A layered microchip conductance detector with through-layer access to detection fields and high sensitivity to dielectric constant.

The present study explores a novel apertured microchip conductance detector (AMCD) that is sensitive to dielectric constant. Fashioned on silicon oxide/silicon using optical microlithography, the detector has novel parallel-plate geometry with a top mesh electrode, a middle apertured insulator, and a bottom conducting electrode. This monolithic apertured architecture is planar and may be provided with a thin insulator layer enabling large capacitances, while the top mesh electrode and middle apertured-insulator enable access to regions of the capacitor where electric fields are strong. Hence, the detector is sensitive yet mechanically robust. To test its response, the AMCD was immersed in various solvents, namely water, methanol, acetonitrile, and hexanes. Its response was found to vary in proportion to the solvents' respective dielectric constants. The AMCD was also able to distinguish quantitatively the presence of various molecules in solution, including molecules with chromophores [such as acetylsalicylic acid (ASA)] in methanol and those without chrompohores [such as polyethylene glycol 200 Daltons (PEG200)] in methanol or water. The universal nature of dielectric constant and the microchip detector's sensitivity point to a wide range of potential applications.

[Usefulness of arousals for the detection of sleep breathing disorder].

Because of the difference of sensitivity among measurement techniques, upper airway obstruction events cannot always be scored as apnea or hypopnea. We hypothesized that arousal accompanied with breathing disturbance is a more sensitive index for the diagnosis of sleep breathing disorders than others. We studied 75 patients with sleep breathing disorder by polysomnograph. Breathing disturbance related arousal (B-Ar) was defined as an arousal accompanied with at least one of the following (apnea, hypopnea, more than 4% oxygen desaturation, snoring), and the breathing disturbance indices were compared. There were close relationships between B-ArI and apnea hypopnea index (AHI), oxygen desaturation index (DI), and percent of total sleep time with SpO2 below 90% in all patients (r = 0.93, r = 0.58, r = 0.92, respectively, all p < 0.001). In 25 patients whose AHI was below 20 per hour, no relationship between B-ArI and AHI was found, and B-ArI was significantly greater than AHI. Thus, B-ArI seemed to be more sensitive than AHI. In all 6 patients whose AHI was below 10, B-ArI was lowered decreased by continuous nasal positive airway pressure therapy. These results suggest that B-ArI may be more sensitive in the detection of sleep breathing disorders than the other indices when AHI is below 20 per hour.

Myocardial uptake of iodine-125-labeled 15-(p-iodophenyl)-3-(R,S)-methyl pentadecanoic acid is decreased in chronic diabetic rats with changes in subcellular distribution.

Iodine-123-labeled 15-(p-iodophenyl)-3-(R,S)-methyl pentadecanoic acid (123I-BMIPP) is widely used to detect myocardial metabolic changes, but the preferred energy substrates in the myocardium would be expected to be altered in the presence of metabolic disorders such as diabetes mellitus (DM). We investigated the metabolism of branched-chain fatty acids in the myocardium of rats with DM. Streptozotocin-induced DM rats were examined 48 h (acute; AD) and 6 weeks (chronic; CD) after injection of streptozotocin. Hearts were excised 15 min or 60 min after injection of 0.185 MBq of 125I-BMIPP, followed by homogenization in an EDTA-Tris buffer. The homogenates were subjected to differential centrifugation to obtain the mitochondrial (MF) and cytoplasmic (CF) fractions. Myocardial 125I uptake tended to increase in the AD group, but the change was not significant. Myocardial 125I uptake at 15 min was significantly lower in the CD group than in the control group, even in the insulin-treated rats [control (CC), 4.4+/-0.4; not treated (CDN), 3.3+/-0.5; insulin-treated (CDI), 3.4+/-0.4 x 10(4) cpm/g, p<0.05 in each case]. The 125I count value corrected for the blood count (counts/min (cpm) per g of protein divided by blood cpm) in the MF decreased by 40% at 60 min in the CC group, but increased by 60% in the CDN group. The results of the present study suggest that the myocardial uptake of branched-chain fatty acids is decreased in rats with chronic diabetes, probably as a result of mitochondrial dysfunction.

Usefulness of arousal for the diagnosis of sleep breathing disorder.

We hypothesize that breathing disorder related arousal index (B-ArI) can differentiate sleep breathing disorder from simple snorer when apnea hypopnea index (AHI) is low. We studied 54 patients using polysomnography. Breathing disorder related arousal (B-Ar) was defined as arousal accompanied by apnea, hypopnea, desaturation or snort. Mean AHI was 44.2+/-34.0/h, and B-ArI correlated significantly with AHI, desaturation index, percentage total sleep time with SpO2 below 90%. Breathing disorder related arousal index was greater than AHI when AHI was below 20. In 11/54 patients, AHI was below 10, and B-ArI more than 10. Nasal continuous positive airway pressure was applied to six patients and showed reduced B-ArI. Breathing disorder related arousal index may be one of the useful indices for the diagnosis of sleep breathing disorder when AHI is less than 10.

Low concentrations of adenosine receptor blocker decrease protection by hypoxic preconditioning in ischemic rat hearts.

UNLABELLED: A role for adenosine in ischemic preconditioning and hypoxic preconditioning (HP) has been established in several species but is controversial in rats, due in part to the inconsistency of the data from the different experimental design. Our objective was to investigate the role of adenosine in the protection of the ischemic myocardium by HP in rats. METHODS: perfused hearts isolated from Sprague-Dawley rats were exposed to 5 min of hypoxic perfusion before 25 min of global ischemia followed by 20 min of reperfusion. The effects of adenosine receptor antagonist, 8-(p-sulfophenyl)-theophylline (8SPT) on HP-based changes in left-ventricular function, energy metabolites, and release of creatine kinase and lactate dehydrogenase were determined. To minimise non-specific effects of 8SPT, low concentrations of agent (0.5 or 1.0 micro mol/l) were used. RESULTS: 8SPT alone had no deleterious effects on normoxically perfused hearts or on ischemic/reperfused hearts. HP improved the recovery of LV function and creatine phosphate, and reduced the release of enzymes during reperfusion. 8SPT (1.0 micromol/l) ameliorated the beneficial effect of HP on cardiac function, but did not reverse the reduction in release of enzymes by HP completely. CONCLUSION: results suggest that the protective effect of HP on myocardial contractile function may be mediated by receptor(s) that can be inhibited by low concentrations of antagonist but may not have a primary role in the reduction of cellular damage by HP in rats.

Effects of alpha 1-adrenoreceptor subtype blockade on ischemia-reperfusion injury.

To clarify the roles of subclasses of alpha 1-adrenoreceptors in ischemic-reperfused myocardium, we compared the effect of the nonselective alpha 1-blocker bunazosin with that of the alpha 1A-blocker WB4101 and the alpha 1B-blocker chlorethylclonidine (CEC) in isolated rat hearts. After 30 min of preperfusion, Langendorff-perfused hearts were subjected to 25 min of global ischemia followed by 30 min of reperfusion. Hearts were randomly divided into 4 groups, with one of the following substances being added to the perfusate: buffer alone (control), 10(-6) mol/L bunazosin, 10(-7) mol/L WB4101, or 10(-7) mol/L CEC. Bunazosin had a negative inotropic effect and preserved the postischemic ATP content, reduced the postischemic increase in intracellular Na+ content and then enhanced postreperfusion recovery of creatine phosphate. Bunazosin also reduced myocardial 45Ca2+ uptake during reperfusion (control 5.2 vs bunazosin 2.5 mumol/g dry weight of tissue (dwt), p < 0.01). However, the recovery of left ventricular developed pressure (DP) was not improved when bunazosin was added to the perfusate during reperfusion. WB4101 had neither a negative inotropic nor an energy-sparing effect, but it improved the recovery of DP (control 43% vs WB4101 56% of preischemic value, p < 0.05) with no reduction in myocardial 45Ca2+ uptake. CEC had a negative inotropic and energy-sparing effect and then reduced myocardial 45Ca2+ uptake (CEC 3.1 mumol/g dwt, p < 0.05), but it did not improve the recovery of DP. These results suggest that the preischemic administration of an alpha 1B-adrenoreceptor subtype blocker protected ischemic-reperfused myocardium via reduction of Ca2+ overload, whereas the selective blockade of the alpha 1A-adrenoreceptor subtype reduced myocardial damage via mechanism(s) other than Ca2+ metabolism.

Changes in ischemic tolerance and effects of ischemic preconditioning in middle-aged rat hearts.

BACKGROUND: Although both clinical and animal studies have shown that ischemic tolerance is reduced in the senescent myocardium, it has not been clarified when myocardium becomes more vulnerable to ischemia. Preconditioning protects the hearts of young adult animals of various species, but its effects are not identical in human studies. We investigated whether ischemic tolerance and the effect of preconditioning decreased in isolated hearts of middle-aged rats. METHODS AND RESULTS: The hearts of young adult rats (12 weeks old: group Y, n = 44) and middle-aged rats (50 weeks old: group M, n = 44) were subjected to global ischemia for 15, 20, or 25 minutes followed by reperfusion. Hearts were also subjected to preconditioning and then to 20 (group Y, n = 22) or 15 (group M, n = 22) minutes of ischemia followed by reperfusion. Left ventricular developed pressure (LVDP) was decreased by 40% to 60%, and the level of ATP was decreased by 60% to 70% in group M compared with group Y. Preconditioning increased LVDP (% LVDP, 40.5% to 72.4%) and levels of high-energy phosphates (ATP, 11.8 to 14.1; creatine phosphate, 17.0 to 23.1 mumol/g dry wt) and reduced left ventricular end-diastolic pressure (LVEDP, 32.8 to 10.3 mm Hg), creatine kinase release (257 to 132 U/g dry wt), and ryanodine-sensitive sarcoplasmic reticulum Ca2+ release after ischemia in group Y. Preconditioning exerted opposite effects in group M (% LVDP, 45.9% to 15.8%; LVEDP, 21.0 to 28.5 mm Hg; ATP, 14.1 to 8.5 mumol/g dry wt; and CK release, 176 to 332 U/g dry wt). Preconditioning was associated with increases in the incidence of reperfusion-induced ventricular fibrillation (0% to 62.5%) and the rate of sarcoplasmic reticulum Ca2+ release in group M. CONCLUSIONS: These results indicate that hearts became more vulnerable to ischemia with age and that the beneficial effects of preconditioning were reversed in middle-aged rat hearts.

[Clinical characteristics and cardiac events in elderly patients with apical hypertrophic cardiomyopathy].

Apical hypertrophic cardiomyopathy (apical HCM) has been believed to be a special type of hypertrophic cardiomyopathy. It usually occurs in middle-aged or elderly men and the prognosis is thought to be good. However, recent reports suggest that approximately 10% of middle-aged patients with apical HCM have cardiac events and poor outcomes. We studied electrocardiograms and echocardiograms, the occurrence of cardiac events, and clinical characteristics in elderly patients with apical HCM (13 men and 7 women, 61 to 95 years old, mean age 74 +/- 7). Three of 20 patients (15%) had cardiac events (sudden death, 1; heart failure, 1; chest pain, 1), 2 had cerebral infarction with atrial fibrillation, and 2 died of non-cardiac causes. There were no differences in age, sex, medication, complications, or in initial values of electrocardiographic or echocardiographic variables between patients who had and did not have cardiac events. However, left ventricular end-systolic dimension (LVEDs) and left atrial diameter at the time of the last evaluation were larger in patients who had cardiac events than in those who did not (26 vs. 34 mm, p = 0.019, 33 vs. 38 mm, p = 0.1325, respectively). These results suggest that the prognosis for patients with apical HCM is not necessarily good, and that enlargement of the LVEDs might be used to predict cardiac events in elderly patients with apical HCM.

Decrease in ischemic tolerance with aging in isolated perfused Fischer 344 rat hearts: relation to increases in intracellular Na+ after ischemia.

While the ischemic tolerance of the myocardium has been reported to decrease with senescence, it is not known when and how this occurs. Our objectives were to determine whether the tolerance to myocardial ischemia in rats decreased before the onset of senescence and whether an increase in myocardial ionic imbalance was associated with an enhanced myocardial injury with aging. Hearts were isolated from Fischer 344 rats categorized as young (12 weeks old), mature adult (24 weeks), middle-aged (50 weeks) or senescent (100 weeks). Hearts were perfused isovolumically by the Langendorff procedure and subjected to 25 min of global ischemia followed by 30 min of reperfusion. In the 50- and 100-week-old rats, the recovery of ventricular function and high-energy phosphate levels was lower and there was increased incidence of ventricular fibrillation after 25 min of global ischemia followed by reperfusion. The release of creatine kinase and lactate dehydrogenase during reperfusion was greater in the 50-and 100-week-old rats than in the 12- and 24-week-old rats, indicating the irreversible myocardial damage due to ischemia-reperfusion increased by middle-age. Intracellular levels of Na+ and K+ before ischemia were higher in the 50- or 100-week-old rats than in the 12-week-old rats. The increase in intracellular Na+ at end of ischemia was greater in the older (50-week-old, 215% of the pre-ischemic value; 100-week-old, 232% of the pre-ischemic value) than in the younger rats (12-week-old, 158% of the pre-ischemic value). Results indicated that the rat heart becomes more vulnerable to ischemia in middle-age. This decrease in ischemic tolerance may be caused by an acceleration of myocardial ionic imbalance with aging.

Protection of ischemic myocardium by inhibition of contracture in isolated rat heart.

Protection of the ischemic myocardium by pretreatment with a high dose of 2,3-butanedione monoxime (BDM) is attributed to the enhancement of glycolytic ATP production rather than to the inhibition of contracture during mild ischemia. Our objective was to investigate whether the inhibition of contracture would protect the arrested heart during prolonged ischemia. Isolated perfused rat hearts were subjected to 30 min of low-flow ischemia followed by reperfusion. Ischemic hearts were treated with BDM (5 mmol/l) after beating stopped. BDM ameliorated the increase in intraventricular pressure after ischemia without significant changes in ATP levels and with a decreased accumulation of lactate. BDM treatment accelerated the recovery of function and high-energy phosphates with reduced myocardial Ca2+ overload. The results of this study suggested that inhibition of contracture can protect the heart from ischemia-reperfusion injury.

[An application of semiquantitative analysis of pulmonary scintigram to pulmonary tuberculosis sequelae].

We performed ventilation-perfusion scintigraphy in 13 patients with pulmonary tuberculosis sequelae and 21 with chronic obstructive pulmonary disease. We used 99mTc-MAA for perfusion scintigram and 133Xe gas for ventilation scintigram. We added the radioactivities during the rebreathing phase of the ventilation scintigram to make a computerized image of the lung volume. Regions of interest (ROIs) were derived from radioactivities on each image. ROIs included each whole lung on lung volume (L) image and areas where radioactivity was greater than 70% of the highest radioactivity on perfusion (P70) image. We counted the area of ROIs on L and P70, and used the ratio of perfusion to lung volume (P70/L) as a parameter of pulmonary perfusion. P70/L in patients with pulmonary tuberculosis sequelae was significantly higher than that in those with COPD. This suggested that the area of high pulmonary perfusion is larger in the patients with pulmonary tuberculosis sequelae as compared with those with COPD.

[Clinical significance and mechanism of ST-segment changes during the post-exercise recovery period in male patients with coronary artery disease].

The treadmill exercise test (TET) is evaluated by exercise-induced ST-segment depression (delta ST). However, the depression sometimes only appears during the post-exercise period. Depression appearing only during the post-exercise period may be as useful as depression during exercise to predict coronary artery disease, but little is known about factors that may affect ST depression after exercise. The clinical significance and mechanism of post-exercise ST depression were investigated in patients with coronary artery disease. Target heart rate- or symptom-limited TET was performed in 531 male patients with definitive effort angina pectoris or myocardial infarction using the Bruce protocol. Patients were divided into four groups according to delta ST during exercise and 1-2 min after exercise; 1) no TET or post-exercise delta ST (Nn, n = 192), 2) only post-exercise delta ST (Np, n = 36), 3) only TET delta ST (Pn, n = 112), 4) both TET and post-exercise delta ST (Pp, n = 66). Patient profiles, parameters during TET, echocardiographic and coronary angiographic findings and outcome during the year after TET were compared between the Nn and Np or Pn and Pp groups. The percentage of patients treated with beta-blocker was higher in the Np than that in the Nn group (Nn: 45%, Np: 64%, p < 0.05) and systolic blood pressure declined at 1 min after exercise from peak exercise in the Nn, but not in the Np group (Nn: 175 --> 167 mmHg, p < 0.05; Np: 170 --> 170 mmHg, not significant). There was no difference in age, other parameters during TET, echocardiographic and coronary angiographic findings and outcome between the Nn and Np group. The incidence of right coronary artery stenosis and that of patients with multi-vessel disease were higher in the Pp than those in the Pn group (Pn: 41%, 58%, Pp: 65%, 73%, both p < 0.05). The occurrence of chest pain during exercise was higher in the Pp than the Pn group in spite of less delta ST at peak exercise. However, systolic blood pressure declined after exercise in the Pn group, but not in the Pp group (Pn: 164 --> 158 mmHg, p < 0.05; Pp: 166 --> 164 mmHg, not significant). These results confirmed that the clinical significance of post-exercise delta ST in patients without TET delta ST differs from that in patients with TET delta ST and suggests that post-exercise delta ST without delta ST during exercise may be associated with an abnormal response to imbalances in the cardiovascular sympathetic system in the post-exercise period rather than with myocardial ischemia.

Intra-arterial administration of the angiogenesis inhibitor TNP-470 blocks liver metastasis in a rabbit model.

We evaluated the best route of administration of TNP-470, an angiogenesis inhibitor, by comparing the anti-tumour effects and toxicity following injection via the hepatic artery, the portal vein, or the jugular vein in a rabbit model of liver metastases. Following the injections of 1 x 10(6) VX2 carcinoma cells into the portal vein of rabbits, 50 mg of TNP-470 was injected continuously into the hepatic artery, portal vein, or jugular vein for 7 days. The number of tumours on the surface of the liver was counted 14 days following the start of the infusion, and the serum glutamic-oxaloacetic transamine (GOT), glutamic-pyruvic transaminase (GPT) and total bilirubin concentrations were examined. In addition, a coloured silicon rubber was injected into the vessels of the liver to visualise the capillary networks around the tumours and assess the degree of suppression of angiogenesis by TNP-470. The mean number of tumours following intra-arterial injection (17.5 +/- 2.9) was significantly less than the control (237.0 +/- 34.0) (P < 0.05). The mean numbers of the tumours following intraportal (89.1 +/- 16.0) and intravenous (140.6 +/- 31.2) injection were both less than the controls (215.3 +/- 45.5, 284.8 +/- 55.4 respectively), but the differences were not significant. We conclude that intra-arterial injection of TNP-470 is the most effective method for preventing liver metastases in this model.

[123I-beta-methyl-iodophenyl-pentadecanoic acid myocardial scintigraphy in diabetic patients without overt ischemic heart disease].

Fatty acid metabolism in the myocardium is affected by metabolic disorders such as diabetes mellitus. We evaluated 123I-beta-methyl-iodophenyl-pentadecanoic acid (BMIPP) myocardial scintigraphy in 15 diabetes mellitus patients without overt coronary heart disease. Patients with overt coronary heart disease were excluded by careful history taking, resting electrocardiography, treadmill exercise testing, echocardiography and resting 201Tl scintigraphy. Patients with remarkably impaired left ventricular (LV) systolic function (%FS < 30%) were also excluded. BMIPP uptake scores as the ratio of heart/mediastinum (H/M) and liver/mediastinum (L/M) at 20 minutes after injection were analyzed and compared with clinical profile, serum parameters, and LV parameters obtained from echocardiography. Five of the 15 patients showed abnormal BMIPP images; two patients showed a decreased uptake in the inferior segments, while three showed a diffuse decrease in BMIPP uptake. Body mass index (BMI), fasting blood sugar (FBS), HbAlc, IRI, and LV end-diastolic diameter (LVEDD) were higher in these five patients with abnormal BMIPP findings (abnormal BMIPP group vs normal BMIPP group, BMI: 29 vs 23 kg/m2, p < 0.05; FBS: 178 vs 114 mg/dl, p < 0.01; HbAlc: 7.6 vs 6.2%, p < 0.01; IRI: 18.5 vs 9.5 microU/ml, p < 0.01; LVEDD: 52 vs 44 mm, p < 0.05). 123I-metaiodobenzyl-guanidine (MIBG) scintigraphy in the five patients with abnormal BMIPP uptake showed more severe defects than in the 10 patients with normal BMIPP imaging. BMIPP scintigraphy demonstrated a significant correlation between H/M and L/M by BMIPP (r = 0.74, p < 0.01). Furthermore, correlation between H/M by BMIPP scintigraphy and clinical parameters (BMI, systolic blood pressure, FBS, HbAlc, IRI) were found, suggesting that diabetes mellitus patients without over coronary heart disease show abnormal BMIPP imaging when their general glucose utility and 123I-MIBG uptake are severely impaired (progression of insulin resistance and sympathetic nerve involvement). BMIPP scintigraphy may be useful in investigating the pathogenesis and subclinical abnormality of diabetic heart.

[A case of complete response by intermittent intra-arterial injection of 5-fluorouracil and carboplatin for liver metastases due to pancreatic cancer].

A 53-year-old woman with multiple liver metastases after pancreato-duodenectomy for pancreas cancer was inserted with a catheter from the left subclavian artery to the proper hepatic artery and an access was placed under the thoracic skin. Using this system, she was injected with 500 mg of 5-fluorouracil and 50 mg of carboplatin once a week. After about 7 months, liver metastases disappeared on ultrasonography and computed tomography scan. The patient is still free from recurrence after about 2 years from the initial chemotherapy. This result suggested that intermittent intra-arterial infusion of 5-fluorouracil and carboplatin is effective for liver metastases of pancreatic cancer, after curative resection of a primary tumor.

Cranial fasciitis of childhood: a case report.

We present a case with cranial fasciitis in childhood and review the literature. A 7-year-old boy presented with hard mass on the scalp. He had sustained a bruise on the right temporal region about 2 years previously. Ultrasonic examination and CT scanning revealed the ossifying soft tissue mass in the right temporal scalp causing erosion and scalloping of the outer table of the skull. At surgery the lesion was firmly attached to the periosteum and the skull. The lesion was completely excised and the lytic bone curettaged. The tumor was composed of immature fibroblasts and diagnosed as cranial fasciitis in childhood. A brief review of the literature is included emphasizing the need to investigate further this completely benign lesion that is frequently confused with a malignant neoplasm.

[Superior mesenteric arterial infusion chemotherapy in patient with both peritoneal carcinomatosis and liver metastasis].

Experimental study of superior mesenteric arterial infusion chemotherapy was done to evaluate the effect of this therapy on metastatic liver tumor. This treatment has been tried clinically for ileus caused by peritoneal carcinomatosis with good result. Moreover, the infused drug is expected to reach the liver via portal route, just like intraportal administration. This study disclosed that superior mesenteric arterial infusion made for a sufficiently high 5-FU concentration of portal blood but the concentration in the metastatic liver tumor was lower when compared with intravenous infusion. However, because the 5-FU concentration in blood of the aorta was lower than in the intravenous administration group, our method may decrease the unfavorable side effects of anti-cancer drugs.

[A case of adenosquamous carcinoma with unknown origin and with superior vena cava syndrome as the first symptom].

This report is concerning a case of adenosquamous carcinoma having unknown origin and showing SVC syndrome as the first symptom. A 44 year-old man was admitted to our hospital because of facial edema at the beginning of April 1990. He was diagnosed as having a mediastinal tumor of the SVC syndrome type. Resection of the SVC tumor and part of the pericardium was performed on June 20, 1990. The operation had extraordinary findings. Lymph nodes adhering to tumor invaded the adjacent right side of the trachea and were situated in a rosette-like form. Furthermore, a part of the tumor stemmed into the lumen of the superior vena cava causing complete obstruction. The pathological diagnosis of the SVC tumor was adenosquamous carcinoma, however, no clinical examinations could identify its original matrix. Mediastinal tumors of unknown origin are reported as about 1% of all mediastinal tumors, and are responsible for 0.68% of all carcinomas in the mediastinum. This was one experience of a rare case of mediastinal tumor having unknown origin and showing SVC syndrome as the first symptom.

Conjugation in Tetrahymena: Ultrastructure of the meiotic prophase of the micronucleus.

The early conjugation process of Tetrahymena thermopbila was studied with particular attention to the fine structure of the "crescent" micronucleus. The stationary macro- and micronuclei are tied together by the fused outer nuclear membrane. Inside the micronucleus, thick chromatin threads form a dense network. The micronucleus becomes detached from the concavity of the macronucleus and swells and loosened chromatin threads form fine threads. Most threads are gathered together in the center to form a large chromatin body, but some threads remain partly dispersed along the periphery. The micronucleus is elongated by extended microtubules below the nuclear membrane. Chromatin threads that are anchored to structures considered to be precursors of kinetochores (PKI) are present in the area that is proximal to the joint region of a conjugant as well as to the inner nuclear membrane at the distal end. These extend together with the microtubules and become dispersed. The PKIs extend their own microtubles to the proximal end, pulling the chromatin threads back into the distal area. In the fully extended U-shaped micronucleus, PKI-microtubules have disappeared, and kinetochores (KI) are located in the vicinity of the inner nuclear membrane. The chromatin threads have become detached from the KI and have reassembled to form a dense network in the distal area.