[Clinicopathological features of gastric carcinomas with NTRK-rearrangement/amplification: report of four cases].

Objective: To investigate the clinicopathological, immunohistochemical and molecular genetic characteristics of gastric carcinoma with NTRK-rearrangement/amplification. Methods: The clinicopathological data of gastric carcinoma cases with NTRK-rearrangement/amplification diagnosed from January 2011 to September 2020 at the Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, China, were collected. The clinicopathological, immunophenotypic and molecular pathological features were analyzed. The relevant literature was reviewed. Results: There were 4 cases of gastric carcinoma with NTRK-rearrangement/amplification. All 4 patients were male, aged 57-67 years (average, 63 years). Tumor sizes ranged from 3.5 to 5.2 cm (average, 4.8 cm). All tumors were in the antrum. All 4 patients underwent radical gastrectomy and were followed up after the surgery. Morphologically, all tumors showed histological features with enteroblastic-differentiated gastric carcinoma. Tumor cells showed predominantly tubular/papillary architecture, with conspicuous vesicular nuclei and pale staining or transparent cytoplasm. Immunohistochemistry showed pan-TRK expression in all cases, with various degrees of positivity in the cytoplasm. All cases were subject to NTRK1/2/3 detection using fluorescence in situ hybridization. There were NTRK translocations in 2 cases and NTRK amplifications in 2 cases. These cases were further verified by RNAseq next generation sequencing which confirmed that NTRK1 gene translocation (TPM3-NTRK1) and NTRK2 gene translocation (NTRK2-SMCHD1) occurred in two cases, respectively. Conclusions: NTRK mutation occurs less frequently in gastric cancer. In this study, the cases mainly occur in the antrum. The morphology has the characteristics of enteroblastic differentiation. The tumors have unique histological, immunophenotypic and molecular characteristics, which require much attention from pathologists to effectively guide clinicians to choose the best treatment.

[Correlation of NTRK genetic fusions with mismatch repair protein deletion in patients with colorectal cancer].

Objective: To investigate the relationship between the expression of four mismatch repair proteins (MLH1, MSH2, MSH6 and PMS2) and NTRK genetic fusions in colorectal cancer. Methods: The paraffin-embedded tissue blocks of 830 cases of colorectal cancer were collected at the Affiliated Drum Tower Hospital, Nanjing University Medical School, China, from 2015 to 2019. Immunohistochemical and fluorescence in situ hybridization(FISH) method were used respectively to detect the expression of mismatch repair proteins and the break-apart of NTRKs; and the relationship between the expression of mismatch repair proteins and the NTRK genetic fusions was analyzed. Results: The overall mismatch repair protein deficiency (dMMR) rate was 9.88% (82/830), the mismatch repair proteins proficiency (pMMR) rate was 90.12%(748/830). The total deficiency rate of MLH1 protein was 9.04% (75/830), hPMS2 protein deficiency rate was 9.04% (75/830), MSH2 protein deficiency rate was 2.53% (21/830), MSH6 protein deficiency rate was 4.10% (34/830), the deficiency rate of synchronous MLH1 and PMS2 were 8.67% (72/830) and the deficiency rate of synchronous MSH2 and MSH6 were 2.17% (18/830). The dMMR group was associated with tumor location, different histological subgroups, tumor differentiation, AJCC stage and N stage (P<0.05). There were six cases (7.32%) carrying NTRK fusion by FISH among the 82 cases of dMMR, but only seven cases (0.94%) carrying NTRK fusion among the 748 cases of PMMR. The NTRKs translocation by FISH in all 13 cases were further confirmed by next generation sequencing. Among the clinicopathological characteristics, only differentiation showed significant difference between NTRK fusion positive and negative groups (P<0.05). More importantly, NTRK fusion was enriched in dMMR group (7.32% vs. 0.94%). Conclusion: In dMMR colorectal cancer group, the prevalence of NTRK fusion is higher than that in pMMR group.

[Study on the safety and clinical efficacy of osteotomy after halo pelvic traction in severe scoliosis accompanied with split cord malformation].

Objective: To investigate the safety and clinical efficacy of osteotomy after halo pelvic traction in severe scoliosis accompanied with split cord malformation. Methods: The clinical data of 14 patients with severe scoliosis accompanied with split cord malformation admitted to the Department of Spinal Surgery, Guizhou Orthopedic Hospital from August 2015 to August 2019 were retrospectively analyzed.There were 6 males and 8 females, aged (19.8±5.0) years (range:13 to 34 years). All patients received spinal orthopedic surgery after halo pelvic traction for 3 to 7 weeks.The data of traction time, height, Cobb angle in the main curved coronal plane and sagittal plane, lung function and nutritional status of the patient were collected before and after the treatment. Paired t test was used to compare the evaluation indexes. Results: The traction time of the 14 patients was (35.2±8.3)days (range:20 to 49 days), and the height of them increased from (156.7±7.6)cm (range:141 to 166 cm) before traction to (167.0±6.4)cm (range:154 to 177 cm) after traction（t=-10.49，P<0.01）. The Cobb angle on the main curved coronal plane decreased from (117.4±17.2) ° (range: 91°to 176°) before traction to (56.4±8.1) ° (range:44°to 68°) after traction（t=13.90，P<0.01）. The sagittal Cobb angle decreased from (92.5±11.6) ° (range:62°to 132°) before traction to (41.7±7.7) °(range:29°to 51°) after traction（t=12.11，P<0.01）. No complications such as loosening of nailing and infection occurred during traction, and no decrease of nerve function occurred. Nine patients underwent single segment acromial transpedicle osteotomy and five underwent double segment adjacent asymmetric shortening osteotomy. None of the patients underwent longitudinal fracture resection. The lung function and nutritional status were improved after traction and surgery(all P<0.01). Postoperative follow-up was (22.5±9.1)months (range:12 to 36 months). At the last follow-up, the coronal Cobb angle was (56.3±7.1) °, and the sagittal Cobb angle was (37.7±6.5) °, showing no statistically significant difference from the angle after traction(t=0.16,P=0.88; t=2.28,P=0.32). There was no loss of orthopedic angle. None of the patients had internal fixation displacement, loosening or fracture. Conclusion: The treatment of severe scoliosis with accompanied with split cord malformation by halo pelvic traction is safe and effective, which is worthy of further confirmation by large sample study.

[Expression of SOX-11 and TFE3 in solid-pseudopapillary tumor of pancreas and its clinical significance].

Objective: To investigate the expression status and diagnostic value of SRY related high mobility group box 11 (SOX-11) and transcription factor E-3 (TFE3) in solid pseudopapillary tumors of pancreas (SPTPs). Methods: Thirty-eight cases of SPTPs, 36 cases of well-differentiated pancreatic neuroendocrine tumors (PanNETs) and six cases of pancreatic acinar cell carcinomas (PACCs) were collected at the Affiliated Drum Tower Hospital of Nanjing University Medical School from 2012 to 2019. The expression of SOX-11, TFE3 and ß-catenin was detected by immunohistochemistry, and the TFE3 gene status was detected by FISH in 18 cases of SPTPs. Results: Among the 38 SPTP patients, 29 were female and 9 were male, with a mean age of 50 years; among 36 PanNET patients, 32 were female and 4 were male, with a mean age of 39 years; for the six PACC patients, four were male and two were female, with a mean age of 60 years. ß-catenin was positive in all 38 SPTPs, but was negative in all 36 PanNETs and 5/6 PACCs. SOX-11 was positive in 35/38 (92.1%) of SPTPs, but was negative in all 36 PanNETs and 6 PACCs. TFE3 was positive in 36/38 (94.7%) of SPTPs, but was negative in all 36 PanNETs and 6 PACCs. Among these three tumors, the specificity and sensitivity of ß-catenin were 97.6% and 100.0%, the specificity and sensitivity of SOX-11 were 92.1% and 100.0%, the specificity and sensitivity of TFE3 were 94.7% and 100.0%, respectively. There was a significant difference of the expression status of all three markers in SPTPs compared with PanNETs and PACCs (P<0.01). The results of SOX-11 and TFE3 immunostaining showed high consistency (Kappa>0.6). No gene rearrangement (0/18) of TFE3 was found in SPTPs. Conclusion: SOX-11 and TFE3 are highly expressed in SPTPs, and their specificity in the differential diagnosis of SPTPs is better than that of ß-catenin.

Long noncoding RNA CRNDE promotes proliferation, migration and invasion in prostate cancer through miR-101/Rap1A.

Prostate cancer (Pca) is the second frequent malignancy in men. Long noncoding RNAs (lncRNAs) have been reported to play essential roles in the progression of cancers, including Pca. LncRNA colorectal neoplasia differentially expressed (CRNDE) has been found to affect tumorigenesis in many cancers. However, the exact role and mechanism of CRNDE in Pca remain poorly understood. 64 Pca patients were recruited in this study. PC3 and 22RV1 cells were used in vitro experiments. The expressions of CRNDE, microRNA-101 (miR-101), and Ras-related protein 1A (Rap1A) were detected in vivo and in vitro by quantitative real-time polymerase chain reaction and western blot, respectively. Cell proliferation, apoptosis, migration, and invasion were investigated through cell counting kit-8, flow cytometry, and Transwell assays, respectively. The interaction between miR-101 and CRNDE or Rap1A was explored by bioinformatics analysis and luciferase reporter assay. High expression of CRNDE was shown in Pca tissues and cells and predicted poor outcomes of patients. Overexpression of CRNDE promoted cell proliferation, migration, and invasion but decreased apoptosis in Pca cells, while its knockdown showed an opposite effect. CRNDE was a decoy of miR-101 and its effect on Pca progression was reversed by miR-101. Rap1A was identified as a target of miR-101 and it attenuated the effect of miR-101 on Pca development. Moreover, the Rap1A protein level was positively regulated by CRNDE, which was weakened by miR-101. CRNDE contributed to cell proliferation, migration, and invasion by regulating the miR-101/Rap1A axis in Pca, providing a novel strategy for Pca treatment.

[Transforming growth factor beta regulates hepatic progenitor cells migration via PI3K/AKT/mTOR/p70S6K pathway].

Objective: To investigate the effect and mechanism of transforming growth factor ß (TGFß) on the migration ability of hepatic progenitor cells in vitro. Methods: Primary hepatic progenitor cells of male wild-type C57BL/6J mice were isolated by two-step perfusion method and stimulated with different concentrations of TGFß .The morphological changes were observed under phase -contrast microscopy. The effects of TGFß on migration ability of hepatic progenitor cells were evaluated by scratch test and transwell method. Expression profiling and signaling phospho antibody array detected the signaling pathways involved in the regulation of TGFß on hepatic progenitor cells. Protein level of PI3K/AKT/mTOR/p70S6K signaling pathway and the localization of each signaling molecules in hepatic progenitor cells were detected. Data comparison between the two groups was performed by independent sample t-test. One-way ANOVA was used for data comparison between multiple groups. Results: TGFß made the liver progenitor cells from oval to long spindle type. Scratch test showed that the scratch healing rates of 24 h control group, and 2 ng/ml and 10 ng/ml TGF-beta groups were 36.48% ± 4.37%, 57.35% ± 4.60%, and 73.14% ± 5.02% (F = 65.87, P < 0.01), respectively. Transwell test showed that the number of migrating cells in 24 h control group, 2 ng/ml and 10 ng/ml TGF-beta groups were 127 ± 16, 230 ± 18, and 385 ±36 (F = 94.99, P < 0.01), respectively. The results of expression profiling showed that TGFß regulates gene expression in hepatic progenitor cells, and differentially expressed genes participate in the PI3K-AKT signaling pathway. Signaling phospho antibody array and western blot showed that TGFß regulated PI3K/AKT/mTOR/p70S6K signaling pathway in hepatic progenitor cells. Concurrently, immunofluorescence assay showed phosphorylation (p) 70s6k, p AKT1 and PI3K and F-actin co-localizations. Conclusion: TGFß can promote hepatic progenitor cell migration through PI3K/AKT/mTOR/p70S6K pathway, and p70S6K, pAKT1 and PI3K signaling molecules are involved in the regulation of morphology and migration of liver progenitor cells.

[Brain derived neurotrophic factor enhances the role of mesenchymal stem cells in inhibiting follicular helper T cells].

Objective: To investigate the effect of brain derived neurotrophic factor (BDNF) on mesenchymal stem cells (MSC) inhibiting follicular helper T cells (Tfh cells). Methods: The contents of indoleamine 2,3-dioxygenase (IDO), IL-10, TGF-ß and IL-21 in MSC culture supernatant were detected by ELISA; The peripheral blood of healthy volunteers were collected, and lymphocyte in peripheral blood was separated by human lymphocyte separation solution; Co-cultures of MSC and lymphocyte were performed by Transwell chamber, and the proportion of CD4(+)CXCR5(+) Tfh cells and their subtypes were detected by flow cytometry. Results: ①The concentrations of IL-10, TGF-ß, and IDO in the supernatant of BDNF group (BDNF-stimulated MSC) were higher than those of the control ones (adding PBS with the same volume) [IL-10: (42.1±4.4) ng/ml vs (19.3±2.1) ng/ml, t=4.761, P=0.009; TGF-ß: (13.9±1.7) ng/ml vs (5.3±0.6) ng/ml, t=5.129, P=0.008; IDO: (441.3±56.9) ng/ml vs (226.7±37.6) ng/ml, t=3.130, P=0.035]; ②The comparisons between BDNF (co-culture of lymphocyte and BDNF-stimulated MSC) and MSC groups (co-culture of lymphocyte and MSC) were detailed as of follows: the proportion of CD4(+) CXCR5(+)Tfh cells were lower [(3.37±0.21)% vs (6.51±0.27)%, t=9.353, P<0.001], the proportion of CD4(+) CXCR5(+)CXCR3(+) CCR6(-) Tfh cells were higher [(41.14±2.04)% vs (26.72±2.57)%, t=4.383, P=0.012], CD4(+)CXCR5(+)CXCR3(-)CCR6(-) Tfh2 cells and CD4(+)CXCR5(+)CXCR3(-)CCR6(+) Tfh17 cells were lower [Tfh2: (30.16±5.38)% vs (43.26±4.11)%, t=4.426, P=0.012; Tfh17: (15.61±1.52)% vs (22.32±0.72)%, t=4.202, P=0.014], the proportion of CD4(+)CXCR5(+)Foxp3(+) Tfr cells were higher [(4.95±0.22)% vs (2.32±0.16)%, t=10.241, P<0.001], the concentration of IL-21 in the lymphocyte supernatant was lower [(0.28±0.03) ng/ml vs (0.85±0.08) ng/ml, t=6.675, P=0.003]. Conclusion: BDNF could enhance the inhibitory effect of MSC on Tfh cells through inhibiting the increasing of Tfh cells and the differentiations of Tfh2 and Tfh17 cells.

[Feasibility and efficacy of transcatheter closure of anastomotic leakage after aortic surgery using Amplatzer Vascular Plug â ¢].

Objective: To investigate the feasibility and efficacy of transcatheter closure of anastomotic leakage after aortic surgery using Amplatzer Vascular Plug Ⅲ (AVP Ⅲ). Methods: A retrospective analysis was performed in 5 patients with anastomotic leakage after aortic surgery, who underwent transcatheter closure in our hospital from January to June 2017 using AVP Ⅲ. Surgeries were performed in 3 cases of Standford type A dissection, 1 case of ascending aortic aneurysm and 1 case of persistent truncus.There were 3 males,and age was (43.8±13.1) years old. Anastomotic leakages located at the ascending aorta in 4 patients, and the other one located between the aortic arch and the stent-graft.Three of them had aorta-right atrium fistula and patients suffered from progressive heart failure. False aneurysm between aorta and pulmonary artery was formed in 1 patient, and patent aortic false lumenwas found in the other patient. All the AVP Ⅲ were deployed based on a femoral arteriosus loop. Patients were followed up after transcatheter closure to observe the clinical results. Results: Six AVP Ⅲ were successfully implanted in the 5 patients. Trivial residual shunt was seen in 1 patient after closure. The patients were followed up 6 (1, 6) months. The cardiac function improved from NYHA class Ⅱ-Ⅳ to class Ⅰ-Ⅱ after the procedure in 3 congestive heart failure patients.The right atrium systolic pressure was significantly reduced after the procedure((8.7±1.8) mmHg (1 mmHg=0.133 kPa) vs. (24.3±2.3) mmHg, P=0.03). The diameter of the false aneurysm reduced in 1 patient after the procedure. Complete thrombosis formation of the thoracic false lumen was observed in 1 patient. Conclusion: Transcatheter closure of anastomotic leakage after aortic surgery using AVP Ⅲ is feasible and effective according to our primary experience.

CCAAT enhancer binding protein ß promotes tumor growth and inhibits apoptosis in prostate cancer by methylating estrogen receptor ß.

The CCAAT enhancer binding protein ß (C/EBPß) is overexpressed at late stages in carcinogenesis of prostate cancer (PCa), suggesting that it could potentially contribute to progression of PCa. Estrogen receptor beta (ERß) is a tumor suppressor gene in PCa. However, whether C/EBPß could regulate ERß by promoter methylation is still poorly understood.In this study, expression levels of C/EBPß and ERß in two PC lines (LNCap and PC-3), prostatic epithelial cell line (RWPE-1), forty-eight paired non-cancerous and cancerous peripheral blood samples were examined via qRT-PCR, western blotting and methylation-specific PCR. In addition, PCa cell line was infected with pCDH-C/EBPß and pLKO.1-C/EBPß and expression levels of C/EBPß, ERß and DNA methyltransferases were detected. Finally, the role of C/EBPß in proliferation and apoptosis of PCa cell lines was examined by MTT and flow cytometer assay. Our results show a higher frequency of promoter methylation of ERß levels in blood samples from PCa patients (16 of 48 cases) compared with that from healthy controls (3 of 48). Besides, elevated expression levels of C/EBPß were found in PCa patients and two PCa lines (LNCap and PC-3) compared to non-cancerous cases or prostatic epithelial cell line (RWPE-1), while opposite expression levels of ERß were found. Overexpression of C/EBPß could regulate ERß expression, DNA methyltransferases expression, cell proliferation and apoptosis. Our results support the conclusion that C/EBPß down-regulated ERß expression through increasing its promoter methylation, and then regulated proliferation and apoptosis in PCa.

[Effect of transcription factor E2F1 expression on the invasion of prostate cancer].

Objective: To investigate the effect of transcription factor E2F1 on the invasion of prostate cancer and its clinical significance. Methods: A stable inhibition of E2F1 prostate cancer cell line PC3 was established. The E2F1 and relative invasion biomarker protein expression level of the transfected cells was detected by Western blot. The PC3 cells were divided into two groups: the control group and sh-E2F1 group, cell invasion assay and cell scratch test were used to detect the number of cell migration in the experiment time. The relationship between E2F1 mRNA expression level and clinical prognostic parameters was analyzed through microarray data of prostate cancer. Results: E2F1 inhibited PC3 cell line was constructed successfully. The results of Western blot showed that the expression of Vimentin, CD147, MMP-2 and MMP-9 protein in E2F1 suppression group was lower than those in control group, while the protein expression of E-cadherin increased. Compared to the control group, inhibiting the expression of E2F1 in prostate cancer cells significantly decreased the invasion and migration, with significant difference (P<0.05). High mRNA expression of E2F1 decreased biochemical recurrence rate and overall survival rate after surgery (P=0.047, 0.035), and the E2F1 expression level was related to pathological stage of prostate cancer. Gleason score and tumor metastasis (P<0.05). Conclusion: E2F1 enhances the invasion and metastasis of prostate cancer through a variety of mechanisms, and its expression level has an important relationship with the adverse prognosis of patients with prostate cancer.

[Comparative study of three different decalcifying solutions in bone metastasis specimens with breast cancer].

Objective: To investigate the optimal strategy for immunohistochemical (IHC) staining in bone metastasis specimens from breast cancer. Methods: Twenty-eight bone metastases specimens from breast cancers were divided into three groups and subjected to different decalcifying agents (group A-10% nitrate, group B-EDTA decalcification, and group C-imported decalcifying solution RapidCal). The effects of those on HE and IHC staining for Ki-67, ER, PR, GATA3, RANK, RANKL, HER2 and HER2 FISH results were assessed. Results: There were no significant differences among three groups in HE morphology and IHC staining. Antigen content in the RapidCal group were all intact; the EDTA group showed a similar staining rate, which was better than the nitrate group (P<0.05). Nitrate group showed marked reduction in nuclear Ki-67 staining, but the loss of cytoplasmic antigens (RANK, RANKL) was less than cell membrane antigen (HER2). For FISH, the RapidCal group and EDTA group showed same results, concordant with IHC staining results. The expression of HER2 protein in the nitric acid group was significantly decreased and chromosome 17 labelling was lost (P<0.05). Conclusions: RapidCal treated bone metastases specimens from breast cancer show excellent sample quality in morphological, IHC and FISH results compared with traditional decalcifying agents. Owing to the longer time of EDTA decalcification, the new decalcifying agent RapidCal plays an important role in quality control and clinical application.

Association of genetic variations in miR-146a rs2910164 and miR-149 rs11614913 with the development of classic Kaposi sarcoma.

Classic Kaposi sarcoma is a type of vascular proliferative inflammatory disease. Previous studies have reported significant associations between microRNAs expression and the development of classic Kaposi sarcoma. Here, we conducted a case-control study to investigate the association between miR-146a and miR-149 genetic polymorphisms and risk of classic Kaposi sarcoma in a Chinese population. Both classic Kaposi sarcoma patients and healthy controls were recruited between December 2013 and October 2015. Genotyping of miR-146a and miR-149 was performed by polymerase chain reaction-coupled with restriction fragment length polymorphism. Results showed that the GG genotype of miR-146a was associated with increased risk to classic Kaposi sarcoma (OR = 6.00, 95%CI = 1.19-30.12), as compared with the CC genotype. In the recessive model, we found that the GG genotype carried a 4.55-fold increased risk to classic Kaposi sarcoma as compared with the CC + CG genotype (OR = 2.06, 95%CI = 1.04-20.29). In conclusion, our study demonstrated that miR-146a, but not miR-149 polymorphism, is associated with risk to classic Kaposi sarcoma in the Chinese population.

Analysis of KIT mutations and c-KIT expression in Chinese Uyghur and Han patients with melanoma.

BACKGROUND: The KIT gene plays an important role in the pathogenesis of malignant melanoma (MM). In recent years, activating mutations in KIT have been recognized as oncogenic. A number of therapies have been established, which provide significant clinical benefits for patients with MM with KIT mutations. Thus, detection of KIT mutations can have profound therapeutic implications. AIM: To investigate KIT gene expression in MMs in Chinese Uyghur and Han patients with mutations in KIT, and to identify the clinical features associated with KIT mutations and c-KIT expression. METHODS: In total, 105 MMs (56 from Uyghur and 49 from Han patients) were selected from patients in the Uyghur Autonomous region. Formalin-fixed, paraffin wax-embedded tumour sections were analysed for c-KIT expression using immunohistochemistry. Exons 11 and 13 of KIT were analysed for the presence of mutations using PCR amplification and DNA sequencing. RESULTS: Of the 105 MMs, 13 (10 Han and 3 Uyghur) were found to have mutations in KIT. Thus, the frequency of KIT mutations in Han patients was significantly higher than that in Uyghur patients (P = 0.02). We detected c-KIT expression in 71.4% and 42.9% of the tumour tissue samples collected from the Uyghur and Han patients, respectively. CONCLUSION: In the Xinjiang Uyghur Autonomous Region in China, chronic sun-induced damage MM is the most prevalent MM among Chinese Uyghur patients, whereas acral and mucosal MMs are the most prevalent in Uyghur patients. Mutations in the KIT gene do not correlate with c-KIT expression.

One hundred and five Kaposi sarcoma patients: a clinical study in Xinjiang, Northwest of China.

BACKGROUND: Kaposi's sarcoma (KS) is an unusual illness that may be associated with human herpes virus 8 (HHV-8) infections, and appears mainly in Jews, Italians and Greeks. There is a lack of patient data in Xinjiang regarding the clinical characteristics of KS. OBJECTIVES: To review the clinical characteristics of a series of patients with KS in Xinjiang, Northwest China, over 16-year period. METHODS: A retrospective analysis of patients referred to a Xinjiang hospital in Northwest China with classic KS (CKS) and AIDS-associated KS (AIDS-KS) between January 1997 and April 2013 was performed. Reviewed information included demographics, clinical features, histopathological traits, treatment and presence of HHV-8 infection. RESULTS: During the study period, 105 patients with a diagnosis of KS, including 77 CKS and 28 AIDS-KS, were referred to our hospital. Mean age at diagnosis was 55.8 ± 16.8 years (range: 25-85 years). There were 70 (90.9%) males and 7 (9.1%) females (male-to-female ratio: 10 : 1) having CKS and 21 (75.0%) males and 7 (25.0%) females (male-to-female ratio: 3 : 1) with AIDS-KS. Most of the patients were Uyghur, including 67 CKS and 24 AIDS-KS. The rate of multifocal lesions at diagnosis was 98.1% (103/105). The most common area of lesions was between 1% and 5% of CKS and AIDS-KS. The main types of lesions were nodules, patches and plaques. The lower extremity and foot were the most common locations for CKS and AIDS-KS. In addition to skin damage, the penis, mouth, lymph nodes and interstitial lung tissues were involved in some cases. No second primary malignancy was diagnosed. Systemic chemotherapy and radiotherapy were effective treatments for CKS. The HHV-8 positivity rate was 98.98% in 98 KS cases. CONCLUSIONS: In Xinjiang, most CKS and AIDS-KS patients were older Uyghur men. AIDS-KS was found predominantly among 30-year-old Uyghur patients, compared with 60 years for those having CKS. The latter exhibited certain characteristics such as disseminated skin disease; in some patients, the condition was accompanied by lymphedema, visceral or lymph node involvement, but no secondary malignancies. In addition, the HHV-8 positivity rate associated with KS was very high.

Inflammation-related genetic variants predict toxicity following definitive radiotherapy for lung cancer.

Definitive radiotherapy improves locoregional control and survival in inoperable non-small cell lung cancer patients. However, radiation-induced toxicities (pneumonitis/esophagitis) are common dose-limiting inflammatory conditions. We therefore conducted a pathway-based analysis to identify inflammation-related single-nucleotide polymorphisms associated with radiation-induced pneumonitis or esophagitis. A total of 11,930 single-nucleotide polymorphisms were genotyped in 201 stage I-III non-small cell lung cancer patients treated with definitive radiotherapy. Validation was performed in an additional 220 non-small cell lung cancer cases. After validation, 19 single-nucleotide polymorphisms remained significant. A polygenic risk score was generated to summarize the effect from validated single-nucleotide polymorphisms. Significant improvements in discriminative ability were observed when the polygenic risk score was added into the clinical/epidemiological variable-based model. We then used 277 lymphoblastoid cell lines to assess radiation sensitivity and expression quantitative trait loci (eQTL) relationships of the identified single-nucleotide polymorphisms. Three genes (PRKCE, DDX58, and TNFSF7) were associated with radiation sensitivity. We concluded that inflammation-related genetic variants could contribute to the development of radiation-induced toxicities.

Detection of acute cerebral hemorrhage in rabbits by magnetic induction

Acute cerebral hemorrhage (ACH) is an important clinical problem that is often monitored and studied with expensive devices such as computed tomography, magnetic resonance imaging, and positron emission tomography. These devices are not readily available in economically underdeveloped regions of the world, emergency departments, and emergency zones. We have developed a less expensive tool for non-contact monitoring of ACH. The system measures the magnetic induction phase shift (MIPS) between the electromagnetic signals on two coils. ACH was induced in 6 experimental rabbits and edema was induced in 4 control rabbits by stereotactic methods, and their intracranial pressure and heart rate were monitored for 1 h. Signals were continuously monitored for up to 1 h at an exciting frequency of 10.7 MHz. Autologous blood was administered to the experimental group, and saline to the control group (1 to 3 mL) by injection of 1-mL every 5 min. The results showed a significant increase in MIPS as a function of the injection volume, but the heart rate was stable. In the experimental (ACH) group, there was a statistically significant positive correlation of the intracranial pressure and MIPS. The change of MIPS was greater in the ACH group than in the control group. This high-sensitivity system could detect a 1-mL change in blood volume. The MIPS was significantly related to the intracranial pressure. This observation suggests that the method could be valuable for detecting early warning signs in emergency medicine and critical care units.