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Masivna opstetrička krvarenja učestali su uzrok smrti rodilja u zemljama u razvoju, ali i u razvijenim zemljama. Najnoviji epidemiološki podatci upozoravaju na njihov trend rasta u razvijenim zemljama, što ukazuje na istinsku potrebu za njihovim dubljim razumijevanjem. Stoga je cilj ovoga narativnog preglednog rada na temelju pretraživanja dostupne literature (baze podataka Web of Science [All Databases] i Scopus) čitateljima dati uvid u najnovije dijagnostičke i terapijske pristupe ovome važnom medicinskom problemu. Utvrdili smo kako uterotonici i dalje čine osnovu liječenja te kako su standardni koagulacijski testovi sve manje zastupljeni u dijagnostici, dok je naglasak stavljen na analize „point of care“ poput tromboelastografije i tromboelastometrije. Zaključno, nužno je poznavanje i usvajanje intervencijskih algoritama masivnih opstetričkih krvarenja te uvježban multidisciplinaran pristup u svakom rodilištu.

It is hard to imagine living in a color-free world, where color is weaved at every moment of life, and used to determine everything from our appearance to our mood. Humans perceive color before shape, words, or movement; the trait of color is to give contrast, contradiction, homogeneity, and harmony in the combination of the overall visual unit of design. This is reflected in trademark design, where choosing its colors correctly helps communicate better and more effectively with the target audience. When choosing the trademark colors, you also choose the feelings and associations that it seeks to evoke with the audience, and the color becomes a shortcut for conveying visual details for that trademark. The subjective experience of the target audience is one of the important factors that influence their perception for color connotations in trademark. It also plays an important role in the process of visual perception, as it helps interpret new things and give them meaning. The subjective experience also affects the interpretation of the symbols used in the trademark; as it gives the target audience the meanings of things he perceives and helps him understand the trademark. This subjective experience is built by many factors such as family, cultural and social environment.The research attempts to clarify the importance of the designer's study of the subjective experience of target audience in order to choose the color of the trademark that is appropriate to them and that does not conflict with their culture or experience.

There is growing demand for separation of 90Y carrier free from 90Sr coexisting to produce high purity 90Y essential for radiopharmaceutical uses. Thus, in this context the sorption profiles of Y3+ and Sr2+ from aqueous solutions containing diethylenetriaminepenta acetic acid (DTPA), ethylenediaminetetra-acetic acid (EDTA), acetic acid, citric acid, or NaCl onto Chelex-100 (anion ion exchange) solid sorbent were critically studied for developing an efficient and low-cost methodology for selective separation of Y3+ from Sr2+ ions (1.0 × 10−5 M). Batch experiments displayed relative chemical extraction percentage (98 ± 5.4%) of Y3+ from aqueous acetic acid solution onto Chelex-100 (anion ion exchanger), whereas Sr2+ species showed no sorption. Hence, a selective separation of Y3+ from its parent 90Sr2+ has been established based upon percolation of the aqueous solution of Y3+ and Sr2+ ions containing acetic acid at pH 1-2 through Chelex-100 sorbent packed column at a 2 mL min−1 flow rate. Y3+ species were retained quantitatively while Sr2+ ions were not sorbed and passed through the sorbent packed column without extraction. The sorbed Y3+ species were then recovered from the sorbent packed column with HNO3 (1.0 M) at a 1.0 mL min−1 flow rate. A dual extraction mechanism comprising absorption associated to “weak-base anion exchanger” and “solvent extraction” of Y3+ as (YCl6)3− and an extra part for “surface adsorption” of Y3+ by the sorbent is proposed. The established method was validated by measuring the radiochemical (99.2 ± 2 1%), radionuclide purity and retardation factor (Rf = 10.0 ± 0.1 cm) of 90Y3+ recovered in the eluate. Ultimately, the sorbent packed column also presented high stability for reusing 2-3 cycles without drop in its efficiency (±5%) towards Y3+ uptake and relative chemical recovery. A proposed flow sheet describing the analytical procedures for the separation of 90Y3+ from 90Sr2+ using chelating Chelex 100 (anion exchange) packed column is also included.

The coccyx, the last segment of the spine, joins the sacrum at the base. It has three to five vertebrae, which are typically fused. In front of the sacrococcygeal junction is the ganglion impar, the only unpaired autonomic ganglion. The two sympathetic chains come to a close there. The impar ganglion is traversed by sympathetic nerves carrying pain fibers from the perineum, distal sections of the rectum, the vagina and the urethra. The painful disorder known as coccygodynia, which affects the tail end of the spine, is frequently brought on by birth trauma or is caused by an unidentified factor. Even though the pain may go away on its own or with therapy, it may also linger and worsen over time. Due to increased stress from the female pelvis on the coccyx, it affects women five times more frequently than it does men. Conservative, invasive or surgical treatment options are available for coccygodynia (partial or total coccygectomy). Rest, nonsteroidal anti-inflammatory medicines (NSAIDs) or COX-2 inhibitors, acupuncture, coccyx cushions, physical therapy, manual therapy and invasive therapy, which involves ganglion impar block with injections of local anesthetic and corticosteroid under fluoroscopy, followed by radiofrequency ablation, spinal cord stimulation (SCS) or peripheral nerve stimulation, are examples of conservative treatments. Coccygectomy is recommended in refractory situations.

Arterial media calcification refers to the pathological deposition of calcium phosphate crystals in the arterial wall. This pathology is a common and life-threatening complication in chronic kidney disease, diabetes and osteoporosis patients. Recently, we reported that the use of a TNAP inhibitor, SBI-425, attenuated arterial media calcification in a warfarin rat model. Employing a high-dimensionality unbiased proteomic approach, we also investigated the molecular signaling events associated with blocking arterial calcification through SBI-425 dosing. The remedial actions of SBI-425 were strongly associated with (i) a significant downregulation of inflammatory (acute phase response signaling) and steroid/glucose nuclear receptor signaling (LXR/RXR signaling) pathways and (ii) an upregulation of mitochondrial metabolic pathways (TCA cycle II and Fatty Acid β-oxidation I). Interestingly, we previously demonstrated that uremic toxin-induced arterial calcification contributes to the activation of the acute phase response signaling pathway. Therefore, both studies suggest a strong link between acute phase response signaling and arterial calcification across different conditions. The identification of therapeutic targets in these molecular signaling pathways may pave the way to novel therapies against the development of arterial media calcification.

Arterial media calcification is an active cell process. This encompasses osteochondrogenic transdifferentiation of vascular smooth muscle cells followed by the deposition of calcium-phosphate crystals. Increasing evidence suggests a significant role for endothelial cells (ECs) in the development of arterial media calcification. This manuscript explores a role for endothelial dysfunction in the disease progression of arterial media calcification. Male rats were randomly assigned to four different groups. The first group received standard chow. The second group was given L-NAME (≈50 mg kg -1 · d -1 ), to induce endothelial dysfunction, in addition to standard chow. The third group and fourth group received a warfarin-supplemented diet to induce mild calcification and the latter group was co-administered L-NAME. Prior to sacrifice, non-invasive measurement of aortic distensibility was performed. Animals were sacrificed after 6 weeks. Arterial media calcification was quantified by measuring aortic calcium and visualized on paraffin-embedded slices by the Von Kossa method. Arterial stiffness and aortic reactivity was assessed on isolated carotid segments using specialized organ chamber setups. Warfarin administration induced mineralization. Simultaneous administration of warfarin and L-NAME aggravated the arterial media calcification process. Through organ chamber experiments an increased vessel tonus was found, which could be linked to reduced basal NO availability, in arteries of warfarin-treated animals. Furthermore, increased calcification because of L-NAME administration was related to a further compromised endothelial function (next to deteriorated basal NO release also deteriorated stimulated NO release). Our findings suggest early EC changes to impact the disease progression of arterial media calcification., (© 2022 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.)

Current treatment strategies for chronic kidney disease (CKD) mainly focus on controlling risk factors. Metformin, a first-line drug for type 2 diabetes, exerts beneficial pleiotropic actions beyond its prescribed use and incipient data have revealed protective effects against the development of kidney impairment. This study evaluated the therapeutic efficacy of metformin and canagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor recently approved by the United States Food and Drug Administration to treat diabetic nephropathy, in slowing the progression of established non-diabetic CKD. Rats with adenine-induced CKD were assigned to different treatment groups to receive either 200 mg/kg metformin, four or five weeks after the start of the adenine diet (established mild-moderate CKD), or 25 mg/kg canagliflozin four weeks after the start of the diet, by daily oral gavage administered during four weeks. Each treatment group was compared to a vehicle group. Chronic adenine dosing resulted in severe CKD in vehicle-treated rats as indicated by a marked rise in serum creatinine levels, a marked decrease in creatinine clearance, and a disturbed mineral metabolism. Metformin, but not canagliflozin, halted functional kidney decline. Additionally, kidneys of metformin-treated animals showed less interstitial area and inflammation as compared to the vehicle group. Proteomic analyses revealed that metformin's kidney-protective effect was associated with the activation of the Hippo signaling pathway, a highly conserved multiprotein kinase cascade that controls tissue development, organ size, cell proliferation, and apoptosis. Thus, metformin demonstrated therapeutic efficacy by halting the progression of established CKD in a rat model., (Copyright © 2022 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Sclerostin is a negative regulator of the Wnt/β-catenin signaling and is, therefore, an important inhibitor of bone formation and turnover. Because ectopic vascular calcification develops in a similar way to bone formation, one might reasonably attribute a role to sclerostin in this pathological process. Ectopic calcification, especially vascular calcification, importantly contributes to mortality in elderly and patients with diabetes, osteoporosis, chronic kidney disease (CKD), and hypertension. The central players in this ectopic calcification process are the vascular smooth muscle cells that undergo dedifferentiation and thereby acquire characteristics of bonelike cells. Therefore, we hypothesize that depletion/deactivation of the Wnt/β-catenin signaling inhibitor sclerostin may promote the development of ectopic calcifications through stimulation of bone-anabolic effects at the level of the arteries. We investigated the role of sclerostin (encoded by the Sost gene) during vascular calcification by using either Sost -/- mice or anti-sclerostin antibody. Sost -/- and wild-type (WT) mice (C57BL/6J background) were administered an adenine-containing diet to promote the development of CKD-induced vascular calcification. Calcifications developed more extensively in the cardiac vessels of adenine-exposed Sost -/- mice, compared to adenine-exposed WT mice. This could be concluded from the cardiac calcium content as well as from cardiac tissue sections on which calcifications were visualized histochemically. In a second experiment, DBA/2J mice were administered a warfarin-containing diet to induce vascular calcifications in the absence of CKD. Here, warfarin exposure led to significantly increased aortic and renal tissue calcium content. Calcifications, which were present in the aortic medial layer and renal vessels, were significantly more pronounced when warfarin treatment was combined with anti-sclerostin antibody treatment. This study demonstrates a protective effect of sclerostin during vascular calcification. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR)., (© 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).)