Preoperative underweight is associated with adverse postoperative events in patients undergoing microvascular reconstruction surgery for oral and maxillofacial cancer.

We aimed to describe the prevalence of postoperative complications and evaluate its relationship with underweight, obesity, preoperative nutritional status, and systemic inflammation status in patients undergoing microvascular reconstruction for oral and maxillofacial cancer. Patients who were ≥20 years old and underwent microvascular reconstruction surgery between January 2009 to June 2019 were investigated. Patient demographics including body mass index, prognostic nutritional status, and neutrophil-lymphocyte ratio were collected. Logistic regression analysis was applied to evaluate these impacts on postoperative complications. A postoperative complication was defined as a Clavien-Dindo classification more than or equal to II. Of the 145 patients included in the analysis, 83 patients (57.2%) experienced postoperative complications, belonging to a Clavien-Dindo classification Ⅱ (n=71), Ⅲb (n=11), and Ⅳa (n=1). Multiple logistic regression revealed that a body mass index less than 18.5 kg/m2 (odds ratio 6.19, 95% confidential interval 1.34-28.6, P=0.02) was related to postoperative complications. Another multiple logistic regression model including all explanatory factors found that underweight (P=0.03) was related to postoperative complications. This retrospective study showed that preoperative underweight was associated with postoperative complications as evaluated by the Clavien-Dindo classification.

Evaluation of screening for drug use using postmortem prolactin levels in serum and cerebrospinal fluid.

Prolactin (PRL) levels can usually be controlled by PRL-inhibiting psychiatric drugs that include anti-dopamine agents. However, the use of dopamine (DA) antagonists may lead to hyperprolactinemia under certain clinical conditions. The aim of this study was to investigate postmortem PRL levels as potential markers of drug abuse, especially that of DA antagonists, in autopsy cases. We examined 121 autopsy cases, excluding cases involving acute hypoxia/ischemia, such as asphyxia, because PRL concentrations are reportedly increased under acute hypoxic conditions. Detected drugs were classified as either DA antagonists, stimulants, psychotropic drugs other than DA antagonists, or other non-psychotropic drugs, and many cases had no detected drugs. Samples comprised blood collected from the right heart chamber and cerebrospinal fluid (CSF). PRL protein level was measured by chemiluminescent immunoassay, and PRL gene expression in the anterior pituitary of autopsy cases was analyzed by reverse transcription-polymerase chain reaction. The PRL-positive cell ratio in the anterior pituitary gland was also measured by immunohistochemical analysis. The results indicated that PRL levels in the serum and CSF were higher in DA antagonist cases than in other cases. PRL levels in the serum and CSF also correlated with the PRL gene expression in cases with abuse of DA antagonists. However, no significant difference in the PRL-positive cell ratio in the anterior pituitary gland was evident between any of the classes of drug-detected and drug-undetected cases. These results suggest that postmortem measurements of PRL transcription levels may be useful for diagnosing cases of DA antagonist use.

[An analysis of nutritional status and pulmonary hypertension in patients with sequela of pulmonary tuberculosis and chronic obstructive pulmonary disease].

The prognostic value of hypercapnia and/or pulmonary hypertension differs in patients with sequela of pulmonary tuberculosis (TBseq) and those with chronic obstructive pulmonary disease (COPD) who are receiving home oxygen therapy (HOT). In an attempt to identify the factors, if any, that might explain this difference, we first compared nutritional status, respiratory function test results, dyspnea indexes, and other data for hypercapnic patients (PaCO2 > or = 45 Torr) and normocapnic patients (PaCO2 < 45 Torr) receiving HOT. Second, we examined the relationship between the degree of pulmonary hypertension and several respiratory function parameters for patients in each disease category. In 44 patients with TBseq, nutritional status estimated by body mass index and serum albumin was significantly better in the hypercapnic patients than in the normocapnic patients. However, this difference was not observed in 37 patients with COPD. In 30 patients with TBseq, the degree of pulmonary hypertension correlated significantly only with PaO2; in 32 patients with COPD, however, significant correlations were observed not only with PaO2 but also with PaCO2, %VC, and FEV1. These differences distinguishing groups of patients with the 2 diseases may provide an explanatory basis for the difference in prognostic value of hypercapnia and/or pulmonary hypertension in patients receiving HOT.

Structure of the L-histidine decarboxylase gene.

Two species of L-histidine decarboxylase (HDC) mRNA were found in the KU-812-F basophilic cell line, but only the 2.4-kilobase (kb) one encodes the functional HDC (Mamune-Sato, R., Yamauchi, K., Tanno, Y., Ohkawara, Y., Ohtsu, H., Katayose, D., Maeyama, K., Watanabe, T., Shibahara, S., and Takishima, T. (1992) Eur. J. Biochem. 209, 533-539). The 3.4-kb one encodes a truncated HDC protein and is also found in human leukemia-derived cell lines HEL and KCL-22. To clarify the mechanisms that regulate transcription of the HDC gene and generate the two species of mRNA, we have isolated genomic DNA clones coding for the HDC from human genomic libraries. Structural analysis of the isolated clones revealed that the human HDC gene is composed of 12 exons spanning approximately 24 kb. Genomic DNA blot analysis suggested that HDC is encoded by a single copy gene. The structural analysis also demonstrated that the heterogeneity of the HDC mRNA is caused by an insertion of the seventh intron sequence and alternative use of the splicing acceptor site at the 12th exon. The transcription start site of the HDC gene and the nucleotide sequences of the promoter and first exon regions were determined. We found a TATA-like sequence, a GC box, four CACC boxes, four GATA consensus sequences, and six leader-binding protein-1 binding motifs in the promoter region of the HDC gene.

Age-related variation of respiratory chemosensitivity in monozygotic twins.

To examine age-related variations in respiratory chemosensitivity to hypoxia and hypercapnia, the magnitudes of within-pair variances for ventilatory responses to hypoxia and hypercapnia were measured in 38 pairs of male monozygotic twins. Mean values for the slope factor of end-tidal PO2-ventilation hyperbola (A) were larger in Group I (13 pairs with a mean age of 16.3 +/- SD 0.9 yr) than those in Group II (12 pairs with a mean age of 29.8 +/- 6 yr), and Group III (13 pairs with a mean age of 46 +/- 7.2 yr). The slope factors for end-tidal PCO2-ventilation line (S) were similar among the 3 groups. Within-pair variances for A, A/body surface area (BSA), and Vo (asymptote for ventilation when end-tidal PO2 is infinite) were larger in Groups II and III than in Group I. Within-pair variances for S and S/BSA were also larger in Groups II and III than in Group I, whereas within-pair variances for B (intercept with end-tidal PCO2) were similar among the 3 groups. These results indicate that variations for respiratory chemosensitivity to hypoxia increase during the period from adolescence to adulthood and stay at a similar level thereafter. Variations of hypercapnic chemosensitivity also increase during this period, attenuating thereafter; however, the variation is 7 times larger than that of hypoxic chemosensitivity in the third and fourth decades.

Pattern of genetic influence on pulmonary function.

Whether genetic factors influence small airway function and lung volume was examined in 20 adolescent (mean age, 16.2 +/- SD 1.1 years) monozygotic twin pairs, 11 adolescent (mean age, 16.7 +/- 0.7 years) dizygotic twin pairs, and 20 adult (mean age, 38.7 +/- 9.3 years) monozygotic twin pairs. Within-pair variances of adolescent dizygotic twins for height, FVC, FEV1/FVC, V50, V25, V50/FVC, FRC, and delta N2 were significantly larger than those of adolescent monozygotic twins, indicating that these pulmonary function variables are influenced predominantly by genetic factors in adolescence. Within-pair variances of adult monozygotic twins were similar to those of adolescent monozygotic twins in terms of V50 and V25, indicating that these pulmonary function variables are influenced predominantly by genetic factors in adulthood. These results indicate that small airway dynamics, in terms of V50 and V25, are influenced in larger part by genetic factors in adolescence as well as adulthood, whereas lung volumes in terms of FRC and FVC are controlled by genetics only in adolescence.

Chemical and behavioral control of breathing in adult twins.

Whether genetic influence on chemical and behavioral control of breathing is still present in adulthood was examined in 28 pairs of monozygotic (mean age, 40 +/- SD 9.9 yr) and 10 dizygotic (35 +/- 9.3 yr) twins. Mean values for hypoxic and hypercapnic ventilatory responses, threshold for perceiving added inspiratory resistance, and respiratory patterns were not different between monozygotic and dizygotic twins. However, within-pair variance ratios (those in monozygotic twins being denominators) for hypoxic response (4.08, p less than 0.005), hypercapnic response (4.89, p less than 0.005), respiratory frequency during air breathing (3.96, p less than 0.005), inspiratory time during air breathing (5.47, p less than 0.005), and inspiratory time during hypoxia (9.08, p less than 0.005) were significantly larger than 1. Within-pair variances for threshold for resistive load perception and respiratory pattern during hypercapnia were equivalent between the 2 groups. These results indicate that ventilatory responses to hypoxia and hypercapnia and respiratory patterns while breathing air include genetically determined factors, whereas perception threshold for added resistance and respiratory patterns during hypercapnia are influenced predominantly by environmental force in adulthood.

Genetic and environmental influence on inspiratory resistive load detection.

To differentiate genetic factors from environmental forces in determining threshold for resistance load detection (RLD), 62 healthy adolescent twins (mean age = 16 years) and 74 healthy adult twins (mean age = 34 years) were studied by the standard psychophysical technique. The zygosity was determined by blood groups, finger prints, and physical appearances. Mean values for age, height, weight, pulmonary functions (FVC, FEV1, FEV1/FVC, Raw, and FRC) were not different between monozygotic (MZ) and dizygotic (DZ) pairs either in adolescent or adult twins. Threshold for RLD was analyzed in terms of added resistance divided by airway resistance plus apparatus resistance (Weber fraction) and mouth pressure (P) at the threshold. Both Weber fraction and P were equivalent between MZ and DZ either in adolescent or adult twins. In adolescence, within-pair variance for P was significantly greater in DZ than in MZ, but within-pair variances for Weber fraction were similar between MZ and DZ, the former indicating that threshold for RLD is predominantly influenced by genetic factors. In adults, within-pair variances for Weber fraction and P were not different between MZ and DZ, indicating that environmental factors predominate over genetic factors. When adolescent and adult twins were lumped together, mean values for Weber fraction and P were not different between male and female. Relationship between P and age was significant both in male and female. P (male) = 0.281 + 0.013 X age (years) +/- SD 0.36 cm H2O, and P (female) = 0.235 + 0.013 X age (years) +/- 0.48 cm H2O. These results indicate that the threshold for RLD is influenced predominantly by genetic factors in adolescence, but environmental factors predominate in the adult. Although sex difference is not clear, P at the threshold increases with age in both sexes.

Respiratory chemosensitivity in smokers. Studies on monozygotic twins.

Whether smoking habits influence ventilatory response to hypoxia and hypercapnia was examined in 23 pairs (8 concordant smoker pairs, 8 concordant nonsmoker pairs, and 7 discordant pairs) of monozygotic twins. Pulmonary function tests were also performed. Smokers (7 subjects) were significantly taller by 2 cm (mean value) than nonsmoker partners (7 subjects). Arterial pH of smokers was significantly lower, although it stayed within normal range. Closing volume to vital capacity ratio tended to be larger in smokers. Ventilatory response to hypoxia (slope factors for ventilation-alveolar Po2 curve and ventilation-arterial O2 saturation line) was significantly higher in smoking than in nonsmoking partners, whereas ventilatory response to hypercapnia (slope factor for ventilation-alveolar Pco2 line) was not different. Intrapair variances for height and ventilatory response to hypoxia were larger in discordant pairs with respect to smoking than in concordant pairs. These results indicate that smoking habits influence the slope, without the parallel shift, of the hypoxic ventilatory response curve.

[Evaluation of pulmonary function parameters in twins].

The purpose of this study was to determine the role of genetic influence on the variability of pulmonary function tests in normal individuals. Thirty-one pairs of twins (20 monozygotes (MZ) and 11 dizygotes (DZ) of both sexes, ranging in age from 15 to 18 years, were tested. Degree of similarity in each parameter was compared between MZ pairs and DZ pairs by within-pair variance ratio (MWDZ/MWMZ). The within-pair variances of MZ were smaller than DZ with respect to FVC, FEV1/FVC, V50, V25, delta N2 and FRC. These parameters were corrected for height; again the within-pair variances of MZ were smaller than DZ with respect to all the parameters except for FRC. The results indicate that these parameters were at least partly determined by genetic factor. However the within-pair variance of FEV1, PF, CV/VC, Raw, Pao2, Paco2, pH, and [HCO3-] were not different between the two groups. To estimate the similarity within MZ pairs, among-pair to within-pair variance ratio (MAMZ/MWMZ) were used. All the parameters of pulmonary mechanics showed similarity within pairs. Arterial pH and Pao2 also disclosed a significant similarity within-pairs, but Paco2 and [HCO3-] did not.

Familial factors affecting arterial blood gas values and respiratory chemosensitivity in chronic obstructive pulmonary disease.

Arterial blood gas determinations in patients with chronic obstructive pulmonary disease (COPD) and respiratory chemosensitivity, and arterial blood gas determinations in their sons were compared. Patients with silicosis (n=17) and their sons (n=22) served as control subjects. Arterial blood gases, pH, and HCO-3 concentration in 25 patients with COPD were averaged from at least 3 determinations (mean sample number, 10.1) to compare with the data on their sons (n-34; mean age, 33.9 yr). The Paco2 obtained during stable stages correlated positively between patients with COPD and their sons. The Pao2 of patients with COPD in stable stages correlated with the hypoxic ventilatory response of their sons. The Paco2 and Paco2 obtained during acute exacerbation of COPD correlated with the hypoxic ventilatory response of the sons. Deviations in FEV1 and V25 from predicted values correlated with deviations in Pao2 in the sons of the patients with COPD. In silicosis, significant relationships between patients and sons were not seen with respect to arterial blood gas determinations and ventilatory responses except for Paco2 of patients and hypercapnic ventilatory responses of sons. Smoking habits did not correlate between patients and sons both in COPD and in silicosis. However, the concordance ratio of smokers or nonsmokers between patients and sons was higher in COPD than in silicosis. These results indicate that familial factors are involved in determining the arterial blood gases and ventilatory response to hypoxia in COPD, and blunted chemosensitivity to hypoxia and incipient airway dysfunction antedate clinically manifest COPD.