Evaluation of a simple loop-mediated isothermal amplification test kit for the diagnosis of tuberculosis.

OBJECTIVE: A new loop-mediated isothermal amplification (LAMP) test kit, including a simple DNA extraction device for the detection of Mycobacterium tuberculosis complex, was developed for commercial use and evaluated for its usefulness in diagnosing tuberculosis (TB). DESIGN: The LAMP test was performed using untreated and N-acetyl-L-cysteine (NALC) NaOH-treated sputum specimen. The efficiency of the kit was compared with other conventional laboratory examinations, including other nucleic acid amplification (NAA) tests. RESULTS: The sensitivity of LAMP using raw sputum (direct LAMP) in smear- and culture-positive specimens was 98.2% (95%CI 94.9-99.4), while the sensitivity in smear-negative, culture-positive specimens was 55.6% (95%CI 43.4-68.0). The diagnostic sensitivity of direct LAMP for the diagnosis of individuals with TB was 88.2% (95%CI 81.4-92.7). The sensitivity values of direct LAMP were slightly, but not statistically significantly lower than those of Cobas Amplicor MTB and TRC Rapid MTB, while the sensitivity of the LAMP test using NALC-NaOH treated sputum was significantly lower than other NAA tests (P < 0.05) for smear-negative, culture-positive specimens. The new commercial version of the LAMP kit was easy to handle and yielded results within 1 h of receiving sputum specimens. CONCLUSIONS: This test is considered a promising diagnostic tool for TB, even for peripheral laboratories with limited equipment, such as those in developing countries.

A female-specific desaturase gene responsible for diene hydrocarbon biosynthesis and courtship behaviour in Drosophila melanogaster.

Drosophila melanogaster shows sexually dimorphic cuticular hydrocarbons, with monoenes produced in males and dienes produced in females. Here we describe a female-specific desaturase gene, desatF. RNAi knock-down led to a dramatic decrease in female dienes and increase in monoenes paralleled with an increase in copulation latency and a decrease in courtship index and copulation attempts by the males. The desatF gene was also expressed in females from D. sechellia, rich in dienes, but not D. simulans, which produce only monoenes. When hydrocarbons were feminized in D. melanogaster males by targeted expression of the transformer gene, the expression of desatF occurred. These results strongly suggest that desatF is a crucial enzyme for female pheromone biosynthesis and courtship behaviour in D. melanogaster.

Effect of human hydrosalpinx fluid on in vitro mouse embryogenesis.

OBJECTIVE: Women with hydrosalpinx have an unfavorable pregnancy rate. As one approach to elucidate the effect of hydrosalpinx on uterine tubal functioning, we examined the effect of hydrosalpinx fluid on early embryo development in mice. METHODS: Hyperovulation was induced in ICR mice, and late 2-cell-stage embryos were harvested 42 hours after administration of human chorionic gonadotropin (hCG). Hydrosalpinx fluid was obtained from patients during surgery after informed consent was obtained. The embryos were cultured in 3 culture fluids: (1) mBWW medium containing 0.3% bovine serum albumin (positive-control medium) (BSA), (2) Ca2+, Mg2+-free phosphate buffered saline (negative-control medium) (PBS), and (3) 100% human hydrosalpinx fluid. The developmental status of the embryos 120 hours after hCG administration was examined. RESULTS: Embryogenesis from a 2-cell-stage embryo to a blastocyst was observed in 98.3% (118/120) of the embryos cultured in the mBWW medium, in 0% (0/120) of the embryos cultured in PBS, and in 98.3% (118/120) of the embryos cultured in 100% human hydrosalpinx fluid. CONCLUSION: In the micro-environment of human hydrosalpinx fluid, late 2-cell embryos of ICR mice developed normally to blastocysts. The present results also suggest that non-species-specific embryogenetic factors might be present in human hydrosalpinx fluid.

Cardioprotective effects of quinapril after myocardial infarction in hypertensive rats.

Although angiotensin-converting enzyme inhibitors are beneficial for patients with congestive heart failure, the appropriate timing and dosage in acute myocardial infarction are still controversial. We examined the hemodynamic effects of quinapril administered before acute myocardial infarction in spontaneously hypertensive rats (SHR). Quinapril (10 mg/kg per day in drinking water) was started 1 week before infarction and continued for 4 weeks after infarction (total duration 5 weeks). The hemodynamic parameters were evaluated by cardiac catheterization 4 weeks after coronary ligation. Sham-operated SHR served as controls. After infarction, left ventricular end-diastolic and right atrial pressures were increased (P < 0.01) and blood pressure and cardiac index were decreased (P < 0.01); the magnitude of blood pressure reduction was similar in the treated and untreated rats with infarction. Quinapril improved these hemodynamic parameters significantly and decreased left and right ventricular weight. These results suggest that a prior treatment with quinapril in SHR with acute myocardial infarction is hemodynamically beneficial.

Ovulation and the suppression of mating in Drosophila melanogaster females: behavioral basis.

Virgin females of Drosophila melanogaster that are ectopically expressing the sex-peptide gene show a high level of ovulation and are unreceptive to males. However, if they are genetically deprived of eggs, receptivity is considerably restored (Fuyama, 1995). These females, whether they have eggs or not, extrude their ovipositors toward courting males as frequently as do fertilized females. However, this rejection behavior was ineffective in suppressing male courtship. Of females with eggs, about half of them could suppress male courtship. Females lacking eggs could not suppress male courtship and continued to elicit vigorous courtship. This difference seems to account for the increased mating frequency in sterilized females. Courtship behavior by mutant males defective in olfaction or learning suggested that females are capable of repelling males by emitting a volatile pheromone(s) with an inhibitory effect on male courtship.

[Internal carotid artery occlusion related to seat belt shoulder strap: report of two cases].

Two cases of traumatic internal carotid artery occlusion probably related to the seat belt shoulder strap are reported. Case 1. A 20-year-old woman was driving and was struck on the right front side of her car by another car. There were neither bruises, abrasions on her neck, nor weakness in her extremities. About 4 hours later, she developed left hemiplegia, and CT scan taken on the following day revealed low density areas in the capsulostriatal area on the right. The right carotid angiography revealed occlusion of the internal carotid artery about 3 cm distal to the bifurcation. Case 2. A 43-year-old man was driving and was struck on the front of his car by a hard iron railing. He sustained a sternum fracture, but there was no disturbance of consciousness or paresis of the extremities. His neck was unremarkable externally. About 50 days later, he developed left hemiplegia. CT scan and MRI revealed a massive infarction in the distribution of the right middle cerebral artery territories. The carotid angiography revealed occlusion of the right internal carotid artery about 3 cm distal to the bifurcation. In each cases, the driver was wearing a three-point shoulder seatbelt when the car was struck on the front or on the right front. Previous experimental studies have revealed in these situations the neck is flexed right anteriorly, and then quickly overextended left posteriorly. The overextension of the neck probably injured the intima of the internal carotid artery ipsilateral to the shoulder fixed in the seatbelt, resulting in the subsequent occlusion by a thrombus.

Comparable effects of angiotensin II and converting enzyme blockade on hemodynamics and cardiac hypertrophy in spontaneously hypertensive rats.

Angiotensin-converting enzyme inhibitors may regress left ventricular hypertrophy (LVH) without decreasing blood pressure (BP). The aim of the present study was to compare the effects of low and high doses of lisinopril and the angiotensin II receptor antagonist TCV116 (TCV) on LVH and hemodynamics in spontaneously hypertensive rats (SHR). Lisinopril (0.5 and 3 mg/kg per day) and TCV (0.3 mg/kg per day) were given to 8-week-old male SHR daily for 2 weeks. Untreated SHR and Wistar-Kyoto rats (WKY) served as controls. Untreated SHR had a greater left ventricular (LV) weight than WKY (p < 0.01). Lisinopril (3 mg/kg per day) decreased both LV weight and BP. Lisinopril (0.5 mg/kg per day) significantly decreased LV weight, but not BP. In contrast, although TCV significantly decreased BP, LVH was not suppressed. Renal blood flow (RBF) in untreated SHR was less than that in WKY (p < 0.05), but was increased with either lisinopril (3 mg/kg per day)-treated rats (p< 0.05). These findings suggest that factors other than afterload reduction play a role in the regression of LVH with lisinopril, whereas a longer duration of treatment and/or a higher dose may be necessary with TCV. Despite the decrease in BP, TCV normalized RBF in SHR, perhaps due to the blockade of renal angiotensin II.

Left ventricular function of the heart regressed by nifedipine in spontaneously hypertensive rats.

Left ventricular (LV) performance of the pharmacologically regressed heart in hypertension is still unclear. We compared LV function of the heart regressed by nifedipine with that of the hypertrophied heart in spontaneously hypertensive rats (SHR). Nifedipine (30 mg/kg/day in food) was given to 15-week-old male SHR for 20 weeks (n = 12). Age- and sex-matched SHR served as controls (n = 12). LV catheterization was performed using a micromanometer and cardiac output was determined by the thermodilution method. Hemodynamic studies were performed after washout of nifedipine (24 h), when blood pressure had returned to the untreated level. Peak pumping ability was assessed during acute volume loading with saline. Nifedipine significantly decreased blood pressure in conscious animals (222 +/- 11 to 201 +/- 12 mmHg, p < 0.01) and reduced LV weight (1.20 +/- 0.07 to 1.07 +/- 0.05g, p < 0.01). After washout of nifedipine, LV systolic and end-diastolic pressures, dp/dtmax and cardiac output determined under pentobarbital anesthesia were similar in the treated and untreated groups. Peak pumping ability during acute preload elevation was also similar in the 2 groups. Plasma norepinephrine was unaltered, and plasma renin activity was significantly lower in the treated rats (p < 0.05). These results indicate that nifedipine regressed LVH with a minimal reduction of blood pressure and without evidence of neurohumoral activation or volume retention. In conclusion, LV function of the heart regressed by nifedipine was preserved after a spontaneous rise in blood pressure and during acute preload elevation.

Converting enzyme inhibition improves congestion and survival in hypertensive rats with high-output heart failure.

The effects of angiotensin-converting enzyme (ACE) inhibitors in high-output heart failure have not yet been well established. We evaluated the effects of lisinopril (3 mg/kg/day) on hemodynamics, neurohormones, and survival in 10-week-old spontaneously hypertensive rats (SHR) with aortocaval fistula. Sham-operated treated and untreated SHR served as controls. Cardiac output (CO) was determined by thermodilution method, and renal blood flow (RBF) was assessed by laser-Doppler flowmetry. In sham-operated SHR, 2-week treatment with lisinopril decreased blood pressure (BP), left ventricular (LV) weight, and total peripheral resistance (TPR) (p < 0.01 each) and increased RBF and plasma renin activity (PRA) (both p < 0.05); CO and LV end-diastolic pressure (LVEDP) were unchanged. Fistula creation induced biventricular hypertrophy and high-output heart failure [increased LVEDP, CO, pulse pressure, and plasma norepinephrine (NE) and decreased RBF] with congestive signs (ascites, tachypnea). Lisinopril decreased LVEDP (p < 0.01), increased RBF, prolonged survival (both p < 0.05), and prevented ascites (0 vs. 46%) and increased PRA (p < 0.05) and attenuated the increase in plasma NE. Heart weight, BP, and CO were not affected by lisinopril. Thus, lisinopril ameliorated congestion and improved survival in SHR with fistula without compromising cardiorenal hemodynamics. Venous and renal dilatation and attenuation of vasoconstrictive systems may have contributed to the beneficial effects.

Effects of renal denervation on pressure-natriuresis in spontaneously hypertensive rats.

To investigate the role of renal sympathetic nerve activity (RSNA) under developing and established hypertension, renal function was studied in chronically renal-denervated and sham-operated male spontaneously hypertensive rats (SHR) and control Wistar Kyoto rats (WKY) at 8 (early hypertensive) and 22 (established hypertensive) weeks of age. To further characterize the renal pressure-natriuresis-diuresis relationship in SHR, renal perfusion pressure (RPP) was reduced by aortic constriction to the level seen in age-matched WKY and the same studies were repeated. After denervation, urinary sodium excretion (UNaV), fractional excretion of sodium (FENa) and urine flow (UF) were increased in 8-week-old SHR (p < 0.01). With the exceptions of UNaV and FENa in denervated 8-week-old SHR, renal cortical blood flow, glomerular filtration rate, UF, UNaV and FENa decreased with the reduction of RPP in all of the SHR groups. These results suggest that RSNA significantly influences renal sodium and fluid handling, thus contributing to the shifting of the arterial pressure-renal sodium excretion curve to the right along the pressure axis and/or to an increase in the steepness of the relationship in 8-week-old SHR. There appeared to be a marked difference in renal sodium handling between 8- and 22-week-old SHR.

Long-term alpha 1 blockade does not reverse cardiac hypertrophy in spontaneously hypertensive rats.

Not all antihypertensive drugs induce regression of left ventricular (LV) hypertrophy in hypertension, although they may equally lower blood pressure. The effects of alpha 1-blockers on regression have been inconsistent. In this study, bunazosin, a selective alpha 1-blocker, (15 mg/kg/day in food) was given to male spontaneously hypertensive rats (SHR) from 15 to 35 weeks of age to evaluate its effects on cardiac hypertrophy, hemodynamics, and neurohumoral factors. Age- and sex-matched SHR served as controls. LV function and cardiac output were determined by a micromanometer and thermodilution, respectively. Bunazosin significantly decreased blood pressure in conscious rats (from 209 to 192 mmHg, p < 0.01) but did not reduce LV mass. Heart rate, LV end-diastolic pressure, dp/dtmax, and cardiac output were similar in the 2 groups. Plasma renin activity was unaltered but plasma norepinephrine levels were higher in the treated rats (p < 0.05). Thus, bunazosin produced a significant relative reduction of blood pressure but did not reverse LV hypertrophy in SHR. Inadequate afterload reduction (8%) due to severe hypertension (> 200 mmHg) may explain the absence of regression. The rise of plasma norepinephrine levels may also offset the beneficial effects of bunazosin.

Haemodynamic and neurohumoral changes in spontaneously hypertensive rats with aortocaval fistulae.

1. Our aim was to evaluate the effects of an aortocaval fistula (1 mm) on cardiorenal haemodynamics, cardiac hypertrophy and neurohumoral factors in spontaneously hypertensive rats and to compare the results with those observed in Wistar rats at 2 weeks after fistulae placement. Sham-operated spontaneously hypertensive rats and Wistar rats served as controls. 2. Heart weight was significantly increased in spontaneously hypertensive rats (34%) and in Wistar rats (43%) at 2 weeks after fistula creation. Left ventricular systolic pressure and dp/dtmax. were significantly decreased (both P < 0.01) in spontaneously hypertensive rats with fistulae which had higher left ventricular end-diastolic pressure than Wistar rats with fistulae (P < 0.01). Signs of circulatory congestion (ascites, tachypnoea, prostration) were observed only in the overloaded spontaneously hypertensive rats (45%). Cardiac index was comparably increased in both fistulae groups due to an increase in stroke index, since heart rate was not increased. 3. Fistulae placement decreased renal blood flow and kidney weight, and increased blood urea nitrogen to a greater degree in spontaneously hypertensive rats (all P < 0.05); serum creatinine levels were unaltered. Plasma noradrenaline concentration was increased in spontaneously hypertensive rats with fistulae (P < 0.05), whereas plasma renin activity was not changed. 4. Thus, spontaneously hypertensive rats with fistulae developed overt haemodynamic signs of high-output heart failure with frequent ascites and dyspnoea, whereas most of these findings were milder or absent in Wistar rats. This model provides an opportunity to evaluate the pathophysiological and pharmacological responses in high-output heart failure.

Hemodynamic and neurohumoral responses to exercise in patients with congestive heart failure.

Hemodynamic and neurohumoral responses to supine bicycle exercise were evaluated in 16 patients with congestive heart failure (New York Heart Association functional class II-III) and in 8 normal controls. We determined cardiac output by the dye-dilution method, and forearm hemodynamics by plethysmography. The patients had lower resting cardiac and stroke indexes (p < 0.05) than the normal controls. During exercise, the increase in the cardiac index due to an increase in heart rate, was less than that in the controls. Resting and exercise systemic vascular resistance indices were higher in the patients (p < 0.05). The patients had lower resting forearm blood flow and higher forearm vascular resistance (p < 0.05), and the increases during exercise were comparable in the 2 groups. However, forearm venous tone and venous pressure increased more in the patients (p < 0.05). Exercise duration was shorter in the patients (p < 0.01). Resting plasma angiotensin II and norepinephrine were similar in the 2 groups, but plasma 6-keto-prostaglandin F1 alpha and atrial natriuretic peptide were higher in the patients. During exercise, all of these neurohumoral parameters rose more in the patients than in the controls (p < 0.05). Thus, the patients exhibited impaired central and peripheral hemodynamics both at rest and during exercise. The excessive exercise responses of all of the neurohumoral factors suggest that both vasoconstrictor and vasodilator systems are activated in heart failure.

Lisinopril reduces cardiac hypertrophy and mortality in rats with aortocaval fistula.

We evaluated the effects of lisinopril (1 mg/kg per day) on hemodynamics, cardiac hypertrophy, and neurohumoral factors in Wistar rats with an abdominal aortocaval fistula. After 4 weeks of treatment, the results were compared with values obtained for untreated rats with a fistula and for sham-operated rats. Volume loading induced biventricular hypertrophy, hemodynamic signs of high-output heart failure (increased cardiac output, left ventricular end-diastolic pressure, and pulse pressure), and impaired renal function (decreased renal blood flow and kidney weight; increased blood urea nitrogen). Lisinopril did not affect these cardiorenal hemodynamics, but decreased left ventricular mass and mortality rate (both P < 0.05). Lisinopril attenuated the increase in plasma norepinephrine, and increased plasma renin activity (both P < 0.05). Thus, lisinopril reduced left ventricular mass and mortality in rats with high-output heart failure without changing the cardiorenal hemodynamics. Neurohumoral inhibition may play a role in the beneficial effects of lisinopril.

Marked increase in plasma interleukin-6 in burn patients.

We measured the levels of interleukin-6 in plasma samples from 18 consecutive burn patients, including three lethal cases, during the early postburn period. In survivors burn injury caused initial increases in interleukin-6 levels that peaked at 6 hours after burn; this was significantly higher than interleukin-6 levels in normal controls (718 +/- 216 vs 70 +/- 4 pg/ml; p < 0.01). The increment in nonsurvivors was even more prominent (11,554 +/- 4,407 pg/ml; p < 0.01). The peak interleukin-6 levels at 6 hours correlated with total burn surface area (r = 0.65, p < 0.025), and tended to be higher in patients with inhalation injury. These data provide evidence that burn injury causes rapid release of interleukin-6 according to the severity of the injury. We also measured acute-phase reactants including fibrinogen, alpha 1-antitrypsin, C1 inhibitor, and alpha 2-plasmin inhibitor. After initial declines, these four proteins increased rapidly in survivors. In addition, the peak interleukin-6 levels correlated well with the increases in fibrinogen (p < 0.025), alpha 1-antitrypsin (p < 0.01), C1 inhibitor (p < 0.01), and alpha 2-plasmin inhibitor (p < 0.0001). In contrast, despite the marked increase in interleukin-6, the levels of acute phase proteins in nonsurvivors remained low. Based on these observations, we suggest that interleukin-6 is released as an alarm signal and has a role for the wound healing in burn patients, and that the levels of interleukin-6 after injury is an indicator of the severity of burn.

Effects of lisinopril upon cardiac hypertrophy, central and peripheral hemodynamics and neurohumoral factors in spontaneously hypertensive rats.

OBJECTIVE: Left ventricular function (LVF) after reversal of left ventricular hypertrophy (LVH) with antihypertensive therapy is still controversial. The present study was undertaken in spontaneously hypertensive rats (SHR) to determine whether LVF of the regressed heart with lisinopril is normally maintained. DESIGN: We compared cardiac function of SHR after reversal of LVH induced by lisinopril with that observed in control SHR and also with effects after a 4-week washout period. METHODS: Administration of lisinopril began at 15 weeks of age and continued for 20 weeks. Cardiac index, renal blood flow, leg muscle blood flow, plasma renin activity, atrial natriuretic peptide level, and norepinephrine concentration were determined. RESULTS: Lisinopril decreased body weight, blood pressure and left ventricular weight and increased leg muscle blood flow; cardiac index and renal blood flow were unaltered. Although norepinephrine concentration was unchanged, plasma renin activity increased and atrial natriuretic peptide decreased in treated SHR. Peak left ventricular pumping ability during volume loading was comparable in the two groups. After a 4-week washout period, left ventricular mass and blood pressure increased but remained lower than controls; cardiac index at rest and during volume loading was similar in the two groups. CONCLUSIONS: These data indicate that LVF of the regressed heart induced by lisinopril was well preserved at rest, during volume loading and also after spontaneous recurrence of hypertension in SHR.

Nifedipine in divided doses does not reverse left ventricular hypertrophy in spontaneously hypertensive rats.

This study investigated whether nifedipine administered in divided daily doses would diminish left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR). We administered nifedipine (12 mg/kg/day) in 3 divided doses by gastric gavage to 15-week-old male SHR (n = 10) for 4 weeks. Age- and sex-matched SHR served as controls (n = 10). Left ventricular (LV) function was evaluated by LV catheterization and cardiac output was determined by the thermodilution method. Plasma renin activity (PRA) and plasma norepinephrine levels were measured. Nifedipine significantly decreased blood pressure (p less than 0.01), shortened time constant T (p less than 0.05), and increased cardiac output (p less than 0.05). Nifedipine did not impair the LV systolic and diastolic indices during acute afterload elevation with angiotensin II. LV weight was similar in the 2 groups of rats. While PRA was unaltered, plasma norepinephrine levels were higher in the nifedipine-treated rats (p less than 0.05). These data indicate that nifedipine in 3 divided doses reduced blood pressure in SHR without compromising cardiac function but did not reverse LVH. The short hypotensive duration of nifedipine and its enhancement of sympathetic nervous activity may be responsible for the failure to reverse LVH, despite adequate blood pressure control.

[Disseminated intravascular coagulation in the early stage after severe burn: the role of excessive thrombin generation].

The pathogenesis of disseminated intravascular coagulation (DIC) in the early stage after burn injury remains still unclear. We investigated 12 burn injured patients by serial determination of anti-thrombin III (AT-III) activities and thrombin-antithrombin III complex (TAT) levels. Of these patients 4 developed DIC (DIC group) and the others had no hematological complications (non-DIC group). The mean levels of TAT increased markedly and peaked at 6 hr; the increment being more pronounced in DIC group (p less than 0.001). A significant correlation was recognized between TAT and Burn Index (r = 0.871, p less than 0.001). We also observed low AT-III activities those inversely related to Burn Index (r = 0.875, p less than 0.001), whereas closely correlated with serum albumin levels (r = 0.864, p less than 0.001), suggesting that this depression might be caused by both massive infusion and shifts of plasma into the extravascular space rather than consumption. These findings suggest that massive thrombin generation and decrease of anticoagulant activity, correlated to the severity of burns, might concurrently develop. Non-DIC group may remain to latent activation of coagulation cascade where anticoagulants could inactivate thrombin generated. This compensatory mechanism may fail in severe burn patients who have Burn Index of more than 90, developing DIC with high levels of TAT (316.3 +/- 104.5 ng/ml) and low AT-III activities (19.5 +/- 8.7%).

[Driver identification of the motorcycle in motorcycle/car accidents].

A series of motorcycle/car collision experiments and in-depth investigations involving motorcycle/car accidents with two riders were carried out in order to study the difference in behavior and injuries between the driver and the passenger of the motorcycle during a collision, and to provide general data for identifying their seat positions on the motorcycle in traffic accidents. In all the tests, two Hybrid II dummies were seated on the double seats of the motorcycle as riders. The motorcycle collided against the front door, front end or rear door of the passenger car at a speed of 50 km/h, at impact angles of 60 degrees, 90 degrees or 120 degrees. The speeds of the passenger car were tested at 0 km/h or 25 km/h. With different speeds of vehicles and different impact angles, the difference in rider behavior between the driver and the passenger was distinctly verified by analysis of high speed films. It is possible to distinguish the driver's injuries from the passenger's. The abrasion and/or contusions in the chest, face and groin area were severe for the drivers, but less serious for the passengers. The typical injuries of the driver can be expected in terms of the rider behavior during collision from 25 ms to about 150 ms after starting contact. The data and information can be used to clarify the question of who was driving in accident reconstruction.

[An experimental study on driver identification of passenger car in vehicle to vehicle accidents].

A series of full-scale vehicle-to-vehicle oblique collision experiments was carried out for providing general data to clarify the question of seating positions. In all test, two unrestrained anthropometric dummies (Hybrid II) were seated on front seats in passenger cars as occupants. The bullet car collided against the target car running with 25 km/h, at 50 km/h, at impact angles of 120 degrees and 150 degrees. Five impact configurations between occupant regions and interior of vehicle were evaluated: head-face/windshield, head-face/A-pillar, chest-abdomen/instrument panel, upper body/inside door and lower extremities/instruments panel. Comparative occupant injuries and vehicle response data were obtained from electronic instrumentation, high-speed movie films and visual observations. No characteristic driver injuries was observed in oblique collision experiments. The crush characteristics of the vehicle interiors and occupant behavior had significant effect in determining the actual injury once contact occurred. The differences of injuries in occupants occurred depend on impact configurations of vehicles. Therefore, on the driver identification, it is important to clarify kinematics of occupants during the impact by an analytical reconstruction. The data and information can be used to determine who was driving in actual traffic accidents for the forensic medicine expert.