Relationship between social support and self-care ability among patients with breast cancer during rehabilitation: The multiple mediating roles of resilience and depression.

AIMS: To identify the multiple mediating effects of resilience and depression between social support and self-care ability among patients with breast cancer during rehabilitation to provide reference for developing and implementing targeted interventions. DESIGN: A cross-sectional study reported according to the STROBE checklist. METHODS: A convenience sample of 320 patients with breast cancer during rehabilitation was recruited from one hospital in China. Data were collected from April to August 2022 using a self-report questionnaire, including the demographic and clinical information, Appraisal of Self-Care Agency Scale-Revised, Multidimensional Scale of Perceived Social Support, Connor-Davidson Resilience Scale-10 item, and Patient Health Questionnaire-9. The mediation analysis was conducted using the SPSS Process macro. RESULTS: Self-care ability was positively associated with social support (ß = .229) and resilience (ß = .290), and negatively associated with depression (ß = -.208). The relationship between social support and self-care ability was mediated by resilience and depression, respectively, and together in serial. The multiple mediating effects accounted for 34.0% of the total effect of social support on self-care ability. CONCLUSION: Our findings identify resilience and depression as multiple mediators between social support and self-care ability and highlight the important roles of social support, resilience and depression in improving self-care ability. RELEVANCE TO CLINICAL PRACTICE: Healthcare providers should pay great attention to the underlying mechanisms of how social support affects patients' self-care ability during breast cancer rehabilitation. Integrated intervention programmes targeted at enhancing social support, building resilience and alleviating depression might be beneficial to the improvement of self-care ability. PATIENT OR PUBLIC CONTRIBUTION: No patient or public contribution. REPORTING METHOD: The Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) checklist for cross-sectional studies was applied to report the results.

[Identification of Fertilized Chicken Eggs Based on Visible/Near-Infrared Spectrum During Early Stage of Incubation].

In the process of chicken egg hatching, some eggs can not be hatched successfully due to the absence of fertilization. These eggs not only cause a lot of waste, but also infect other normal eggs with bacteria. In the study, the fertilized eggs and clear eggs is identified by using the visible/near-infrared spectrum. It is of great necessity to get the best time of identifying the clear eggs in the early of hatching, so the variation of eggs' quality in the condition of hatching over time is studied. The results show that eggs are fresh after 24 hours' hatching and eggs can not be eaten after 72 hours' hatching while the best time of identification is within 36 hours. Static acquisition system is developed based on visible/near-infrared transmission spectrum for acquiring spectrum. Comparing the effect of the model of the different samples of same breed and samples of different breed, the different part of spectrum among fertilized eggs and clear eggs is deleted which caused by the color of eggshell and yolk, the effective spectral band are 355～590 and 670～1 025 nm. Adopting the pretreatment of PCA and comparing the accuracy of the various mathematical models with different time and the number of principal components decide the best number of principal components. Considering the production efficiency and comparing the different pretreatment methods of spectrum, for examples, SNV, MSC, Derivative correction and PCA, and various mathematical models are combined to establish the most efficient discriminant model. The result shows that the most efficient discriminant model is established with Fisher and based on the pretreatment of PCA after 24 hours' hatching. And the precision rate is 87.18%. The study provides a new way for nondestructive and online identification of the fertilized eggs and clear eggs.

[Prediction of storage time of fresh beef with multi-index using visible and near-infrared spectroscopy].

The prediction model of beef's storage time was established based on multi indexes of fresh beef, such as TVB-N, colony total, pH value, and L* parameter. Visible and near-infrared spectroscopy (Vis/NIR) combined with interval PLS (iPLS)and genetic algorithm(GA) was investigated for establishing PLS calibration model of above 4 indexes, respectively, and rapid and nondestructive prediction of the storage time of fresh beef stored at 4 degrees C was realized. PLS models of 4 indexes were built with full spectrum and effective variables selected by iPLS and iPLS-GA method, respectively. The performance of each model was evaluated according to two correlations coefficients(R) and standard error (SE) of calibration and prediction sets. Experimental results showed that the performance of all models built with effective variable selected by iPLS-GA was better than full spectrum and iPLS. The storage time of calibration and prediction sets of beef samples was predicted by storage time model with predicted values of above 4 indexes, and was achieved as follows: R(c) = 0.903, R(p) = 0.897, SEC = 1.88 and SEP = 2.24. The study demonstrated that the beef's storage time can be synthetically predicted with multi-index by using visible and near-infrared spectroscopy combined with the prediction model of beef's storage time. This provides a new method for rapid and nondestructive detection of beef's storage time or shelf life.

Ewing sarcoma-primitive neuroectodermal tumor of the uterus: a clinicopathologic, immunohistochemical and ultrastructural study of one case.

INTRODUCTION: Ewing sarcoma-primitive neuroectodermal tumors (ES/PNET) constitute a family of neoplasms characterized by a continuum of neuroectodermal differentiation. ES/PNET of the uterus is rare. There are 43 cases published in the English literature as far as we know. We describe an additional case. CASE REPORT: A 56-year-old woman presented with a 2-month history of irregular menopausal vaginal bleeding. After surgical excision, microscopic, immunohistochemical and electron microscopic examination suggested the diagnosis of ES/PNET. The patient underwent combined chemotherapy consisting of ifosfamide, etoposide, and cisplatin. She was alive with no evidence of recurrence or metastasis after 41 months of the initial operation. DISCUSSION: In spite of the rarity of ES/PNET, we should consider it in the differential diagnosis of small cell neoplasms of the uterus.

Transurethral resection in women with symptomatic keratinizing squamous metaplasia of urinary bladder: A retrospective study of 92 cases.

OBJECTIVES: To investigate the efficacy of transurethral resection (TUR) on relieving urinary symptoms in patients with keratinizing squamous metaplasia (KSM) of the urinary bladder. METHODS: Data were analyzed from a retrospective study of patients receiving transurethral bipolar plasma resection (bi-TUR) treatment for symptomatic KSM. Urinary symptoms were assessed by the International Prostate Symptom Score (IPSS) and a numeric rating scale pain score. Efficacy was assessed using the IPSS to determine changes from baseline in lower urinary tract symptoms (LUTS). Self-reported quality of life (QoL) was assessed by the last question of the IPSS questionnaire. RESULTS: A total of 92 female patients were included in the analysis. The median age was 42 years. LUTS, pain, and hematuria were the most common symptoms that affected patients. The median follow-up duration was 51 months. There were significant improvements in LUTS from baseline IPSS after TUR (P < .001). The percentage of the patients with moderate to severe LUTS went down from 52.2% to 18.5%. The median Numeric Rating Scale (NRS)-11 pain score reduced from 3 at baseline to 0 at the last visit. Twenty-one out of 40 patients reported that the pain symptoms disappeared completely. No patients reported hematuria symptoms at the final follow-up. Improvement of self-reported QoL was significant (P < .001). A total of 57.6% of patients reported an improvement, 26.1% of patients reported no improvement, and 16.3% reported deterioration. CONCLUSIONS: Bi-TUR therapy significantly relieved urinary symptoms in women with KSM. Improvement of QoL was acceptable with a success rate of 57.6%. Considering the very low complication rate, our study supported bi-TUR as an alternative treatment for patients who are resistant to medical therapy.

[Effects of glucagon like peptide-1 treatment on the alveolar capillary basal lamina in Otsuka Long-Evans Tokushima Fatty rats].

OBJECTIVE: To observe and quantitatively analyze the effect of glucagon like peptide-1 (GLP-1) on the alveolar capillary basal lamina in spontaneous type 2 diabetes mellitus animal model Otsuka Long-Evans Tokushima Fatty (OLETF) rats. METHODS: Experimental rats were divided into three groups: OLETF group, GLP-1-treated group (OLETF/G group), and Long-Evans Tokushima Otsuka group (LETO group) as control. The ultrastructure and thickness of the alveolar capillary basal lamina in the rats were examined by transmission electron microscopy and morphometry methods. RESULTS: The fused basal lamina (F-BL) of the alveolar capillary endothelium and type I epithelial basal lamina, and the alveolar capillary endothelium basal lamina (Cap-BL) were thickened in OLETF rats than those of LETO rats [(110.60+/-14.14) nm vs (57.30+/-11.08) nm, and (118.40+/-19.12) nm vs (66.80+/-8.63) nm, P<0.01]. F-BL and Cap-BL were thinned in the OLETF/G group as compared with OLETF group [(79.70+/-5.44) nm vs (110.60+/-14.14) nm and (69.80 +/-3.32) nm vs (118.40+/-19.12) nm, P<0.01]. CONCLUSION: Our studies suggest the existence of ultrastructural changes of alveolar capillary basal lamina in OLETF rats. GLP-1 intervention decreases the damage of alveolar capillary basal lamina in OLETF rats.

[Establishment of Mongolian gerbil model of long-term Helicobacter pylori infection].

OBJECTIVE: To establish a model of long-term infection with Helicobacter pylori (Hp) in Mongolian gerbil (Meriones unguiculatus), and to investigate if Hp combined with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) has a synergistic effect to induce gastric mucosa injury. To investigate pathological changes of gastric mucosa during long-term Hp infection in Mongolian gerbil model. METHODS: 90 healthy male Mongolian gerbils were randomly divided into 4 groups: Hp group (n = 24) undergoing gastric perfusion of Hp suspension of the line NCTC11637 in brain-heart infusion (BHI) 10(8)-10(9) CFU/ml once a day for 10 days and then gastric perfusion of 1 ml normal saline (NS) once a day for 10 days since the 4th week after Hp perfusion, Hp + MNNG group (n = 24) undergoing gastric perfusion of Hp solution once a day for 10 days and then MNNG 1 ml (2 mg/ml) once a day for 10 days, MNNG group (n = 20) undergoing gastric perfusion of BHI once a day for 10 days and then gastric perfusion of MNNC once a day for 10 day since the 4th week after BHI perfusion, and control group (n = 22) undergoing gastric perfusion of BHI once a day for 10 days and then gastric perfusion of NS again once a day for 10 day since the 4th week after the BHI perfusion. 4 and 8 weeks 1 gerbil from the control group and 2 gerbils from the Hp and Hp + MNNG groups each were killed to observe the pathological changes and Hp colonization by liquid-based urease test and Warthin-Starry silver staining. 20 and 40 weeks after the Hp inoculation 10 gerbils from each group were killed to observe the pathology of the gastric mucosa. RESULTS: (1) A Mongolian gerbil model of long-term Hp infection was successfully established. (2) Hp induced the process progressing from normal gastric mucosa --> chronic atrophic gastritis --> intestinal metaplasia --> dysplasia. Until 40 weeks after Hp infection, the gastric mucosa of the control group remained normal. Twenty weeks after Hp infection 3 gerbils in the Hp group and 1 gerbil in the Hp + MNNC group showed glandular atrophy and intestinal metaplasia respectively, and 40 weeks after infection, glandular atrophy, intestinal metaplasia, and dysplasia at different degrees in the gastric mucosa were seen in the three experimental groups. The pathological changes of the Hp + MNNG group were the most severe. The incidence rates of precancerous lesions of the Hp + MNNG group were significantly higher than those of the other groups, but no gastric carcinoma was found in the experimental animals. CONCLUSION: Hp colonizes stably in the glandular gastric mucosa of Mongolian gerbils. The histological changes after infection are similar to those of the Hp infected human being. Hp and MNNG both cause the injury of gastric mucosa. With synergistic effect, the two pathogenic agents attack the gastric mucosa, they cause more severe injury.

[Effects of sulfur dioxide on cardiac function of isolated perfusion heart of rat].

OBJECTIVE: To observe the effects of sulfur dioxide (SO2) on cardiac function of isolated perfused heart of rat and to explore the physiological regulation of endogenous SO2 on myocardial action. METHODS: The hearts of 64 Wistar rats were isolated, perfused with Krebs-Henseleit (KH) solution through Langendorff apparatus, and randomly divided into 8 equal groups: Four groups underwent perfusion of SO2 of the concentrations 1, 10, 100, 1000 micromol/L respectively for 5 min and then perfused with KH solution for 15 min. Eight hearts underwent perfusion of SO2 of the physiological concentration (10 micromol/L) for 20 min. The control group underwent perfusion of KH solution for 20 min. Eight hearts of the nicardipine group underwent perfusion of nicardipine, a L-type calcium channel blocker, 2.5 micromol/L for 5 min, SO2 10 micromol/L for 5 min, and then KH solution for 10 min. The heart in the hydroxamate (HDX) group underwent perfusion of HDX, an inhibitor of SO2 endogenous generating enzymes, for 5 min, and then perfused by KH solution for 15 min. The heart rate (HR), difference of left ventricular pressure (LVP), left ventricular peak rate of contraction (+ dp/dtmax), peak rate of relaxation (- dp/dtmax), and coronary flow (CF) were measured. Then transmission electron microscopy was conducted. RESULTS: SO2 concentration-dependently inhibited the left ventricular +/- dp/dtmax, LVP, HR, and CF (all P < 0.01). The left ventricular +/- dp/dtmax, LVP, and HR were inhibited (P < 0.05) by the physiological concentration (10 micromol/L) SO2 donor continuous perfusion for 20 min. During perfusion 20 min, the LVP, + dp/dtmax, - dp/dtmax, and HR after perfusion for 20 min of the physiological concentration (10 micromol/L) SO2 donor continuous perfusion group were (15 +/- 3) mm Hg, (485 +/- 74) mm Hg/s, (339 +/- 64) mm Hg/s, and (114 +/- 26)/min respectively, all significantly lower than those 5 min after perfusion [(23 +/- 7) mm Hg, (595 +/- 93)mm Hg/s, (436 +/- 83) mm Hg/s, and (159 +/- 31)/min, all P < 0.05]. The LVP, + dp/ dtmax, -dp/dtmax, and HR of the nicardipine group were(37 +/- l0)mm Hg, (1025 +/- 287)mm Hg/s, (570 +/- 181)mm Hg/s, and (139 +/- 48)/min respectively, all not significantly different from those of the control group. The LVP, + dp/dtmax, - dp/dtmax, and CF after perfusion of the HDX group were (50 +/- 11)mm Hg, (1167 +/- 270) mm Hg/s, (889 +/- 72) mm Hg/s, and (6.3 +/- 1.9) ml/min respectively, all significantly lower than those before perfusion [(69 +/- 16) mm Hg, (1579 +/- 315) mm Hg/s, (1186 +/- 263) mm Hg/s, and (9.5 +/- 1.3) ml/min, all P < 0.05]. CONCLUSION: Exogenous SO2 has negative inotropic effect on myocardium. by the mechanism related to voltage-gated calcium channel. Nicardipine blocks the inhibitory effect of SO2 at physiological concentration.

[Effects of dexamethasone on acute lung injury in rats induced by lipopolysacharide].

OBJECTIVE: To study the difference between the preventive and therapeutic effects of dexamethasone on acute lung injury models induced by lipopolysacharide (LPS) in different phases. METHODS: Forty adult male Wistar rats were randomly divided into four groups: (1)control group to receive intraperitoneal NS injection (2 mL/kg). (2)LPS group to receive intraperitoneal LPS injection (5 mg/kg). (3)one-hour group to receive intraperitoneal dexamethasone injection (2 mg/kg) one hour after LPS injection. (4)three-hour group to receive intraperitoneal dexamethasone injection (2 mg/kg) three hours after LPS injection. Then histopathology, arterial blood gases, lung permeability, wet-to-dry weight ratio and immunohistochemistry AQP1 were performed 24 hours later. RESULTS: Dexamethasone could improve biological indexes. Lung permeability, wet-to-dry weight ratio and immunohistochemistry AQP1 were (5.73+/-1.37), (4.92+/-0.23), (19.92+/-6.47) in LPS group, (2.4+/-0.51), (4.89+/-0.21), (33.47+/-9.41) in one-hour group and (2.15+/-0.63), (4.57+/-0.14), (40.69+/-9.18) in three-hour group, respectively. Dates in three-hour group were prior to those of one-hour group, and there was slight but no significant difference between the two groups. CONCLUSION: Dexamethasone can improve lung permeability and reduce lung edema. There is no need to be treated with glucocorticoids in advance.

[Effect of Interleukin-17 on neutrophil apoptosis].

OBJECTIVE: To study the effect of Interleukin(IL)-17 on neutrophil apoptosis and try to explain the possible mechanism involved. METHODS: Neutrophils isolated from healthy donors were incubated in enriched RPMI 1640 cell culture medium at 37 degrees C in 5% carbon dioxide. Subgroups were incubated with IL-17, heat-denatured IL-17 (X-IL-17), dexamethasone (DEX), or buffer alone. Apoptosis was assessed by morphologic changes, by detecting DNA strand breaks. Production of proapoptotic protein Bax by neutrophils was evaluated by immunocytochemistry. RESULTS: At the time of neutrophil incubation, neutrophils in the control subsets exhibited morphologic evidence of apoptosis. A steady rise in apoptosis index (AI) was noted, with (1.54+/-0.08)% for 0 h, (11.48+/-1.80)% (compared with 0 h, P<0.05) for 12 h and (34.19+/-1.92)% (compared with 0 h, P<0.01) for 24 h, respectively. IL-17 at concentration of 50 microg/L resulted in increased AI of neutrophils, with (1.43+/-0.17)% (compared with control 0 h, P>0.05) for 0 h, (20.47+/-6.22)% (compared with control 12 h, P<0.01) for 12 h and (40.74+/-3.48)% (compared with control 24 h, P<0.05) for 24 h, respectively. While at concentrations of 5 mug/L and 0.5 microg/L, IL-17 resulted in decreased AI, with (14.24+/-4.26)% (compared with control 24 h, P<0.01) for 24 h, and (19.86+/-4.39)% (compared with control 24 h, P<0.01) for 24 h, respectively. AI of neutrophils treated with X-IL-17 at concentration of 50 ng/ml for 24 h was (33.22+/-1.61)% (compared with control 24 h, P>0.05). Neutrophils apoptosis was accompanied by DNA fragmentation. In all groups, the increasing of Bax immunoreactivity was strongly related with more apoptotic neutrophils (r=0.932, P<0.01). CONCLUSION: In vitro, IL-17 modulates apoptosis of neutrophils. At higher concentrations, it accelerates neutrophils apoptosis. At lower concentrations, it delays neutrophils apoptosis. Modulation of the expression of Bax by IL-17 may be one of the possible inner mechanisms.

[Impact of hydrogen sulfide donor on experimental pulmonary hypertension induced by high pulmonary flow and endogenous carbon monoxide/heme oxygenase pathway].

OBJECTIVE: To explore the possible impact of hydrogen sulfide donor-NaHS (sodium hydrosulfide) on experimental pulmonary artery structural remodeling induced by high pulmonary flow and endogenous carbon monoxide/heme oxygenase pathway. METHODS: Thirty-two male SD rats were randomly divided into shunt group (n=8), shunt+NaHS group (n=8), sham group (n=8) and sham+NaHS group (n=8). Rats in shunt group and shunt+NaHS group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. In the sham group and sham+NaHS group, rats experienced the same experimental processes except the shunting procedure. After 11 weeks of operation, systolic pulmonary artery pressure (SPAP) was detected using a right cardiac catheterization procedure. The percentage of muscularized artery (MA), partly muscularized artery (PMA) and non-muscularized artery (NMA) was calculated. Relative medial thickness (RMT) and relative medial area (RMA) of MA were observed under optical-microscope, respectively. The ultra-structure of pulmonary arteries was observed under electro-microscope. Lung tissue carbon monoxide (CO) was measured. Western-blot was used to analyze lung tissue heme oxygenase (HO-1) protein expression. RESULTS: After 11 weeks of shunt, compared with sham group, SPAP in shunt group increased by 48.6%.The percentages of MA and PMA increased by 74.2% and 90.9%, but the percentage of NMA decreased 32.2%, respectively, in rats of shunt group as compared with that of sham group. In contrast to those in sham group, RMT and RMA in median MA and small MA of rats in shunt group increased by 83.6%, 86.9%, and 74.4%, 39.9%, respectively. Ultra-structural changes in rats of shunt group showed that endothelial cells were swollen and denatured, inner elastic membrane became irregular, and smooth muscle cells became synthetic phenotype. The sham and shunt groups did not differ significantly in CO and HO-1 protein expression of lung tissues. In contrast to that of shunt group, SPAP in rats of shunt+NaHS group decreased by 19.8%. The percentages of MA and PMA decreased by 14.4% and 12.2%, but the percentage of NMA increased 13.9%, respectively, in rats of shunt+NaHS group as compared with that of shunt group. In contrast to those of shunt group, RMT and RMA in median MA and small MA in rats of shunt+NaHS group decreased by 16.2%, 14.3%, and 26.9%, 14.3%, respectively. For rats in shunt+NaHS group ultra-structural changes showed that flat endothelial cells, inner elastic membrane became regular, and smooth muscle cells were contractile phenotype. The content of CO increased by 25.5% and the HO-1 protein expression increased by 114.3% in shunt+NaHS group as compared with those of shunt group. CONCLUSION: NaHS might prevent pulmonary hypertension and pulmonary artery structural remodeling induced by high pulmonary flow, and its mechanism might be associated with the changes in endogenous CO/HO pathway.

[The pathological characters and its clinical significance of internal hemorrhoids].

OBJECTIVE: To investigate the pathological characters and the corresponding clinical significance of internal hemorrhoids tissues. METHODS: Normal anal cushion and internal haemorrhoids tissue samples were obtained after stapled haemorrhoidectomy procedure from 24 grade III hemorrhoidal patients. The macroscopically normal cushions served as own controls and the normal cushions from a patient without a history of haemorrhoids as quality control. Routine Hematoxylin-Eosin and orcein were performed for elastic fibers. RESULTS: Compared with the corresponding normal anal cushions, the subepithelial vessels especially the cavernous vessels of the hemorrhoidal tissues showed obvious structural impair, retrograde changes, and the internal elastic lamina were ruptured and discontinuous. In addition, thrombosis and subsequent ischemic changes were observed. The Trietz's muscle and the fibro-elastic tissues showed hypertrophy, distortion, rupture and tortility. Obvious mucosal injury was observed in the mucous of hemorrhoidal tissues. Venous dilatation was infrequent in the hemorrhoidal tissues. CONCLUSIONS: The anal cushions of hemorrhoids disease patients show significant pathological changes. The pathological changes include structural impair, retrograde changes of the cavernous vessels and the hypertrophy, distortion, rupture and tortility of the Trietz's muscle and the fibroelastic tissues, and mucosal injury of the mucous membranes. These pathological changes are the basis of pathogenesis and development of hemorrhoids.

[Changes of pulmonary artery structural remodeling in pulmonary hypertension induced by high pulmonary flow in rats].

UNLABELLED: To explore the changes of time-dependent pulmonary artery structural remodeling in pulmonary hypertension induced by high pulmonary flow in rats. METHODS: Eighty male SD rats were randomly divided into control group (n =40) and shunt group (n = 40). Rats in shunt group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. In the control group, rats experienced the same experimental processes except the shunting procedure. After 1 day, 3 days, 1 week, 4 weeks, and 8 weeks of experiment, systolic pulmonary artery pressure (SPAP) and mean pulmonary artery pressure (MPAP) of each rat were evaluated by using a right cardiac catheterization procedure. Heart tissues were separated as right ventricle (RV) and left ventricle plus septum (LV+SP), and the ratio of RV to LV+SP [RV/ (LV+ SP)] was calculated. The morphologic changes including micro- and ultra-structural changes of pulmonary arteries of rats were observed under optical microscope and electro-microscope, respectively. The percentages of muscularized artery (MA), partial muscularized artery (PMA) and non-muscularized artery (NMA) in small pulmonary arteries and median pulmonary arteries were calculated. The changes of relative medial thickness (RMT) and relative medial area (RMA) of pulmonary arteries were examined. RESULTS: Compared with control group, SPAP and MPAP did not change on day 1, day 3, and week 4. However, in week 1 and week 8 of experiment, SPAP and MPAP increased significantly (P < 0.01). Meanwhile, in week 8 of experiment, RV/ (LV+SP) increased significantly (P < 0.05). In contrast to control group, the percentages of MA, PMA, and NMA did not change in day 1, day 3 and week 1. But in week 4 and week 8, the percentages of MA and PMA increased significantly (P < 0.01) but that of NMA decreased significantly (P < 0.01). RMT and RMA did not change in day 1, day 3, week 1 and even week 4 in shunt group as compared with those of control group, but they increased significantly in week 8 (P < 0.05). The changes of ultra-structure of pulmonary arteries included that endothelial cells became swollen and large in size on day 3, smooth muscular cells increased in size besides the change of endothelial cells in week 1, and they changed from contractile phenotype to synthetic phenotype in week 4. Collagen deposited in pulmonary arteries markedly in week 8. CONCLUSION: Pulmonary artery structural remodeling develops in a time-dependent manner. Endothelial cells of pulmonary arteries become swollen firstly, followed by the proliferation of smooth muscular cells and finally by remodeling of extra cellular matrix.

[An experimental study on gastric mucosal damage induced by duodenogastric reflux in rats].

OBJECTIVE: Duodenogastric reflux (DGR) is an important factor causing gastric mucosal damage, but whether short-term DGR cause gastric damage and its characteristics remain unclear. The aim of the study is to investigate the damage of gastric mucosa and its characteristics due to short-term DGR in a rat model. METHODS: Healthy, male SD rats were divided into three groups: a DGR group, a pylorus ligation group and a control group. The rats were sacrificed three weeks after the operation. The damage of gastric mucosa was observed macroscopically and microscopically. The pH value and bilirubin level of the gastric fluid were examined. The tight junctions between antral mucosal cells were evaluated under transmission electronmicroscopy. The serum gastrin concentration was investigated with radioimmune assay. Myeloperoxidase (MPO) was examined with chemical method. RESULTS: Macroscopically, there were significant mucosal lesions such as erosions, ulcers and bleeding spots in the DGR group. Microscopically, short-term DGR can cause faveolar hyperplasia, but no apparent intestinal metaplasia and atrophy were observed. There was scarcely presence of acute and chronic inflammatory cell infiltration and MPO activity remained unchanged. The pH value and bilirubin level of gastric fluid increased significantly and the serum gastrin concentrations did not change a lot. Short-term DGR can cause destruction of tight junction, which was shorter in duration, less in deformation and might even disappear at the time of examination. CONCLUSIONS: It is suggested that short-term DGR can induce gastric damage, faveolar hyperplasia and tight junction destruction without inflammatory cell infiltration and MPO activity changes.

[The clinicopathological features of early renal amyloidosis].

OBJECTIVE: To investigate the clinicopathological manifestations of early renal amyloidosis (AL) and its diagnostic criteria. METHODS: Fifteen cases with early renal amyloidosis admitted from 1994 to 2001 were collected from the hospital, and their clinical and pathological features were reviewed. Of them, the initial diagnoses were not made by depending findings from the light microscopy (LM) and immunofluorescense (IF), but confirmed by electron microscopy (EM) afterwards. Immuno-electron microscopy (IEM) were applied for amyloidosis typing. RESULTS: Most patients of early renal AL were in the middle to old age. Nephrotic syndrome was the most prominent symptoms and signs accompanying with rare microscopic hematuria and hypertension. Most of them had a normal renal function. Pathological examinations of renal biopsies using LM and IF showed mild mesangial proliferation and mild thickening of glomerular basement membrane (GBM). Immunoglobulins and complements were negative or only scanty in certain cases, but in all cases there was a light chain protein deposition homogeously. There were 4 cases of minimal change glomerulopathy, 5 cases of mild mesangial proliferative glomerulonephritis, 5 cases of stage I membranous nephropathy, and 1 case of cast nephropathy diagnosed with LM. The amyloid fibrils (diameter 8 - 10 nm) were randomly distributed in the mesangium, along GBM and at the arteriolar wall under EM. Additionally, Congo red staining was positive. IEM demonstrated that amyloid fibrils labeled with colloid gold was combined with a kind of light chain protein which was confirmed as the light chain type of AL. CONCLUSIONS: The diagnosis of early renal AL was occasionally neglected by depending only findings of LM and LF. However, special amyloid fibrils can be detected using EM. EM observation is an indispensable technique for the diagnosis of early renal AL and the typing of AL may further be determined by using IEM.

[Pathological features of light chain nephropathy].

OBJECTIVE: To investigate the pathologic features and diagnostic algorithm of light chain nephropathy (LCN). METHODS: Seven cases of LCN were studied by light microscopy, electron microscopy and immunolabeling of light chains (kappa, lambda) by immunofluorescence and immunoelectron microscopy. RESULTS: The histopathology of 7 cases by light microscopy was variable, with 3 cases showing nodular glomerulosclerosis, 1 case showing mild to moderate mesangial proliferation, and 3 cases showing cast nephropathy with minimal glomerular change. Immunofluorescence study revealed positive staining of a single type of light chain in mesangium (nodular pattern) or along glomerular basement membrane (linear), along tubular basement membrane and around arteriolar walls in all the 7 cases. Ultrastructurally, electron-dense granular deposits were identified in mesangium, subendothelial aspect of glomerular basement membrane, outer aspect of tubular basement membrane and arteriolar walls. Immunogold labeling of light chains showed distinct labeling of a single type light chain in the granular electron-dense materials (5 cases being kappa-positive and 2 being lambda-positive). CONCLUSIONS: LCN typically shows nodular glomerulosclerosis. The ultrastructural change is characteristic and important for diagnosis. Immunolabeling of light chains by immunofluorescence and immunoelectron microscopy carries further diagnostic value, especially in cases with minimal light microscopic change.

[A case report of cystic fibrosis and review of 16 cases of cystic fibrosis in Chinese patients].

OBJECTIVE: To report a case of cystic fibrosis (CF) in a Chinese and to review the clinical features, gene mutations, diagnosis and outcome of CF in Chinese patients. METHODS: A 14-year-old Chinese girl presenting with recurrent productive cough since birth with parasinusitis and otitis media was confirmed to have CF in Peking University First Hospital. Chest CT scan showed bronchiectasis, more severe in the right upper lobe. Sweat tests were taken three times, and the values of Na(+) and Cl(-) were (126.6 +/- 5.4) mmol/L and (108.9 +/- 3.3) mmol/L, respectively. The examination of the pancreas showed no remarkable cystic changes on CT scan and there was no pancreatic insufficiency. Sixteen patients with CF in Chinese reported from 1974 to 1999 were reviewed. RESULTS: Sixteen of the 17 patients (7 males and 9 females, aged from 6 months to 25 years) had clinical data available for analysis. Eleven of them had died, nine before the age of 13. They all suffered from frequent episodes of pneumonia, while 14 had malnutrition and 4 had jaundice. The diagnostic procedures included clinical features, sweat test and autopsy. Four of them had DNA screened and four kinds of novel mutations in the cystic fibrosis transmembrane conductance regulator gene were found. CONCLUSIONS: Chinese patients with CF show similar clinical manifestations to patients in the European and North American populations, but the CFTR mutation was different.

Hydrogen sulfide regulates vascular endoplasmic reticulum stress in apolipoprotein E knockout mice.

BACKGROUND: Atherosclerosis is an important cardiovascular disease, becoming a major and increasing health problem in developed countries. However, the possible underlying mechanisms were not completely clear. In 2009, our research group first discovered that hydrogen sulfide (H(2)S) as a novel gastrotransmitter played an important anti-atherosclerotic role. The study was designed to examine the regulatory effect of hydrogen sulfide (H(2)S) on endoplasmic reticulum stress (ERS) in apolipoprotein E knockout (apoE(-/-)) mice fed a Western type diet. METHODS: C57BL/6 mice and homozygous apoE(-/-) mice were fed a Western type diet. C57BL/6 mice were injected intraperitoneally with normal saline (5 ml/kg per day) as control group. The apoE(-/-) mice were treated with the same dose of normal saline as the apoE(-/-) group, injected intraperitoneally with sodium hydrosulfide (NaHS, an H(2)S donor, 56 µmol/kg per day) as the apoE(-/-) + NaHS group and injected intraperitoneally with DL-propargylglycine (PPG, a cystathionine-γ-lyase inhibitor, 50 mg/kg, per day) as the apoE(-/-) + PPG group. After 10 weeks, the mice were sacrificed and the plasma lipids were detected. Sections of aortic root from these animals were examined for atherosclerotic lesions by HE and oil red O staining. The aortic ultrastructure and microstructure were analyzed with the help of light and electronic microscope. Glucose-regulated protein 78 (GRP78), caspase-12, copper-andzinc-containing superoxide dismutase (Cu/ZnSOD) and Mn-containing superoxide dismutase (MnSOD) protein expression in aortic tissues were detected with immunohistochemistry. The level of intracellular reactive oxygen species (ROS) were measured by using a commercial assay kit. RESULTS: Compared with control mice, apoE(-/-) mice showed increased plasma levels of total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL), decreased high density lipoprotein (HDL), increased aortic plaque size, destroyed ultra-structure of aortic tissue, and increased expression of GRP78 and caspase-12 proteins. Compared with apoE(-/-) mice, H(2)S donor-treated apoE(-/-) mice showed a decreased plasma LDL level, lessened plaque necrosis and attenuated aortic ultra-structural disorder. H(2)S donor-treatment induced GRP78 expression but suppressed caspase-12 expression in aortic lesions. However, compared with apoE(-/-) mice, PPG treated apoE(-/-) mice showed enlarged plaque size, more severe ultrastructural disorder of the aortic tissue and reduced GRP78 staining in aortic lesions. The plasma lipids and the staining of caspase-12 in apoE(-/-) + PPG rats did not significantly differ from those in the apoE-/-mice. Consistently, H(2)S induced SOD expression, accompanied by a reduced level of ROS. CONCLUSION: H(2)S plays a regulatory role in aortic ERS and reduces atherosclerotic lesions in apoE(-/-) mice fed with a Western type diet.

Effects of N-acetylcysteine on Clara cells in rats with cigarette smoke exposure.

BACKGROUND: The number of Clara cells and the Clara cell 16-kDa protein (CC16) levels of the lung decrease in patients with chronic obstructive pulmonary disease (COPD). N-acetylcysteine (NAC) is a powerful antioxidant and can reduce the frequency of acute exacerbations of COPD. But the exact mechanism is unclear. The present study was designed to investigate the effects of NAC on Clara cells in rats with cigarette smoke exposure. METHODS: Eighteen adult male Wistar rats were randomly divided into 3 groups, 12 exposed to cigarette smoke (CS) thrice a day, 10 cigarettes for 30 minutes each time for 1 week, without (CS group) or with (CS + NAC group) oral intake of NAC 80 mg x kg(-1) x d(-1), and another 6 rats exposed to fresh air (control group). Clara cells were observed by an electron microscope. The mRNA expression of CC16 and CC16 protein in lungs were determined by reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry respectively. The glutathion (GSH) level in plasma and lung tissue were tested by fluorimetry assay. RESULTS: Compared with the controls, the pathologic score of small airways significantly increased in the CS exposed rats (20.3 +/- 14.7 vs. 53.7 +/- 11.5, P < 0.05). The Clara cell particles in cytoplasm decreased in the CS group (P < 0.05). The percentage of CC16-positive cells in bronchioles in the CS group (27.8 +/- 4.3 and 29.5 +/- 2.4 in terminal bronchioles and respiratory bronchioles, respectively) significantly decreased as compared with the control group (37.1 +/- 3.8 and 43.8 +/- 5.8 in terminal bronchioles and respiratory bronchioles, respectively) (P < 0.05). No significant difference was observed in GSH level ((181 +/- 26) nmol/L in the control group vs. (170 +/- 18) nmol/L in the CS group) between the two groups. After treatment with NAC, the pathologic score of small airways (24.1 +/- 17.5) decreased (P < 0.05). Clara cell particles in cytoplasm of Clara cells increased and GSH level in plasma ((213 +/- 40) nmol/L vs. (170 +/- 18) nmol/L in the CS group) increased too (P < 0.05), while the increase in the proportions of CC16 positive cells in bronchioles (30.1 +/- 6.4 and 34.3 +/- 6.3 in terminal bronchioles and respiratory bronchioles, respectively) did not reach the statistical significance (P > 0.05). No significant difference was found in the expression of CC16 mRNA among the three groups. Correlation analysis indicated that the percentage of CC16-positive cells in bronchioles negatively correlated with the pathologic score of small airways (r = -0.592, P < 0.05), but not with GSH level. CONCLUSIONS: One-week CS exposure decreased the number of Clara cells and the expression of CC16 in bronchioles in rats. NAC might provide protection of the Clara cells from oxidative damage and possibly through the elevation of the synthesis and secretion of CC16. These data indicate that NAC decreases airway inflammation induced by CS via induction of CC16.

Hydrogen sulfide regulates cardiac function and structure in adriamycin-induced cardiomyopathy.

BACKGROUND: The present study was designed to investigate if hydrogen sulfide (H2S), a novel gasotransmitter, might have a regulatory effect on cardiac function and structure, as well as oxidative stress, in adriamycin (ADR)-induced cardiomyopathy. METHODS AND RESULTS: Hemodynamic measurements, histopathological examination and stereological ultrastructural analysis of mitochondria in ADR-treated rats showed characteristics of cardiomyopathy with remarkable greater size and smaller number of cardiomyocytic mitochondria and a significantly low H2S content in plasma and myocardium, but increased levels of thiobarbituric acid reactive substance (TBARs) and decreased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in plasma and myocardium compared with controls (P<0.01). However, administration of the H2S donor, NaHS, markedly improved cardiac function, as demonstrated by elevated left ventricular developed pressure (+/-LVdp/dtmax; P<0.01) with ameliorated morphological alterations in the myocardium. Myocardial TBARs content decreased, whereas the activities of SOD and GSH-Px increased (P<0.01 and P<0.05, respectively). CONCLUSIONS: Downregulation of endogenously-generated H2S is probably involved in the pathogenesis of ADR-induced cardiomyopathy, whereby H2S reduces lipid peroxidation, increases antioxidation, and inhibits oxidative stress injury.