Biomedical subjects

J Lindroth

Publications and source records attributed to J Lindroth.

5 recordsLinked to original sources

PubMed2001

Obsessive compulsive disorder: a case report.

A general dentist often will find the most challenging aspect of dentistry is patient management. In the controlled environment of a dental school, many students are not exposed to certain patient populations. It is likely that their first experience with particular patient pools will be in private practice. One such group of patients is those suffering from Obsessive Compulsive Disorder (OCD). This article reviews the clinical signs and symptoms of this group of patients.

Adult↗

PubMed1995

The relationship between forward head posture and temporomandibular disorders.

This study investigated the relationship between forward head posture and temporomandibular disorder symptoms. Thirty-three temporomandibular disorder patients with predominant complaints of masticatory muscle pain were compared with an age- and gender-matched control group. Head position was measured from photographs taken with a plumb line drawn from the ceiling to the lateral malleolus of the ankle and with a horizontal plane that was perpendicular to the plumb line and that passed through the spinous process of the seventh cervical vertebra. The distances from the plumb line to the ear, to the seventh vertebra, and to the shoulder were measured. Two angles were also measured: (1) ear-seventh cervical vertebra-horizontal plane and (2) eye-ear-seventh cervical vertebra. The only measurement that revealed a statistically significant difference was angle ear-seventh cervical vertebra-horizontal plane. This angle was smaller in the patients with temporomandibular disorders than in the control subjects. In other words, when evaluating the ear position with respect to the seventh cervical vertebra, the head was positioned more forward in the group with temporomandibular disorders than in the control group (P < .05).

Adolescent↗

PubMed1993

Changes in diastolic function during development and correction of chronic LV volume overload produced by mitral regurgitation.

BACKGROUND: Mitral regurgitation (MR) causes an augmentation in left ventricular (LV) diastolic function, increasing early diastolic filling rate and decreasing LV stiffness. Whether these changes in diastolic function persist, return to normal, or become abnormal after mitral valve replacement (MVR) is unknown. METHODS AND RESULTS: Simultaneous LV echocardiography and catheterization studies were performed in six dogs in the baseline state (baseline), 3 months after creation of MR (chronic MR), and 3 months after MVR. Chronic MR caused LV dilation (end-diastolic dimension increased from 4.5 +/- 0.1 cm in baseline to 5.8 +/- 0.1 cm in chronic MR, p < 0.05) and eccentric LV hypertrophy (LV-to-body weight ratio increased from 3.6 +/- 0.2 g/kg in baseline to 4.9 +/- 0.4 g/kg in chronic MR, p < 0.05). Chronic MR caused an increase in LV early diastolic filling rate (peak rate of increase in minor-axis dimension increased from 11 +/- 1 cm/sec in baseline to 18 +/- 1 cm/sec in chronic MR, p < 0.05), did not change the time constant of myocardial relaxation (tau was 31 +/- 4 msec in baseline and 30 +/- 2 msec in chronic MR), and caused a decrease in the modulus of regional chamber stiffness from 7.7 +/- 1.2 in baseline to 2.4 +/- 0.03 in chronic MR, p < 0.05. MVR caused the resolution of LV dilation (end-diastolic dimension returned to normal [4.8 +/- 0.2 cm]), but three months after MVR, regression of LV hypertrophy was incomplete (LV-to-body weight ratio remained elevated [4.4 +/- 0.5 g/kg]). After MVR, LV early diastolic filling rate (8 +/- 1 cm/sec), the relaxation time constant (31 +/- 2 msec), chamber stiffness (7.1 +/- 1.8), myocardial stiffness (11.2 +/- 3.1), and LV end-diastolic pressure (8 +/- 1 mm Hg) returned to normal. CONCLUSIONS: The enhanced diastolic function seen in chronic MR returned to normal after correction of the chronic volume overload by MVR.

Animals↗

PubMed1992

MIPSY: real-time morphometry to quantify the time course of rapid epithelial restitution.

The gastrointestinal mucosa has the ability to repair itself rapidly following superficial mucosal injury by rapid epithelial restitution. The mechanism consists of cell migration and does not involve mitosis. This study reports the mechanisms of rapid epithelial restitution in the rabbit colon in vivo and in the human colon in vitro, describes a new computerized real-time morphometry system to investigate the time course of restitution and presents a new method to calculate the migration speed of epithelia during the repair process. Superficial mucosal damage to the rabbit colon in vivo was produced by luminal exposure to 100 mM HCl for 5 min (80% of mucosal surface), a comparable injury in the human colon in vitro was obtained by luminal exposure to 10 mM HCl for 10 min (96% of mucosal surface). After detachment of the damaged tissue the intact epithelial cells in the vicinity of the necrosis extended pseudopodia and migrated over the denuded basal lamina. The morphological appearance of rapid epithelial restitution was the same in the rabbit and the human, only the time course was postponed in the human. The time course of rapid restitution was assessed by a newly developed computerized morphometry system (MIPSY). When tissues were examined after various time points following acid damage, 61% of the mucosa were damaged in the rabbit after 1 h, 10% after 2 hs and 20% after 5 hs. In the human colon 85% of the mucosal surface were damaged after 2 hs and 20% 5 hs after the end of acid exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effects of left ventricular volume overload produced by mitral regurgitation on diastolic function.

We hypothesized that the left ventricle's ability to compensate for the volume overload produced by mitral regurgitation (MR) depends, at least in part, on associated changes in left ventricular (LV) diastolic function. Indexes of the rate of LV pressure decline, the rate and extent of early diastolic filling, and LV diastolic stiffness were measured with simultaneous echocardiography and catheterization in the baseline state (baseline), immediately after creation of MR (acute MR), and 3 mo after creation of MR (chronic MR). Data are means +/- SD. MR caused LV dilation; end-diastolic dimension increased from 4.3 +/- 0.4 in baseline to 4.7 +/- 0.5 in acute MR and 5.8 +/- 0.1 cm in chronic MR (P less than 0.05 vs. baseline for both). Chronic MR caused eccentric LV hypertrophy; LV-to-body weight ratio increased from 3.6 +/- 0.3 in baseline to 4.5 +/- 0.2 g/kg in chronic MR (P less than 0.05 vs. baseline). Acute MR increased LV end-diastolic pressure from 8 +/- 4 in baseline to 15 +/- 3 mmHg (P less than 0.05 vs. baseline); chronic MR did not further increase LV end-diastolic pressure (14 +/- 4 mmHg). MR increased the transmitral pressure gradient from 5 +/- 1 in baseline to 14 +/- 3 in acute MR and 20 +/- 6 mmHg in chronic MR (P less than 0.05 vs. baseline for both). MR increased LV early diastolic filling rate; peak rate of increase in minor axis dimension increased from 11 +/- 2 baseline to 18 +/- 2 in acute MR and 19 +/- 2 cm/s in chronic MR (P less than 0.05 vs. baseline for both). Acute MR did not change LV stiffness constants. Chronic MR decreased LV stiffness; the modulus of chamber stiffness decreased from 7.1 +/- 2.8 in baseline to 2.9 +/- 1.6 in chronic MR (P less than 0.05 vs. baseline). Thus MR caused compensatory changes in LV diastolic function. These changes resulted from an increased transmitral pressure gradient and increased LV distensibility.

Animals↗