Smoking is a risk factor for pulmonary metastasis in colorectal cancer.

AIM: The hepatic microenvironment, which may include chronic inflammation and fibrosis, is considered to contribute to the pathogenesis of liver metastases of colorectal cancer. A similar mechanism is anticipated for pulmonary metastases, although no reports are available. Smoking causes pulmonary inflammation and fibrosis. Thus, we hypothesized that smokers would be especially affected by pulmonary metastases of colorectal cancer. In this study, we attempted to clarify the impact of smoking on pulmonary metastasis of colorectal cancer. METHOD: Between September 2005 and December 2010 we reviewed 567 patients with pathological Stage I, II or III colorectal cancer, whose clinicopathological background included a preoperative smoking history, pack-year history from medical records. Univariate and multivariate analyses using the Cox proportional hazard model were performed to determine the independent prognostic factors for pulmonary metastasis-free survival. RESULTS: Pulmonary metastases occurred in 39 (6.9%) patients. The smoking histories revealed 355 never smokers, 119 former smokers and 93 current smokers among the subjects. Multivariate analysis revealed that being a current smoker (hazard ratio = 2.72, 95% CI 1.18-6.25; P = 0.02) was an independent risk factor for pulmonary metastases. CONCLUSION: Smoking may be a risk factor for pulmonary metastasis of colorectal cancer. Cessation of smoking should be recommended to prevent pulmonary metastasis, although further basic and clinical studies are required.

Size and orientation of masticatory muscles in patients with mandibular laterognathism.

Size measurements of jaw muscles reflect their force capabilities and correlate with facial morphology. Using MRI, we examined the size and orientation of jaw muscles in patients with mandibular laterognathism in comparison with a control group. We hypothesized that the muscles of the deviated side would be smaller than those of the non-deviated side, and that the muscles of both sides would be smaller than in controls. In patients, a comparison of deviated and non-deviated sides showed, in orientation, differences for masseter and medial pterygoid muscles, but, in size, differences only for the masseter muscle. Nevertheless, muscle sizes in patients were much smaller than in controls. Lateral displacement of the mandible can explain the orientation differences, but not the smaller muscle size, in patients. It is possible that the laterodeviation initiates an adaptive process in the entire jaw system, resulting in extensive atrophy of the jaw muscles.

In vivo cross-sectional area of human jaw muscles varies with section location and jaw position.

Muscle cross-sectional area (CSA) is used as a measure for maximum muscle force. This CSA is commonly determined at one location within the muscle and for one jaw position. The purpose of this study was to establish a method to standardize the analysis of the CSA of the masticatory muscles in vivo, and to compare the CSAs along their entire length for two different jaw positions (opened and closed). The CSAs in the planes perpendicular to the long axes of the masseter, medial, and lateral pterygoid muscles were measured in ten normal young adult subjects by magnetic resonance imaging. Our results showed large differences among the muscles and a non-uniform change in CSA after jaw-opening. The method enables the CSA measurement to be standardized in vivo, and allows for a correct comparison of CSAs in different skull morphologies.

Volume changes in human masticatory muscles between jaw closing and opening.

Most jaw muscles are complex, multipennate with multiple components. The morphologic heterogeneity of masticatory muscles reflects their functions. We hypothesized that the volume of masticatory muscles changes between jaw closing and opening, and that there is a difference in the volume change among the muscles. Magnetic resonance images of the entire head were obtained in ten normal young adult subjects before and after maximum jaw opening. The volume changes of the masseter, medial, and lateral pterygoid muscles were measured. Only slight changes were seen in the masseter and medial pterygoid muscles. The lateral pterygoid muscle, however, significantly decreased its volume during jaw opening. The results provide normative values of muscle volume in living subjects, and suggest that the volume changes differ among jaw muscles.

[Effects of exogenous adenosine on myocardial recovery after acute hemorrhage].

This study was designed to investigate whether reperfusion with adenosine had an effect on myocardial high energy phosphate levels and cardiac function in hearts extracted from acutely hemorrhaged rats. Rats were bled to a mean arterial pressure of 0 mmHg for 5, 10 or 15 minutes and hearts were removed and assigned to one of three groups: 1) Hearts freeze clamped for measuring high energy phosphates; 2) Hearts perfused by Langendorff method at a constant perfusion pressure of 90 mmHg for 30 minutes followed by freeze clamping and determining high energy phosphates and; 3) Hearts perfused with adenosine (20 microM) and treated in the same way as in group 2. In group 1 myocardial ATP was significantly reduced as compared with control. When reperfusion started within 10 min, ATP contents recovered to the levels of control, and there were no significant changes between groups 2 and 3. LVP and LV dp/dt in group 3 were significantly higher than those in group 2. When reperfusion started after 15 min, ATP remained at a low level and few hearts could be resuscitated. These findings suggest that early resuscitation with adenosine might facilitate cardiac recovery following acute hemorrhage.

[Alterations in number of rabbit myocardial beta-adrenergic receptors in endotoxic shock: down regulation in hyperdynamic sepsis model and effects of cytokines administration].

We investigated alterations in myocardial beta- and beta 1-adrenergic receptor (BAR and B1AR) number during hyperdynamic state induced by endotoxin or cytokines. [METHODS] Twenty-nine Japanese White rabbits were divided into 2 groups. Hearts were removed 18 h after intraperitoneal administration of sterile saline (SAL) or E. coli endotoxin (LPS; 50 micrograms/kg) (Group E, n = 12), or 3 h after intravenous injection of SAL or cytokines (interleukin 1-beta; 5 micrograms/kg followed by 25 ng/kg/min for 2 h, or tumor necrosis factor; 5 micrograms/kg) (Group C, n = 17). BAR and B1AR numbers were determined in myocardial membranes from rabbit left ventricles with techniques of radioactive ligand binding study. We used [3H] dihydroalprenolol (3H-DHA) as radioactive ligand, and specific 3H-DHA binding to BARs was defined as the difference between the presence and the absence of 10 microM propranolol. B1AR number was assessed through the specific binding of 3H-DHA in the presence of ICI 118, 551 (5 x 10(-8) M), a highly selective beta 2-adrenergic receptor antagonist. In Group E, mean arterial blood pressure (MAP), heart rate (HR), and cardiac output (CO) (by thermodilution) were measured under pentobarbital sodium anesthesia before excision of hearts. [RESULTS] In Group E, CO was significantly (p less than 0.05) increased in rabbits injected with LPS (E-LPS) as compared with that in rabbits injected with SAL (E-SAL) (E-LPS; 0.75 +/- 0.02 l.min-1, E-SAL; 0.61 +/- 0.05 l.min-1, mean +/- SEM). MAP and HR were slightly decreased in E-LPS but not significantly. Maximum binding (Bmax) of 3H-DHA to BARs was significantly (p less than 0.05) decreased by 18% in myocardial membranes from E-LPS compared to E-SAL (E-LPS; 48.2 +/- 4.3 fmol/mg protein, E-SAL; 58.9 +/- 2.9 fmol/mg protein, mean +/- SEM). Similarly, Bmax of 3H-DHA to B1ARs was decreased by 18% in E-LPS, although no statistical significance was detected. In Group C, both BAR and B1 AR number was slightly, but not significantly decreased 3 h after administration of cytokines. [CONCLUSION] These data suggest that down regulation of cardiac BARs may occur during hyperdynamic stage of endotoxic shock.

Decreased beta-adrenergic receptor density in rat myocardium during hemorrhagic shock.

We investigated alterations in the number and affinity of cardiac beta-adrenergic receptors during hemorrhagic shock. Forty male Wistar rats were divided into two groups: (1) a shock group (n = 20), in which mean arterial blood pressure was decreased to 40-50 mmHg by bleeding and kept constant for 6 h; and (2) a control group (n = 20), which underwent a sham operation. We used (-)[(3)H]dihydroalprenolol for the determination of the number and affinity of beta-adrenergic receptors in myocardial membranes. An additional 25 rats were used for determination of plasma epinephrine and norepinephrine concentrations. Scatchard analysis showed a 20% reduction ( P < 0.05) in beta-adrenergic receptor density in the shock group (70.3 +/- 3.5 fmol.mg(-1) protein) compared to the control group (90.0 +/- 4.8 fmol.mg(-1) protein) but no significant change in the affinity (2.52 +/- 0.06 vs. 2.31 +/- 0.09 nmol. l(-1), control vs. shock). Plasma catecholamine concentrations were increased significantly at 1, 2, 4 and 6 h after the start of hypotension. These data suggest that increased levels of plasma catecholamines in hemorrhagic shock may be correlated a significant loss of beta-adrenergic receptors in rat myocardium.

[Changes in myocardial energy charge following cardiac arrest and subsequent resuscitation].

Cardiac resuscitation becomes more difficult as time of arrest is prolonged. This study was designed to investigate changes in energy charge (EC) during cardiac arrest and subsequent resuscitation periods. The experiment was divided into 2 parts. In the first part, 36 rats were divided into 6 groups. Control rats were anesthetized only with pentobarbital and the heart was extirpated. In other rats, an acute exsanguination was carried out until mean arterial pressure (MAP) fell to 0, and then the rats were divided into 5 groups according to the time of extirpation following the cardiac arrest: 1, 5, 10, 15 and 20 minutes, respectively. The extirpated hearts were rapidly frozen with liquid nitrogen. ATP, ADP and AMP were enzymatically measured and EC was calculated. ECG was monitored to ascertain complete electrical arrest. Disappearance of ECG activity was observed about 9 minutes after MAP reaching zero. In the second part; 36 rats were also divided into 6 groups. After the same manipulation as in the first part, the extirpated heart was perfused for 30 minutes using Langendorff method and both cardiac function (LVP, LV dp/dt and HR) and EC were investigated. Total adenine nucleotide (TAN) was already diminished at 1 minute and decreased progressively. On the contrary, EC was well maintained around control level until ECG activity disappeared completely, and an abrupt decrease in EC occurred after electrical arrest. When the heart was perfused about 30 minutes, EC recovered almost to the control level in the groups in which perfusion was started within 10 minutes, but its recovery was incomplete in the groups in which perfusion was begun after 10 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Sensory nerve conduction velocities in the cutaneous afferents of the ulnar and peroneal nerves of the dog: tissue temperature-dependent reference ranges.

Sensory nerve conduction velocities in the cutaneous afferents of the ulnar and peroneal nerves of the neurologically normal adult dog were determined by stimulation at stimulus intensities of 15, 20 and 25 V through subcutaneously placed electrodes and by the averaged evoked response technique. Stimulus intensities of 15 V for the ulnar nerve and 20 V for the peroneal nerve were adequate to measure the sensory nerve conduction velocities of these nerves. A linear relationship was seen between sensory nerve conduction velocity (y in m/s) and tissue temperature (x in degree C) and the regression equations were expressed as follows: y = 1.6x + 12.3 at a stimulus intensity of 15 V for the ulnar nerve and y = 2.0x - 10.6 at 20 V for the peroneal nerve, respectively. The 95% confidence limits of the regressions of the sensory nerve conduction velocities against tissue temperature, obtained at a stimulus intensity of 15 V for the ulnar nerve or at a stimulus intensity of 20 V for the peroneal nerve, were proposed for a tissue temperature-dependent reference range to enable the clinician to evaluate graphically the sensory nerve conduction velocity in a diseased dog.

Evaluation of shock-related cardiotoxic peptide.

The aim of the present work is to confirm the presence of MDF (myocardial depressant factor), which has long been postulated to be one of the cardiotoxic substances in the shock state. Twenty male mongrel dogs were divided into two groups, a hemorrhagic shock group (n = 10) and an endotoxic shock group (n = 10). Blood samples were obtained from each animal at 1, 2, 4, and 7 h after hypotensive events occurred. Inotropic properties of the plasma samples were evaluated by the isometric contraction of a cat papillary muscle preparation, and chromatographic analysis was performed on the peptides in the plasma. Developed tension of the muscle was increased significantly by changing the bathing medium from Krebs-Henseleit solution to plasma obtained 1 to 4 h after the onset of hemorrhagic and endotoxin induced hypotension. The positive inotropic change was associated with a significant increase in plasma epinephrine concentration. None of these plasma samples possessed a negative inotropic effect (i.e., the property of MDF activity). The elution profile by gel column chromatography of samples obtained from shocked animals was almost identical to that recognized as MDF. However, the presence of MDF was not confirmed by column parameters and color development by the ninhidrin reaction. In conclusion, we found no evidence to support the presence of cardiotoxic peptide in plasma of shocked animals.

[Superovulation-induced transient hyperprolactinemia in human in vitro fertilization and embryo transfer].

To examine the effects of transient hyperprolactinemia on in vitro fertilization and embryo transfer, 61 cycles in 50 euprolactinemic ovulatory women with irreparable tubal diseases were stimulated with clomiphene (CC) alone or CC and human menopausal gonadotropin followed by human chorionic gonadotropin (hCG). Serum prolactin (PRL) increased after hCG administration with peak values of 45.4 +/- 4.2 ng/ml on the day of laparoscopic oocyte aspiration. The highest serum estradiol (E2) concentration was found on the day before PRL peak and serum progesterone (P) began to increase after hCG injection concomitant with the PRL rise. The group having 50 ng/ml or more of PRL (34 cycles) had significantly higher levels of E2 during preovulatory and early luteal phase compared to those of the group having less than 50 ng/ml of PRL (27 cycles) but there was no significant difference between the P levels in the two groups. In the higher PRL group 72 (62.1%) of 116 collected oocytes were fertilized and 6 (20.0%) conceived. In the lower PRL group 45 oocytes (58.4%) of 77 were fertilized and 3 (12.5%) became pregnant. These data suggest that elevated serum PRL concentrations may have no effect on fertilization of oocytes in vitro or embryonic development.

[Clomiphene-HMG ovarian stimulation in human in vitro fertilization and embryo transfer].

In a program for in vitro fertilization and embryo transfer, laparoscopies for oocyte aspiration were performed in 40 cycles in 36 normally menstruating women with irreparable tubal diseases (IVF patients) who received clomiphene citrate (CC) and human menopausal gonadotropin (hMG). An intramuscular injection of human chorionic gonadotropin (hCG) was given to all patients after completion of follicular maturation. Fourteen cycles in 13 spontaneously ovulating women (control patients), also stimulated with CC and hMG, were adequately monitored to identify the appearance of the spontaneous luteinizing hormone (LH) surge. The follicular maturation was followed by daily ovarian ultrasonographic examination and serum estradiol estimations. Just before the LH surge the diameter of the leading follicle was 20.2 +/- 0.7 (mean +/- S.E.) mm and the serum estradiol concentration per follicle was 384.1 +/- 16.3pg/ml in the control patients. In the IVF patients the former was 20.6 +/- 0.3mm and the latter was 305.8 +/- 13.3pg/ml prior to hCG administration. When the relationship of follicular size to the rates of oocytes recovery, maturation, fertilization and cleavage was examined, larger follicles (3ml less than or equal to follicular fluid volume) showed good results. Of the 152 oocytes that were recovered from these IVF patients, 96 (63.2%) were fertilized and 79 (52.0%) cleaved. Three pregnancies resulted from 35 embryo transfers.