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The MTP Temporary Hospital in Poznań operated within the nationally adopted model of dealing with the COVID-19 epidemic, being one of the largest clinics of this type in the country. It has become an essential element in the fight against the pandemic in the region. The article presents the basic principles and organizational framework for the functioning of this makeshift hospital, which fulfilled its medical and social role thanks to the persistent work of a wide range of competent employees and well-used infrastructure.

Selectins and their ligands play an important role in atherosclerosis. The role of these adhesion molecules in the pathogenesis of obstructive sleep apnea (OSA) may be of clinical relevance. Therefore, the aim of this study was to assess the serum content of platelet P-selectin (P-SEL) and P-selectin glycoprotein ligand 1 (PSGL-1) in different OSA stages. The study was performed in nondiabetic patients, aged 32-71, in whom OSA was verified by polysomnography. The apnea/hypopnea index (AHI) was used to stratify OSA stages: AHI 5, no sleep pathology (OSA-0); AHI 5-15, (OSA-1); AHI 16-30, (OSA-2); and AHI 30, (OSA-3). There were 16 patients in each group. P-SEL and PSGL-1 were assessed by ELISA kits. There were no appreciable differences in the patients' glucose or high-specificity C-reactive protein content. We found that P-SEL and PSGL-1 significantly increased from OSA-0 to OSA-3. There were the following positive associations in all OSA patients: P-SEL vs. AHI, PSGL-1 vs. AHI, and P-SEL vs. PSGL-1. In addition, the adhesion molecules are associated with the anthropometric parameters, oxygen saturation, and sleep architecture in the OSA-1 group. We conclude that the adhesion molecules consistently increase in the blood of nondiabetic OSA patients, along with progression of disorder severity.

Selectins and their ligands play an important role in atherosclerosis. The role of these adhesion molecules in the pathogenesis of obstructive sleep apnea (OSA) may be of clinical relevance. Therefore, the aim of this study was to assess the serum content of platelet P-selectin (P-SEL) and P-selectin glycoprotein ligand 1 (PSGL-1) in different OSA stages. The study was performed in nondiabetic patients, aged 32–71, in whom OSA was verified by polysomnography. The apnea/hypopnea index (AHI) was used to stratify OSA stages: AHI 30, (OSA-3). There were 16 patients in each group. P-SEL and PSGL-1 were assessed by ELISA kits. There were no appreciable differences in the patients’ glucose or high-specificity C-reactive protein content. We found that P-SEL and PSGL-1 significantly increased from OSA-0 to OSA-3. There were the following positive associations in all OSA patients: P-SEL vs. AHI, PSGL-1 vs. AHI, and P-SEL vs. PSGL-1. In addition, the adhesion molecules are associated with the anthropometric parameters, oxygen saturation, and sleep architecture in the OSA-1 group. We conclude that the adhesion molecules consistently increase in the blood of nondiabetic OSA patients, along with progression of disorder severity.

Oxidative stress underlies both obstructive sleep apnea (OSA) and atherosclerosis. The aim of the study was to assess the markers of oxidative stress in plasma at different stages of OSA in non-smoking obese Caucasian males aged 41-60, with normal oral glucose tolerance test. All patients were subjected to clinical and polysomnographic examinations. The stage of OSA severity was set according to the following criteria of the apnea-hypopnea index (AHI): AHI5/h - no disease (OSA-0; n = 26), AHI 5-15/h - mild disease (OSA-1; n = 26), AHI 16-30/h - moderate disease (OSA-2: n = 27), and AHI 30/h obstructive episodes per hour - severe disease (OSA-3; n = 27). Plasma total antioxidant status (TAS) and thiobarbituric acid-reacting substances (TBARS), reflecting the level of lipid peroxides, were determined spectrophotometrically. We found that TAS decreased and TBARS increased significantly from OSA-0 to OSA-3. We conclude that the oxidative stress markers are conducive to setting the severity of OSA in normoglycemic patients.

Oxidative stress underlies both obstructive sleep apnea (OSA) and atherosclerosis. The aim of the study was to assess the markers of oxidative stress in plasma at different stages of OSA in non-smoking obese Caucasian males aged 41–60, with normal oral glucose tolerance test. All patients were subjected to clinical and polysomnographic examinations. The stage of OSA severity was set according to the following criteria of the apnea-hypopnea index (AHI): AHI 30/h obstructive episodes per hour – severe disease (OSA-3; n = 27). Plasma total antioxidant status (TAS) and thiobarbituric acid-reacting substances (TBARS), reflecting the level of lipid peroxides, were determined spectrophotometrically. We found that TAS decreased and TBARS increased significantly from OSA-0 to OSA-3. We conclude that the oxidative stress markers are conducive to setting the severity of OSA in normoglycemic patients.

Thrombophilia-hypofibrinolysis may play an important role in rare premature (or = age 45 years) arterial occlusive events in atherothrombotic cardiovascular (ATCVD) disease, particularly in normolipidemic patients. Whether thrombophilia-hypofibrinolysis contributed to ATCVDor = age 45 years was assessed in 78 men and 40 women with 230 ATCVD events (myocardial infarction (MI) [n = 60], coronary artery bypass graft [CABG, n = 33], angioplasty [n = 52], chronic angina [n = 41], ischemic stroke [n = 11], transient ischemic attack [TIA, n = 24], claudication [n = 9]). Cases were compared with healthy normal adult controls (44 men and 76 women). In men, the Factor V Leiden mutation was present in 6/63 (10%) cases versus 0/44 (0%) controls (P = 0.042), Factor VIII was high (150%) in 16/60 (27%) cases versus 1/42 (2%) controls (P = 0.001), Factor XI was high (150%) in 9/57 (16%) cases versus 0/42 (0%) controls (P = 0.009), and plasminogen activator inhibitor activity (PAI-Fx) was high (21.1 U/mL) in 15/63 (24%) cases versus 3/43 (7%) controls (P = 0.023). In women, protein C was low (73%) in 4/26 (15%) cases versus 0/74 (0%) controls (P = 0.004), and free protein S was low (66%) in 5/27 (19%) cases versus 2/74 (3%) controls (P = 0.014). In women, Factor XI was high (150%) in 3/27 (11%) cases versus 1/74 (1%) controls (P = 0.057), and the lupus anticoagulant was present in 9/32 (28%) cases versus 2/51 (4%) controls (P = 0.002). In patients with ATCVDor = age 45 years, thrombophilias (Factor V Leiden, Factor VIII, Factor XI, protein C and S deficiency, lupus anticoagulant) and hypofibrinolysis (PAI-Fx, Lp[a]) may promote arterial thrombosis, which is synergistic with atherosclerotic endothelial injury.

Leptin is an adipocyte-derived hormone regulating energy homeostasis and body weight. Leptin concentration is increased in patients with the obstructive sleep apnea syndrome (OSAS). Leptin receptor (LEPR) is a single transmembrane protein belonging to the superfamily of cytokine receptors related by a structure to the hemopoietin receptor family. The aim of the present study was to evaluate the frequency of distribution of leptin receptor gene polymorphism GLN223ARG in OSAS patients compared with healthy controls. The examined group included 179 subjects: 102 OSAS patients (74 men and 28 women) and 77 non-apneic controls (39 men and 38 women). Genomic DNA was isolated with the use of a column method and genotyping of DNA sequence variation was carried out by restriction enzyme analysis of PCR-amplified DNA. The results revealed a significant correlation between the polymorphism of LEPR and OSAS. Carriers of Arg allele in homozygotic genotype Arg/Arg and heterozygotic genotype Gln/Arg were more often obese and developed OSAS than the group of carriers of homozygotic Gln/Gln genotype. This tendency was observed in the whole examined population and in the group of obese women. We also found the highest levels of total cholesterol, LDL, HDL, and triglycerides in the group of homozygotic Arg/Arg genotype carriers, lower in heterozygotic Gln/Arg genotype carriers, and the lowest in the group of persons carring homozygotic Gln/Gln genotype. The presence of Arg allel seems linked to a higher risk of obesity and higher lipid levels in OSAS patients. OSAS may have a strong genetic basis due to the effects from a variety of genes including those for leptin receptor.

Background: In 35 adolescent females (17 ± 2 years) with polycystic ovary syndrome (PCOS), median body mass index (BMI) 30.8 kg/m 2 , we assessed effeicacy of metformin-diet for 1 year for reduction of weight, insulin, HOMA insulin resistance (IR), cholesterol, triglycerides, and resumption of regular menses. Methods: Calories (26% protein, 44% carbohydrate) were targeted to 1,500-1,800/day if BMI was

Patients with high levels of low-density lipoprotein cholesterol (LDL-C) might not tolerate 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors ("statins") because of adverse effects (AEs) and might not respond well enough to nonstatin lipid-lowering therapies (LLTs) to meet LDL-C goals.The purpose of this study was to assess the acceptability, effectiveness, and safety profile of rosuvastatin 5 and 10 mg/d in consecutively referred patients with primary high LDL-C who were unable to tolerate other statins because of myalgia and, subsequently in some cases, unable to reach LDL-C goals with nonstatin LLT.This prospective, open-label pilot study was conducted in consecutively referred male and female patients aged 38 to 80 years with primary high LDL-C (mean, 177 mg/dL) at The Cholesterol Center, Jewish Hospital, Cincinnati, Ohio. Patients were instructed in the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) therapeutic lifestyle changes diet. Rosuvastatin 5 mg/d was administered to patients categorized by NCEP ATP III risk stratification as moderately high risk, and rosuvastatin 10 mg/d was administered to patients categorized as high or very high risk. End points included acceptability (assessed using patient-initiated discontinuation of rosuvastatin), effectiveness (absolute and percentage reductions in LDL-C and triglycerides), and safety profile (aspartate and alanine aminotransferases [AST and ALT, respectively]3 times the laboratory upper limit of normal [xULN] or elevations in creatine kinase [CK]10xULN).A total of 61 patients were enrolled (41 women, 20 men; mean [SD] age, 60 [10] years; 5-mg/d dose, 25 patients; 10-mg/d dose, 36 patients). Myalgia, a predominant AE, had caused 50 patients to previously discontinue treatment with atorvastatin; 30, simvastatin; 19, pravastatin; 5, fluvastatin; 2, ezetimibe/simvastatin; and 1, lovastatin. Eighteen patients subsequently failed to reach LDL-C goals with nonstatin LLT(s) alone (colesevelam, 10 patients; ezetimibe, 8; niacin extended release, 2; and fenofibrate, 1). After a median treatment duration of 16 weeks, rosuvastatin 5 mg/d+diet was associated with a mean (SD) decrease from baseline in LDL-C of 75 (34) mg/dL (mean [SD] %Delta, -42% [18%]) (P0.001 vs baseline). After a median treatment duration of 44 weeks, rosuvastatin 10 mg/d+diet was associated with a mean (SD) decrease from baseline in LDL-C of 79 (49) mg/dL (mean [SD] %Delta, -42% [24%]) (P0.001 vs baseline). Of the 61 patients, 1 receiving the 10-mg/d dose discontinued rosuvastatin treatment because of unilateral muscular pain after 4 weeks; no AST or ALT levels were3xULN, and no CK levels were10xULN.In these 61 hypercholesterolemic patients unable to tolerate other statins and, subsequently in some cases, unable to meet LDL-C goals while receiving nonstatin LIT monotherapy, these preliminary observations suggest that rosuvastatin at doses of 5 and 10 mg/d+diet was well tolerated, effective, and had a good safety profile.

In 74 women with polycystic ovary syndrome, treated for 4 years with metformin (MET) and diet, we prospectively assessed whether, and to what degree, weight loss, reduction of insulin resistance, and amelioration of coronary heart disease risk factors could be sustained. We hypothesized that response to MET-diet would not differ by pretreatment body mass index (BMI) classes25 (normal),or =25 to30 (overweight),or =30 to40 (obese), andor =40 (extremely obese). [table: see text] Metformin-diet was successful in producing stable approximately 8% weight reduction for all 4 years (trend P.0001). Percentage of reductions in weight on MET-diet was significant (P.05) and did not differ among the 3 highest BMI categories (or =40,or =30 to40,or =25 to30), but were not significant in the normal-weight category (BMI,25). On MET-diet, median homeostasis model assessment of insulin resistance (HOMA-IR) was 33% lower than entry at 1 year, 50% at 2 years, 51% at 3 years, and 50% at 4 years (trend, P.0001). On MET-diet, median low-density lipoprotein cholesterol (LDL-C) was 6% lower than entry at year 1, 6% at year 2, 7% at year 3, and 11% at year 4 (trend P.0001). On MET-diet, median high-density lipoprotein cholesterol (HDL-C) was 3% higher than entry at year 2, 8% higher at year 3, and 11% higher at year 4 (trend P.0001). Percentage of reductions in HOMA-IR, LDL-C, triglyceride, and systolic blood pressure, and increments in HDL-C did not differ (P.1) in the 4 BMI categories. By stepwise regression, weight loss was a significant (Por = .01) positive explanatory variable for reduction in HOMA-IR for all 4 follow-up years. Metformin-diet in women with polycystic ovary syndrome effectively and safely reduces weight and LDL-C while raising HDL-C, and maintains these outcomes stable over 4 years.

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We have tentatively identified colostrinines as novel cytokines produced by the mammary gland after delivery and detectable in colostrum. The primary colostrinine, the proline-rich polypeptide, was isolated from ovine colostrum in 1974. It is generally understood that the various factors present in colostrum play a pivotal role in transmitting of passive or active immunity from mother to child. We have found previously that both ovine and human colostrinines are inducers of interferon (IFN) gamma and other cytokines. In this paper, we reported that the leukocytes isolated from human colostrum donated by healthy mothers at 1-9 days after delivery, produced IFNs and tumor necrosis factors (TFNs) spontaneously. The release of IFNs and TNFs coincided with production of a colostrinine that has been isolated from the human colostrum samples and partially characterized. Our results suggest that the maximum production of colostrinine occurs 3 days after delivery. The tolerance (hyporeactivity) of the colostral leukocytes to IFN inducers and the modulation of the TNF response may be the late effects of the colostrinine release.

In 10 normolipidemic patients with 1 or more myocardial infarctions (MI) 35 in men and > 40 mg/dL in women, and triglycerides (TG) 150%) was present in 4 of 7 (57%) cases vs 0/36 controls ( p = .0003). Of 14 hyperlipidemic patients having an arterial event 150%) vs 0/36 controls ( p = .004), 2 of 11 (18%) had high factor XI (> 150%) vs 0/61 controls ( p = .022), and 5 of 13 (38%) had hypofibrinolytic high PAI-Fx (> 21.1 U/mL) vs 4/61 (7%) controls ( p = .007). In both normo- and hyperlipidemic patients sustaining an arterial thrombotic event before age 45, and especially before age 35, we speculate that heritable thrombophilias (factors VIII, XI, factor V Leiden) or hypofibrinolysis (PAI-Fx) may contribute to endothelial damage or altered hemostatic equilibrium and thus promote arterial thrombotic events. In patients with thrombophilia and/or hypofibrinolysis-mediated arterial thrombotic events before age 45, we speculate that thromboprophylaxis might have value in secondary prevention of subsequent arterial thrombotic events.

Buerger9s disease (BD) etiologies are poorly understood. Beyond smoking cessation, medical-surgical treatments have limited success. We hypothesized that mutations associated with arterial vasospasm (stromelysin-1 5A/6A, eNOS T-786C) and C677T-A1298C methylenetetrahydrofolate reductase (MTHFR) interacted with cigarette-cannabis smoking, reducing vasodilatory nitric oxide (NO), promoting arterial spasm-thrombosis. Of 19 smoking BD patients (13 men [2 siblings], ± women, 18 Caucasian, 1 African American), compared to 200 healthy Caucasian controls, BD patients were more likely to have 6A6A stromelysin-1 homozygosity (7/19 [37%] vs 46/200 [23%]) and to have eNOS T-786C homozygosity (3/19 [16%] vs 22/200 [11%]), but these patient-control differences were not significant, p = .4, 0.5. C677T MTHFR homozygosity or compound C677T-A1298C heterozygosity did not differ in patients vs controls (6/19 [32%] vs 70/200 [35%]), p = .8. In 9 patients who stopped and 1 who continued smoking, all stromelysin-1 5A/6A and/or eNOS heterozygotes-homozygotes, lower limb gangrenous ulcers, and intractable ischemic rest pain with arterial occlusion progressed despite conventional medical therapy, threatening amputation. In these 10 patients, to increase vasodilatory NO via endothelial NO synthase, L-arginine (15 g/day) was given, along with folic acid 5 mg, vitamin B6 (100 mg), and B12 (2,000 μg/day) to optimize homocysteine metabolism and reduce asymmetric dimethylarginine, a NO synthase inhibitor. Unexpectedly quickly and strikingly, within 8 weeks to 8 months on L-arginine-folic acid, all 10 treated patients improved with uniform pain reduction, ulcer healing, and in 5, full recovery of previously absent peripheral pulses. In smokers homo-heterozygous for stromelysin-1 5A/6A, eNOS T-786C, and C677T-A1298C MTHFR mutations, we speculate that the development and severity of BD are related to a gene-environment vasospastic interaction with reduced NO-mediated vasodilatation. Increasing NO production by L-arginine while optimizing homocysteine metabolism by folic acid-B6-B12 may have therapeutic benefit. Further blinded, placebo-controlled studies are needed to determine whether our observations can be generalized to larger BD cohorts.

In 40 women (36 white, 1 black, 3 other) with polycystic ovary syndrome (PCOS) not optimally responsive to metformin (MET 2.55 g/day) for 1 year, endocrine and menstrual response to MET (2.55 g) with added pioglitazone (PIO 45 mg/day) for 1 year were compared to outcomes on MET alone. Before MET, 35% of women were obese with BMI 30.0 to .1), and rose to 27 on MET-PIO (p 0.1), but then fell to 13.1 μU/mL on MET-PIO (p .1), but then fell to 2.74 on MET-PIO (p .1), but then fell to 159 on MET-PIO (p .1), rose to 44 mg/dL on MET-PIO (p

To report interaction of Cymbalta (duloxetine hydrochloride) with warfarin leading to persistent, severe elevation of an INR. A 44 year old woman, homozygous for the factor V Leiden mutation, receiving warfarin (10 mg/day) for 1 year after an ischemic stroke, with a stable INR (2.17 ± 0.51) for the year, was evaluated by us 30 days after development of petechiae-purpura (day 94, Fig. 1). Serial measures were taken for INR and liver function tests (LFTs), and plasma warfarin was measured on day 85. Measures were taken on day 94 for fibrinogen, vitamin K-dependent clotting factors, and with repeat measures of factors II and X on day 98 (Fig. 1). No drugs taken daily over the previous year were changed (warfarin, atorvastatin, lamotrigine, topiramate, clorazepam, albuterol); however, Cymbalta (30 mg/day), a selective serotonin and norepinephrine reuptake inhibitor (SSNRI), was added by the psychiatrist at day 0 and was continued until day 94. Having unexpectedly high INR (5.0) on day 55, warfarin was stopped, but Cymbalta was continued. Despite cessation (documented by pill count) of warfarin, INR continued to rise to > 19 on day 85, when plasma warfarin level was 5.3 μg/mL (therapeutic range 2-8 μg/mL), 30 days after the last warfarin dose. INR was briefly reduced to 2.7 only by vitamin K (IV) on day 85. On day 94, with INR 6.4, 39 days after stopping warfarin, factors II, VII, and X had low values; LFTs and fibrinogen remained normal. On day 94, duloxetine was stopped, and by day 98, INR had fallen to 1.2, with factor II increasing to 48% and factor X to 54%. On day 105, INR was 0.9. The metabolism of warfarin involves several CY P450 isoenzymes (CY P 1A2, 2D6, 2C9, 2C19, and 3A4). Duloxetine inhibits CYP1A2 and CYP2D6 and could potentially interact with warfarin. Duloxetine is also highly protein bound in plasma (> 90%) and when given with warfarin, another highly protein-bound drug, could displace warfarin, possibly resulting in a toxic effect. Our case emphasizes the need to closely monitor for the toxic drug interactions between the 2 drugs.

In 296 women with polycystic ovary syndrome (PCOS) treated with metformin (MET 2.3 ± 0.4 g/day [Rx]) and diet (1,500 calories/day if BMI Despite pretreatment (Pre-Rx) group severe obesity, MET-diet was successful in producing group weight reductions of 5.9% at 1 year, 5.8% at 2 years, and 6.3% at 3 years. Weight loss $ 5% was realized by 55% of women at 1 year, 55% at 2 years, and 58% at 3 years, with 15% or more weight loss in 11% of women at 1 year, 14% at 2 years, and 16% at 3 years. At years 1-3 on Rx, weight fell (p

In 35 postmenarchal adolescent females (17 ± 2 years, range 14-19) with polycystic ovary syndrome (PCOS), in a case-series prospective description, we assessed effectiveness of metformin-diet for 1 year for reduction of weight, insulin, HOMA insulin resistance (IR), cholesterol, triglycerides, and resumption of regular menses. By selection, all 35 girls met the 2003 consensus criteria for diagnosis of PCOS; all 35 had clinical hyperandrogenism, 37% were amenorrheic, and 60% oligomenorrheic. Pretreatment median weight was 82.7 kg, BMI 30.8 kg/m2, and 19 (54%) girls had BMI > the CDC age-gender-specific 95th percentile (overweight). Calories (26% protein, 44% carbohydrate) were targeted to 1,500-1,800/day if BMI was

Statins as a class are well tolerated. We assessed acceptability, efficacy, and safety of rosuvastatin in 57 euthyroid patients with primary high LDL cholesterol (LDLC) who, serially, could not tolerate most other statins or cholesterol-lowering drugs, primarily because of myocitis. Of the 57 patients, 44 could not tolerate atorvastatin, 27 simvastatin, 15 pravastatin, 7 fluvastatin, 2 lovastatin, 1 Vytorin, 10 WelChol, 5 Zetia, 2 TriCor, and 2 Niaspan. Rosuvastatin (5 mg/day)-diet was given to 24 patients (3 men, 21 women, 21 white, 3 black, 3 type 2 diabetics, mean ± SD age 61 ± 9 years, BMI 31.7 ± 4.2, LDLC 179 ± 32 mg/dL). On rosuvastatin 5 mg-diet for a median of 5 months, weight fell 3.0 ± 7.7 lb ( p = .016), LDLC fell 76 ± 35 mg/dL ( p

In children aged 3 years without malocclusion the dental arches were studied for the occurrence, position and size of diastemata (interdental clefts). In the studied children most arches had diastemata (in 95% of cases in the upper arch and in 80% in the lower arch). It is concluded that the behaviour of the contact points between teeth is not a characteristic feature of the teeth of children aged 3 years. It seems that the presence of "closed" dental arches--without diastemata, and "open" with diastemata, confirms the presence of two types of dental arches of milk teeth.

The dental arches were analysed in 3-year-old children without malocclusion evaluating the shape of arches, measuring their with, length and depth. The index of the dental arch and the palatal index were calculated. In children aged 3 years the shape of the upper dental arch was in most cases similar to a semi-ellipse and that of the lower arch approached parabole. This suggests that the semicircular shape of dental arches is not characteristic of this period of occlusion development.