Resting and total energy expenditure in patients with ischemic heart disease.

Total energy expenditure (TEE) was measured by doubly labeled water in 13 preoperative patients undergoing elective coronary artery surgery and compared to resting energy expenditure (REE) measured by indirect calorimetry (IC) calculated from the Harris-Benedict (HB) formula or from formulas based on midarm circumference and arm muscle circumference. Mean REE measured by IC and calculated from the HB, midarm circumference, arm muscle circumference formulas were 62, 75, 62, and 69%, respectively, of TEE measured by doubly labeled water. REE measured by IC correlated significantly with that predicted by the HB (p = 0.006) but not the anthropometric formulas. The relationship between REE derived from anthropometric predictive formulas and REE measured by IC is altered in ischemic heart disease.     

Procalcitonin''s amino-terminal cleavage peptide is a bone-cell mitogen.

The parafollicular-cell (C-cell) hormone calcitonin (CT) can preserve or even augment skeletal mass by inhibiting osteoclast-mediated bone resorption. The possibility of an additional anabolic skeletal influence has also been raised: C cells might, via CT or other secretory products, affect osteoblast-mediated bone formation. The 57-residue amino-terminal procalcitonin cleavage peptide, N-proCT, has recently been identified in human and rat C cells, where it is made and secreted in equimolar amounts with CT. The coelaboration of N-proCT and CT and N-proCT's sequence conservation during evolution prompted us to investigate the potential skeletal bioactivity of N-proCT. We found that synthetic human N-proCT, at nanomolar concentrations, stimulated proliferation of normal and neoplastic human osteoblasts. At maximally effective doses, human N-proCT caused more than a 100% increase above the control rate of DNA synthesis, an effect comparable to the maximal growth effect of insulin, a potent mitogen for osteoblasts. Human N-proCT exerted a similar maximal mitogenic effect in chicken osteoblast cultures but at 1000-fold greater concentrations than in human bone-cell cultures. The bone-cell action of N-proCT was potentiated with insulin with a greater than 200% increase in DNA synthesis at high insulin concentrations. In sharp contrast to these findings for N-proCT, the other bioactive C-cell peptides, CT and somatostatin, showed no mitogenic effects in human or chicken osteoblast cultures. Our results indicate that the action of N-proCT on cultured bone cells is separate from and potentiated by insulin, a known growth factor. Unlike insulin and related growth factors such as insulin-like growth factor I, N-proCT is not mitogenic in skin fibroblast cultures. We propose that N-proCT is a C-cell hormone that promotes bone formation via stimulatory actions on osteoblasts and preosteoblasts.     

头皮电烧伤骨外露带毛发皮瓣修复

目的：探讨头皮电烧伤骨外露用头皮扩张皮瓣移植修复的临床效果。方法：采用早期扩创,保留部分坏死骨质,用邻近头皮扩张使带毛发的头皮面积扩大后移植覆盖创面,电性失活骨质在血循环良好的皮瓣覆盖下,为周边及基底健康骨质生长起到支架作用,皮瓣扩张到一定面积后移植到裸露骨质上,使其得以修复。结果：在治疗的9例中,除1例皮瓣边缘在1．5cm×1．5cm坏死外,其余皮瓣全部成活,未发生感染坏死,创面均一次性封闭。结论：头皮电烧伤骨外露扩张后皮瓣带毛发修复,可缩短创面愈合时间,外形较好,易掌握,效果较为满意。     

多济敷对面部磨削创面愈合的临床疗效观察

目的：本研究采用多济敷外用于面部皮损磨削术后创面,观察其对创面愈合时间、皮肤色素沉着等的变化。方法：采用区域神经阻滞或局部浸润麻醉,对不同类型的面部皮损34例进行皮肤磨削治疗,术后创面应用多济敷或凡士林纱布作为底层敷料包扎创面,术后换药一次,保留底层敷料。结果：2001年8月至2003年9月间,通过自身对照,34例面部磨削术后采用多济敷治疗组较凡士林纱布组创面愈合时间缩短(P＜0．05),经过6个月至2年的随访,皮肤色素沉着也有明显改善。结论：多济敷有利于缩短面部磨削术后创面愈合时间,改善面部色素沉着,外观满意。     

麦冬类中药组织切片计算机三维重建图鉴

利用计算机技术实现麦冬类中药组织连续切片三维重建与动态显示,为计算机辅助生药学鉴定和教学提供了新的三维图像技术和研究资料。     

Cylindrical spirals of myofilamentous origin associated with exertional cramps and rhabdomyolysis

We describe the presence of cylindrical spirals on muscle biopsy from a 31-year-old man who developed rhabodomyolysis following a long run. He had a prior history of exertional cramps and myoglobinuria. His maternal grandfather had similar symptoms. Transmission electron micrographs demonstrated continuity between the lamellae of the cylindrical spirals and native myofilaments. Whether these unusual structures confer a derangement in myofilament function is uncertain.     

Toxic shock syndrome after inguinal hernia repair. Report of a case with patient survival

A 40-year-old man developed fulminant multisystem failure several days after elective repair of an inguinal hernia. Toxic shock syndrome (TSS) was diagnosed. There was, however, no evidence of wound infection at the time of multisystem failure. Only later in his hospital course did the wound drain. Staphylococcus aureus was cultured from the wound and was the presumed etiologic agent in the patient's life-threatening illness. The patient recovered fully with supportive care, antibiotics, and surgical debridement of the inguinal hernia site. This case is discussed in the context of existing literature on the toxic shock syndrome. The site of infection is typically nonsuppurative, but the systemic manifestations are typically life threatening. The responsible organism is commonly believed to be a strain of S. aureus that expresses a toxin (TSS toxin-1) that effects multisystem failure, but which also diminishes the local inflammatory response and explains the benign appearance of the wound. Although this is a rare clinical entity, elective surgical procedures complicated by fatal TSS have been reported. Surgeons should understand this disease and the management necessary to avert mortality.     

Evidence for arsenic as the immunosuppressive component of gallium arsenide.

Gallium arsenide (GaAs) has been shown previously to suppress the in vivo antibody-forming cell (AFC) response to sheep erythrocytes (SRBC) when administered intratracheally at concentrations between 50 and 200 mg/kg. In the present studies, direct addition of GaAs to in vitro-generated antibody cultures resulted in dose-dependent suppression of the primary antibody response, and was only seen when GaAs was added within 36 hr following immunization. Using atomic absorption spectrophotometry on tissue samples from mice exposed to 200 mg/kg GaAs, arsenic concentrations were found to peak in the spleen at 24 hr and decline, whereas gallium concentrations continue to rise through 14 days. Concentrations of each metal in the spleen at 24 hr are comparable to the concentrations achieved for each metal when GaAs is added at 25 microM to the in vitro model system. The 24 hr time point was chosen for comparison because all in vivo-in vitro studies were conducted using spleens from mice 24 hr after GaAs exposure. NaAsO2 and Ga(NO3)3 suppressed the AFC response dose-dependently, and in a time-dependent manner similar to GaAs when added to the in vitro system. However, based on IC50 values for each salt, the role of the gallium component in the immunosuppression appears weak. Oxalic acid (OA) and meso-2,3-dimercaptosuccinic acid (DMSA), chelators of gallium and arsenic respectively, were added to cultures with GaAs to confirm that arsenic was the primary immunosuppressive component. DMSA dose-dependently blocked GaAs-induced immunosuppression in vitro, while OA had no effect. The metal-binding compounds were determined to be specific for the metals used in these studies and did not cross-react with one another. DMSA was evaluated for its ability to prevent suppression of the AFC response in splenocytes from GaAs-exposed mice and was able to block GaAs-induced suppression of the AFC response when given sc every 4 hr beginning 1 hr prior to GaAs exposure. These data indicate that the arsenic component of GaAs is the major contributor to the GaAs-induced immunosuppression and that this effect occurs within the first 36 hr of the 5-day culture period in a concentration-dependent manner.