Transient ischemic attack without self-awareness of symptoms witnessed by bystanders: analysis of the PROMISE-TIA registry.

BACKGROUND AND PURPOSE: A transient ischemic attack (TIA) can occur without self-awareness of symptoms. We aimed to investigate characteristics of patients with a tissue-based diagnosis of TIA but having no self-awareness of their symptoms and whose symptoms were witnessed by bystanders. METHODS: We used data from the multicenter registry of 1414 patients with a clinical diagnosis of TIA. For patients without evidence of ischemic lesions on imaging, clinical characteristics were compared between patients with and without self-awareness of their TIA symptoms. RESULTS: Among 896 patients (559 men, median age of 70 years), 59 (6.6%) were unaware of their TIA symptoms, but had those symptoms witnessed by bystanders. Patients without self-awareness of symptoms were older and more frequently female, and more likely to have previous history of stroke, premorbid disability, and atrial fibrillation, but less likely to have dyslipidemia than those with self-awareness. Patients without self-awareness of symptoms arrive at hospitals earlier than those with self-awareness (P < 0.001). ABCD2 score was higher in patients without self-awareness of symptoms than those with self-awareness (median 5 vs. 4, P = 0.002). Having no self-awareness of symptoms was a significant predictor of ischemic stroke within 1 year after adjustment for sex, ABCD2 score, and onset to arrival time (hazard ratio = 2.44, 95% confidential interval: 1.10-4.83), but was not significant after further adjustment for arterial stenosis or occlusion. CONCLUSIONS: Patients with a TIA but having no self-awareness of their symptoms might have higher risk of subsequent ischemic stroke rather than those with self-awareness, suggesting urgent management is needed even if patients have no self-awareness of symptoms.

Spin structure and spin Hall magnetoresistance of epitaxial thin films of the insulating non-collinear antiferromagnet SmFeO3.

We report a combined study of imaging the antiferromagnetic (AFM) spin structure and measuring the spin Hall magnetoresistance (SMR) in epitaxial thin films of the insulating non-collinear antiferromagnet SmFeO3. X-ray magnetic linear dichroism photoemission electron microscopy measurements reveal that the AFM spins of the SmFeO3(1 1 0) align in the plane of the film. Angularly dependent magnetoresistance measurements show that SmFeO3/Ta bilayers exhibit a positive SMR, in contrast to the negative SMR expected in previously studied collinear AFMs. The SMR amplitude increases linearly with increasing external magnetic field at higher magnetic fields, suggesting that field-induced canting of the AFM spins plays an important role. In contrast, around the coercive field, no detectable SMR signal is observed, indicating that the SMR of the AFM and canting magnetization components cancel out. Below 50 K, the SMR amplitude increases sizably by a factor of two as compared to room temperature, which likely correlates with the long-range ordering of the Sm ions. Our results show that the SMR is a sensitive technique for non-equilibrium spin systems of non-collinear AFMs.

Features of cardioembolic stroke with persistent and paroxysmal atrial fibrillation - a study with the Japan Stroke Registry.

BACKGROUND AND PURPOSE: The stroke severity on admission and clinical outcomes were compared between ischaemic stroke patients with non-valvular atrial fibrillation (NVAF) of the persistent (PeAF) and paroxysmal (PAF) types. METHODS: The study comprised 9293 patients with cardioembolic stroke and NVAF who were registered in the Japanese stroke databank: 6522 had PeAF (70.2%) and 2771 had PAF (29.8%). Stroke severity on admission and the clinical outcomes on discharge were retrospectively compared between these patient groups. RESULTS: The National Institutes of Health Stroke Scale score on admission (median, interquartile range) was 10 (3-20) for PeAF patients and 7 (2-17) for PAF patients, indicating that stroke severity on admission was significantly worse in PeAF patients than PAF patients (P < 0.001). Good outcomes (modified Rankin scale score ≤2) were achieved by 45% PeAF patients and 53% PAF patients. Thus, PeAF patients had significantly poorer clinical outcomes than PAF patients (P < 0.001). In-hospital mortality was significantly higher amongst PeAF patients (11%) than PAF patients (8%) (P < 0.001). Multivariate analysis of factors contributing to clinical outcomes showed that PeAF was a contributing factor for in-hospital mortality (odds ratio 1.261; 95% confidence interval 1.011-1.652; P = 0.045). CONCLUSIONS: Amongst cardioembolic stroke patients with NVAF, those with PeAF have significantly higher stroke severity on admission than those with PAF, and PeAF is a factor contributing to in-hospital mortality. Thus, our study suggests that the type of atrial fibrillation affects stroke severity and clinical outcomes following cerebral infarction.

Functional dissociation between Kana and Kanji: agraphia following a thalamic hemorrhage.

We report the case of a 61-year-old woman with a left thalamic hemorrhage causing agraphia of Kanji (morphograms). Single-photon emission computed tomography (SPECT) showed a decrease in the blood flow in the left thalamus from the superior temporal convolution to the parietal lobe, as well as in the frontal lobe while computed tomography showed no remarkable lesions in the cortex. The agraphia in this case may be due to the thalamic lesion itself, but the SPECT findings strongly suggest that a secondary cortical lesion may be involved in producing the higher cognitive disorder.

Usefulness of MRA-DWI mismatch in neuroendovascular therapy for acute cerebral infarction.

BACKGROUND: This study evaluated the usefulness of MR angiography (MRA)-diffusion-weighted imaging (DWI) mismatch in neuroendovascular therapy over 3 h after onset of acute cerebral infarction. METHODS: The subjects were 14 cases (age, 73 ± 8.4 years) who had an anterior circulation deficit on DWI/MRA on arrival and underwent neuroendovascular therapy over 3 h after onset. MRA-DWI mismatch (MDM) (+) was defined as 'major artery lesion (+) and diffusion-weighted image-Alberta Stroke Program Early CT Score (DWI-ASPECTS) ≥6'; MDM (-) was defined as 'major artery lesion (+) and DWI-ASPECTS <6'. RESULTS: Reperfusion was achieved in nine of 14 patients (64%) undergoing neuroendovascular therapy. Within the reperfusion group, in the five MDM (+) patients and the four MDM (-) patients, the outcome was a favorable clinical response in the MDM (+) group. The modified Rankin Scale (mRS) scores after 90 days were 0-2 in 3 (60%) and 3-6 in 2 (40%) of the MDM (+) group patients and 0-2 in 0 (0%) and 3-6 in 4 (100%) of the MDM (-) group patients. In the MDM (+) group, a good outcome was achieved. However, the number of cases was small, so this was not a significant difference. Within the non-reperfusion group, in the three MDM (+) patients and the two MDM (-) patients, the mRS scores after 90 days were 0-2 in 1 (33%) and 3-6 in 2 (67%) of the MDM (+) group patients and 0-2 in 0 (0%) and 3-6 in 2 (100%) of the MDM (-) group patients. In both groups, the outcome was poor. CONCLUSIONS: With neuroendovascular therapy, a good outcome with reperfusion was achieved in the MDM (+) group compared to the MDM (-) group. This suggests that the presence or absence of MDM may be useful in determining prognosis after reperfusion.

Functional outcome in patients with pontine infarction after acute rehabilitation.

We examined the clinical features of patients with pontine infarction in the acute stage and the factors affecting functional prognosis and outcome. Lesions, neurological manifestations at initial physical status examinations, cognitive function, swallowing function and outcome [activities of daily living (ADL), status of nutritional intake at discharge and destination after discharge] were evaluated in 68 patients (47 males and 21 females) who had pontine lesions with acute phase cerebral infarction. The mean length of stay was 24.4 days. The symptoms (number of patients) observed included paralysis (50), dysarthria (47), ataxia (18), diplopia (11), dysphagia (49) and poor cognitive performance (37). The types of lesions (number of patients) included lacunar infarcts in the ventral pontine area (15), lacunar infarcts in the dorsal pontine area (13) and large lacunar infarcts (LLIs) (41). After hospital discharge, 23 patients were discharged home, 44 were transferred to another hospital and 1 died. Twenty-three patients were on a regular diet, 22 were receiving a dysphagia diet and 22 were on enteral feeding at discharge. Patients with LLIs more frequently had poor cognitive performance, paralysis, dysphagia at discharge and a tendency for a longer length of stay compared with patients who had lacunar infarct. Most patients who returned home were those who were younger in age, had fewer neurological symptoms, had better cognitive function and ADL performance, and could ingest food. In an acute hospital, age, neurological symptoms, ADL, cognitive function, and dysphagia were considered important factors for determining the outcome in patients with pontine infarction.

Enhanced dechlorination of chlorobenzene and in situ dry sorption of resultant Cl-compounds by CaO and Na2CO3 sorbent beds incorporated with Fe2O3.

The dechlorination of C(6)H(5)Cl and the in situ dry sorption of Cl-compounds produced by C(6)H(5)Cl decomposition in an alkaline sorbent of CaO or Na(2)CO(3) incorporated with Fe(2)O(3) were studied. A sample gas containing C(6)H(5)Cl at an initial concentration of 500 ppm balanced by either N(2), O(2) (5%)-N(2) or H(2)O (10%)-N(2) carrier gas was introduced into a lab-scale quartz tube reactor where CaO or Na(2)CO(3) sorbent was packed with Fe(2)O(3). Subsequently, the effect of Fe(2)O(3) addition to CaO or Na(2)CO(3) on the removal of C(6)H(5)Cl, achieved by the decomposition of C(6)H(5)Cl as well as the dry sorption of Cl-compounds produced by C(6)H(5)Cl decomposition, was investigated. It was found that the decomposition of C(6)H(5)Cl in CaO or Na(2)CO(3) sorbent bed incorporated with Fe(2)O(3) occurred in the lower temperatures, compared to the case when only CaO or Na(2)CO(3) sorbent bed was used. Thus, Fe(2)O(3) was found to play a catalytic role in the oxidative decomposition of C(6)H(5)Cl. Further, the decomposition of C(6)H(5)Cl in a bed containing only Fe(2)O(3) was promoted by the presence of O(2) and H(2)O in the reaction atmosphere. Moreover, a higher amount of Cl was absorbed in the combined CaO/Fe(2)O(3) and Na(2)CO(3)/Fe(2)O(3) beds, compared to the absorption of Cl-compounds in only CaO or Na(2)CO(3) sorbent bed. Finally, the comparison of CaO and Na(2)CO(3) sorbents showed that the decomposition of C(6)H(5)Cl and the in situ dry sorption of the resultant Cl-compounds in the combined Na(2)CO(3) and Fe(2)O(3) beds were higher than those in the combined CaO and Fe(2)O(3) beds.

Astroglial swelling in the neuronal depolarization ensemble.

The coupling between neuronal depolarization and astroglial swelling was examined. First, previous in vitro data for the swelling of cultured neurons (N18; rat neuroblastoma) and astroglia (C6; rat astroglyoma) upon exposure to a hypoosmotic solution were reappraised. Neurons swelled rapidly, forming blisters, and easily burst. whereas astroglia resisted swelling and slowly assumed a large full-moon shape. The time constant of swelling was 35.2 +/- 7.8 s for N18 and 594.8 +/- 554.0 s for C6. The glial plasmic membrane was found to be much stronger than the neuronal one, presumably due to a well-developed cytoskeleton. To overcome such neuronal membranous weakness, strong astroglial processes need to cover the neurons including the cell body and synapses, as demonstrated electron-microscopically. Next, in situ astroglial swelling was investigated in rats. During K(+)-induced cortical spreading depression, increases or decreases of a wave-ring spread of light (550 nm) transmission through a 1 mm-thick cerebral cortical layer was observed. The moving local optical density decrease in the cortex was attributable to local vascular bed compression induced by astroglial swelling, since concomitant occurrence of colocated dynamic capillary flow stall was confirmed by a hemodilution technique. Astroglial swelling may occur in an ensemble acting during neuronal depolarization, suggesting that neurons and astroglia behave like a unit complex.

Notch3 gene polymorphism and ischaemic cerebrovascular disease.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a type of hereditary stroke and dementia. More than 90% of patients with CADASIL have mutations in the Notch3 gene. All mutations either create or destroy a cysteine residue in the epidermal growth factor-like repeats. In addition, five polymorphisms, which lead to amino acid substitutions, have been identified within the Notch3 coding sequence. However, whether these polymorphisms affect Notch signalling or are involved in cerebrovascular diseases is unknown. In the present study, we investigated a possible association between a T6746C polymorphism in the Notch3 coding region and the occurrence of symptomatic ischaemic cerebrovascular disease (CVD) was investigated. Two hundred and thirty five patients with CVD, as confirmed by brain CT or MRI, and 315 age and sex matched control subjects were analyzed for genotype frequencies of the T6746C polymorphism in Notch3. The genotype distributions were: patients with CVD, C/C 14.0%, C/T 45.5%, and T/T 40.4%; controls, C/C, 14.3%; C/T, 47.9%; T/T, 37.8%. The Japanese population has a higher C allele frequency of the T6746C polymorphism than European populations. There was no significant difference between the T6746C polymorphism in patients with CVD and controls (chi(2)=0.414, p=0.813). This was confirmed by the results of multiple logistic regression analysis including established risk factors (chi(2) =4.65, p=0.311). In conclusion, the results indicate that T6746C polymorphism in the intracellular domain of the Notch3 gene is not associated with an increased risk for CVD.

Immunoproteasome assembly and antigen presentation in mice lacking both PA28alpha and PA28beta.

Two members of the proteasome activator, PA28alpha and PA28beta, form a heteropolymer that binds to both ends of the 20S proteasome. Evidence in vitro indicates that this interferon-gamma (IFN-gamma)-inducible heteropolymer is involved in the processing of intracellular antigens, but its functions in vivo remain elusive. To investigate the role of PA28alpha/beta in vivo, we generated mice deficient in both PA28alpha and PA28beta genes. The ATP-dependent proteolytic activities were decreased in PA28alpha(-/-)/beta(-/-) cells, suggesting that 'hybrid proteasomes' are involved in protein degradation. Treatment of PA28alpha(-/-)/beta(-/-) cells with IFN-gamma resulted in sufficient induction of the 'immunoproteasome'. Moreover, splenocytes from PA28alpha(-/-)/beta(-/-) mice displayed no apparent defects in processing of ovalbumin. These results are in marked contrast to the previous finding that immunoproteasome assembly and immune responses were impaired in PA28beta(-/-) mice. PA28alpha(-/-)/beta(-/-) mice also showed apparently normal immune responses against infection with influenza A virus. However, they almost completely lost the ability to process a melanoma antigen TRP2-derived peptide. Hence, PA28alpha/beta is not a prerequisite for antigen presentation in general, but plays an essential role for the processing of certain antigens.

Role of platelet glycoprotein IIb/IIIa in ADP-activated platelet adhesion to aortic endothelial cells in vitro: observation with video-enhanced contrast microscopy.

Intravascular thrombus formation downstream of cerebral arterial occlusion may result in necrosis of ischemic tissue. To clarify the causative mechanisms, interaction between adenosine-5'-diphosphate (ADP)-activated platelets and cultured human aortic endothelial cells (HAEC) was examined by employing video enhanced contrast-differential interference contrast (VEC-DIC) microscopy. The numbers of (1) control/platelets, (2) ADP-activated platelets, (3) ADP-activated, anti-platelet GP Ibalpha antibody (GUR20-5)-treated platelets, and (4) ADP-activated, platelet GP IIb/IIa antagonist (TAK-029)-treated platelets, associated with HAEC after superfusion and wash-out were counted in visual fields of 30 x 30 microm2. Many ADP-activated platelets adhered to HAEC directly, while almost no platelets adhered to HAEC in the control. The adhesion was almost completely blocked by the GP IIb/IIIa antagonist, but not by GP Ibalpha antibody. We conclude that initial binding of ADP-activated platelets to HAEC is mediated by platelet GP IIb/IIIa in this in vitro system.

Adhesion of adenosine diphosphate-activated platelets to human brain microvascular endothelial cells under flow in vitro is mediated via GPIIb/IIIa.

Employing video-enhanced contrast (VEC) microscopy, we examined whether TAK-029 (GPIIb/IIIa antagonist) inhibits the adhesion of activated platelets to human brain microvascular endothelial cells (HBEC) in vitro. HBECs were cultured on a coverglass and put in the observation chamber of VEC microscopy. Then, activated platelets by adenosine diphosphate (ADP) (2 microM) were perfused over HBEC at a low shear rate of 10 s(-1) for 30 min and washed out. Platelets adhered directly to HBEC. However, platelet adhesion to HBEC was suppressed when platelet rich plasma with ADP (2 microM) plus TAK-029 (GPIIb/IIIa antagonist; 1 microM) was perfused over HBEC for 30 min and washed out. Anti-GPIbalpha antibody (GUR20-5) did not inhibit adhesion of ADP-activated platelets to HBEC. The above results showed adhesion of ADP-activated platelets to HBEC under flow in vitro is mediated via GPIIb/IIIa

The ATP-dependent CodWX (HslVU) protease in Bacillus subtilis is an N-terminal serine protease.

HslVU is a two-component ATP-dependent protease, consisting of HslV peptidase and HslU ATPase. CodW and CodX, encoded by the cod operon in Bacillus subtilis, display 52% identity in their amino acid sequences to HslV and HslU in Escherichia coli, respectively. Here we show that CodW and CodX can function together as a new type of two-component ATP-dependent protease. Remarkably, CodW uses its N-terminal serine hydroxyl group as the catalytic nucleophile, unlike HslV and certain beta-type subunits of the proteasomes, which have N-terminal threonine functioning as an active site residue. The ATP-dependent proteolytic activity of CodWX is strongly inhibited by serine protease inhibitors, unlike that of HslVU. Replacement of the N-terminal serine of CodW by alanine or even threonine completely abolishes the enzyme activity. These results indicate that CodWX in B.subtilis represents the first N-terminal serine protease among all known proteolytic enzymes.

Polymorphism in the promoter of lipopolysaccharide receptor CD14 and ischemic cerebrovascular disease.

BACKGROUND AND PURPOSE: A growing amount of evidence suggests that infectious and inflammatory processes may be involved in the initiation of arteriosclerosis, but the mechanisms are conceivably multifactorial and complex. Two European groups have recently demonstrated that a C(-260)-->T polymorphism in the promoter of the CD14 lipopolysaccharide receptor may be a risk factor for coronary artery disease (CAD). The T allele of this polymorphism reportedly increases the expression of CD14 and may be involved in atherogenesis. In the present study we investigated a possible association between the C(-260)-->T polymorphism in the CD14 promoter and the occurrence of symptomatic ischemic cerebrovascular disease (CVD). METHODS: Genotype frequencies of the C(-260)-->T polymorphism in the CD14 promoter were determined in 235 patients with CVD, as confirmed by brain CT and/or MRI, and 309 age- and sex-matched control subjects. RESULTS: The distribution of genotypes was as follows: CVD patients, T:/T: 24.3%, C:/T: 53.2%, and C:/C: 22. 6%; controls, T:/T: 26.9%, C:/T: 50.2%, and C:/C: 23.0%. There was no significant difference between the CD14 promoter genotypes of the CVD patients and the controls (chi(2)=0.601, P:=0.741). We also measured the concentration of serum soluble CD14 and the density of membranous CD14 on monocytes in the CVD patients, but the polymorphism was not associated with either the concentration of soluble CD14 or the density of membranous CD14 (P:=0.358, P:=0.238, respectively). CONCLUSIONS: Our results indicate that the C(-260)-->T polymorphism in the CD14 promoter is not associated with an increased risk for CVD.

Tissue distribution of constitutive proteasomes, immunoproteasomes, and PA28 in rats.

We investigated the expression of standard proteasomes, immunoproteasomes, and their regulators, PA28, and PA700, in rat tissues. Immunoproteasomes (with subunits LMP2, LMP7, and MECL1) were abundant in the spleen but almost absent in the brain. In contrast, standard proteasomes (with X, Y, and Z) were highly expressed in the brain but not in the spleen. Both proteasome types were present in the lung and the liver. PA700 subunits (p112, S5a, and p45) were found in all tissues. PA28alpha, PA28beta, and PA28gamma were also expressed in all tissues, except for the brain which contained very little PA28beta. The results did not depend on rat sex or age. The cleavage specificity for peptide substrates differed greatly between brain and spleen proteasomes. Hybrid proteasomes, containing both PA28alphabeta and PA700, were not present in the brain but in all other tissues examined.

A 35-year-old man with cerebral hemorrhage and pheochromocytoma: the second brain-dead organ donor in Japan.

A 35-year-old man was brought into the emergency room of Keio University Hospital by ambulance because of a sudden onset of coma. His Glasgow Coma Scale was 3 and his blood pressure 150/100 mmHg. CT scanning revealed a subcortical hemorrhage 8 cm in diameter. His respiration deteriorated rapidly, and an emergency craniotomy was performed for hematoma removal and cerebral decompression. Postoperatively the patient remained in a deep coma (GCS = 3) requiring respiratory support. The family presented an organ donor card previously signed by the patient, and brain death was confirmed in accordance with Japan's transplant law. As a result of two tests conducted six hours apart brain death was confirmed on the 5th postoperative day. With the family's consent, the donor's heart, kidneys and skin were removed for organ transplantation to be performed in other institutions. An autopsy was performed after the removal of the organs and skin. An extensive subgaleal hemorrhage was found in the left cerebral hemisphere, and microscopic examination revealed extensive necrosis with karyolysis of neuronal cells, but no viable neuronal cells were found in the cerebrum. The brain stem was marked by edema, hemorrhage, infarction necrosis and neuronal cell loss. The cerebellum was swollen and congested and showed autolysis of the granular layer. These findings suggested brain death syndrome with respirator brain. Other autopsy findings included a huge pheochromocytoma in the right adrenal gland, bilateral bronchopneumonia, liver congestion and fatty metamorphosis with four cavernous hemangiomas, and mild chronic lymphocytic thyroiditis. This patient was the second brain-dead organ donor and the first brain-dead patient to undergo postmortem examination in Japan.

A nonproteolytic function of the proteasome is required for the dissociation of Cdc2 and cyclin B at the end of M phase.

Inactivation of cyclin B-Cdc2 kinase at the exit from M phase depends on the specific proteolysis of the cyclin B subunit, whereas the Cdc2 subunit remains present at nearly constant levels throughout the cell cycle. It is unknown how Cdc2 escapes degradation when cyclin B is destroyed. In Xenopus egg extracts that reproduce the exit from M phase in vitro, we have found that dissociation of the cyclin B-Cdc2 complex occurred under conditions where cyclin B was tethered to the 26S proteasome but not yet degraded. The dephosphorylation of Thr 161 on Cdc2 was unlikely to be necessary for the dissociation of the two subunits. However, the dissociation was dependent on the presence of a functional destruction box in cyclin B. Cyclin B ubiquitination was also, by itself, not sufficient for separation of Cdc2 and cyclin B. The 26S proteasome, but not the 20S proteasome, was capable of dissociating the two subunits. These results indicate that the cyclin B and Cdc2 subunits are separated by the proteasome through a mechanism that precedes proteolysis of cyclin B and is independent of proteolysis. As a result, cyclin B levels decrease on exit from M phase but Cdc2 levels remain constant.

New optical method for analyzing cortical blood flow heterogeneity in small animals: validation of the method.

In pentobarbital-anesthetized male Sprague-Dawley rats, a small cranial window was trephined, and the cortex was transilluminated with a fine glass fiber inserted into the brain parenchyma. The light intensity at the surface area of 2 x 2 mm was recorded during intracarotid injection of 25 microl of carbon black (CB) solution. The region of interest (ROI) was divided into a 50 x 50 matrix, and the mean transit time of CB transport was calculated in each matrix element. We found rapid transits of CB along the microvasculature, with considerable heterogeneity in the avascular area, and heterogeneous efficiency in autoregulatory capacity in the ROI during hypotension. The method was validated by comparison with laser-Doppler flowmetry. The average mean difference was 0.03 +/- 0. 05%. Five percent CO(2) inhalation increased the flow by 85%, but heterogeneously. We concluded that the technique is exclusively sensitive to indicator transits in a very small area on the brain surface with potential usefulness in detecting regional heterogeneity in blood flow.

New crystal forms and low resolution structure analysis of 20S proteasomes from bovine liver.

20S proteasomes from higher eukaryotes have immunological functions rather than those from archibacteria or yeast. To clarify the mechanism of the sorting and production of antigen-presenting peptides, it is important and worthwhile to determine the structure of mammalian proteasomes using a third generation synchrotron radiation source. Here we report new crystal forms of 20S proteasomes from bovine liver and preliminary structure analysis of them. The crystals belong to the same space group but have different cell dimensions. One crystal (form I) belongs to space group P2(1)2(1)2(1) with unit cell dimensions of a = 124.8, b =197.4, c =323.8 A, and diffracts to 3.0 A resolution. The other crystal (form II) belongs to the same space group with a =115.1, b =205.6, c =316. 0 A, and diffracts to 4.0 A resolution. The diffraction data for the form I crystal provided an interpretable electron density map for presenting the structural differences from yeast proteasomes.