TNF-alpha augments the expression of RhoA in the rat bronchus.

While nonspecific airway hyperresponsiveness (AHR) is a central feature of allergic bronchial asthma, the mechanism underlying the development of AHR is not clearly understood. We have previously demonstrated in vitro hyperresponsiveness of bronchial smooth muscle to acetylcholine (ACh) in rats that were actively sensitized and repeatedly challenged with aerosolized antigen. It has also been demonstrated that the ACh-induced, RhoA-mediated Ca(2+) sensitization is markedly augmented concomitantly with an increased expression and activation of RhoA protein in the bronchial smooth muscle of the antigen-treated rats. In the present study, we have investigated whether TNF-alpha, a proinflammatory cytokine which is involved in bronchial asthma, causes upregulation of RhoA mRNA and protein in the rat bronchus. Treatment of rat bronchial smooth muscle preparations with TNF-alpha (300 ng/ml for 24 hr) significantly shifted the concentration-response curve to ACh upwards, but did not alter the response to high K(+), when compared to that of control tissues. Levels of RhoA mRNA and protein in the TNF-alpha-treated bronchus were significantly greater than those in the control group. In conclusion, it is suggested that the augmentation of the ACh-induced contractile response evoked by TNF-alpha might be mediated by an upregulation of RhoA in rat bronchial smooth muscle.     

Human parvovirus-induced transient anemia and leukopenia after delivery]

A 30-year-old female at 27 weeks' gestation, was hospitalized on September 24 1990 because of the premature rupture of the amniotic sac. She underwent Caesarean section on the same day with 700 ml blood loss, but no blood transfusion was required. For several days after the operation, her hemoglobin level remained 7.8 g/dl and did not increase significantly in spite of parenteral iron therapy. On the 9th postoperative day, chills and pyrexia developed with leukopenia. Bone-marrow aspiration revealed severe erythroblastopenia with giant proerythroblasts, suggesting recent HPV infection, which was confirmed by the presence of anti-HPV IgM and HPV antigen by ELISA. The hemoglobin level gradually decreased to 6.0 g/dl by the 21st day, then began to increase rapidly. The serum of acute-phase containing HPV antigens inhibited BFU-E and CFU-E but not CFU-GM. The serum of convalescent-phase inhibited neither erythroid colony growth nor myeloid colony growth. These results indicate that the inhibitory effect of HPV in colony assay is highly specific for erythropoiesis and that HPV play a role in transient cessation of erythropoiesis. The reason, however, for leukopenia in HPV infection remained unclear. This case shows that HPV infection may induce severe hematological disorders even in normal person under erythropoietic stress.     

Thrombosed aneurysm of the middle cerebral artery with occlusion of the distal parent artery--case report.

A 54-year-old female presented with subarachnoid hemorrhage due to rupture of a small middle cerebral artery aneurysm, found to be thrombosed at surgery and not visualized on the preoperative angiograms. One major branch of the middle cerebral artery was found to be occluded near the trifurcation. The lumen of the branch proximal to the occlusion had appeared as the aneurysmal opacification on the preoperative angiograms.     

Placental alkaline phosphatase as a tumor marker for primary intracranial germinoma

A sensitive enzyme-linked immunosorbent assay (ELISA) was used in a retrospective study of placental alkaline phosphatase (PLAP) levels in serum, cerebrospinal fluid (CSF), and intratumoral cyst fluid in primary intracranial germinoma. The ELISA showed no cross-reactivity with intestinal alkaline phosphatase except in very high concentrations, after samples had been heat-treated. Three patients with germinoma were studied for serum PLAP levels and in all the levels were elevated (3.78, 0.52, and 2.11 IU/liter). Two of the germinoma patients were studied for PLAP levels in the CSF, and both had elevated levels (0.83 and 9.83 IU/liter). The intratumoral cyst fluid in one case of germinoma was tested for PLAP and the level was found to be very high (603 IU/liter). These PLAP levels decreased concomitantly with the reduction in tumor size during irradiation. Serum PLAP levels were measured in 40 control adult male individuals and in the CSF of 20 nonpregnant patients with subarachnoid hemorrhage. The upper normal limits were 0.20 and 0.11 IU/liter in the serum and the CSF, respectively. All PLAP levels measured in the serum of patients with various brain tumors were 0.18 IU/liter or less. This study strongly suggests that PLAP is a clinically useful tumor marker for primary intracranial germinoma.     

Sialolipoma of the hard palate

Sialolipoma is a new variant of salivary gland lipoma, which was first proposed by Nagao et al. (Histopathology 2001; 38: 30) in 2001. We report this rare case of sialolipoma in the hard palate. A 60-year-old Japanese woman was referred to our department complaining of a painless swelling on the right side of the hard palate. Intra-oral examination revealed a soft, elastic, dome-shaped mass with 1 cm in diameter located in the posterior part of the hard palate. Magnetic resonance imaging examination revealed high intensity on T(1)-weighted image and isointensity on T(2)-weighted image. Incisional biopsy revealed that the tumor was encapsulated by fibrous tissue, consisted of adipose tissue, and also contained normal salivary gland tissue peripherally. First diagnosed as an ordinary lipoma of the hard palate, the tumor was excised. According to the recent criteria of histologic findings of sialolipoma, we rediagnosed the tumor as sialolipoma of the hard palate.     

Climbing exercise increases bone mass and trabecular bone turnover through transient regulation of marrow osteogenic and osteoclastogenic potentials in mice.

To investigate the relationship between the effects of bone turnover and bone marrow cell development in bone cells, we developed a mouse voluntary climbing exercise model. Climbing exercise increased bone volume and transient osteogenic potential of bone marrow. This model would be suitable for investigating the mechanistic roles of mechanical loading. INTRODUCTION: The relationship between bone mass gain and local bone formation and resorption in mechanically loaded bone is not well understood. MATERIALS AND METHODS: Sixty-five C57BL/6J mice, 8 weeks of age, were assigned to five groups: a baseline control and two groups each of ground control and climbing exercise mice for 2 and 4 weeks. Mice were housed in a 100-cm tower and had to climb toward a bottle placed at the top to drink water. RESULTS: Compared with the ground control, bone mineral density of the left femur increased in the climbing mice at 4 weeks. At 2 and 4 weeks, bone formation rate (BFR/BS) of periosteal surface, the cross-sectional area, and moment of inertia were increased in the climbing mice, whereas BFR/BS and eroded surface (ES/BS) of endosteal surface did not differ. The trabecular bone volume (BV/TV) of the proximal tibia increased in climbing mice, and osteoclast surface (Oc.S/BS) and osteoclast number decreased at 2 weeks. At 4 weeks, there were increases in BV/TV and parameters of bone formation, including mineralized surface, mineral apposition rate, and bone formation rate. In marrow cell cultures from the tibia, the number of alkaline phosphatase+ colony forming units-fibroblastic and the area of mineralized nodule formation in climbing mice were increased, and the number of osteoclast-like TRACP+ multinucleated cells was lower at 2 weeks. At 4 weeks, these parameters recovered to the levels of the ground controls. CONCLUSION: Our results indicate that climbing increased trabecular bone volume and reduced bone resorption, with a subsequent increase in bone formation. Intermittent climbing downregulates marrow osteoclastogenic cells and upregulates osteogenic cells initially, but further exercise seemed to desensitize them. Cortical envelopes were enlarged earlier, but the response seems to differ from trabecular bone.     

Congestive heart failure in elderly readmitted patients]

The clinical features of congestive heart failure in the elderly were investigated in 104 patients (57 males, 47 females, mean age of 79.2). Patients were divided into two subgroups, the readmission group, 33 patients who were readmitted within 6 months after discharge, and the non-readmission group. Chief complaints were dyspnea, edema, chest pain, loss of appetite, chest compression, and palpitation. Heart failure was caused by infection, myocardial ischemia, arrhythmia, inappropriate drug usage including poor drug compliance, the use of beta-blockers, excessive intake of sodium, and anemia. Careful use of drug was essential especially in the readmission group. Major underlying heart disease were ischemic heart disease (39.4%), valvular disease (26.9%), hypertensive heart disease (9.6%), with cardiomyopathy, congenital heart disease seen in the minority. There was no statistically significant difference in underlying heart diseases between the two groups. Supraventricular arrhythmias such as atrial fibrillations, paroxysmal atrial fibrillations, paroxysmal supraventricular tachycardias, and premature atrial contractions were noted in 85.3% of the cases. Drugs for treatment were diuretics, digitalis, isosorbide dinitrate, calcium antagonists. ACE inhibitors and alpha-blockers were also used, showing that vasodilators were more extensively used than before. The major complications were hypertension (39.4%), renal dysfunction (27.9%), cerebrovascular disease (26.9%), diabetes mellitus (16.5%), arteriosclerosis obliterans (7.7%). Renal dysfunction, arteriosclerosis obliterans was seen significantly more frequently in the readmission group. The prognosis at one year after admission was significantly worse in the readmission group. In summary, the major underlying diseases were ischemic heart disease, valvular disease, and hypertensive heart disease. Ischemic heart disease was seen more frequently than in previous investigations at our hospital.(ABSTRACT TRUNCATED AT 250 WORDS)     

Multiple intracerebral hemorrhages due to cerebral amyloid angiopathy after head trauma

Cerebral amyloid angiopathy (CAA) is an important cause of intracerebral hemorrhage and ischemic cerebrovascular disease in some normotensive elderly patients. The diagnosis is made by proof of amyloid deposition in the vessel wall. A case of recurrent and multiple intracerebral hemorrhages due to cerebral amyloid angiopathy after head injury is reported. A 74-year-old female was referred to our hospital because of head injury. CT scan showed traumatic subarachnoid hemorrhage and intraventricular hematoma. Her consciousness was clear but slight disorientation was recognized. Conservative therapy was performed. During the course subcortical hemorrhages occurred five times and during the second one, right frontal and right parietal hemorrhages occurred simultaneously. Her consciousness deteriorated. The second subcortical hemorrhage was especially complicated by a ventriculoperitoneal shunt operation. A biopsy of the cortex was performed and pathological examination revealed amyloid deposition in the walls of small pial and cortical vessels. Occasional duplicated wall, obliterative intimal proliferation and disappearance of elastic lamina were recognized. The patient sank into a vegetative state due to recurrent and multiple hemorrhages. CAA results in two possibilities, hemorrhage and ischemic cerebrovascular disease. When lobar or subcortical hemorrhage is encountered in a normotensive elderly patient, the possibility of a CAA-related hemorrhage should be considered. The author carefully emphasizes that there is indication for neurosurgical treatment in CAA patients and proposes that therapy for ischemic cerebrovascular disease should be given special attention.