The energy expended while playing tennis was determined from the players heart rate and from the amount of oxygen they consumed. This study was made using eight healthy but unathletic male college students. Expired air was collected for 2 minute periods during each game by the Douglas bag method. Samples were collected when serving and receiving. The air collected was measured using a wet test gas meter. The amount of air collected was expressed in STPD. Oxygen consumption was determined by measuring the oxygen content of the expired air with a Orzat gas analyzer. The energy expended during the tennis games was calculated indirectly. The caloric coefficient of oxygen was multiplied by the volume of oxygen consumed. The caloric coefficient of oxygen varied from 4.6 to 5.1 kcal/liter of oxygen. In this study the value of 5 kcal/liter of oxygen was used in the calculations. The accuracy of the measurements of energy expended was tested using regression analysis of the measured volume of oxygen. The mean values of heart rate, oxygen consumed and energy expended did not vary when the activity of serving and receiving was compared. The mean value of oxygen consumed during play was 1.4329+/-282 ml/min or 21.6+/-4.0 ml/kg/min. The energy expended was 7.15+/-1.46 kcal/min or 6.45+/-1.23 kcal/kg/min. The values were equivalent to 5.5 mets. When the levels of oxygen consumed were estimated using the formulas, they were found to be higher than the measured levels. The estimated amounts, however, were within 25% of the measured amounts.
Heart Rate* ; Heart* ; Humans ; Male ; Oxygen Consumption ; Oxygen* ; Tennis*

BACKGROUND: Tumor angiogenesis is required for tumor growth and metastasis. In this study, we investigated the correlation between the intensity of angiogenesis and stage, nodal status, histologic type, metastasis and survival rate of non-small cell lung cancer. METHOD: Formalin fixed, paraffin embedded surgical specimens of 45 patients who had surgically resected primary non-small cell lung cancers without pre or post perative adjuvant chemotherapy or radiotherapy were examined. The microvessel count(MVC) was demonstrated by immunohistochemical staining for CD31(platelet ednothlial cell adhesion molecule, PECAM). RESULTS: Microvessel counts(MVCs)in stage IIIA and IIIB were higher than in stage I and II(p<0.05). The MVC in patients with lymph node metastasis was higher than that in patients without lymph node metastasis, although the difference was not statistically significant(p>0.05). However, in adenocarcinoma, the MVC in patients with lymph node metastasis was significantly higher than that seen in patients without lymph node metastasis(p<0.05). The MVC in adenocaricinoma was higher than that in squamous cell carcinoma(p<0.05). The difference between the MVCs of adenocarcinoma and squamous cell carcinoma was not statistically significant in stage Iand II or NO stage(p>0.05). However, in stage IIIA and IIIB or N1~3 stage, the MVC in adenocarcinoma was higher than that in squamous cell carcinoma(p<0.05). MVC was more increased when metastasis developed within 12 months. In the same histologic type and stage, the duration of survival time in patients with high MVC was shorter than in patients with low MVC, however the difference was not statistically significant(p>0.05). The survival rate in patients with high MVCs was lower than that in patients with low MVCs(P<0.05). CONCLUSION: In non-small cell lung cancer, MVC correlated relatively well with pathologic stage, nodal status (limited in patients with adenocarcinoma), histologic type, postoperative metastasis and survival rate. However, in the same histologic type and stage, MVC was not significantly related to the duration of survival. Therefore the assessment of the intensity of angiogenesis in non-small cell lung cancer may be helpful in predicting prognosis and in selecting patients for systemic adjuvant therapy of potential metastasis according to the results.
Adenocarcinoma ; Carcinoma, Non-Small-Cell Lung* ; Carcinoma, Squamous Cell ; Cell Adhesion ; Chemotherapy, Adjuvant ; Formaldehyde ; Humans ; Lung Neoplasms ; Lymph Nodes ; Microvessels ; Neoplasm Metastasis ; Paraffin ; Prognosis* ; Radiotherapy ; Survival Rate

BACKGROUND: Hypoxia inducible factor-1alpha(HIF-1alpha) is a transcription factor for various target genes that are involved in adapting cells to hypoxia. It promotes cell proliferation and survival via modulation of such cell cycle regulators such as cyclin A1 and cyclin B1 in response to hypoxia. This is associated with local failure of radiotherapy, which renders a poor prognosis for cervical carcinoma. METHODS: Using the tissue histologic sections and a tissue microarray of the archived biopsy and surgical specimens of uterine cervical carcinoma from 57 patients who were treated with radiation therapy alone, we performed immunohistochemical staining for HIF-1alpha and cyclin A1 and B1 to evaluate the correlations between the expressions of these proteins in tumors and the clinicopathologic parameters associated with the prognosis. RESULTS: The large tumor cell nests and invasive front margins of the tumors showed comparatively intense immunoreactivity of HIF-1alpha. There was no significant correlation between the HIF-1alpha, cyclin A1 and cyclin B1 expressions and the clinicopathologic factors. CONCLUSIONS: The HIF-1alpha expression showed marked intra-tumoral heterogeneity. The HIF-1alpha expression is neither a powerful predictor of resistance to radiotherapy nor is it a poor prognostic marker in cervical carcinoma patients who are treated with radiotherapy. The expressions of cyclin A1 and cyclin B1 are neither independently associated with the response of radiation therapy nor are they associated with the prognostic parameters of uterine cervical carcinoma.
Anoxia ; Biopsy ; Cell Cycle ; Cell Proliferation ; Cyclin A ; Cyclin A1 ; Cyclin B ; Cyclin B1 ; Cyclins ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; Population Characteristics ; Prognosis ; Proteins ; Transcription Factors ; Uterine Cervical Neoplasms

No abstract available.
Acute Kidney Injury* ; Hemoglobinuria, Paroxysmal*

A variety of intrinsic and extrinsic factors have been studied to explain the pathogenesis of rhinosinusitis. Recently biofilms are emerging as an important cause. Biofilms are highly organized structures composed of a protective extracellular matrix and bacterial colonies, and provide the means for bacterial survival and virulence. Biofilms are known to be associated with intractable cases of rhinosinusitis and antibiotic resistance. Patients diagnosed with biofilm-related rhinosinusitis tend to suffer more severe disease that those without biofilms. Biofilm severity can also influence the prognosis of rhinosinusitis. We present two cases of pseudomonas-induced macroscopic biofilms (bioballs) of the maxillary sinuses. These bioballs cause intractable chronic rhinosinusitis as well, but unlike traditional biofilms, they can be surgically removed by endoscopy, and thus have a better prognosis than traditional biofilms. This is the first report of visible biofilms (bioballs) found in the maxillary sinuses.
Bacteria ; Biofilms ; Drug Resistance, Microbial ; Endoscopy ; Extracellular Matrix ; Humans ; Maxillary Sinus ; Prognosis ; Pseudomonas ; Virulence

Primary lung cancer can metastasize by a direct local extension, hematogenous dessemination, and lymphatic spread. However, it less commonly metastasizes via a transbronchial invasion. A pproximately half of all patients with lung cancer have metastases at the initial presentation. Autopsy data showed that there are an average of 4.8 metastatic sites. The most common sites for metastases include the lymph nodes, liver, adrenal gland, bone, and brain. However, clinically significant metastases isolated in the small bowel seldom occur. Here we report a case of lung cancer with a small bowel metastasis.
Adrenal Glands ; Autopsy ; Brain ; Humans ; Liver ; Lung Neoplasms ; Lung* ; Lymph Nodes ; Neoplasm Metastasis*

Purpose: This study aimed to establish baseline morphological and functional data for normal mouse kidneys via a clinical 33 MHz ultra-high-frequency (UHF) transducer, compare the data with the findings from fibrotic mice, and assess correlations between ultrasonography (US) parameters and fibrosis-related markers. Methods: This retrospective study aggregated data from three separate experiments (obstructive nephropathy, diabetic nephropathy, and acute-to-chronic kidney injury models). Morphological parameters (kidney size, parenchymal thickness [PT]) and functional (shear-wave speed [SWS], stiffness, resistive index [RI], and microvascular imaging-derived vascular index [VI]) were assessed and compared between normal and fibrotic mouse kidneys. Semi-quantitative histopathologic scores were calculated and molecular markers (epithelial cadherin), Collagen 1A1 [Col1A1], transforming growth factor-β, and α-smooth muscle actin [α-SMA]) were evaluated using western blots. Correlations with US parameters were explored. Results: Clinical UHF US successfully imaged the kidneys of the experimental mice. A three-layer configuration was prevalent in the normal mouse kidney parenchyma (34/35) but was blurred in most fibrotic mouse kidneys (33/40). US parameters, including size (11.14 vs. 10.70 mm), PT (2.07 vs. 1.24 mm), RI (0.64 vs. 0.77), VI (22.55% vs. 11.47%, only for non-obstructive kidneys), SWS (1.67 vs. 2.06 m/s), and stiffness (8.23 vs. 12.92 kPa), showed significant differences between normal and fibrotic kidneys (P<0.001). These parameters also demonstrated strong discriminative ability in receiver operating characteristic curve analysis (area under the curve, 0.76 to 0.95; P<0.001). PT, VI, and RI were significantly correlated with histological fibrosis markers (ρ=-0.64 to -0.68 for PT and VI, ρ=0.71-0.76 for RI, P<0.001). VI exhibited strong negative correlations with Col1A1 (ρ=-0.76, P=0.006) and α-SMA (ρ=-0.75, P=0.009). Conclusion Clinical UHF US effectively distinguished normal and fibrotic mouse kidneys, indicating the potential of US parameters, notably VI, as noninvasive markers for tracking fibrosis initiation and progression in mouse kidney fibrosis models.

Purpose: This study aimed to establish baseline morphological and functional data for normal mouse kidneys via a clinical 33 MHz ultra-high-frequency (UHF) transducer, compare the data with the findings from fibrotic mice, and assess correlations between ultrasonography (US) parameters and fibrosis-related markers. Methods: This retrospective study aggregated data from three separate experiments (obstructive nephropathy, diabetic nephropathy, and acute-to-chronic kidney injury models). Morphological parameters (kidney size, parenchymal thickness [PT]) and functional (shear-wave speed [SWS], stiffness, resistive index [RI], and microvascular imaging-derived vascular index [VI]) were assessed and compared between normal and fibrotic mouse kidneys. Semi-quantitative histopathologic scores were calculated and molecular markers (epithelial cadherin), Collagen 1A1 [Col1A1], transforming growth factor-β, and α-smooth muscle actin [α-SMA]) were evaluated using western blots. Correlations with US parameters were explored. Results: Clinical UHF US successfully imaged the kidneys of the experimental mice. A three-layer configuration was prevalent in the normal mouse kidney parenchyma (34/35) but was blurred in most fibrotic mouse kidneys (33/40). US parameters, including size (11.14 vs. 10.70 mm), PT (2.07 vs. 1.24 mm), RI (0.64 vs. 0.77), VI (22.55% vs. 11.47%, only for non-obstructive kidneys), SWS (1.67 vs. 2.06 m/s), and stiffness (8.23 vs. 12.92 kPa), showed significant differences between normal and fibrotic kidneys (P<0.001). These parameters also demonstrated strong discriminative ability in receiver operating characteristic curve analysis (area under the curve, 0.76 to 0.95; P<0.001). PT, VI, and RI were significantly correlated with histological fibrosis markers (ρ=-0.64 to -0.68 for PT and VI, ρ=0.71-0.76 for RI, P<0.001). VI exhibited strong negative correlations with Col1A1 (ρ=-0.76, P=0.006) and α-SMA (ρ=-0.75, P=0.009). Conclusion Clinical UHF US effectively distinguished normal and fibrotic mouse kidneys, indicating the potential of US parameters, notably VI, as noninvasive markers for tracking fibrosis initiation and progression in mouse kidney fibrosis models.