Tubo-ovarian abscess caused by Clostridioides difficile after eight months of surgery: Case report and review of extraintestinal abdominal abscess cases.

We present a case of tubo-ovarian abscess (TOA) caused by Clostridioides difficile (CD) in a 43-year-old female. Despite lacking a history of sexually transmitted diseases, the patient had undergone paraovarian cystectomy nine months before admission. Transvaginal ultrasonography performed eight months post-surgery revealed left ovarian enlargement, accompanied by subsequent lower abdominal pain and fever exceeding 38 °C. As oral antibiotic treatment was ineffective, the patient was admitted to our hospital. Computed tomography upon admission revealed a massive TOA. Surgical drainage of the abscess was performed, and CD was identified in the culture from the pus. The TOA was treated with a three-month course of metronidazole and oral amoxicillin/clavulanic acid. While CD is commonly associated with colitis, extraintestinal manifestations are exceptionally rare. This case represents the inaugural report of TOA resulting from CD. A literature review on abdominal and pelvic CD abscesses found that patients undergoing surgical drainage had a favorable prognosis. Therefore, surgical intervention plays an important role in the management of CD abscesses.

Effects of intensity, frequency, and time window of exercise on sleep quality among community-dwelling adults aged 65-86 years.

BACKGROUND: Although the effects of exercise training (ET) on sleep problem have been reported, the effects according to the components of exercise, including intensity, frequency, and time window, are unknown. Thus, in this study, we aimed to assess the effects of ET on sleep quality in community-dwelling older adults with sleep problems. METHODS: We evaluated individuals aged ≥65 years whose Pittsburgh sleep quality index was >5 points at baseline. The participants were allocated to either the control group or the ET group and underwent interval walking training (IWT) for 5 months. Information regarding intensity, frequency, and time window of ET were obtained using a waist-worn accelerometer. RESULTS: Overall, 63 participants (24 men [mean ± standard deviation age: 75.1 ± 4.6 years] and 39 women [74.7 ± 5.2 years]) and 65 participants (24 men [75.2 ± 4.0 years] and 41 women [73.6 ± 4.2 years]) were included in the ET and control groups, respectively. The change in Pittsburgh sleep quality index was not significantly different between the two groups for both sexes. In the ET group, women who exercised 3-8 h before bedtime, men who did ET > 8 h before bedtime and more than 1 h after waking up, and men who did ET ≥ 5.05 days/week experienced significant improvements compared to the baseline. CONCLUSIONS: IWT does not significantly improve sleep quality. To obtain improvements in sleep quality, it might be necessary to consider the time window of performing ET for both sexes and ET frequency for men.

Effect of high-intensity interval walking on microvascular endothelial function among community-dwelling older people.

AIM: To investigate the effects of high-intensity interval exercise training on microvascular endothelial function among community-dwelling older people. METHODS: We analyzed the data from a nonrandomized controlled trial. This study's participants were 48 men (aged 75 ± 5 years; exercise training group, n = 24; control group, n = 24) and 83 women (aged 75 ± 4 years; exercise training group, n = 36; control group, n = 47). The exercise training group underwent a high-intensity interval walking training for 5 months. RESULTS: In the exercise group, 100% and 91.7% of men and women, respectively, achieved brisk walking times ≥50 min/week. The change in the reactive hyperemia index significantly differed between the groups of men, whereas that in the control group was not significant; however, a significant increase was observed in the exercise training group. Among women, changes in the reactive hyperemia index were not significant in either group; however, for women in the exercise training group, these changes negatively and positively correlated with the change in body mass index (Spearman's rho = -0.342; P = 0.041) and baseline body mass index (rho = 0.362, P = 0.030), respectively. Additionally, the distribution of body mass index was broader in women than in men. CONCLUSIONS: Interval walking training increased the reactive hyperemia index in men rather than in women. A higher variation in baseline body mass index may be associated with no statistical increase in reactive hyperemia index in women. Geriatr Gerontol Int 2023; 23: 103-110.

Urine neutrophil gelatinase-associated lipocalin as a biomarker of adult pyelonephritis.

BACKGROUND: Pyelonephritis is a common infection at any age. Urine neutrophil gelatinase-associated lipocalin (NGAL), a novel biomarker of acute renal failure, is related to pyelonephritis in pediatric patients, although the significance of this urine biomarker in adult patients are not clear. We investigated the relationship between urine NGAL of pyelonephritis and non-pyelonephritis. PATIENTS AND METHODS: We prospectively enrolled adult patients who were hospitalized due to pyelonephritis or non-pyelonephritis. Pyelonephritis was diagnosed in patients with fever and bacteriuria, with no any other infection focuses. Non-pyelonephritis was diagnosed in patients who had fever and another infection focus without bacteriuria. Urine samples were collected on days 0, 3 and 7. Urine NGAL levels were measured by ELISA. RESULTS: There were 35 patients in the pyelonephritis group and 19 patients in the non-pyelonephritis group. Urine NGAL level were significantly higher in the pyelonephritis group than the non-pyelonephritis group on day 0 (median 302 ng/mL vs 25 ng/mL, p = 0.006). The area under the receiver operating characteristic curve of NGAL was 0.78 (p = 0.006). Urine NGAL level had a specificity of 66.7% and sensitivity of 87.0% at the cut-off level of 250 ng/mL for diagnosing pyelonephritis. CONCLUSIONS: Urine NGAL level at the diagnosis of infection are elevated in adult patients with pyelonephritis, but not in those with non-pyelonephritis. Urine NGAL might be a supportive biomarker for the diagnosis of pyelonephritis.

Effects of interval-walking training on blood pressure in community-dwelling Japanese older adults.

BACKGROUND: The hypotensive effects of high-intensity interval training have been reported; however, studies on older adults are few. This study aimed to examine whether interval-walking training (IWT), a home-based program of high-intensity interval training, reduces blood pressure (BP) levels when compared with a non-intervention group in community-dwelling older adults. METHODS: An intervention study was conducted with 55 men (age, 75±5 years; IWT/control groups, N.=27/28) and 100 women (75±5 years; N.=47/53). The IWT regimen was as follows: fast (high-intensity) walking at 70-85% of the peak aerobic capacity and normal (light-intensity) walking at approximately 40% of the peak aerobic capacity for 3 min each, ≥5 times/walking day, and ≥4 days/week for 5 months. Systolic, diastolic, and mean arterial BPs (SBP, DBP, and MAP, respectively) were measured in the supine posture. RESULTS: The mean baseline SBP/DBP was 132/78 mmHg in men and 131/72 mmHg in women. Five-month changes in SBP, DBP, or MAP did not significantly differ between the IWT and control groups in either sex. The weekly fast-walking time in the IWT group was negatively correlated with changes in DBP (Spearman's ρ=-0.383, P=0.049) and MAP (ρ=-0.444, P=0.021) only in men. CONCLUSIONS: Though present findings did not indicate significant hypotensive effects of IWT in community-dwelling older adults, men with longer fast-walking times experienced greater BP decreases. Further studies with sufficient sample sizes are needed to determine the factors modulating the effects of the proposed training program.

First case of necrotizing fasciitis and bacteremia caused by Bifidobacteriumbreve.

We report the first case of necrotizing fasciitis and bacteremia caused by Bifidobacterium breve. Some Bifidobacterium breve strains are known as probiotic bacterium. However, it causes bacteremia in infants and immunocompromised patients. Our patient developed necrotizing fasciitis which was thought to have been infected from chronic diabetic foot ulcers. Bifidobacterium breve was isolated from the patient's blood and soft tissue sample. The patient underwent amputation and intravenous antibiotics administration.

High D-glucose levels induce ACE2 expression via GLUT1 in human airway epithelial cell line Calu-3.

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters the host cell by binding to angiotensin-converting enzyme 2 (ACE2) receptors. ACE2 is expressed on human airway epithelial cells. Increased ACE2 expression may be associated with potentially high risk of COVID-19. However, the factors responsible for the regulation of ACE2 expression in human airway epithelial cells are unknown. Furthermore, hyperglycemia is a risk factor for poor disease prognosis. RESULTS: In this study, we investigated the effects of D-glucose on ACE2 mRNA and protein expressions in Calu-3 bronchial submucosal cells. The cells were cultured in minimal essential medium containing different D-glucose concentrations. After 48 and 72 h of high D-glucose (1000 mg/dL) treatment, ACE2 mRNA expressions were significantly increased. ACE2 protein expressions were significantly increased after 24 h of high D-glucose treatment. ACE2 mRNA expression was enhanced by a D-glucose concentration of 550 mg/dL or more after 72 h of treatment. In addition, we investigated the role of glucose transporters (GLUTs) in Calu-3 cells. ACE2 mRNA and protein expressions were suppressed by the GLUT1 inhibitor BAY-876 in high D-glucose-treated Calu-3 cells. GLUT-1 siRNA was also used and ACE2 mRNA expressions were suppressed in high D-glucose-treated Calu-3 cells with GLUT-1 knockdown. CONCLUSIONS: This is the first report indicating that high D-glucose levels induced ACE2 expression via GLUT1 in bronchial submucosal cells in vitro. As hyperglycemia can be treated appropriately, these findings could help reduce the risk of worsening of coronavirus disease 2019.

Combined Treatment with Hydrophilic and Lipophilic Statins Improves Neurological Outcomes Following Experimental Cardiac Arrest in Mice.

BACKGROUND: Global ischemia due to cardiac arrest (CA) followed by cardiopulmonary resuscitation (CPR) causes significant neuronal damage in vulnerable areas in the brain. Currently, a majority of patients eventually die after successful CPR due to neurological injury. Statins have pleiotropic effects including anti-inflammatory and/or antioxidant responses. These pleiotropic effects can have a beneficial role in the post-CPR phase. We tested whether two different types of statins, hydrophilic pravastatin and lipophilic simvastatin, attenuated neurological injury following CA/CPR. The efficacy of pravastatin and simvastatin combination treatment was also assessed. METHODS: Isoflurane-anesthetized adult male wild-type C57Bl/6 mice subjected to 8-min CA/CPR were randomized into four groups: control, 2 mg/kg pravastatin, 20 mg/kg simvastatin, or a combination of 3 mg/kg pravastatin and 10 mg/kg simvastatin. Neurobehavioral assessment and histological analyses were performed to assess overall general health condition and neuronal injury, respectively. RESULTS: Combination treatment with pravastatin and simvastatin significantly reduced neuronal injury in the striatum and hippocampus, reduced cerebral edema, and improved general health at 4 days after CA/CPR. Combination statin treatment upregulated endothelial nitric oxide synthase mRNA in the brain. Pravastatin alone, but not simvastatin alone, improved general health after CA/CPR. Pravastatin was less potent than simvastatin at reducing neuronal injury in the brain. CONCLUSION: Combination treatment with two different types of statins at the correct dose may be a promising approach to neuroprotection following CA/CPR.

Role of Cranial Temperature in Neuroprotection by Sodium Hydrogen Sulfide After Cardiac Arrest in Mice.

The hydrogen sulfide donor sodium hydrogen sulfide (NaHS) is recognized as a neuroprotective agent, which induces a hibernation-like metabolic state and hypothermia. However, it remains unclear whether it is the sulfide itself or the hypothermia induced by the sulfide that mediates treatment outcomes following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). We therefore tested whether NaHS improved outcomes following CA/CPR in mice maintained at 35.0°C by active warming during recovery. Adult male mice were subjected to 8 minutes CA/CPR and randomly treated intraperitoneally with either implantation of miniosmotic pump with NaHS (50 µmol/kg/day) for 3 days or vehicle 30 minutes after CPR. A normothermia group had cranial temperatures kept >35.0°C for 6 hours with a heat pad, and a hypothermia group was allowed to spontaneous hypothermia at room temperature (26.0°C). Behavioral testing and histological evaluation of neurons in the CA1 hippocampal region and striatum were performed on days 4 and 12 after CA/CPR. Both cranial and body temperature decreased following CA/CPR in the hypothermia group, and this was enhanced by NaHS treatment. In the active warming (normothermia) group, NaHS protected striatal neurons and improved long-term survival, which was comparable to the hypothermia groups. No differences were found in the CA1 region. Following CA/CPR, NaHS treatment decreased the heart rate, but not the mean arterial pressure. Our study demonstrated that post-CPR treatment with NaHS exerted neuroprotection in mice while maintaining a normal cranial temperature, indicating that NaHS-related neuroprotection is independent of the known protective effect of spontaneous hypothermia.

Glibenclamide and Therapeutic Hypothermia Have Comparable Effect on Attenuating Global Cerebral Edema Following Experimental Cardiac Arrest.

BACKGROUND: Cerebral edema is one of the major causes of mortality following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). A subunit of the sulfonylurea receptor 1-transient receptor potential M4 (Sur1-TRPM4) channel has been implicated in the pathogenesis of ischemia-evoked cerebral edema. In this study, we examined whether glibenclamide (GBC), a Sur1-TRPM4 channel inhibitor, attenuates cerebral edema following CA/CPR and further examined the efficacy of GBC combined with therapeutic hypothermia. METHODS: Isoflurane-anesthetized adult male wild-type C57Bl/6 mice subjected to 7-min CA/CPR were randomized into five groups: sham operation, control with normothermia, GBC with normothermia, control with hypothermia, and GBC with hypothermia. The primary outcome was to evaluate regional brain water content; the secondary outcome was to measure blood glucose level, Sur1-TRPM4 expression, and pro-inflammatory factor expression. RESULTS: Compared with normothermia, GBC treatment or hypothermia significantly attenuated brain water content in mice subjected to CA/CPR. GBC combined with hypothermia had no additional effects on attenuating cerebral edema. Pro-inflammatory factor messenger RNA expression (TNF-α and IL-6), NFκß activation, and SUR1-TRPM4 levels were upregulated after CA/CPR. Compared with normothermia, hypothermia, but not GBC, partly suppressed these factors' expression. CONCLUSIONS: GBC attenuated cerebral edema following CA/CPR by blocking Sur1-TRPM4 channels upregulated by CA insult. The effect of GBC was comparable with that of therapeutic hypothermia alone. These results suggest that GBC is an alternative approach for treating CA-evoked cerebral edema.

Single administration of soluble epoxide hydrolase inhibitor suppresses neuroinflammation and improves neuronal damage after cardiac arrest in mice.

Cardiac arrest (CA) causes ischemia-reperfusion injury in the whole body among victims. Especially in the brain, inflammation and neuronal cell death can lead to irreversible dysfunction. Our goal was to determine whether a single administration of soluble epoxide hydrolase inhibitor (AS2586144-CL) has a neuroprotective effect and decreases the inflammatory response after CA and cardiopulmonary resuscitation (CPR). Global cerebral ischemia was induced in male C57BL/6 mice with 8min of CA. Thirty minutes after recovery of spontaneous circulation, the mice were randomly assigned to three groups and administered AS2586144-CL: 1mg/kg (n=25), 10mg/kg (n=25), or 0mg/kg (vehicle, n=25). At 6 and 7 days after CA/CPR, behavioral tests were conducted and brains were removed for histological evaluation. Analysis of histological damage 7 days after CA/CPR revealed that 10mg/kg of AS2586144-CL protected neurons, and suppressed cytokine production and microglial migration into the hippocampus. Two hours after CA/CPR, 10mg/kg of AS2586144-CL suppressed serum tumor necrosis factor-α and hippocampal nuclear factor κB expression. Our data show that 10mg/kg of AS2586144-CL administered following CA/CPR suppresses inflammation and decreases neuronal damage.

Osmotherapy With Hypertonic Saline Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest via Perivascular Pool of Aquaporin-4.

OBJECTIVES: We tested the hypothesis that osmotherapy with hypertonic saline attenuates cerebral edema following experimental cardiac arrest and cardiopulmonary resuscitation by exerting its effect via the perivascular pool of aquaporin-4. We used mice with targeted disruption of the gene encoding α-syntrophin (α-Syn) that demonstrate diminished perivascular aquaporin-4 pool but retain the non-endfoot and ependymal pools. DESIGN: Laboratory animal study. SETTING: University animal research laboratory. INTERVENTIONS: Isoflurane-anesthetized adult male wild-type C57B/6 or α-Syn mice were subjected to cardiac arrest/cardiopulmonary resuscitation and treated with either a continuous IV infusion of 0.9% saline or various concentrations of hypertonic saline. Serum osmolality, regional brain water content, blood-brain barrier disruption, and aquaporin-4 protein expression were determined at 24 hours after cardiac arrest/cardiopulmonary resuscitation. MEASUREMENTS AND MAIN RESULTS: Hypertonic saline (7.5%) treatment significantly attenuated water content in the caudoputamen complex and cortex compared with 0.9% saline treatment in wild-type mice subjected to cardiac arrest/cardiopulmonary resuscitation. In contrast, in α-Syn mice subjected to cardiac arrest/cardiopulmonary resuscitation, 7.5% hypertonic saline treatment did not attenuate water content. Treatment with 7.5% hypertonic saline attenuated blood-brain barrier disruption at 24 hours following cardiac arrest/cardiopulmonary resuscitation in wild-type mice but not in α-Syn mice. Total aquaporin-4 protein expression was not different between 0.9% saline and hypertonic saline-treated wild-type mice. CONCLUSIONS: Following experimental cardiac arrest/cardiopulmonary resuscitation: 1) continuous hypertonic saline therapy maintained to achieve serum osmolality of ≈ 350 mOsm/L is beneficial for the treatment of cerebral edema; 2) perivascular pool of aquaporin-4 plays a critical role in water egress from brain; and 3) hypertonic saline attenuates blood-brain barrier disruption via perivascular aquaporin-4 pool.

Conivaptan, a Selective Arginine Vasopressin V1a and V2 Receptor Antagonist Attenuates Global Cerebral Edema Following Experimental Cardiac Arrest via Perivascular Pool of Aquaporin-4.

BACKGROUND: Cerebral edema is a major cause of mortality following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Arginine vasopressin (AVP) and water channel aquaporin-4 (AQP4) have been implicated in the pathogenesis of CA-evoked cerebral edema. In this study, we examined if conivaptan, a V1a and V2 antagonist, attenuates cerebral edema following CA/CPR in wild type (WT) mice as well as mice with targeted disruption of the gene encoding α-syntrophin (α-syn(-/-)) that demonstrate diminished perivascular AQP4 pool. METHODS: Isoflurane-anesthetized adult male WT C57Bl/6 and α-syn(-/-) mice were subjected to 8 min CA/CPR and treated with either bolus IV injection (0.15 or 0.3 mg/kg) followed by continuous infusion of conivaptan (0.15 mg/kg/day or 0.3 mg/kg/day), or vehicle infusion for 48 h. Serum osmolality, regional brain water content, and blood-brain barrier (BBB) disruption were determined at the end of the experiment. Sham-operated mice in both strains served as controls. RESULTS: Treatment with conivaptan elevated serum osmolality in a dose-dependent manner. In WT mice, conivaptan at 0.3 mg dose significantly attenuated regional water content in the caudoputamen (81.0 ± 0.5 vs. 82.5 ± 0.4% in controls; mean ± SEM) and cortex (78.8 ± 0.2 vs. 79.4 ± 0.2% in controls), while conivaptan at 0.15 mg was not effective. In α-syn(-/-) mice, conivaptan at 0.3 mg dose did not attenuate water content compared with controls. Conivaptan (0.3 mg/kg/day) attenuated post-CA BBB disruption at 48 h in WT mice but not in α-syn(-/-) mice. CONCLUSIONS: Continuous IV infusion of conivaptan attenuates cerebral edema and BBB disruption following CA. These effects of conivaptan that are dependent on the presence of perivascular pool of AQP4 appear be mediated via its dual effect on V1 and V2 receptors.

Extraction of the pharmacological treatment features in literature-based discovery by applying cluster analysis.

Literature-based discovery (LBD) facilitates the extraction of hidden relationships between a disease and chemical substances. As a methodology of LBD, we had previously proposed to apply cluster analysis to analyze the intermediate concepts between them. In this study, we compared the ranks of chemical substances predicted by our methodology to the original rank so as to validate possibilities for extraction of the heterogeneity in the relationships. As a result, we obtained two clusters. The rank for one cluster was similar to the original rank (ρ=0.956), but another was different (ρ=0.580). The different features from the original rank were obtained on Pharmacological Action Terms of MeSH terms.

Mutation accumulation in a selfing population: consequences of different mutation rates between selfers and outcrossers.

Currently existing theories predict that because deleterious mutations accumulate at a higher rate, selfing populations suffer from more intense genetic degradation relative to outcrossing populations. This prediction may not always be true when we consider a potential difference in deleterious mutation rate between selfers and outcrossers. By analyzing the evolutionary stability of selfing and outcrossing in an infinite population, we found that the genome-wide deleterious mutation rate would be lower in selfing than in outcrossing organisms. When this difference in mutation rate was included in simulations, we found that in a small population, mutations accumulated more slowly under selfing rather than outcrossing. This result suggests that under frequent and intense bottlenecks, a selfing population may have a lower risk of genetic extinction than an outcrossing population.

[Group A streptococcus-induced toxic shock syndrome in pregnancy: a case report of cesarean section].

Group A streptococcus (GAS)-induced toxic shock syndrome (TSS) in pregnancy is rare, but its clinical course is fulminant. The mortality rates of mother and fetus are reported to be 58 and 66%, respectively. We report a case of GAS-TSS after cesarean section. A 38-year-old pregnant woman of 38 weeks gestation was admitted to our hospital because of vomiting, fever of 39 degrees C, and continuous abdominal pain with scanty genital bleeding. She had complained of sore throat several days before. One hour after admission, external fetal monitoring revealed periodic pulse deceleration to 90 x beats min(-1). The emergent cesarean section was performed under general anesthesia. Approximately 8 hours after the cesarean section, she developed coma, shock and respiratory insufficiency requiring intubation. Streptococcus pyogens were isolated from her blood sample and the patient met criteria for GAS-TSS. She was treated with antibiotics (penicillin and clindamycin), antithrombin III, recomodulin, catecholamins, and continuous hemodialysis with filtration of toxins. Although the patient recovered and was discharged on 63rd day, the infant died on postpartum day 4. Early recognition and intensive treatment for GAS is recommended in a late stage pregnancy with an episode of sore throat, vomiting, high fever, strong labor pain, and DIC signs.

Fluoxetine has neuroprotective effects after cardiac arrest and cardiopulmonary resuscitation in mouse.

AIMS: Fluoxetine, a selective serotonin reuptake inhibitor, is protective in a rat focal ischaemia model via anti-inflammatory mechanisms. Cardiac arrest and cardiopulmonary resuscitation (CA/CPR) were performed in mice to test the hypothesis that fluoxetine protects the brain following global cerebral ischaemia, even when administered after an insult. METHODS: Global cerebral ischaemia was induced with 8 min CA/CPR in C57BL/6 male mice. Thirty minutes after recovery of spontaneous circulation, the mice were randomly assigned into 3 groups and administered fluoxetine; fluoxetine (5 mg/kg: n=15, 10 mg/kg: n=15) or vehicle (NaCl: n=15). Three days after CA/CPR, sensorimotor evaluations were conducted and brains were removed for histological evaluation of the hippocampus and caudate putamen. RESULTS: Analysis of histological damage 72 h after resuscitation revealed that low dose fluoxetine (5 mg/kg) did not protect, while high dose (10 mg/kg) fluoxetine protected neurons in the caudate putamen. In contrast, there were no protective effects in the hippocampus at either dose. In agreement with histological observations of neuronal damage in the caudate putamen, high dose fluoxetine decreased sensorimotor deficits following CA/CPR compared to vehicle-treated animals. CONCLUSIONS: Our data showed that 10mg/kg fluoxetine administered following global cerebral ischaemia decreases neuronal damage. Although long-term neuroprotection needs further study, the results of our study suggest that fluoxetine may have therapeutic potential when administered after global cerebral ischaemia, cardiac arrest and cardiopulmonary resuscitation.

Normothermic cardiac arrest and cardiopulmonary resuscitation: a mouse model of ischemia-reperfusion injury.

Acute Kidney Injury (AKI) is a common, highly lethal, complication of critical illness which has a high mortality and which is most frequently caused by whole-body hypoperfusion. Successful reproduction of whole-body hypoperfusion in rodent models has been fraught with difficulty. Models which employ focal ischemia have repeatedly demonstrated results which do not translate to the clinical setting, and larger animal models which allow for whole body hypoperfusion lack access to the full toolset of genetic manipulation possible in the mouse. However, in recent years a mouse model of cardiac arrest and cardiopulmonary resuscitation has emerged which can be adapted to model AKI. This model reliably reproduces physiologic, functional, anatomic, and histologic outcomes seen in clinical AKI, is rapidly repeatable, and offers all of the significant advantages of a murine surgical model, including access to genetic manipulative techniques, low cost relative to large animals, and ease of use. Our group has developed extensive experience with use of this model to assess a number of organ-specific outcomes in AKI.

[Comparison of diagnostic criteria for the metabolic syndrome among Japanese university faculty].

OBJECTIVES: Diagnostic criteria for the metabolic syndrome (Mets) in Japan have been set by the Medical Committee of the Japanese Association of Medical Sciences (Med), the National Health and Nutrition Examination Survey (Nat), specific health checkups (Ckup), and second medical examination by Worker's Accident Compensation Insurance System (Wor). The purpose of this study was to compare classification of the metabolic syndrome by different organizational criteria and to investigate underlying differences. METHODS: All faculty members of a university in Osaka, Japan, underwent mandatory health checkups in September 2008. The demographic distribution included 769 males (mean age, 49 +/- 12 years) and 415 females (mean age, 43 +/- 10 years). Using the Med, Nat, Ckup and Wor criteria, individuals were assessed for the MetS and pre-metabolic syndrome (pre-Mets), strongly suspected metabolic syndrome (S-Mets) and assumed pre-metabolic syndrome (A-pre-Mets), as well as a positive support level (PSL) and a motivational support level (MSL). All faculty members were categorized into a morbid group (Mets, S-Mets, PSL, and FB) or a pre-morbid group (pre-Mets, A-pre-Mets, and MSL) based on medical data and smoking habits. The incidence of morbid and pre-morbid individuals was compared across the four criteria and analyzed based on gender and age (under 40 and 40 or over). RESULTS: Male incidences for the morbid and pre-morbid classifications were 17% and 20% with Med, 9% and 23% with Nat, 27% and 14% with Ckup, and 1.4% and 0% with Wor. There were significant differences across criteria sets in both the morbid and pre-morbid groups, with significantly greater numbers of males than females, and higher prevalences in those aged 40 or over than in their younger counterparts. Males aged under 40 classified into the pre-morbid group comprised 18% in Med, 16% in Nat, and 13% in Ckup. CONCLUSION: The different disease incidences found between Med and Ckup data in males aged 40 or over might be attributed to varying criteria for blood glucose levels, while Wor data may be influenced by the higher level of blood pressure set as a criterion with this approach. It will be important to continuously validate currently established criteria to identify the actual prevalence of MetS in Japan. Furthermore, incorporation of waist circumference and BMI for females, and a positive approach for young males, may be critical for future developments.