Rigid spine syndrome with respiratory failure.

The pathogenesis and therapy of respiratory failure in the rigid spine syndrome are discussed in two cases who improved with respiratory assistance. In both cases, the partial pressures of oxygen and carbon dioxide were reversed in arterial blood gas analysis and %VC was less than 30%. Remission from respiratory failure has been obtained by the use of a ventilator during the night. The cause of the respiratory failure in both cases was severe restrictive respiratory dysfunction due to extreme flattening of the chest and fixation of the thorax during respiration as a result of contracture of costovertebral joints. All the previously reported cases of the rigid spine syndrome with respiratory failure died. Appropriate use of the ventilator can improve the prognosis.     

Mesangial cell behavior in a three-dimensional extracellular matrix.

To understand the role of mesangial matrix in regulating responses of mesangial cells (MCs), particularly as a cause of disease, we examined the behavior of MCs cultured in a three-dimensional extracellular matrix (ECM). Mouse and rat MCs were incorporated into ECM composed of type I collagen gel matrix (CGM) and basement membrane-type gel matrix (BGM), and their shape and proliferation were assessed. The effect of gel matrix on MC migration was also studied. MCs exhibited marked elongation and proliferation in CGM, whereas these behavior were inhibited by increasing the ratio of BGM. Although CGM allowed MC migration, BGM restricted it to a great extent. To identify the cause of our findings, we examined the effects of ECM components in our experimental system. Laminin, fibronectin, type IV collagen, and heparin-like proteoglycans (heparan sulfate and heparin) were each mixed separately with CGM at a concentration of 50 micrograms/ml gel. Whereas fibronectin promoted MC elongation and proliferation, and laminin inhibited MC migration, type IV collagen and heparin-like proteoglycans inhibited all three activities of MCs. Our findings suggest that basement membrane-type mesangial matrix is important in regulating the behavior of MCs in vivo.     

Effects of inhibitors of some mediators on the paw-edema induced by acetyl glyceryl ether phosphorylcholine in rats

The characterization of acetyl glyceryl ether phosphorylcholine (AGEPC)-induced paw edema in rats was explored. Edema formation was maximum at 45 min after the injection of AGEPC. The dose for maximal response was 1 microgram/site, while edema was suppressed at higher doses. The systemic administration (s.c.) of cyproheptadine (CH, 10 mg/kg) did not inhibit this edema differently from serotonin-induced edema, while the local treatment of CH suppressed AGEPC-induced edema in a dose-dependent manner. The combination of local treatments with pyrilamine and methysergide also suppressed this edema. The s.c. injection of indomethacin (IM, 10 mg/kg) did not inhibit AGEPC edema differently from carrageenin-induced edema, while locally given IM suppressed it partially. The local treatment with caffeic acid and esculetin, lipoxygenase inhibitors, or with FPL 55712, an antagonist of SRS-A, suppressed AGEPC edema slightly. Various combinations of local treatment with IM and lipoxygenase inhibitors gave synergistic suppression of this edema. Dexamethasone strongly suppressed AGEPC edema when given both systemically and locally 3 hr before the injection of AGEPC. However, phospholipase A2 (PLA2) inhibitors, i.e. mepacrine, p-bromophenacyl bromide, chlorpromazine and tetracaine, did not show the same effect as dexamethasone. These results suggest that the edema formation induced by AGEPC may involve not only the combined action of histamine and serotonin but also the synergistic action of cyclooxygenase and lipoxygenase products. Dexamethasone may inhibit this edema by mechanisms other than the inhibitory action of PLA2.     

Medical therapy in patients with left main coronary artery stenosis]

To elucidate the long-term prognosis of medically-treated patients with left main coronary artery (LMCA) lesions, 119 consecutive patients with LMCA lesions undergoing coronary angiography were analyzed retrospectively. Among these, 3 patients died soon after angiography and were excluded from this study. Among the remaining 116 patients, 22 were treated medically (Group M) for the following reasons: profound left ventricular (LV) dysfunction (3 patients), effective pharmacological treatment (10), and patients' refusal of surgical therapy (9). Among 94 patients who underwent coronary artery bypass graft (CABG), 83 patients survived (Group S). During the follow-up period, cardiac events occurred in 5 patients in Group M; cardiac deaths in 3, non-fatal myocardial infarction (MI) in one and late application of CABG in one. Two-year cardiac event-free rate after diagnosis was 77%, which remained unchanged thereafter. The cumulative survival rate was 83%. The incidence of cardiac events in Group M was higher than that in Group S (p < 0.01). However, cardiac event rates were similar between these 2 groups for patients with good collateral circulations to the left coronary arteries, no preceding MI and LV end-diastolic pressure less than 15 mmHg. We concluded that the Japanese patients with severe LMCA lesions who respond favorably to pharmacological intervention have unexpectedly good prognoses, however, obstructed collateral circulation to the left coronary system, the presence of preceding MI and high LV end-diastolic pressure were all high-risk factors for medically-treated patients.     

A case of brainstem encephalitis caused by herpes simplex virus type 1 with possible infection via trigeminal nerve]

A 24-year-old man was admitted to our hospital because of consciousness disturbance, a stiff neck and various brainstem symptoms including a right one-and-a-half syndrome and right peripheral facial palsy a week after an episode of pharyngitis and right facial herpes simplex. Magnetic resonance imaging of the brain on admission showed high-signal intensities in the right pontine tegmentum, right cerebellar peduncle and vermis on fluid-attenuated inversion recovery imaging. Examination of cerebrospinal fluid yielded mononuclear pleocytosis, elevated protein and increased IgM antibodies to herpes simplex virus (HSV) by enzyme immunoassay. HSV-1 specific antibodies also were detected in serum by neutralization test. We gave a diagnosis of brainstem encephalitis caused by HSV-1. The patient was successfully treated with high dose of acyclovir, steroid and intravenous immunoglobulin. He was discharged without any neurologic sequelae. We herein presented a case of atypical encephalitis due to HSV-1 involving mainly the brainstem with possible infection via right trigeminal nerve and summarized recent 35 cases with herpetic brainstem encephalitis since 1990.     

Regulatory Effects of Gamma-Interferon on IL-6 and IL-8 Secretion by Cultured Human Keratinocytes and Dermal Fibroblasts

Gamma-interferon (IFN-γ) is produced by T cells and plays an important role in immunological and inflammatory processes. To determine the effects of IFN-γ on interleukin (IL)-6 and IL-8 secretion, normal human keratinocytes (NHKs), human squamous cell carcinoma cell line (HSC-1) cells, and human dermal fibroblasts (HDFs) were incubated with 100 U/ml of recombinant (r) IFN-γ in the presence of various stimulants. HSC-1 cells and HDFs spontaneously secreted both IL-6 and IL-8 into the culture medium. NHKs secreted detectable levels of IL-8, but not of IL-6, and IL-8 secretion increased over 20 fold by stimulation with 10 nM of phorbol 12-myristate 13-acetate (PMA). rIFN-γ inhibited IL-8 secretion in both HSC-1 cells and PMA-stimulated NHKs. On the other hand, it enhanced IL-1α- and TNFα-induced IL-8 secretion in NHKs. In HDFs, rIFN-γ inhibited IL-8 secretion, but enhanced secretion of IL-6, regardless of whether they were stimulated with IL-1α or PMA. These results suggest that IFN-γ has different regulatory effects on IL-6 and IL-8 secretion in NHKs and HDFs, depending on the stimulus.     

Bone loss in a rat model of non-insulin-dependent diabetes mellitus, the OLETF (Otsuka Long-Evans Tokushima fatty strain) rat

A long-term investigation of bone metabolism was conducted in a newly developed strain, the OLETF (Otsuka Long-Evans Tokushima fatty strain) rat, which spontaneously develops non-insulin-dependent diabetes (NIDDM). The OLETF rats used in this study developed hyperglycemia before the age of 24 weeks and overt diabetes before 40 weeks. The bone mineral density (BMD) of the lumbar spine peaked at the age of 24 weeks in the OLETF rats, and declined rapidly after 40 weeks. In addition, the BMD of the tibial proximal metaphysis and diaphysis and the bone strength of the femoral diaphysis peaked at 40 weeks, then declined rapidly. In contrast, the BMD and the bone strength of the LETO (Long-Evans Tokushima Otsuka) rats, used as a control, peaked at 24 weeks, and did not change thereafter. The serum vitamin D metabolites [25-hydroxy vitamin D (25-OHD), 24,25-dihydroxyvitamin D (24,25(OH)₂D), and 1,25-dihydroxy vitamin D (1,25(OH)₂D)] levels for the OLETF rats declined with age, and were significantly lower than those of the control LETO rats. The level of serum bone-specific alkaline phosphatase (Alp) activity and serum tartrate-resistant acid phosphatase (Tr-Acp) activity in the OLETF rats increased remarkably with age from 24 weeks, and there were significant differences in the 56- and the 69-week values between the OLETF rats and the age-matched control LETO rats. These results suggested that this strain can serve as a useful model for NIDDM with osteopenia. Received: Dec. 12, 1997/Accepted: April 14, 1998     

Cystatin C and apolipoprotein E immunoreactivities in CA1 neurons in ischemic gerbil hippocampus

The distribution patterns of cystatin C and apolipoprotein E (apo E) were studied immunocytochemically in the gerbil hippocampus before and after 5 min ischemia. In the controls, cystatin C was distributed mainly in astrocytes. In addition, a large number of dots positive for cystatin C were observed around the outlines of neuronal perikarya in the CA1 subfields. One day after ischemia, cystatin C-positive stainings outlining neuronal cell bodies disappeared. On the fourth day, intense stainings for cystatin C appeared in atrophied pyramidal neurons and these stainings in neurons disappeared by the 14th day. A remarkable increase in the number of cystatin C-positive astrocytes occurred on the fourth day and thereafter these spread over the whole of the CA1 subfield. Apo E was also distributed in astrocytes in the control specimens. From the fourth day, extra- and/or intracellular distribution of apo E-immunoreactivities was noted in the stratum pyramidale. Apo E-positive astrocytes disappeared transiently on the fourth day and then reappeared and increased remarkably by the 14th day. These findings indicate that cystatin C and apo E are involved in the degeneration process of brain neuronal cells.