No abstract available.
Pregnancy*

No abstract available.
Humans ; Infant, Newborn* ; Lipoproteins* ; Plasma*

OBJECTIVE: Recently, we have demonstrated that embryonic ventral spinal cord motor neurons(ESMNs), transplanted into the distal stump of the axotomized tibial nerve, can grow into the denervated gastrocnemius muscle and form neuromuscular junctions. Our interest in study was to see whether these newly formed neuronal connections are physiologically active, and to electrophysiologically characterize the reinnervated motor units. MATERIAL AND METHODS: Three to eight weeks after transplantation rats were prepared for electrophysiological recording. Motor unit (MU) action potential and gross EMG were monitored. In eleven out of sixteen transplanted animals single unit and gross EMG were recorded after electrical stimulation of the transplant site. Total of 63 motor units were analyzed for their stimulus threshold (ST), latency and stimulus intensity, which is required to produce maximum firing. RESULTS: ST intensities activating MUs were significantly higher in transplanted animals than in controls. Maximum firing of MUs occurred at less than 1.2×T in the control but greater variation was observed in the transplanted animals ranging from 1.1×T to 1.6×T. No significant differences were found in the latencies of MU's firing following stimulation. MU firing was reversibly blocked by infusion of succinylcholine. CONCLUSION: we characterized the temporal, morphological and electrophysiological parameters of denervated skeletal muscle reinnervated by dissociated grafts of embryonic ventral spinal cord cells. MUs reinnervated by the embryonic motoneuronal transplant were physiologically active, with some properties similar to the MUs of the normal.
Action Potentials ; Animals ; Electric Stimulation ; Fires ; Mice ; Motor Neurons ; Muscle, Skeletal ; Neuromuscular Junction ; Neurons ; Rats ; Spinal Cord ; Succinylcholine ; Tibial Nerve ; Transplants

No abstract available.
Anterior Cruciate Ligament* ; Rupture*

No abstract available.
Humans ; Infant* ; Infant, Newborn* ; Radial Artery*

No Abstract Available.
Case-Control Studies*

No abstract available.
Fertilization in Vitro* ; Gonadotropin-Releasing Hormone*

3T3-L1 adipocytes express the B-cell-activating factor (BAFF) and three different BAFF receptors (BAFF-Rs). Furthermore, BAFF expression is regulated by inflammatory modulators, such as tumor necrosis factor-alpha and rosiglitazone. Here we investigated the function of BAFF in 3T3-L1 adipocytes and RAW 264.7 macrophages. We examined adipokine expression in 3T3-L1 adipocytes treated with 10 ng ml-1 BAFF. We also examined inflammatory molecule expression in RAW 264.7 macrophages treated with 10 or 100 ng ml-1 BAFF. We examined BAFF expression in the coculture of 3T3-L1 adipocytes and RAW 264.7 macrophages, as well as in white adipose tissue (WAT) of diet-induced obese (DIO) mice. We found that BAFF decreases leptin and adiponectin expression, but increases the expression of proinflammatory adipokines monocyte chemotactic protein-1, interleukin-6 (IL-6), cyclooxygenase-2 (COX-2) and haptoglobin. Coculturing the two cell types resulted in increased BAFF mRNA and protein expression, as well as modulation of BAFF-R mRNA expression in both cell types. These data indicate that BAFF might mediate adipocyte and macrophage interaction. When RAW 264.7 macrophages were treated with BAFF, BAFF-R expression was modulated as in coculture, and nitric oxide synthase and IL-6 expression increased. BAFF expression also increased in WAT of DIO mice. We propose that BAFF can regulate adipokine expression and possibly mediate adipocyte and macrophage interaction.
3T3-L1 Cells ; Adipocytes/drug effects/*metabolism ; Adipokines/genetics/*metabolism ; Adiponectin/genetics/metabolism ; Animals ; B-Cell Activating Factor/*metabolism/pharmacology ; Chemokine CCL2/genetics/metabolism ; Coculture Techniques ; Gene Expression Regulation/drug effects ; Haptoglobins/genetics/metabolism ; Inflammation Mediators/metabolism ; Interleukin-6/genetics/metabolism ; Leptin/genetics/metabolism ; Macrophages/drug effects/*metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; RNA, Messenger/genetics/metabolism

We present a case of acquired tracheoesophageal fistula (TEF) which was found during induction of general anesthesia for clipping of aneurysm. The patient had been intubated with endotracheal tube for 10 days and then done tracheotomy for 45 days. Thereafter, TEF was confirmed by MRI and treated with fistula repair and tracheal fenestration. Acquired TEF can occur under the condition of prolonged tracheal intubation with high cuff pressure (>30 mmHg) and can also result from intratracheal neoplasm, mediastinitis, and other tracheal or esophageal damages. If unrecognized during anesthetic induction, TEF can cause gastric dilatation and rupture, pulmonary aspiration and respiratory failure. So early diagnosis and proper management is very important whenever TEF is suspected during anesthetic induction.
Anesthesia, General ; Aneurysm ; Early Diagnosis ; Fistula ; Gastric Dilatation ; Humans ; Intubation ; Magnetic Resonance Imaging ; Mediastinitis ; Respiratory Insufficiency ; Rupture ; Tracheoesophageal Fistula* ; Tracheotomy

Obesity is recognized as a chronic low-grade inflammatory state due to adipose tissue expansion being accompanied by an increase in the production of proinflammatory adipokines. Our group is the first to report that B-cell-activating factor (BAFF) is produced from adipocytes and functions as a proinflammatory adipokine. Here, we investigated how loss of BAFF influenced diet-induced obesity in mice by challenging BAFF-/- mice with a high-fat diet for 10 weeks. The results demonstrated that weight gain in BAFF-/- mice was >30% than in control mice, with a specific increase in the fat mass of the subcutaneous region rather than the abdominal region. Expression of lipogenic genes was examined by quantitative real-time PCR, and increased lipogenesis was observed in the subcutaneous adipose tissue (SAT), whereas lipogenesis in the epididymal adipose tissue (EAT) was reduced. A significant decrease in EAT mass resulted in the downregulation of inflammatory gene expression in EAT, and more importantly, overall levels of inflammatory cytokines in the circulation were reduced in obese BAFF-/- mice. We also observed that the macrophages recruited in the enlarged SAT were predominantly M2 macrophages. 3T3-L1 adipocytes were cultured with adipose tissue conditioned media (ATCM), demonstrating that EAT ATCM from BAFF-/- mice contains antilipogenic and anti-inflammatory properties. Taken together, BAFF-/- improved systemic inflammation by redistributing adipose tissue into subcutaneous regions. Understanding the mechanisms by which BAFF regulates obesity in a tissue-specific manner would provide therapeutic opportunities to target obesity-related chronic diseases.
3T3-L1 Cells ; Adipocytes/drug effects/metabolism ; Adiposity/*genetics ; Animals ; B-Cell Activating Factor/*genetics ; Cells, Cultured ; Culture Media, Conditioned/pharmacology ; Diet, High-Fat ; Disease Models, Animal ; Gene Knockout Techniques ; Inflammation/*genetics ; Lipogenesis/genetics ; Macrophages/metabolism ; Male ; Mice ; Mice, Knockout ; Obesity/*etiology