Independent and combined effects of smoking, drinking and depression on periodontal disease.

BACKGROUND: Periodontitis is a complex chronic inflammatory disease that is particularly associated with health-related conditions such as smoking, excessive drinking and depression. This research aimed to investigate the interaction between these lifestyles factors on periodontitis risk. METHODS: This study included participants who participated in the National Health and Nutrition Examination Survey in the United States between 2009 and 2014. They had completed oral health-periodontal examination, Smoking-Cigarette Use Questionnaire, Alcohol Use Questionnaire, and Patient Health Questionnaire. Periodontal clinical attachment loss (CAL) of 3 mm or more and Patient Health Questionnaire-9 (PHQ-9) of 10 scores or more were used to identify periodontitis and depression, respectively. Daily alcohol consumption in the past year was classified into three levels: low (1 drink or less), moderate (between 1 and 3 drinks), and heavy drinking (4 drinks or more), while smoking was defined as having smoked at least 100 cigarettes in one's lifetime. Then, the logistic regression combined with interaction models were used to analyze the independent and combined effects of smoking, drinking and depression on periodontitis risk. RESULTS: The results indicated a statistically significant multiplicative interaction between smoking and depression in relation to the development of periodontitis, both in the overall population (P = 0.03) and among male participants (P = 0.03). Furthermore, among individuals experiencing depression, smoking was found to significantly increase the prevalence of periodontitis by 129% in the younger age group compared to non-smokers (odds ratio [OR]: 2.29; 95% confidence interval [CI]: 1.10 to 4.76). However, the interaction between smoking and alcohol consumption was only significant among females (P < 0.05). There was a dose-dependent relationship between drinking frequency and smoking on periodontitis prevalence. In the smoking population, occasional drinking (OR: 1.70; 95% CI: 1.22 to 2.37) and regular drinking (OR: 2.28; 95% CI: 1.68 to 3.11) significantly increased the prevalence of periodontitis compared to individuals without these two factors. CONCLUSION: These results suggested that there were interactive effects between smoking, drinking and depression on periodontitis risk and policies aimed at healthy behaviours and mental health may be beneficial for our oral health.

[Diagnostic value of contrast-enhanced ultrasound in hepatic epithelioid hemangioendothelioma].

Objective: To investigate the features of contrast-enhanced ultrasound (CEUS) in hepatic epithelioid hemangioendothelioma (HEHE) in order to improve the preoperative diagnosis rate. Methods: CEUS images of 32 pathologically-proven cases of hepatic epithelioid hemangioendothelioma from January 2004 to August 2021 were collected. Lesions were analyzed to observe the features of enhancement mode, enhancement intensity, and distinct enhancement phases. Results: Among the 32 cases, one had a solitary lesion, 29 had multiple lesions, and two had diffuse-type lesions. Contrast-enhanced ultrasound revealed a total of 42 lesions in 32 cases. In terms of arterial phase enhancement, 18 lesions had overall enhancement, six lesions had uneven dendritic enhancement, 16 lesions had rim-like enhancement, and two lesions had just slight peripheral spot enhancement around the lesions. Among the three cases, there were multiple lesions that had overall enhancement and ring enhancement. In terms of the enhancement phase, 20 lesions showed "fast progression", 20 lesions showed "same progression", and two lesions showed "slow progression". During the late arterial or early portal venous phases with rapid washout, all lesions manifested as hypoechoic. With peaked enhanced intensity, 11 lesions had a lower enhancement intensity than the surrounding normal liver parenchyma; 11 lesions had the same enhancement degree as the surrounding normal liver parenchyma; and 20 lesions had a higher enhancement degree than the surrounding normal liver parenchyma. All 16 ring-enhancing lesions had marked hyperenhancement. In the typical enhancing lesions, four showed hyperenhancement, five showed low enhancement, and nine showed isoenhancement. In the dendrite-enhancing lesions, there were two isoenhancing and four hypoenhancing. Contrast-enhanced ultrasound delineated the boundaries of all lesions more clearly than two-dimensional ultrasound. Conclusion: Contrast-enhanced ultrasound has certain value in the diagnosis of hepatic epithelioid hemangioendothelioma.

[Association between inflammation activity of left atrial epicardial adipose tissue measured by 18F-FDG PET/CT and atrial fibrillation].

Objective: To explore the association between inflammation activity of left atrial epicardial adipose tissue (LA-EAT) measured by 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) and atrial fibrillation (AF). Methods: A total of 78 patients with AF, who underwent 18F-FDG PET/CT in the Nuclear Medicine Department of the Third Affiliated Hospital of Soochow University due to abnormally elevated levels of tumor indicators or malignant tumors from March 2018 to December 2019, were enrolled in this retrospective study. According to the examination date of PET/CT and basic characteristics of AF patients (gender, age), a 1∶1 propensity score matching was used to enroll a non-AF control group (78 patients). The maximum standard uptake value of left atrial epicardial tissue (LA-EAT FDG SUVmax) and total EAT volume (V-EAT) were measured by 18F-FDG PET/CT. Left ventricular ejection fraction (LVEF) and left atrial diameter (LAD) were obtained by echocardiography. Blood lipids and biomarkers of inflammation were measured. The differences of clinical data and EAT-related indicators were compared between the AF group and control group. Logistic multivariate regression analysis was used to determine the related factors of AF. Then the receiver operating characteristic (ROC) curve was used to determine the cutoff value of LA-EAT FDG SUVmax on the diagnosis of AF. Univariate and multivariate logistic regression analysis were used to analyze the relationship between the increase of LA-EAT FDG SUVmax and AF. Results: The age was (66.9±10.2) years and there were 55 males (70.5%) in the AF group. The age was (66.9±8.0) years, and there were 52 males (66.7%) in the control group (both P>0.05). The LAD ((44.2±5.8) mm vs. (35.4±4.4) mm), V-EAT ((122.1±42.0) cm3 vs. (91.6±34.5) cm3), and LA-EAT FDG SUVmax ((1.6±0.3) vs. (1.4±0.2)) values were significantly higher, while LVEF ((60.1±4.7)% vs. (63.9±2.9)%) was lower in the AF group than in the control group (P all<0.001). Multivariate logistic regression analysis showed that LAD (OR=1.340, 95%CI 1.195-1.502), V-EAT (OR=1.016, 95%CI 1.001-1.031), and LA-EAT FDG SUVmax (OR=1.375, 95%CI 1.095-1.723) were positively correlated with AF, LVEF (OR=0.781, 95%CI 0.659-0.926) was negatively correlated with AF(P all<0.05). The area under the ROC curve of LA-EAT FDG SUVmax for diagnosis of AF was 0.680 (95%CI 0.597-0.764, P<0.001), and the best cut-off value was 1.415 with a sensitivity of 65.4% and specificity of 61.5%. After adjusting for high-density lipoprotein cholesterol, LVEF, LAD and V-EAT, LA-EAT FDG SUVmax≥1.415 was independently associated with AF (OR=2.982, 95%CI 1.122-7.926, P=0.010). Conclusions: The inflammatory activity of LA-EAT measured by 18F-FDG PET/CT is an independent risk factor of AF, and the increased inflammatory activity of LA-EAT is positively correlated with AF.

Long noncoding RNA OR3A4 promotes cisplatin resistance of non-small cell lung cancer by upregulating CDK1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA OR3A4 promotes cisplatin resistance of non-small cell lung cancer by upregulating CDK1, by J. Shang, Y.-D. Xu, Y.-Y. Zhang, M. Li, published in Eur Rev Med Pharmacol Sci 2019; 23 (10): 4220-4225-DOI: 10.26355/eurrev_201905_17926-PMID: 31173293" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17926.

[Clinical analysis and prognosis factors of malignancy in the patients with mucinous cystic neoplasms of the pancreas].

Objective: To examine clinic pathological features of mucinous cystic neoplasms (MCN) of the pancreas and explore the prognosis factors associated with malignant transformation of MCN of the pancreas. Methods: This multicenter retrospective study included all patients with pancreatic MCN underwent surgery at Department of Pancreatic Surgery, Zhongshan Hospital of Fudan University between January 2008 and December 2018 and patients with MCN who confirmed by postoperative pathology from Multicenter Pancreatic Cystic Tumor Database. There were 50 males (14.4%) and 297 females (85.6%) and the mean age was 48.6 years (range: 24-77 years). According to the pathological results, all patients were divided into benign lesion group (including MCN and which associated with low/medium grade dysplasia) and malignant lesion group (including MCN with high-grade dysplasia or invasive carcinoma) . The preoperative clinical pathology and imaging features of the two groups were analyzed, and the risk factors associated with malignant transformation of MCN were statistically analyzed. Results: This multicenter retrospective study included 347 patients. Twenty-four of the 347 patients were malignant, including 7 males and 17 females. Univariate analysis showed that age, gender, carcino-embryonic antigen (CEA) , CA19-9, CA125, tumor maximum diameter, and tumor location were remarkably different in the two groups (P<0.05) . Logistic regression analysis found that the preoperative tumor maximum diameter (OR=1.023, 95% CI: 1.002-1.045, P=0.035) was an independent risk factor for MCN malignant transformation. Conclusions: Age, gender, CEA, CA19-9, CA125, tumor maximum diameter, and tumor location are important features of MCN malignant lesions.The maximum diameter of the preoperative tumor is an independent risk factor for MCN malignant transformation.

LncRNA SNHG5 promotes cisplatin resistance in gastric cancer via inhibiting cell apoptosis.

OBJECTIVE: To elucidate the function of long non-coding RNA (lncRNA) SNHG5 in cisplatin-resistant gastric cancer (GC), and its potential mechanism. PATIENTS AND METHODS: We detected the expressions of SNHG5, apoptosis-specific genes (Bax and Bcl-2) and drug resistance-specific genes (MDR1 and MRP1) in cisplatin-sensitive and cisplatin-resistant GC patients. The expression levels were also detected in cisplatin-resistant GC cell lines (BGC823/DDP, SGC7901/DDP) and GC cell lines (BGC823 and SGC7901). Through the liposome transfection, the regulatory effects of SNHG5 on proliferative potential and apoptosis were examined by cytotoxicity assay and flow cytometry assay, respectively. The protein levels of apoptosis-related genes and drug resistance-related genes influenced by SNHG5 were detected by Western blot. RESULTS: Compared with cisplatin-sensitive GC patients, SNHG5 expression was remarkably higher in cisplatin-resistant GC patients. Besides, higher SNHG5 expression was observed in BGC823/DDP and SGC7901/DDP cells relative to that of their parental cells. Proliferative rate (OD450) and IC50 decreased, but the apoptotic rate increased in BGC823/DDP and SGC7901/DDP cells with SNHG5 knockdown. It is found that SNHG5 overexpression reduced cisplatin sensitivity in BGC823 and SGC7901 cells. Decreased cisplatin cytotoxicity, elevated IC50 and inhibited apoptotic rate were observed in GC cells overexpressing SNHG5. Moreover, the expression levels of Bax, MDR1 and MRP1 were upregulated, while Bcl-2 downregulated in BGC823 and SGC7901 cells overexpressing SNHG5. CONCLUSIONS: SNHG5 is highly expressed in cisplatin-resistant GC. SNHG5 promotes cisplatin resistance in GC by regulating apoptosis-related genes and drug resistance-related genes.

Long noncoding RNA OR3A4 promotes cisplatin resistance of non-small cell lung cancer by upregulating CDK1.

OBJECTIVE: Numerous studies have proved that long non-coding RNAs (lncRNAs) have an important role in malignant tumors, including non-small cell lung cancer (NSCLC). LncRNA olfactory receptor family 3 subfamily A member 4 (OR3A4) was explored to identify how it functions in resistance of NSCLC patients to cisplatin. MATERIALS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect OR3A4 expression in NSCLC patients. Then, we conducted Cell Counting Kit-8 (CCK-8) assay and flow cytometric analysis to detect the function of OR3A4 on the resistance of NSCLC cells to cisplatin. Furthermore, the potential mechanism was explored by mechanism assays. RESULTS: Compared with OR3A4 expression of paired A549 cells, OR3A4 expression of A549/DDP cells was higher. Moreover, the functional assay showed that after OR3A4 was silenced in A549/DDP cells, cell cycle arrest and cell apoptosis was induced, and resistance to cisplatin was reversed. Furthermore, it was found that CDK1 expression was suppressed in A549/DDP cells by knockdown of OR3A4. CONCLUSIONS: The present work suggests that OR3A4 participates in regulating cell cycle, cell apoptosis of NSCLC cells and the resistance to cisplatin via upregulating CDK1, indicating that OR3A4 could be identified as a potential therapeutic target for NSCLC patients.

LncRNA SNHG14 promotes the development of cervical cancer and predicts poor prognosis.

OBJECTIVE: The aim of this study was to explore the role of long non-coding RNA (LncRNA) small nucleolar RNA host gene 14 (SNHG14) in cervical cancer, and to further understand the possible underlying mechanism. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of SNHG14 in cervical cancer. The relationship between SNHG14 expression with clinic-pathological features and prognosis of patients was analyzed. Cell Counting Kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) and flow cytometry were used to evaluate the proliferation and apoptosis of cells. At the same time, the changes in the expression of apoptosis-related proteins after SNHG14 knockdown were detected. RESULTS: Compared with normal cervical tissues, the expression of SNHG14 was significantly higher in cervical cancer tissues. The prognosis of patients with higher expression of SNHG14 was worse than those with a lower level. The relationship between the expression of SNHG14 and clinicopathological features of patients with cervical cancer was further analyzed. The results demonstrated that a higher expression level of SNHG14 indicated later tumor stage and higher incidence of lymph node metastasis. Compared with normal cervical epithelial cell line End1/E6E7, the level of SNHG14 in cervical cancer cell lines (including SW756, SiHa and HeLa) was markedly up-regulated. Among them, SW756 and SiHa cells exhibited the highest level of SNHG14. After knocking down SNHG14, the viability and proliferation ability of SW756 and SiHa cells were remarkably decreased, while cell apoptosis was increased. Subsequently, we investigated the possible underlying mechanism. The results found that the knockdown of SNHG14 enhanced the activation of caspases-3, and increased the protein expression of Bax, JAK2 and STAT3, whereas decreased the expression of Bal-2 and Bid. CONCLUSIONS: LncRNA SNHG14 was highly expressed in cervical tumor tissues or cells, which could promote the progression of cervical cancer. Furthermore, SNHG14 might be associated with the activation of the JAK-STAT pathway.

LncRNA DANCR accelerates the development of multidrug resistance of gastric cancer.

OBJECTIVE: The development of multidrug resistance (MDR) is a key issue for tumor recurrence and metastasis, leading to treatment failure of gastric cancer (GC). Long non-coding RNA (lncRNA) DANCR has been shown to be highly expressed in GC patients, which accelerates growth and metastasis of GC cells. This study aims to elucidate the role of DANCR in regulating MDR of GC. PATIENTS AND METHODS: The mRNA level of DANCR in GC patients with or without DDP-resistance was determined by quantitative Real-time polymerase chain reaction (qRT-PCR). DANCR expression in GC cell lines (SGC7901, BGC823) and cisplatin (DDP)-resistant cell lines (SGC7901/DDP, BGC823/DDP) was determined as well. Knockdown or overexpression of DANCR in GC cells with or without DDP-resistance was achieved by siRNA interference technology or stable transfection of lentivirus, respectively. The regulatory effects of DANCR on cytotoxicity and apoptosis were examined by cytotoxicity assay and flow cytometry method (FCM), respectively. In addition, we detected the expressions of MDR1, MRP1, mechanistic target of rapamycin (mTOR) and hypoxia inducible factor-1α (HIF-1α) in GC cells overexpressing DANCR by qRT-PCR and Western blot. RESULTS: DANCR expression remained high in DDP-resistant GC tissues or cells. SGC7901/DDP and BGC823/DDP cells transfected with si-DANCR presented decreased survival and increased apoptosis. On the contrary, SGC7901/DDP and BGC823/DDP cells overexpressing DANCR showed increased survival and decreased apoptosis. In addition, DANCR overexpression could upregulate expressions of MDR1 and MRP1 in DDP-induced SGC901 and BGC823 cells. CONCLUSIONS: Upregulation of DANCR can accelerate the MDR development of GC, which may become a potential target for treating GC with MDR.

[The facial nerve study of multi-slice spiral computed tomography in congenital abnormality of external and middle ear].

Objective:Images of temporal bone are obtained on Siemens 64 slices spiral CT scanner with high resolution scanning to describe the course of facial nerve for better preoperative evaluation of CAEMA.Method:To describe the course of facial nerve on rectangular coordinate system from three silce on HRCT, 29 patients(35 ears) are enrolled in our study in ENT department from November 2005 to March 2007 in the second affiliated hospital of sun yan sen university, who are all diagnosed not acquired deformity but CAEME, associated with no congenital deformity syndromes and no middle ear or mastoid operations before. Patients with bilateral ears deformity are 6, and unilateral ears deformity are 23 (13 right and 10 left) in the study group. The control group is the normal ears of unilateral ear deformity.Result:In the study group, the shortest distance from FN tympanic segment to oval window is shorter than that of the normal group (P< 0.05). In CAEME of unilateral ears the FN mastoid segment displaces anteriorly about 2.7 mm, and in CAEME of bilateral ears displaces 3.0mm, compared with the normal ears (P< 0.05). The deformity degree of auricle has correlations with anteriorly displacement of facial nerve mastoid segment (P< 0.05).Conclusion:The FN mastoid segment is anteriorly displacement in both bilateral and unilateral ear deformity. The deformity degree of auricle has correlations with anteriorly displacement of facial nerve mastoid segment. The lateral displacement of facial nerve doesn't occur usually in CAEME. The shortest distance between oval window and tympanic segment of FN become shorter than normal ears.

[Feasibility study of transplantation of penile corpus cavernosum and major pelvic ganglion in renal subserous region].

OBJECTIVE: To study the feasibility of transplantation of normal rat penile corpus cavernosum and major pelvic ganglion (MPG) into the renal subserous region of a Nu/Nu mouse based on allograft technology. METHODS: Penile corpus cavernosum and MPG, harvested from Sprague-Dawley (SD) rats under sterile condition, were transplanted underneath the kidney capsule of Nu/Nu mice through the microsurgery instruments and surgery microscope. The histopathologic changes and cellular proliferation in the transplanted penile corpus cavernosum and MPG were then analyzed at the end of 1week and 4 weeks after transplantation. Histological staining and immunohistochemical staining were used to evaluate the main outcome measures. RESULTS: After 1 week, the tissue morphology of the transplanted corpus cavernosum underneath the kidney capsule of Nu/Nu mice was consistent with normal penile corpus cavernosum, and blood could be observed in the penis cavernous sinus of the graft; after 4 weeks, the mophorlogy of the tranplanted corpus cavernosum near the kidney was consistent with normal penile corpus cavernosum, while fibrosis was noteworthy in the graft away from the kidney, but blood could still be seen in the penis cavernous sinus. After 1 week, the tissue morphology of the transplanted MPG was consistent with normal MPG, multiple islet-like cell clusters could be seen in the transplanted MPG in the renal subserous region, and angiogenesis could be observed near the kidney; after 4 weeks, a network of blood vessels was clearly visible away from the kidney, and islet-like cell clusters were still clearly observed in the transplanted MPG. In addition, ki67 positive cells were observed in the transplanted penile corpus cavernosum and MPG after 4 weeks of transplantation, which indicated that there was still cell proliferation activity in the grafts. CONCLUSION: The transplanted corpus cavernosum and MPG underneath the kidney capsule of Nu/Nu mice could survive at least 4 weeks. Moreover, the inner structure of the transplanted corpus cavernosum and MPG was close to the normal tissue. The underlining mechanism may be related to the local microenvironment underneath the kidney capsule of Nu/Nu mice and the neovascularization in the transplanted grafts.

[A clinical study into the vestibular function and therapy of patients with chronic positional symptoms after acute vestibular syndrome].

Objective:To investigate the status of the vestibular function of the patients with chronic positional symptoms after peripheral acute vestibular syndrome (AVS) and the curative effect of the vestibular rehabilitation therapy (VRT). Method:Using caloric test (CT), head shaking nystagmus test (HST), cervical vestibular evoked myogenic potentials as well as ocular vestibular evoked myogenic potentials to estimate the function of semicircular canal and otolith organs. The patients with normal VEMPs are divided as Group A. Otherwise are as Group B. Both groups are treated with VRT. The curative effect is estimated by vestibular symptom index (VSI) and Berg balance scale (BBS). Result:Thirty-three of 37 patients (86.5%) had an abnormal result of CT and HST, with 23 of these patients (65.7%) had an abnormal of both test. Twenty-two patients (59.5%) were in Group A and 15 (40.5%) in Group B. Before the therapy, Group B had a higher score of the balance and dizziness symptoms of VSI (P<0.05), and Group A had a higher score of the BBS (P<0.05). After the therapy, the VSI scores of both groups dropped and scores of the BBS raised. Conclusion:Patients with chronic positional symptoms after peripheral AVS have dynamic vestibular lesions to different extents. Those with otolith organs lesions tend to have a worse function of balance. Nevertheless, patients have a better off after VRT.

[A clinical analysis for sudden sensorineural hearing loss withcontralateral sensorineural hearing loss].

Objective:To analyze the clinical characteristics and prognosis,and to learn the impact factors of patients with sudden sensorineural hearing loss with contralateral sensorineural hearing loss(SSHLwCSHL).Method:Clinical data of 63 cases of patients with SSHLwCSHL were analyzed systematically,including all the clinical manifestations,audiologic characteristics and the effect assessment,and compared with that of unilateral sudden sensorineural hearing loss(USSHL) and bilateral sudden sensorineural hearing loss(BSSHL).Base on those,we summarized comprehensively the development and prognosis characteristics of the disease.Result:The incidence of SSHLwCSHL was 8.3 percent of overall patients with SSNHL.SSHLwCSHL occurs more commonly in male patients,with more vertigo,diabetes mellitus,and lipid panel abnormalities compared with other groups.Hearing curve and the degree of hearing loss of the prevalence ear of SSHLwCSHL was statistically significant difference with USSHL(P<0.05).Most common reason of the contralateral hearing loss was sudden sensorineural hearing loss(49%),and 59% patients of SSHLwCSHL suffered hearing loss of other ear after 2-10 years after contralateral hearing loss.The total effective rate was 14.3%,1 in 63 patients cured,1 excellence and 6 effective.The total effective rate was 9.5% in patients with severe or profound sensorineural hearing loss in the contralateral ear,which was lower than that of patients with moderate and moderately severe sensorineural hearing loss in the contralateral-ear(P=0.021).Conclusion:SSHLwCSHL has complex condition.The prognosis for improvement is poor.Recognition of similarities and differences between bilateral and unilateral SSNHL can help in counseling and managing the patients.

[Feasibility study of transplantation of penile corpus cavernosum and major pelvic ganglion in renal subserous region].

OBJECTIVE: To study the feasibility of transplantation of normal rat penile corpus cavernosum and major pelvic ganglion (MPG) into the renal subserous region of a Nu/Nu mouse based on allograft technology. METHODS: Penile corpus cavernosum and MPG, harvested from Sprague-Dawley (SD) rats under sterile condition, were transplanted underneath the kidney capsule of Nu/Nu mice through the microsurgery instruments and surgery microscope. The histopathologic changes and cellular proliferation in the transplanted penile corpus cavernosum and MPG were then analyzed at the end of 1week and 4 weeks after transplantation. Histological staining and immunohistochemical staining were used to evaluate the main outcome measures. RESULTS: After 1 week, the tissue morphology of the transplanted corpus cavernosum underneath the kidney capsule of Nu/Nu mice was consistent with normal penile corpus cavernosum, and blood could be observed in the penis cavernous sinus of the graft; after 4 weeks, the mophorlogy of the tranplanted corpus cavernosum near the kidney was consistent with normal penile corpus cavernosum, while fibrosis was noteworthy in the graft away from the kidney, but blood could still be seen in the penis cavernous sinus. After 1 week, the tissue morphology of the transplanted MPG was consistent with normal MPG, multiple islet-like cell clusters could be seen in the transplanted MPG in the renal subserous region, and angiogenesis could be observed near the kidney; after 4 weeks, a network of blood vessels was clearly visible away from the kidney, and islet-like cell clusters were still clearly observed in the transplanted MPG. In addition, ki67 positive cells were observed in the transplanted penile corpus cavernosum and MPG after 4 weeks of transplantation, which indicated that there was still cell proliferation activity in the grafts. CONCLUSION: The transplanted corpus cavernosum and MPG underneath the kidney capsule of Nu/Nu mice could survive at least 4 weeks. Moreover, the inner structure of the transplanted corpus cavernosum and MPG was close to the normal tissue. The underlining mechanism may be related to the local microenvironment underneath the kidney capsule of Nu/Nu mice and the neovascularization in the transplanted grafts.

Surgical treatment of osteoradionecrosis of the temporal bone in patients with nasopharyngeal carcinoma.

OBJECTIVE: To investigate methods of treating diffuse osteoradionecrosis of the temporal bone in cases of nasopharyngeal carcinoma, following radiotherapy. STUDY DESIGN: Retrospective. METHODS: Fourteen post-irradiation nasopharyngeal carcinoma patients (n = 14 ears) with diffuse osteoradionecrosis received surgical treatment from March 1994 to May 2005. The patients underwent radical mastoidectomy (five ears), extensive radical mastoidectomy (one ear), or radical mastoidectomy and obliteration with local vascularised fascia flaps (eight ears). RESULTS: Six ears fully recovered; two ears were still infectious but sequestrum had not re-formed; five ears (50 per cent) still had repeated suppuration and did not epithelialise; and one ear had local re-formation of sequestrum requiring periodic dressing changes. CONCLUSION: Diffuse osteoradionecrosis of the temporal bone following radiotherapy for nasopharyngeal carcinoma is difficult to treat surgically. The main objective of surgery is to facilitate drainage and to prevent complications. Radical mastoidectomy and obliteration with local vascularised flaps is an effective method.

Regulation of the effects of TGF-beta 1 by activation of latent TGF-beta 1 and differential expression of TGF-beta receptors (T beta R-I and T beta R-II) in idiopathic pulmonary fibrosis.

BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is characterised by subpleural fibrosis that progresses to involve all areas of the lung. The expression of transforming growth factor-beta1 (TGF-beta 1), a potent regulator of connective tissue synthesis, is increased in lung sections of patients with IPF. TGF-beta 1 is generally released in a biologically latent form (L-TGF-beta 1). Before being biologically active, TGF-beta must be converted to its active form and interact with both TGF-beta receptors type I and II (T beta R-I and T beta R-II). TGF-beta latency binding protein 1 (LTBP-1), which facilitates the release and activation of L-TGF-beta 1, is also important in the biology of TGF-beta 1. METHODS: Open lung biopsy samples from patients with IPF and normal controls were examined to localise T beta R-I, T beta R-II, and LTBP-1. Alveolar macrophages (AM) and bronchoalveolar lavage (BAL) fluid were examined using the CCL-64 bioassay to determine if TGF-beta is present in its active form in the lungs of patients with IPF. RESULTS: Immunoreactive L-TGF-beta 1 was present in all lung cells of patients with IPF except for fibroblasts in the subepithelial regions of honeycomb cysts. LTBP-1 was detected primarily in AM and epithelial cells lining honeycomb cysts in areas of advanced IPF. In normal lungs LTBP-1 immunoreactivity was observed in a few AM. AM from the upper and lower lobes of patients with IPF secreted 1.6 (0.6) fmol and 4.1 (1.9) fmol active TGF-beta, respectively, while AM from the lower lobes of control patients secreted no active TGF-beta (p< or =0.01 for TGF-beta in the conditioned media from AM obtained from the lower lobes of IPF patients v normal controls). The difference in percentage active TGF-beta secreted by AM from the lower lobes of patients with IPF and the lower lobes of control patients was significant (p< or =0.01), but the difference between the total TGF-beta secreted from these lobes was not significant. The difference in active TGF-beta in conditioned media of AM from the upper and lower lobes of patients with IPF was also not statistically significant. BAL fluid from the upper and lower lobes of patients with IPF contained 0.7 (0.2) fmol and 2.9 (1.2) fmol active TGF-beta, respectively (p< or =0.03). The percentage of active TGF-beta in the upper and lower lobes was 17.6 (1.0)% and 78.4 (1.6)%, respectively (p< or =0.03). In contrast, BAL fluid from control patients contained small amounts of L-TGF-beta. Using immunostaining, both T beta R-I and T beta R-II were present on all cells of normal lungs but T beta R-I was markedly reduced in most cells in areas of honeycomb cysts except for interstitial myofibroblasts in lungs of patients with IPF. TGF-beta 1 inhibits epithelial cell proliferation and a lack of T beta R-I expression by epithelial cells lining honeycomb cysts would facilitate repair of the alveoli by epithelial cell proliferation. However, the presence of both T beta Rs on fibroblasts is likely to result in a response to TGF-beta 1 for synthesis of connective tissue proteins. Our findings show that biologically active TGF-beta 1 is only present in the lungs of patients with IPF. In addition, the effects of TGF-beta 1 on cells may be further regulated by the expression of T beta Rs. CONCLUSION: Activation of L-TGF-beta 1 and the differential expression of T beta Rs may be important in the pathogenesis of remodelling and fibrosis in IPF.

[Cholangioplasty by using a patch of bovine pericardium in the treatment of stricture of extrahepatic bile duct].

From Sept. 1989 to Jan. 1994, processed fresh bovine pericardium was used for the repairment of stricture of extrahepatic bile duct in 6 cases (7 times). All patients have been followed up for 8 approximately 52 months (average 24 months). One case reoperated on for recurrent jaundice on 26th month postoperation. All cases are alive and in good health, without any clinical symptom.

The initiation-promotion-progression model of rat hepatocarcinogenesis.

Carcinogenesis is a multistage process consisting of the three distinct stages: initiation, promotion, and progression. The initiation-promotion-progression (IPP) protocol models these stages and establishes a method whereby agents that possess a carcinogenic risk can be classified as acting primarily at any one or combination of these stages. In one hepatocarcinogenesis IPP protocol, rats were initiated with 10 mg of diethylnitrosamine/kg body wt at 5 days of age, started on the promoting agent phenobarbital at weaning, subjected to a 70% partial hepatectomy at 6 months, and, at the peak of proliferation, given a putative progressor agent, ethylnitrosourea ([ENU] 100 mg/kg, ip) or hydroxy-urea ([HU] 3 x 150 mg/kg, ip). Administration of the promoting agent was discontinued after the progressor agent was given, and the rats were sacrificed 6 months later. The number and volume fraction of promoter-independent (growth in the absence of the promoting agent) altered hepatic foci (AHF) were then determined by quantitative stereology. The number of such AHF increased with either ENU or HU treatment compared with animals not given a progressor agent. In addition, hepatocytes isolated from animals subjected to an IPP regimen with ENU as the progressor agent exhibited a greater degree of chromosomal breakage and aneuploidy than animals not given a second initiator. A variation of this model, in which the promoting agent was maintained after administration of the progressor agent, was examined. In this IPP model, the number of heterogeneous AHF (foci-in-foci) increased after application of the progressor agent (ENU or HU). An increased incidence of hepatocellular carcinoma was also observed in animals subjected to the IPP protocol when promotion was maintained until sacrifice. Thus, the characteristics of progression--increased chromosomal damage, aneuploidy, growth of AHF in the absence of continued tumor promotion, the presence of foci-in-foci, and an increased incidence of malignant neoplasia--have been used as end points for the demonstration of progressor activity by ENU. In addition, the potential progressor activity of HU and benzene has been demonstrated with the IPP model of rat hepatocarcinogenesis.

The effect of the format of administration and the total dose of phenobarbital on altered hepatic foci following initiation in female rats with diethylnitrosamine.

The effect of changing the format of administration as well as the total dose of the promoting agent phenobarbital (PB) on the development of altered hepatic foci (AHF) was determined in an initiation-promotion protocol with female rats fed the purified AIN-76 diet. Effects on the total number of AHF and the volume percentage of liver occupied by AHF were determined for four histochemical markers, the placental form of glutathione S-transferase, gamma-glutamyl-transpeptidase canalicular ATPase, and glucose-6-phosphatase after 16 and 60 weeks of promotion with varying doses and formats of PB, as well as for a further 16-week period in which no PB was administered. At the 16-week point, animals fed 0.1% PB continuously exhibited the largest number and volume percentage of AHF, whereas rats fed 0.1% PB for 4 days followed by 10 days of no PB with continuous repetition of this pattern during the 16-week treatment period exhibited no increase in the number of AHF over control and only a slight increase in volume percentage. Rats fed a continuous repetition of 0.2% PB for 2 days followed by 12 days of no PB exhibited an intermediate increase in the number of AHF as well as the volume percentage fraction after 16 weeks of this regimen. After 60 weeks of feeding PB by these three different formats, the numbers of AHF observed in these groups were equivalent and had increased above those seen after 16 weeks of feeding. The volume percentage occupied by the AHF in these three groups was also similar, although animals receiving 0.2% PB intermittently showed a significantly lower volume percentage than animals receiving 0.1% PB continuously for 60 weeks. When animals were maintained for an additional 16 weeks without PB feeding, the numbers of AHF decreased dramatically, much more so in animals fed PB intermittently, whereas the volume percentage fraction of AHF in livers of animals receiving 0.1% PB continuously for 60 weeks almost doubled. In contrast, the volume percentage fraction of AHF in livers of animals receiving PB intermittently for 60 weeks followed by 16 weeks of no PB was slightly less. Examination of the individual size classes of AHF showed little change in their distribution at 16 and 60 weeks, but after 16 weeks of PB withdrawal (76 weeks total time), the distribution of AHF in animals that had received 0.1% PB continuously for 60 weeks exhibited a decidedly greater shift to larger AHF than animals receiving PB intermittently for the 60-week period.(ABSTRACT TRUNCATED AT 400 WORDS)

Tumor promotion as a target for estrogen/antiestrogen effects in rat hepatocarcinogenesis.

Tamoxifen is a well-tolerated palliative and adjuvant treatment for human breast cancer and requires continuous, long-term administration for optimal therapeutic effectiveness. A two-stage model of experimental hepatocarcinogenesis, based upon the natural history of cancer development, has been employed to assess the carcinogenic potential of tamoxifen. In this study, the effectiveness of tamoxifen both as an initiator and a promoter in hepatocarcinogenesis was assessed in female F-344 rats. Tamoxifen was tested as an initiator at a single intragastric dose of 40 mg/kg, followed by promotion with 0.05% phenobarbital. The number and size of the resulting altered hepatic lesions were quantified, and tamoxifen was found to lack initiating action at the dose tested. Other groups of animals were initiated with a nonnecrogenic, subcarcinogenic dose of diethylnitrosamine (10 mg/kg) and were fed tamoxifen at either 250 or 500 mg/kg in the AIN-76A purified diet for 6 months. The livers of these animals showed an increase in the size and number of altered hepatic lesions compared with those animals that were initiated but not exposed to tamoxifen; this indicates that tamoxifen acts as a tumor promoter in the rat liver. The promotion index of tamoxifen, a measure of relative potency, was less than one-tenth that of ethinyl estradiol and more than four times that of phenobarbital, an agent commonly employed as a representative promoting agent in experimental carcinogenesis. Since tamoxifen lacked initiating activity in the rat liver at the dose tested, the mechanism of tumor induction in long-term feeding studies by tamoxifen may be due to its promotion of spontaneously initiated hepatocytes. The chronic therapeutic use of tamoxifen should therefore be limited by the potential carcinogenic risk of this agent as an effective tumor promoter.