Kinematic analysis of hyolaryngeal complex movement in patients with dysphagia development after pneumonectomy.

PURPOSE: Aim of the study was to investigate the swallowing kinematics of patients with dysphagia which developed after pneumonectomy. METHODS: We investigated the swallowing kinematics of patients with dysphagia development after pneumonectomy and compared them with age- and gender-matched normal controls. The following swallowing parameters were compared: (1) maximum anterior and superior displacement (mm) of the hyoid bone; (2) maximum anterior and superior displacement (mm) of the larynx; (3) maximum epiglottic rotation angle ( degrees ); and (4) pharyngeal delay time (PDT) (sec) using videofluoroscopy. RESULTS: Significant differences were found in the maximum superior displacement of the hyoid bone ( P = 0.028) and larynx ( P = 0.001). Pharyngeal delay time showed a significant difference between the two groups ( P = 0.001). When we dichotomized patients to vocal cord palsy and non-palsy subgroups, no significant difference was found in all parameters. CONCLUSION: Our results indicate that dysphagia development after pneumonectomy is characterized by reduced hyolaryngeal elevation during swallowing and delay of the pharyngeal swallowing reflex. Further study must be done to reveal the exact mechanism of this phenomenon.

Roles of histidine residues in tobacco acetolactate synthase.

Acetolactate synthase (ALS) catalyzes the first common step in the biosynthesis of valine, leucine, and isoleucine in plants and microorganisms. ALS is the target of several structurally diverse classes of herbicides, including sulfonylureas, imidazolinones, and triazolopyrimidines. The roles of three well-conserved histidine residues (H351, H392, and H487) in tobacco ALS were determined using site-directed mutagenesis. Both H487F and H487L mutations abolished the enzymatic activity as well as the binding affinity for the cofactor FAD. Nevertheless, the mutation of H487F did not affect the secondary structure of the ALS. The K(m) values of H351M, H351Q, and H351F are approximately 18-, 60-, and fivefold higher than that of the wild-type ALS, respectively. Moreover, the K(c) value of H351Q for FAD is about 137-fold higher than that of wALS. Mutants H351M and H351Q showed very strong resistance to Londax (a sulfonylurea) and Cadre (an imidazolinone), whereas mutant H351F was weakly resistant to them. However, the secondary structures of mutants H351M and H351Q appeared to be different from that of wALS. The mutation of H392M did not have any significant effect on the kinetic parameters nor the resistance to ALS-inhibiting herbicides. These results suggest that the His487 residue is located at the active site of the enzyme and is likely involved in the binding of cofactor FAD in tobacco ALS. Mutational analyses of the His351 residue imply that the active site of the ALS is probably close to its binding site of the herbicides, Londax and Cadre.

Multiple peripheral nerve compressions related to malignantly transformed hereditary multiple exostoses.

Autosomal dominantly transmitted hereditary multiple exostoses is an uncommon disorder consisting of multiple projections of bone capped by cartilage. The lesions are most numerous in the metaphyses of long bones but may appear on flat bones. Sarcomatous transformation occurs in 1-25% of patients. We report a 33-year-old man with sciatica, previously diagnosed as hereditary multiple exostoses, presenting with multiple peripheral nerve compressions. Electrodiagnostic studies showed profound axon-loss multiple neuropathies involving the sciatic, superior gluteal, and inferior gluteal nerves. Magnetic resonance imaging of the left pelvis showed a large mass in the sacral area that was suggestive of a chondrosarcoma. An open intralesional excision biopsy confirmed chondrosarcoma transformed from chondromatosis. Excision of the lesion was effective in eliminating the impingement of nerves and retarding progressive osseous growth. We suggest that malignant transformation be suspected in cases with focal compression neuropathy of patients known to have multiple exostoses. Osteochondroma as a possible cause for compression neuropathy is discussed.

Fetal exposure to an intra-amniotic inflammation and the development of cerebral palsy at the age of three years.

OBJECTIVE: The aim of this study was to determine whether fetal exposure to intra-amniotic inflammation and a systemic fetal inflammatory response (funisitis) are associated with the development of cerebral palsy at the age of 3 years. STUDY DESIGN: This cohort study included 123 preterm singleton newborns (gestational age at birth, /=3 years. The presence of intra-amniotic inflammation was determined by elevated amniotic fluid concentrations of proinflammatory cytokines such as interleukins 6 and 8 and by amniotic fluid white blood cell count. Cytokine concentrations were measured with sensitive and specific immunoassays. Funisitis was diagnosed in the presence of neutrophil infiltration into the umbilical vessel walls or Wharton jelly. Cerebral palsy was diagnosed by neurologic examination at the age of 3 years. RESULTS: Newborns with subsequent development of cerebral palsy had a higher rate of funisitis and were born to mothers with higher median concentrations of interleukins 6 and 8 and higher white blood cell counts in the amniotic fluid compared with newborns without subsequent development of cerebral palsy (funisitis: 75% [9/12] vs 23% [24/105]; interleukin 6: median, 18.9 ng/mL; range, 0. 02-92.5 ng/mL; vs median, 1.0 ng/mL; range, 0.01-115.2 ng/mL; interleukin 8: median, 13.0 ng/mL; range, 0.1-294.5 ng/mL; vs median, 1.2 ng/mL; range, 0.05-285.0 ng/mL; white blood cell count: median, 198 cells/mm(3); range, 0->1000 cells/mm(3); vs median, 3 cells/mm(3); range, 0-19,764 cells/mm(3); P <.01 for each). After adjustment for the gestational age at birth, the presence of funisitis and elevated concentrations of interleukins 6 and 8 in amniotic fluid significantly increased the odds of development of cerebral palsy (funisitis: odds ratio, 5.5; 95% confidence interval, 1.2-24.5; interleukin 6: odds ratio, 6.4; 95% confidence interval, 1. 3-33.0; interleukin 8: odds ratio, 5.9; 95% confidence interval, 1. 1-30.7; P <.05 for each). CONCLUSION: Antenatal exposure to intra-amniotic inflammation and evidence of a systemic fetal inflammatory response (funisitis) are strong and independent risk factors for the subsequent development of cerebral palsy at the age of 3 years.

Chronic gastrointestinal problems and bowel dysfunction in patients with spinal cord injury.

Amongst complications arising from spinal cord injury (SCI), chronic gastrointestinal (G-I) problems and bowel dysfunction have not received as much research attention as many other medical and rehabilitation problems, even although their incidence is not negligible. We therefore investigated chronic G-I problems and bowel dysfunction in SCI patients where the degree of these was such that activities of daily living (ADL) were significantly affected and/or long-term medical management was required. Detailed semi-structured individual interviews were conducted with 72 traumatic SCI patients. The history of SCI was longer than 6 months, bowel habits had settled, and neurological recovery was completed. The incidence of chronic G-I problems was very high (62.5%), most were associated with defecation difficulties such as severe constipation, difficult with evacuation, pain associated with defecation, or urgency with incontinence. These problems had an extensive impact on ADL, and in particular, restricted diet (80%), restricted outdoor ambulation (64%) and caused unhappiness with bowel care (62%). Bowel care was performed once per 2.85 +/- 1.96 days and occupied an average of 42.1 +/- 28.7 min. To improve bowel habits, 43% of the patients took oral medication, and 36.1% controlled their diet. The usual methods of bowel care were anal massage (34.7%), unaided self-defecation with or without oral medication and abdominal massage (29.2%), finger enema (18.1%), rectal suppository (15.2%) and in two patients a colostomy tube had been inserted because of rectal cancer and traumatic colorectal injury. These chronic G-I symptoms were vague and very subjective, but significant enough to affect the quality of life. Bowel dysfunction was not related to age, duration of, or the neurological level of injury, ASIA score of ADL level, and bowel habits had generally settled within 6 months of SCI. With regard to frequency, time, and method of defection, bowel care habits varied considerably amongst individuals, and in relation to the extent to which practical results matched the level of expectation generated by physicians' recommended care program. Individual satisfaction was also very subjective. We therefore suggest that during the early stage of rehabilitation, an appropriate bowel program should be properly designed and adequate training provided.