominantly expressed isoform from FGFR2-IIIb to -IIIc, concomitant with the decreased expression of ΔNp63 and TAp63, which changes might partially account for abnormal epidermis and appendages in keloids. In addition, we found that TGF-ß1-induced hair follicle outer root sheath keratinocytes (ORSKs) and normal skin epithelial cells underwent EMT in vitro with ORSKs exhibiting more obvious EMT changes and more similar expression profiles for EMT-associated and skin homeostasis-related genes as in keloid tissues, suggesting that ORSKs might play crucial roles in the EMT in keloids. Our study provided insights into the molecular mechanisms mediating the EMT pathogenesis of keloids.

miR-196a targets netrin 4 and regulates cell proliferation and migration of cervical cancer cells.

Recent research has uncovered tumor-suppressive and oncogenic potential of miR-196a in various tumors. However, the expression and mechanism of its function in cervical cancer remains unclear. In this study, we assess relative expression of miR-196a in cervical premalignant lesions, cervical cancer tissues, and four cancer cell lines using quantitative real-time PCR. CaSki and HeLa cells were treated with miR-196a inhibitors, mimics, or pCDNA/miR-196a to investigate the role of miR-196a in cancer cell proliferation and migration. We demonstrated that miR-196a was overexpressed in cervical intraepithelial neoplasia 2-3 and cervical cancer tissue. Moreover, its expression contributes to the proliferation and migration of cervical cancer cells, whereas inhibiting its expression led to a reduction in proliferation and migration. Five candidate targets of miR-196a chosen by computational prediction and Cervical Cancer Gene Database search were measured for their mRNA in both miR-196a-overexpressing and -depleted cancer cells. Only netrin 4 (NTN4) expression displayed an inverse association with miR-196a. Fluorescent reporter assays revealed that miR-196a inhibited NTN4 expression by targeting one binding site in the 3'-untranslated region (3'-UTR) of NTN4 mRNA. Furthermore, qPCR and Western blot assays verified NTN4 expression was downregulated in cervical cancer tissues compared to normal controls, and in vivo mRNA level of NTN4 inversely correlated with miR-196a expression. In summary, our findings provide new insights about the functional role of miR-196a in cervical carcinogenesis and suggested a potential use of miR-196a for clinical diagnosis and as a therapeutic target.

Mechanism of RBBP8-mediated homologous recombination repair in gastric cancer synthetic lethal.

Background: It is of great clinical significance to further explore new strategies and potential combined therapeutic targets for gastric cancer. This study aimed to investigate the synthetic lethal effect of RBBP8 molecular intervention combined with a poly ADP ribose polymerase (PARP) inhibitor in non-BRCA mutant gastric cancer and clarify the mechanism by which RBBP8 regulates homologous recombination repair. Methods: The role of RBBP8 in DNA damage repair was observed using bioinformatic analysis, western blot analysis, and immunofluorescence. The synthetic lethal effect was verified using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt (MTS)and flow cytometry apoptosis experiments. Results: Among the patients with gastric cancer treated with chemotherapy, the prognosis of patients with high RBBP8 expression levels was worse (homologous recombination [HR] = 1.54, p = 0.028). RBBP8 knockdown induced DNA damage and had a synergistic effect with PARP inhibitor treatment on cell viability inhibition and cell apoptosis in AGS (generic code for human gastric adenocarcinoma cells) (t = 11.154, p < 0.001) and N87 (t = 6.362, p < 0.001) cells. RBBP8 knockdown inhibited RAD51 activation and DNA terminal excision in homologous recombination repair. Conclusion: RBBP8 is involved in homologous recombination repair, and molecular intervention into RBBP8 could achieve a synthetic lethal effect with PARP inhibitor treatment in gastric cancer cells.

Comparison of clinical outcomes in critical patients undergoing different mechanical ventilation modes: a systematic review and network meta-analysis.

Purpose: To evaluate the effects of different mechanical ventilation modes on critical patients. Methods: PubMed, Embase, Web of science, and Cochrane Library databases were searched from their inception to November 15, 2022 for randomized controlled trials on the application of different mechanical ventilation modes in critical patients. Two researchers independently screened the literature, extracted data, and assessed the risk of bias in the included studies. R4.2.1 was used for this network meta-analysis. Results: Twenty-eight RCTs involving 3,189 patients were included. The interventions in these RCTs included NAVA (neurally adjusted ventilatory assist), PAV (proportional assist ventilation), ASV (adaptive support ventilation), Smartcare/PS (Smartcare/pressure support), PSV (pressure support ventilation), PSV_ATC (pressure support ventilation_automatic tube compensation), and SIMV (synchronized intermittent mandatory ventilation). The network meta-analysis showed that, compared with the PSV group, there was no significant difference in duration of mechanical ventilation, duration of ICU stay, and hospital stay between NAVA, SIMV, AVS, PAV, Smartcare/PS, and PSV_ATC groups. Compared with PSV, PAV improved the success rate of withdrawal of ventilator [OR = 3.07, 95%CI (1.21, 8.52)]. Compared with PSV and PAV, NAVA reduced mortality in the ICU [OR = 0.63, 95%CI (0.43, 0.93); OR = 0.45, 95%CI (0.21, 0.97)]. Conclusion: NAVA can reduce mortality in ICU, and PAV may increase the risk of withdrawal of the ventilator. There was no significant difference between PSV and other mechanical ventilation modes (NAVA, SIMV, AVS, PAV, Smartcare/PS, and PSV_ATC) in the duration of mechanical ventilation, duration of ICU stay, or hospital stay. Due to the limitations, more high-quality studies are needed to verify these findings.

Cortistatin-14 Exerts Neuroprotective Effect Against Microglial Activation, Blood-brain Barrier Disruption, and Cognitive Impairment in Sepsis-associated Encephalopathy.

Sepsis-associated encephalopathy (SAE) is a life-threatening deterioration of mental status in relation to long-term and disabling cognitive dysfunction that is common in intensive care units worldwide. Cortistatin-14 is a neuropeptide structurally resembling somastostatin, which has been proven to play a crucial role in sepsis. The present study aimed to explore the neuroprotective role of cortistatin-14 in sepsis-associated encephalopathy and its underlying mechanisms in a mouse model. A septic mice model was established using the cecal ligation and puncture (CLP) method. The novel object recognition test (NORT), open field test (OFT), elevated plus maze test (EPMT), and tail suspension test (TST) were used to explore the behavioral performance of the mice. Transmission electron microscopy was used to observe the microstructure of the blood-brain barrier (BBB). Evans Blue staining was used to examine the integrity of the BBB. Immunofluorescence was used to examine the morphology and infiltration of microglia. A multiplex cytokine bead array assay was used to determine cytokine and chemokine levels in mouse serum and brain tissues. NORT revealed that cortistatin treatment improved cognitive impairment in septic mice. OFT, EPMT, and TST indicated that cortistatin-14 relieved the anxiety-related behaviors of CLP mice. In addition, cortistatin-14 treatment decreased the levels of various inflammatory cytokines, including interleukin-1ß, interleukin-6, interferon-γ, and tumor necrosis factor-α in both the serum and brain of septic mice. Cortistatin reduced sepsis-induced blood-brain barrier disruption and inhibited microglial activation after the onset of sepsis. Cortistatin exerts neuroprotective effects against SAE and cognitive dysfunction in a CLP-induced mouse model of sepsis.

Factors associated with progression of different prediabetic status to Diabetes: A Community-based cohort study.

AIMS: To examine the predictive factors associated with the progression of different prediabetic status to diabetes. METHODS: A two-year retrospective cohort study was conducted on 5741 participants aged 40 years or older. Finally, 1685 participants with prediabetes defined by IFG (impaired fasting glucose), IGT (impaired glucose tolerance) and CGI (combined IFG and IGT) were included. Logistic regression model was used to evaluate the risk of prediabetes progression to diabetes. RESULTS: Of the 1685 subjects with prediabetes at baseline, 212 (12.6%) subjects progressed to diabetes and 1473 (87.4%) subjects did not. Logistic regression analysis demonstrated that people with CGI were associated with an increased risk of progressing to diabetes compared to those with IFG (OR, 95% CI: 3.127, 2.047-4.776). Moreover, males, obese people, people with increased BMI and WHR (Waist/ Hip ratio), and hypertension were positively associated with the progression to diabetes, while HOMA-ß was negatively associated with the progression to diabetes. CONCLUSIONS: Subjects with CGI are prone to progressed to diabetes compared to those with IFG or IGT in middle-aged and older person in China. More attention should be paid to male and obese prediabetic subjects, and measures should be taken to control the increase in their BMI and WHR.

LAPTM4B promotes the progression of bladder cancer by stimulating cell proliferation and invasion.

Bladder cancer is a highly metastatic tumor and one of the most common malignant tumors originating in the urinary system. Due to the complicated etiology and lack of significant early symptoms, the diagnosis and treatment of bladder cancer is difficult. Lysosome-associated transmembrane protein 4ß (LAPTM4B) was reported to be involved in the development and progression of several types of tumor, however, its potential effect on the development and metastasis of bladder cancer is still unclear. Immunohistochemistry was performed to detect the protein expression level of LAPTM4B in bladder cancer tissues and short hairpin RNAs targeting LAPTM4B were transfected into bladder cancer cells to knockdown its expression. MTT and colony formation assays were performed to detect cell proliferation, while wound healing and Transwell invasion assays were performed to detect cell migration and invasion, respectively. In addition, tumor growth assays were performed to confirm the effects of LAPTM4B in mice. The present study demonstrated that LAPTM4B was associated with the prognosis of patients with bladder cancer. In addition, LAPTM4B was associated with clinical characteristics, including tumor stage and recurrence. The results further showed that LAPTM4B knockdown could suppress the proliferation of bladder cancer cell lines. In addition, the migration and invasion of T24 and 5637 cells was suppressed following LAPTM4B knockdown in vitro. The in vivo data confirmed that knockdown of LAPTM4B markedly inhibited tumor growth and metastasis in mice. In summary, the results from the present study provide strong evidence of the effects of LAPTM4B in bladder cancer progression.

Knockdown of lncRNA X inactive specific transcript (XIST) radiosensitizes non-small cell lung cancer (NSCLC) cells through regulation of miR-16-5p/WEE1 G2 checkpoint kinase (WEE1) axis.

Long non-coding RNA (lncRNA) X inactive specific transcript (XIST) is reported to play an oncogenic role in non-small cell lung cancer (NSCLC). However, the role of XIST in regulating the radiosensitivity of NSCLC cells remains unclear. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of XIST and miR-16-5p in NSCLC in tissues and cells, and Western blot was used to assess the expression of WEE1 G2 checkpoint kinase (WEE1). Cell counting kit-8 (CCK-8), colony formation and flow cytometry assays were used to determine cell viability and apoptosis after NSCLC cells were exposed to different doses of X-rays. The interaction between XIST and miR-16-5p was confirmed by StarBase database, qRT-PCR and dual-luciferase reporter gene assays. TargetScan database was used to predict WEE1 as a target of miR-16-5p, and their targeting relationship was further validated by Western blot, qRT-PCR and dual-luciferase reporter gene assays. XIST was highly expressed in both NSCLC tissue and cell lines, and knockdown of XIST repressed NSCLC cell viability and cell survival, and facilitated apoptosis under the irradiation. MiR-16-5p was a target of XIST, and rescue experiments demonstrated that miR-16-5p inhibitors could reverse the role of XIST knockdown on radiosensitivity in NSCLC cells. WEE1 was validated as a target gene of miR-16-5p, and WEE1 could be negatively regulated by XIST. XIST promotes the radioresistance of NSCLC cells by regulating the expressions of miR-16-5p and WEE1, which can be a novel target for NSCLC therapy.

Challenge in the new era: Translational medicine in gastrointestinal endoscopy and early cancer.

Translational medicine is a new medical model that has emerged over the past 20 years and is dedicated to bridging the gap between basic and clinical research. At the same time, the diagnosis and treatment of digestive diseases, especially gastrointestinal endoscopy, have been rapidly developed. The emergence of new techniques for gastrointestinal endoscopy has changed the therapeutic spectrum of some diseases and brought huge benefits to patients. Targeted therapy has positively affected the individualized and precise treatment of patients with advanced gastrointestinal cancer. The construction of a standardized biobank provides a strong guarantee for clinicians to conduct translational medical research. Translational medicine has brought good development opportunities, but it also faces challenges. The training of translational medicine researchers and the transformation of educational models require sufficient attention for further development.

Increased Serum ANGPTL8 Concentrations in Patients with Prediabetes and Type 2 Diabetes.

The objectives of the study were to investigate serum ANGPTL8 concentrations in different glucose metabolic statuses and to explore the correlations between serum ANGPTL8 levels and various metabolic parameters. Serum ANGPTL8 levels were determined using ELISA in 22 subjects with NGT (normal glucose tolerance), 74 subjects with IGR (impaired glucose regulation), and 33 subjects with T2DM (type 2 diabetes mellitus). Subjects with IFG, IGT, CGI, and T2DM had higher levels of serum ANGPTL8 than subjects with NGT. Serum ANGPTL8 was positively correlated with FPG, fasting C-peptide, and postprandial C-peptide and negatively correlated with BETA/IR when adjusted for age and BMI. Multivariate analysis suggested FPG and fasting C-peptide as independent factors associated with serum ANGPTL8 levels. Serum ANGPTL8 concentrations were significantly increased in IGR and T2DM. Serum ANGPTL8 might play a role in the pathological mechanism of glucose intolerance.

Nonalcoholic Fatty Liver Disease and Associated Metabolic Risks of Hypertension in Type 2 Diabetes: A Cross-Sectional Community-Based Study.

The mechanisms facilitating hypertension in diabetes still remain to be elucidated. Nonalcoholic fatty liver disease (NAFLD), which is a higher risk factor for insulin resistance, shares many predisposing factors with diabetes. However, little work has been performed on the pathogenesis of hypertension in type 2 diabetes (T2DM) with NAFLD. The aim of this study is to investigate the prevalence of hypertension in different glycemic statuses and to analyze relationships between NAFLD, metabolic risks, and hypertension within a large community-based population after informed written consent. A total of 9473 subjects aged over 45 years, including 1648 patients with T2DM, were enrolled in this cross-sectional study. Clinical and biochemical parameters of all participants were determined. The results suggested that the patients with prediabetes or T2DM were with higher risks to have hypertension. T2DM with NAFLD had significantly higher levels of blood pressure, triglyceride, uric acid, and HOMA-IR than those without NAFLD. Data analyses suggested that hypertriglyceridemia [OR = 1.773 (1.396, 2.251)], NAFLD [OR = 2.344 (1.736, 3.165)], hyperuricemia [OR = 1.474 (1.079, 2.012)], and insulin resistance [OR = 1.948 (1.540, 2.465)] were associated with the higher prevalence of hypertension independent of other metabolic risk factors in type 2 diabetes. Further studies are needed to focus on these associations.

Multifractals embedded in short time series: An unbiased estimation of probability moment.

An exact estimation of probability moments is the base for several essential concepts, such as the multifractals, the Tsallis entropy, and the transfer entropy. By means of approximation theory we propose a new method called factorial-moment-based estimation of probability moments. Theoretical prediction and computational results show that it can provide us an unbiased estimation of the probability moments of continuous order. Calculations on probability redistribution model verify that it can extract exactly multifractal behaviors from several hundred recordings. Its powerfulness in monitoring evolution of scaling behaviors is exemplified by two empirical cases, i.e., the gait time series for fast, normal, and slow trials of a healthy volunteer, and the closing price series for Shanghai stock market. By using short time series with several hundred lengths, a comparison with the well-established tools displays significant advantages of its performance over the other methods. The factorial-moment-based estimation can evaluate correctly the scaling behaviors in a scale range about three generations wider than the multifractal detrended fluctuation analysis and the basic estimation. The estimation of partition function given by the wavelet transform modulus maxima has unacceptable fluctuations. Besides the scaling invariance focused in the present paper, the proposed factorial moment of continuous order can find its various uses, such as finding nonextensive behaviors of a complex system and reconstructing the causality relationship network between elements of a complex system.

Preparation and characterization of polyclonal antibodies against VLDL receptor.

The polyclonal antibodies against VLDL receptor were prepared and identified. Rabbits were immunized with polypeptide fragment of VLDL receptor as antigen. The collected blood serum of the immunized rabbits was analyzed and identified by using ELISA and Western Blot. The results showed that the rabbit against mouse and human VLDL receptor antibodies were obtained with high titer and could recognize the natural VLDL receptors through Western blot. The prepared polyclonal antibodies against VLDL receptor provide a new tool to study the protein of VLDL receptor.

ADAM10 overexpression in human non-small cell lung cancer correlates with cell migration and invasion through the activation of the Notch1 signaling pathway.

A disintegrin and metalloproteinase 10 (ADAM10) was identified as a key protease in the ectodomain shedding of various substrates, such as Notch1 protein, ErbB2 and E-cadherin, which are important in the development of non-small cell lung cancer (NSCLC). The aim of this study was to investi-gate the role of ADAM10 in NSCLC metastasis.We characterized the expression of ADAM10 and Notch1 in human NSCLC tissues in vivo. Immunohistochemical analysis indicated that ADAM10 expression was significantly increased in the NSCLC tissues, particularly in the metastatic tissues. Futhermore, ADAM10 overexpression positively correlated with Notch1 expression in the NSCLC tissues. The in vitro downregulation of ADAM10 expression using ADAM10 short hairpin RNA (shRNA) reduced the migration and invasion of NSCLC cells. We present further evidence that ADAM10 promotes NSCLC cell migration and invasion via the activation of the Notch1 signaling pathway. Taken together, our results suggest that ADAM10 may serve as a potential target for the therapeutic intervention of NSCLC metastasis. The data provided in this study may aid in the further understanding of the function of ADAM10 in the progression of NSCLC and open new perspectives for the diagnosis and treatment of NSCLC.

[Association between p53 gene codon 72 polymorphism and keloid in Chinese population].

OBJECTIVE: To investigate the relationship between p53 gene codon 72 polymorphism and genetic predisposition to keloid in Chinese population. METHODS: PCR-based restriction fragment length polymorphism (PCR-RFLP) analysis was used to detect p53 gene codon 72 genotypes of 60 keloid samples and 102 whole blood samples from healthy controls in China. RESULTS: There was no significant difference in the distribution of p53 gene codon 72 polymorphism between the keloid patients and the healthy controls (X2 = 2.910, P = 0.233), nor did the frequencies for Pro and Arg alleles (X2 = 0.882, P = 0.348), and there was no significant difference in the distribution of p53 gene codon 72 polymorphism in keloid patients and normal controls from China and Japan respectively (X2 = 3.942, P = 0.139; X2 = 3.260, P = 0.196). But the Arg/Arg genotype was significantly higher than the Pro/Pro genotype among the patients with keloid in shoulder and back (P < 0.01). CONCLUSIONS: There was no significant association between the distribution of p53 gene codon 72 polymorphism and keloid in Chinese population, but Arg/Arg genotype may affect the formation of keloids in shoulder and back compared to others. Further research should be done to investigate the relationship between p53 gene codon 72 polymorphism and keloids in different sites.