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Hisako Karube, Koju Kamoi, Kyoko Ohno-Matsui Department of Ophthalmology and Visual Science, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan Background: Ocular symptoms in Behçet’s disease (BD) begin mostly before 30 years of age according to international surveys, and BD activity may decrease with age. Information regarding the treatment of ocular symptoms in elderly BD patients is thus scant. Anti-TNFα antibody has recently demonstrated strong effects against recurrent uveitis in BD, but the efficacy and safety of anti-TNFα therapy in elderly patients remain unclear. We report herein the case of an elderly patient with long-standing uveitis due to BD who was successfully treated with two types of anti-TNF therapy. Case: An 81-year-old Japanese man presented with a 33-year history of ocular inflammation due to BD. As immunosuppressive agents, such as cyclosporine A, were difficult to use because he had undergone removal of the left kidney due to cancer, he was treated with colchicine. However, attacks of ocular inflammation persisted around nine times a year. After colchicine had been changed to infliximab, ocular inflammation was fairly well controlled, but ocular attacks still occurred once or twice a year. As soon as intestinal hemorrhage related to BD occurred, infliximab was switched to adalimumab. After this switch, ocular attacks resolved and visual acuity was maintained at 1.0. Intestinal lesions were also well controlled, and no side effects were seen. Conclusion: This represents the first report of the application of two types of anti-TNFα therapy for ocular attacks in an elderly BD patient. In addition to infliximab, adalimumab appears to offer an alternative therapy for refractory, long-standing BD-related uveitis in elderly patients. Keywords: Behçet’s disease, anti-tumor necrosis factor-α antibody, infliximab, adalimumab, elderly patient

Chronic hepatic encephalopathy (CHE) is a neurological syndrome caused by liver disease. It results when products of digestion escape breakdown by liver processes and enter the circulation. Ammonia, a product of protein metabolism, is a probable contributor to CHE. CHE is usually treated by restricted dietary protein and by lactulose, a synthetic sugar that alters colonic bacteria and is a cathartic, but such treatment is not always effective. Vancomycin, an antibiotic, has previously been shown to be effective in treating CHE. The effects of vancomycin on 12 patients with cirrhosis and lactulose-resistant CHE was studied. Encephalopathy resolved completely in 10 patients within two to three days, and only minimum grade encephalopathy persisted in the other patients. When patients who had improved were given lactulose again, and vancomycin was not use, their condition worsened. The medical improvement correlated with a decrease in blood ammonia levels and colonic anaerobic bacteria. The study suggests that the colonic bacteria may be responsible for a large part of the ammonia levels found in encephalopathy. Other mechanisms may also be important in the disorder as well. Further study is needed to determine why vancomycin is so effective in treating lactulose-resistant CHE. (Consumer Summary produced by Reliance Medical Information, Inc.)

Introduction: HTLV-1 (human T-cell lymphotropic virus type 1) is a retrovirus that infects approximately 20 million people worldwide. Many diseases are caused by this virus, including HTLV-1-associated myelopathy, adult T-cell leukemia, and HTLV-1 uveitis. Intraocular anti-vascular endothelial growth factor (VEGF) antibody injection has been widely used in ophthalmology, and it is reportedly effective against age-related macular degeneration, complications of diabetic retinopathy, and retinal vein occlusions. HTLV-1 mimics VEGF 165 , the predominant isoform of VEGF, to recruit neuropilin-1 and heparan sulfate proteoglycans. VEGF 165 is also a selective competitor of HTLV-1 entry. Here, we investigated the effects of an anti-VEGF antibody on ocular status under conditions of HTLV-1 infection in vitro ., Methods: We used MT2 and TL-Om1 cells as HTLV-1-infected cells and Jurkat cells as controls. Primary human retinal pigment epithelial cells (HRPEpiCs) and ARPE19 HRPEpiCs were used as ocular cells; MT2/TL-Om1/Jurkat cells and HRPEpiCs/ARPE19 cells were co-cultured to simulate the intraocular environment of HTLV-1-infected patients. Aflibercept was administered as an anti-VEGF antibody. To avoid possible T-cell adhesion, we lethally irradiated MT2/TL-Om1/Jurkat cells prior to the experiments., Results: Anti-VEGF antibody treatment had no effect on activated NF-κB production, inflammatory cytokines, chemokines, HTLV-1 proviral load (PVL), or cell counts in the retinal pigment epithelium (RPE) under MT2 co-culture conditions. Under TL-Om1 co-culture conditions, anti-VEGF antibody treatment did not affect the production of activated NF-κB, chemokines, PVL, or cell counts, but production of the inflammatory cytokine IL-6 was increased. In addition, anti-VEGF treatment did not affect PVL in HTLV-1-infected T cells., Conclusion: This preliminary in vitro assessment indicates that intraocular anti-VEGF antibody treatment for HTLV-1 infection does not exacerbate HTLV-1-related inflammation and thus may be safe for use., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer MM declared a shared affiliation with the authors to the handling editor at the time of review., (Copyright © 2023 Zong, Kamoi, Kurozumi-Karube, Zhang, Yang and Ohno-Matsui.)

Human T-cell lymphotropic virus type 1 (HTLV-1) was the first retrovirus identified as the causative agent of human diseases, such as adult T-cell leukemia, HTLV-1-associated myelopathy, and HTLV-1 uveitis (HU). HU is one of the most frequent ocular inflammatory diseases in endemic areas, which has raised considerable public health concerns. Approximately 30% of HU patients develop secondary glaucoma, which is higher than the general uveitis incidence. We therefore investigated the mechanism underlying the high incidence of glaucoma secondary to HU in vitro. After contact with HTLV-1-producing T cells (MT-2), human trabecular meshwork cells (HTMCs) were infected. The infected cells increased in number, and nuclear factor (NF)-κB expression was activated. Contact between MT-2 cells and HTMCs resulted in significantly upregulated production of inflammatory cytokines, such as IL-6, and chemokines, such as CXCL10, CCL2, and CXCL-8. These findings indicate that the mechanism underlying secondary glaucoma in HU may involve proliferation of trabecular meshwork tissue after contact with HTLV-1-infected cells, resulting in decreased aqueous humor outflow. Upregulated production of inflammatory cytokines and chemokines simultaneously disrupts the normal trabecular meshwork function. This mechanism presumably leads to increased intraocular pressure, eventually resulting in secondary glaucoma., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Zong, Kamoi, Ando, Kurozumi-Karube and Ohno-Matsui.)

HTLV-1 uveitis (HU) is the third clinical entity to be designated as an HTLV-1-associated disease. Although HU is considered to be the second-most frequent HTLV-1-associated disease in Japan, information on HU is limited compared to that on adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy (HAM). Recent studies have addressed several long-standing uncertainties about HU. HTLV-1-related diseases are known to be caused mainly through vertical transmission (mother-to-child transmission), but emerging HTLV-1 infection by horizontal transmission (such as sexual transmission) has become a major problem in metropolitan areas, such as Tokyo, Japan. Investigation in Tokyo showed that horizontal transmission of HTLV-1 was responsible for HU with severe and persistent ocular inflammation. The development of ATL and HAM is known to be related to a high provirus load and hence involves a long latency period. On the other hand, factors contributing to the development of HU are poorly understood. Recent investigations revealed that severe HU occurs against a background of Graves' disease despite a low provirus load and short latency period. This review highlights the recent knowledge on HU and provides an update on the topic of HU in consideration of a recent nationwide survey.

Adalimumab (ADA), a fully human monoclonal tumor necrosis factor (TNF)-α antibody, is one of the most widely used biologics in the treatment of inflammatory diseases. However, ADA can exacerbate infectious conditions, induce paradoxical reactions such as inflammation, and cause neoplasia. Human T-cell leukemia virus type 1 (HTLV-1) is an infectious agent that induces inflammation and neoplastic infiltration in the eye. To date, numerous HTLV-1 carriers have been treated with adalimumab to suppress inflammation out of necessity, when standard anti-inflammatory drugs such as steroids and immunosuppressive agents have proven inadequate to control the inflammation. Here, we clarify the safety of adalimumab for the eye under HTLV-1 infectious conditions in vitro . We used the adult retinal pigment epithelial cell line (ARPE)-19 cell line as ocular resident cells, and used MT2 and TL-Om1 as HTLV-1-infected cells. ARPE-19 and MT2/TL-Om1 were co-cultured, and then adalimumab was administered. Production of cytokines and chemokines, TNF-α receptor (TNF-R), HTLV-1 proviral load (PVL), and apoptosis were measured to assess the effects of adalimumab. Contact between ARPE-19 and MT2/TL-Om1 produced inflammatory cytokines such as TNF, interleukin (IL)-6, IL-8 and IL-10, and transduced chemokines such as interferon-inducible protein-10 (IP-10), monocyte chemotactic protein-1 (MCP-1), monokine induced by interferon-γ (MIG), and regulated on activation, normal T cell expressed and secreted (RANTES). No inflammatory cytokines and chemokines were exacerbated by adalimumab. Expression of TNF-R on ARPE-19 and MT2/TL-Om1 cells, HTLV-1 PVLs of MT2/TL-Om1 cells, and cell growth rate and apoptotic rate of ARPE-19 were unaffected by adalimumab. In conclusion, adalimumab does not appear to exacerbate HTLV-1-associated inflammatory conditions in the eye or increase PVL in HTLV-1-infected T cells. These data suggest that adalimumab could be used safely for the eye under HTLV-1 infectious conditions from the perspective of in vitro assessment., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2020 Kurozumi-Karube, Kamoi, Ando, Uchida, Hamaguchi and Ohno-Matsui.)

Infliximab (IFX) was the first biologic introduced for refractory uveitis treatment in Behçet's syndrome (BS). However, there have been few reports on the safety and efficacy of IFX monotherapy over follow-up periods of more than 10 years. This retrospective study evaluated the 10-year safety and efficacy of IFX monotherapy compared to IFX combination therapies with colchicine or corticosteroid for refractory uveitis in BS patients. Monotherapy was performed in 30 eyes of 16 patients while combination therapies were performed in 20 eyes of 11 patients. Continuation of IFX occurred in 70.3% of enrolled patients for 10 years without any significant difference noted in the retention rate between the monotherapy and combination therapies (p = 0.86). Reduction of ocular inflammatory attacks and improvement of best corrected visual acuity occurred in the monotherapy group after 10 years, which was equivalent to that for the combination therapies. Although adverse events (AEs) or therapy discontinuation occurred during the initial 5 years in both therapies, no AEs were observed for either therapy after 6 years. Our results suggested that IFX monotherapy proved to be effective and not inferior to combination therapies over a 10-year follow-up. Although loss of response and AEs may be noticed during the initial 5-year period, a safe and effective continuation can be expected thereafter.

Rationale: Proliferation of retinal pigment epithelium (RPE) is typically observed in limited ocular disorders, in connection with the local mechanism of RPE proliferation-mediated wound repair. Bilateral and diffuse type RPE proliferation is considered to be associated with paraneoplastic syndromes, such as a bilateral diffuse uveal melanocytic proliferation. However, other reported diseases that induce bilateral diffuse RPE proliferation are quite rare, especially for patients who are considered to have a non-malignant status., Patient Concerns: The bilateral eyes of a 47-year-old woman with bilateral ocular inflammation, presented united multiple small to medium white retinal lesions during the disease progress., Diagnoses: Optical coherence tomography showed scattered serous retinal detachments, choroidal folds, choroidal thickening and diffuse RPE proliferation. As autofluorescence and angiography showed a "giraffe pattern", bilateral diffuse uveal melanocytic proliferation was suspected. However, systemic investigations identified no malignancy. In consideration of the above findings, choroidal inflammation was thought to be the major cause of this condition., Interventions: The patient was administered intensive systemic steroids. Over the next 2 months, the amount of steroid was tapered off., Outcomes: After administration, the bilateral diffuse RPE proliferation settled down. During the 2-year follow-up, there was no recurrence of ocular inflammation and diffuse RPE proliferation, or any other malignancy found., Lessons: This finding demonstrates that bilateral diffuse RPE proliferation can be generated as a secondary phenomenon of choroidal inflammation in patients with a non-malignant status.

Use of biologics has been widely advocated for inflammatory diseases recently. Anti-tumor necrosis factor (TNF)-α antibody therapy is reportedly effective against ocular inflammation. However, side effects of TNF-α inhibition have been reported, particularly in the form of exacerbation of infections such as tuberculosis. Paradoxical reactions such as exacerbated inflammation are also well known. Around 20 million humans are infected with human T-cell leukemia virus type 1 (HTLV-1) globally, and this virus can cause adult T-cell leukemia, HTLV-1-associated myelopathy and HTLV-1 uveitis. As for ophthalmic concerns, it has not been identified whether anti-TNF-α antibody stimulates HTLV-1-infected cells and ocular cells to induce HTLV-1 uveitis in HTLV-1 carriers. Here we investigated the effects of anti-TNF-α antibody on ocular status under HTLV-1 infectious conditions using ocular cells and HTLV-1-infected cells in vitro . We used the ARPE-19 human retinal pigment epithelial cell line as ocular cells considered to play an important role in the blood-ocular barrier, and the MT2 HTLV-1-infected cell line. Jurkat cells were used as controls. Infliximab (IFX) was used as an anti-TNF-α antibody to achieve TNF-α inhibition. We evaluated the production of inflammatory cytokines and intercellular adhesion molecule (ICAM)-1, proliferation of ARPE-19, expression of TNF-α receptor (TNF-R) and HTLV-1 proviral DNA, and the percentage of apoptotic ARPE-19. Inflammatory cytokines such as interleukin (IL)-6, IL-8, TNF, and ICAM-1 were significantly elevated through contact between ARPE-19 and MT2. Treatment with IFX tented to inhibit TNF production, although the level of production was low, but changes in IL-6, IL-8, and ICAM-1 remained unaffected. Expression of TNFR was unaltered by IFX treatment. HTLV-1 proviral DNA was not significantly changed with treatment. No change in cell growth rate or apoptotic rate of ARPE-19 was seen with the addition of IFX. In conclusion, IFX did not exacerbate production of inflammatory cytokines, and did not affect expression of TNFR, proliferation of ARPE-19, HTLV-1 proviral load, or apoptosis of ARPE-19. These results suggest that IFX does not exacerbate HTLV-1-related inflammation in the eye and represents an acceptable treatment option under HTLV-1 infectious conditions., (Copyright © 2019 Uchida, Kamoi, Ando, Wei, Karube and Ohno-Matsui.)

A new species of the genus Ochthebius , O. (O.) sasakii sp. nov. , is described from the Ogasawara Islands, Japan, with a description of the larva. This record is the first of the family Hydraenidae from the Ogasawara Islands. This species belongs to the punctatus species group and is similar to two Japanese species, O. (O.) inermis Sharp, 1884 and O. (O.) danjo Nakane, 1990, but it differs from them in both adult and larval characters. The larva of O. (O.) inermis is also described for comparison.

Background: Carcinoma of unknown primary site (CUP) is said to account for approximately 3 to 5% of all carcinomas. However, an isolated lesion in the abdominal cavity is rare, and there are no reports describing associated abscess formation., Case Presentation: A 76-year-old woman had consulted a previous physician complaining of fever and right lower quadrant abdominal pain. Enhanced computed tomography (CT) showed an abscess formation around the cecum. She was treated conservatively with antibiotics, but the symptoms relapsed and she consulted our hospital. Enhanced CT showed a persistent abscess, a tumorous lesion in the mesentery and right hydronephrosis. Because malignancy could not be ruled out, surgical treatment was selected. At laparotomy, encapsulated abscesses were found on the mesenteric side and outside of the ileocecal region. When we raised the ileocecal region, a tumor was found to be fixed to the right ureter, and there was leakage of white, solid tumor content. This tumor content was submitted to intraoperative frozen section diagnosis which revealed a carcinoma. Ileocecal resection with D3 lymph node dissection and retroperitoneal tumor resection was thus performed. There were no abnormal findings in the uterus and adnexa, nor any evidence of peritoneal dissemination. We regarded this case as an incomplete resection and chemotherapy with paclitaxel and carboplatin was administered. The patient has remained alive and disease-free for almost one year since the primary operation., Conclusion: We described a case with mesenteric CUP discovered during surgery for an intra-abdominal abscess. It is necessary to pay attention to treatment-resistant intraperitoneal abscesses as they may accompany a tumor.

Exposure of alpha-synuclein (alphaS), a major component of Lewy bodies in Parkinson's disease, to polyunsaturated fatty acids (PUFAs) triggers the formation of soluble alphaS oligomers. Here, we demonstrate that PUFA binds recombinant alphaS protein through its N-terminal region (residues 2-60). In HEK293 cells, alphaS mutants lacking the N-terminal region failed to form oligomers in the presence of PUFA. The PUFA-induced alphaS oligomerization was accelerated by C-terminal truncation or Ser129 phosphorylation of alphaS; however, this effect was abolished by deletion of the N-terminus. The results indicate that the N-terminus of alphaS is essential for the PUFA-induced alphaS oligomerization.

Sporadic Parkinson's disease (sPD) is a common neurodegenerative disorder, characterized by selective degeneration of dopaminergic neurons in the substantia nigra. Although the pathogenesis of the disease remains undetermined, phosphorylation of alpha-synuclein and its oligomer formation seem to play a key role. However, the protein kinase(s) involved in the phosphorylation in the pathogenesis of sPD has not been identified. Here, we found that G-protein-coupled receptor kinase 5 (GRK5) accumulated in Lewy bodies and colocalized with alpha-synuclein in the pathological structures of the brains of sPD patients. In cotransfected cells, GRK5 phosphorylated Ser-129 of alpha-synuclein at the plasma membrane and induced translocation of phosphorylated alpha-synuclein to the perikaryal area. GRK5-catalyzed phosphorylation also promoted the formation of soluble oligomers and aggregates of alpha-synuclein. Genetic association study revealed haplotypic association of the GRK5 gene with susceptibility to sPD. The haplotype contained two functional single-nucleotide polymorphisms, m22.1 and m24, in introns of the GRK5 gene, which bound to YY1 (Yin Yang-1) and CREB-1 (cAMP response element-binding protein 1), respectively, and increased transcriptional activity of the reporter gene. The results suggest that phosphorylation of alpha-synuclein by GRK5 plays a crucial role in the pathogenesis of sPD.

Gallium arsenide (GaAs), a chemical compound of gallium and arsenic, causes various toxic effects including pulmonary diseases in animals. Since the toxicity is not completely investigated, GaAs has been used in workplaces as the material of various semiconductor products. The present study was conducted to clarify the toxicity of GaAs particles in the alveolar macrophages of hamsters using magnetometry, enzyme release assays and morphological examinations. Alveolar macrophages obtained from hamsters by tracheobronchial lavage and adhered to the disks in the bottom of wells were exposed to ferrosoferric oxide and GaAs particles. Ferrosoferric oxide particles were magnetized externally and the remanent magnetic field was measured. Relaxation, a fast decline of the remanent magnetic fields radiated from the alveolar macrophages, was delayed and decay constants were decreased dose-dependently due to exposure to GaAs. Because the relaxation is thought to be associated with cytoskeleton, the exposure of GaAs may have impaired the motor function of them. Enzyme release assay and morphological findings indicated the damage to the macrophages. Thus the cytotoxicity causes cytostructural changes and cell death. According to DNA electrophoresis and the TUNEL method, necrotic changes occur more frequently than apoptotic changes.

Dogs were exposed to 1% (v/v) (10,000 ppm) vapor of 1,1,1-Trichloroethane (1,1,1-TCE) by inhalation for 3 min repeated four times at 4 hr intervals under continuous anesthesia. Changes in the 1,1,1-TCE concentration in blood with time, as well as distribution of 1,1,1-TCE in the organs and tissues (lungs, liver, kidneys, heart, brain, and fat around the kidneys and on the abdominal wall) upon completion of the four exposures were studied. Concentrations of 1,1,1-TCE in blood showed the highest level immediately after exposure, and fairly decreased in about 30 min after exposure. The half life of 1,1,1-TCE in blood was 4-12 min after exposure. Upon completion of the exposures (3 min inhalations repeated four times), 1,1,1-TCE concentrations per gram wet weight of each organ ranged from 0.1 to 0.5 microgram/g in the lungs, liver, kidneys, heart and brain. On the other hand, the 1,1,1-TCE concentration in fat ranged from 16.9 to 54.6 micrograms/g, greatly exceeding those in other organs.

Regarding colophony, the use in industries, adverse effects, diagnosis, pathophysiology and control are reviewed. Colophony is an unhomogeneous mixture of resin acids as like abietic acid and neutral substances. Colophony is used everywhere, in industry, daily life and medical supplies. Soldering workers are exposed to the colophony fumes heated up to the temperature of soldering irons. The effects of exposure to colophony are classified into bronchial asthma and contact dermatitis. Colophony fumes cause bronchial asthma by its nonspecific irritation. Inhalation challenge test and repeated spirometry during working day may help the diagnosis of colophony induced asthma. Improvement of working environment for soldering and development of new flux instead of colophony will be necessary. A study on contact dermatitis revealed that colophony and its related compounds are one of major causes for contact dermatitis. Cases of dermatitis by depilatory agents used to remove hair from slaughtered swine, anti-slipping cream for ballet shoes or resin for cello strings have been reported. Patch test may contribute to the diagnosis of dermatitis caused by colophony.

Objective: To evaluate the effectiveness of IVF treatment in endometriosis-associated infertility., Design: Nonrandom retrospective study., Setting: Department of Gynecology and Obstetrics, Akita University School of Medicine., Main Outcome Measure(s): Cumulative pregnancy rate., Patient(s): One hundred eighteen infertile patients in whom diagnosis of endometriosis was established by laparoscopic examination., Intervention(s): The prognoses of 60 patients (IVF group) who started IVF treatment within 6 months after laparoscopy were compared with those of 58 patients who were managed expectantly without IVF treatment during the same period., Result(s): The cumulative conception rates at 36 months after laparoscopy were 62% in the IVF group and 43% in the control group, and the difference was not significant (a log-rank test). For patients > or = 32 years of age, the conception rates were significantly higher in the IVF group (59% versus 29%). A relatively large but nonsignificant difference in the conception rate between the two groups was observed in patients with endometriosis at stages III or IV (52% versus 27%)., Conclusion(s): In vitro fertilization treatment provides better prognosis in patients > or = 32 years of age and is recommended for such patients. The benefits of treatment appear to be greater in patients with more advanced stages of endometriosis.

Objective: To elucidate characteristic changes of plasma hemostatic markers in ovarian hyperstimulation syndrome (OHSS) cycles., Design: Prospective study., Setting: The IVF-ET program of the Department of Obstetrics and Gynecology, The University of Akita, School of Medicine., Patients: Forty cycles of 40 IVF patients, including 12 cycles in which a severe form of OHSS occurred., Interventions: Blood samples were taken during IVF treatment to determine the levels of blood markers that reflect activation of the coagulation and fibrinolytic systems., Main Outcome Measures: Thrombin-antithrombin III complexes, plasmin-alpha 2 antiplasmin complexes, and other hemostatic markers related to the coagulation and fibrinolytic system activation., Results: In the OHSS cycles, the levels of thrombin-antithrombin III and plasmin-alpha 2 antiplasmin complexes in the plasma began to rise within a few days after hCG administration and demonstrated significantly higher levels during the midluteal phase. In OHSS cycles with pregnancy, elevation of these markers continued for > or = 3 weeks after the onset of disease. There were some characteristic changes in OHSS cycles in other hemostatic markers, such as a decrease in the levels of antithrombin III and prekallikrein and shortened activated partial thromboplastin time., Conclusion: These data demonstrate the status of the coagulation and fibrinolytic systems in OHSS cycles and provide insight into the mechanism of activation in the hemostatic system.

Objective: To investigate whether a patient with ovarian hyperstimulation syndrome (OHSS) demonstrated characteristic changes in the blood hemostatic markers before she developed thromboembolism., Design: Patients with OHSS had blood drawn to determine hemostatic markers and related factors., Patients: Twenty-three OHSS patients, including a case complicated with thromboembolism., Setting: The IVF-ET program of the Department of Obstetrics and Gynecology, The University of Akita, School of Medicine., Main Outcome Measures: Blood hemostatic markers and related factors., Results: The patient with thromboembolism demonstrated marked leukocytosis and higher levels of activation in the blood markers related to fibrinolytic system, such as alpha 2 plasmin inhibitor, plasmin-alpha 2 antiplasmin complexes, and D-dimers, before the onset of this episode., Conclusion: Marked leukocytosis and higher levels of activation of the fibrinolytic system may be the signs of imminent thromboembolism in OHSS patients.

Intratracheal instillation of GaAs suspension has been histopathologically shown to induce a diffuse pulmonary response. In the present study, magnetometry was used to evaluate the effects of intratracheally instilled GaAs on the behavior of externally magnetized iron particles instilled in rabbit lung. Magnetometric evaluation of the effects of GaAs in rabbits dosed with 30 mg or 300 mg/animal showed significant decreased relaxation of iron particles at 1, 3, 7, 14, 21 and 28 days following instillation compared with the controls. Relaxation indicates a rapid decrease of remanent magnetic field following magnetization of the lungs due to random rotation of phagocytized iron particles in macrophages. Clearance of the iron particles was measured by serial determinations of the remanent magnetic field at the end of magnetization estimated from relaxation curves. Clearance was significantly impaired in rabbits exposed to both doses of GaAs at 14, 21 and 28 days after instillation. Dose-effect relationships were observed in both cases. Histological examination of lungs instilled with these doses indicated active phagocytosis of GaAs and iron particles by alveolar macrophages.