Italy was the rst, among all the European countries, to be strongly hit by the Covid-19 pandemic outbreak caused by the severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2). The virus, proven to be very contagious, infected more than 9 million people worldwide (in June 2020). Nevertheless, it is not clear the role of air pollution and meteorological conditions on virus transmission. In this study, we quantitatively assessed how the meteorological and air quality parameters are correlated to the Covid-19 transmission in Lombardy (Northern Italy), the region epicenter of the virus outbreak. Our main ndings highlight that temperature and humidity related variables are negatively correlated to the virus transmission, whereas air pollution (PM 2.5) shows a positive correlation. In other words, Covid-19 pandemic transmission prefers dry and cool environmental conditions, as well as polluted air. For these reasons, the virus might easier spread in un ltered air-conditioned environments. Those results will be supporting decision makers to contain new possible outbreaks.

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CONCLUSION: LCVP is easily achievable in technique.Maintenance of CVP ≤ 4 mmHg can help reduce blood loss during hepatectomy, shorten the length of hospital stay, and has no detrimental effects on hepatic or renal function. INTRODUCTIONHepatectomy remains as the treatment of choice for hepatocellular carcinoma (HCC). Intra-operative blood loss is one of the major causes for post-operative morbidity and mortality. Various techniques, such as Pringle's maneuver and unilateral hepatic hilum occlusion, have been used to control bleeding from hepatic arterial and portal venous systems during hepatectomy in clinical settings. However, for excision of HCC adjacent to major blood vessels, hepatic system could be the major source of hemorrhage, especially after the application of Pringle's maneuver. Hence, effective control of hepatic venous hemorrhage is crucial to minimize intraoperative blood loss. This prospective randomized clinical trial aims at evaluating the role of low central venous pressure (LCVP) in reducing blood loss during hepatectomy for HCC. MATERIALS AND METHODS Patients'data and groupingFrom June 2002 to December 2003, a total of 50 consecutive patients with HCC (40 men and 10 women) underwent hepatectomy by the same group of surgeons at our hospital. By the sealed envelope method, the patients were blindly randomized into LCVP group (n = 25) and control group (n = 27) at the beginning of the operation. Two patients in the control group were excluded from the study because hepatectomy was given up due to cardiac arrest in one and unclear tumor demarcation in the other. Eventually, there were 25 patients in each group. The demographic data of the patients are shown in Table 1

Lithium treatment for 4 wk caused severe polyuria, dramatic downregulation in aquaporin-2 (AQP-2) expression, and marked decrease in AQP-2 immunoreactivity with the appearance of a large number of cells without AQP-2 labeling in the collecting ducts after lithium treatment. Surprisingly, this was not all due to an increase in AQP-2-negative principal cells, because double immunolabeling revealed that the majority of the AQP-2-negative cells displayed [H+]ATPase labeling, which identified them as intercalated cells. Moreover, multiple [H+]ATPase-labeled cells were adjacent, which was never seen in control rats. Quantitation confirmed a significant decrease in the fraction of collecting duct cells that exhibited detectable AQP-2 labeling compared with control rats: in cortical collecting ducts, 40 ± 3.4 vs. 62 ± 1.8% of controls ( P < 0.05; n = 4) and in inner medullary collecting ducts, 58 ± 1.6 vs. 81 ± 1.3% of controls ( P < 0.05; n = 4). In parallel, a significant increase in the fraction of intercalated ([H+]ATPase-positive) cells was shown. Urine output, whole kidney AQP-2 expression, cellular organization, and the fractions of principal and intercalated cells in cortex and inner medulla returned to control levels after 4 wk on a lithium-free diet following 4 wk on a lithium-containing diet. In conclusion, lithium treatment not only decreased AQP-2 expression, but dramatically and reversibly reduced the fraction of principal cells and altered the cellular organization in collecting ducts. These effects are likely to be important in lithium-induced nephrogenic diabetes insipidus.

. Increased expression and apical targeting of renal ENaC subunits in puromycin aminonucleoside-induced nephrotic syndrome in rats.

Bilateral ureteral obstruction (BUO) is associated with marked changes in the expression of renal aquaporins (AQPs) and sodium transport proteins. To examine the role of prostaglandin in this response, we investigated whether 24-h BUO changed the expression of cyclooxygenases (COX-1 and -2) in the kidney and tested the effect of the selective COX-2 inhibitor parecoxib (5 mg.kg(-1).day(-1) via osmotic minipumps) on AQPs and sodium transport. Sham and BUO kidneys were analyzed by semiquantitative immunoblotting, and a subset of kidneys was perfusion fixed for immunocytochemistry. BUO caused a significant 14-fold induction of inner medullary COX-2 (14.40 +/- 1.8 vs. 1.0 +/- 0.4, n = 6; P < 0.0001) and a reduction in medullary tissue osmolality, whereas COX-1 did not change. Immunohistochemistry confirmed increased COX-2 labeling associated with medullary interstitial cells. COX isoforms did not change in cortex/outer medulla after 24-h BUO. In BUO kidneys, inner medullary AQP2 expression was reduced, and this decrease was prevented by parecoxib. In the inner stripe of outer medulla, the type 3 Na(+)/H(+) exchanger (NHE3) and apical Na(+)-K(+)-2Cl(-) cotransporter (BSC-1) were significantly reduced by BUO, and this decrease was significantly attenuated by parecoxib. Immunohistochemistry for AQP2, NHE3, and BSC-1 confirmed the effect of parecoxib. Parecoxib had no significant effect on the Na-K-ATPase alpha(1)-subunit, type II Na-P(i) cotransporter, or AQP3. In conclusion, acute BUO leads to marked upregulation of COX-2 in inner medulla and selective COX-2 inhibition prevents dysregulation of AQP2, BSC-1, and NHE3 in response to BUO. These data indicate that COX-2 may be an important factor contributing to the impaired renal water and sodium handling in response to BUO.