We examined the changes in pulmonary function values in 27 patients who underwent a lobectomy due to cystic lung disease and compared the results regarding such factors as disease type, age at operation, and preoperative infections. Percent vital capacity (%VC) decreased immediately after lobectomy, but recovered to normal values within 2 postoperative years and remained within or above the normal range. The ratio of residual volume to total lung capacity (RV/TLC) rose temporally with the increase in %VC, but then remained normal after 2 postoperative years. There was no difference in %VC and RV/TLC between diseases, while bronchial atresia showed a significantly lower correlation with percent of forced expiratory volume at 1 s. The older group operated upon at over 4 years of age and the group that had infections before operation showed relatively low %VC and high RV/TLC. Some patients demonstrated extremely low %VC along with funnel chest deformities. Our study suggests that overinflation of the remaining lung compensates VC in the early period after lobectomy while subsequently alveolar multiplication occurs. Factors affecting compensatory lung growth were considered to be operation later than 4 years of age, preoperative infection, and a thoracic deformity.

5-Fluorouracil (FU) and its masked compounds tegafur (FT) and carmofur (HCFU) were administered orally to Beagle dogs daily for 6 months, and their chronic neurotoxic effects were examined morphologically. In ten dogs that survived the 6-month treatment large vacuoles produced by splitting of the intraperiod line of myelin were observed in the fornix in the wall of the third ventricle. In severely affected dogs large vacuoles developed in the medial preoptic area, medial portion of the internal capsule, the area around the subthalamic nucleus and the mammillo-thalamic tract. Axons of myelinated fibers affected by vacuolation were generally well maintained, and destruction of myelin was not detected. Though proliferation of glia cells or abnormality of oligodendroglia was not detected, a lipid deposit covered by a single layer membrane was observed in the cell bodies and processes of astrocytes. No abnormality was detected by electron microscopy in the cerebrum, inferior colliculus, cerebellum, or pons. Of eight dogs that died during the treatment period, large vacuoles were observed in the fornix in the wall of the third ventricle of four dogs treated for more than 1 month, and large vacuoles were present in the inferior colliculus in two dogs of the FT group in the above four dogs. In the HCFU group, the interruption of treatment for 6 months resulted in alleviation or disappearance of the vacuolar lesions. The above findings suggest that the neurotoxicity of FU and its masked compounds FT and HCFU in long-term treatment produces changes morphologically identical with one another in respect to the site of their manifestation and nature of lesion, that their common degraded product alpha-fluoro-beta-alanine (FBAL) plays a crucial role in their neurotoxic actions, and that vacuolar lesions, to which myelin was more vulnerable than neurons, can develop where the toxic substance readily deposits and accumulates.

No abstract

Primary erythermalgia is a rare neuropathy characterized by attacks of burning pain and redness in the extremities in response to warm stimuli. We describe here a boy with erythermalgia whose painful attacks began in infancy. We found a novel mutation of SCN9A, which is a responsible gene for primary erythermalgia in this case. In his teens, he developed wintry hypothermia with resultant neurological dysfunction and recurrent pneumonia. During the course of pneumonia, he had transient encephalopaty with a reversible lesion in the splenium of the corpus callosum. In addition to excessive cooling, a defect in central thermoregulation may have caused hypothermia in this patient.

Smoking increases the risk of atherosclerosis-related events, such as myocardial infarction and ischemic stroke. Recent studies have examined the expression levels of altered microRNAs (miRNAs) in various diseases. The profiles of tissue miRNAs can be potentially used in diagnosis or prognosis. However, there are limited studies on miRNAs following exposure to cigarette smoke (CS). The present study was designed to dissect the effects and cellular/molecular mechanisms of CS-induced atherosclerogenesis. Apolipoprotein E knockout (ApoE KO) mice were exposed to CS for five days a week for two months at low (two puffs/min for 40 min/day) or high dose (two puffs/min for 120 min/day). We measured the area of atherosclerotic plaques in the aorta, representing the expression of miRNAs after the exposure period. Two-month exposure to the high dose of CS significantly increased the plaque area in aortic arch, and significantly upregulated the expression of atherosclerotic markers (VCAM-1, ICAM-1, MCP1, p22phox, and gp91phox). Exposure to the high dose of CS also significantly upregulated the miRNA-155 level in the aortic tissues of ApoE KO mice. Moreover, the expression level of miR-126 tended to be downregulated and that of miR-21 tended to be upregulated in ApoE KO mice exposed to the high dose of CS, albeit statistically insignificant. The results suggest that CS induces atherosclerosis through increased vascular inflammation and NADPH oxidase expression and also emphasize the importance of miRNAs in the pathogenesis of CS-induced atherosclerosis. Our findings provide evidence for miRNAs as potential mediators of inflammation and atherosclerosis induced by CS.