Impact of the COVID-19 pandemic on the incidence of surgical site infection after orthopaedic surgery: an interrupted time series analysis of the nationwide surveillance database in Japan.

BACKGROUND: During the COVID-19 pandemic, hygiene awareness was increased in communities and hospitals. However, there is controversy regarding whether such circumstances affected the incidence of surgical site infections (SSIs) in the orthopaedic surgical field. AIM: To examine the impact of the COVID-19 pandemic on the incidence of SSIs after orthopaedic surgery. METHODS: The medical records of patients having undergone orthopaedic surgery were extracted from the nationwide surveillance database in Japan. The primary outcomes were the monthly incidences of total SSIs, deep or organ/space SSIs, and SSIs due to meticillin-resistant Staphylococcus aureus (MRSA). Interrupted time series analysis was conducted between pre-pandemic (January 2017 to March 2020) and pandemic (April 2020 to June 2021) periods. RESULTS: A total of 309,341 operations were included. Interrupted time series analysis adjusted for seasonality showed no significant changes in the incidence of total SSIs (rate ratio 0.94 and 95% confidence interval 0.98-1.02), deep or organ/space SSIs (0.91, 0.72-1.15), or SSIs due to MRSA (1.07, 0.68-1.68) along with no remarkable slope changes in any parameter (1.00, 0.98-1.02; 1.00, 0.97-1.02; and 0.98, 0.93-1.03, respectively). CONCLUSIONS: Awareness and measures against the COVID-19 pandemic did not markedly influence the incidence of total SSIs, deep or organ/space SSIs, or SSIs due to MRSA following orthopaedic surgery in Japan.

15 N DILUTION METHOD FOR ESTIMATING THE ABSORPTION OF ATMOSPHERIC NO2 BY PLANTS.

The 15 N dilution method was used for the quantitative estimation of nitrogen dioxide (NO2 ) absorbed by Helianthus annuus and Zea mays during a relatively long period. The relationships between the amount of NO2 absorbed and the concentration of NO2 and length of exposure were investigated, in order to ascertain the reliability of this method. The total amount of NO2 -nitrogen absorbed by the plants over two weeks (from two to four weeks after the sowing) increased with increasing concentrations of NO2 . The rate of absorption of NO2 per unit leaf area also increased linearly with increasing concentrations of NO2 from 0 to 1 µl l-1 . This means that the diffusive resistances of stomata or mesophyll tissues were not changed by the continuous exposure to NO2 at 1 µl l-1 for two weeks. The absorption rate per unit leaf area in H. annuus was about three times greater than that in Z. mays. The total amount of NO2 -nitrogen absorbed by the plants which were continuously exposed to 0.5 µl l -1 NO2 rose not linearly but exponentially as the exposure time increased from zero to three weeks. This might in part have reflected the growth characteristics of the plants, since dry weight and leaf area increased exponentially during the period of exposure to the pollutant. The absorption rate per unit leaf area remained constant during the first two weeks, but thereafter increased significantly, probably due to the uptake of NO2 -nitrogen through the air-soil-root pathway. These results demonstrated that the values estimated by the15 N dilution method were reliable, and this method can be recommended for the quantitative determination of NO2 absorbed by plants during a long period.

[Ultrasonography in the diagnosis of liver cirrhosis].

Ultrasound is now widely used in the diagnosis of liver diseases. Applications of ultrasound in the diagnosis of liver cirrhosis are reviewed in this paper. Characteristic findings of liver cirrhosis in ultrasound are nodular liver surface, round edge, and hypoechoic nodules in liver parenchyma which represent regenerative nodules of cirrhotic liver. Detection of hypoechoic nodule more than 10 mm is important in the early diagnosis of hepatocellular carcinoma. Detection of splenomegaly, ascites, and portosystemic collaterals is possible by ultrasound. Evaluation of portosystemic collaterals is beneficial in the management of esophagogastric varices and portosystemic encephalopathy. Ultrasound is useful in the non-invasive diagnosis and long-term management of cirrhotic patients.

Tofogliflozin, a sodium/glucose cotransporter 2 inhibitor, attenuates body weight gain and fat accumulation in diabetic and obese animal models.

OBJECTIVE: Tofogliflozin, a highly selective inhibitor of sodium/glucose cotransporter 2 (SGLT2), induces urinary glucose excretion (UGE), improves hyperglycemia and reduces body weight in patients with Type 2 diabetes (T2D). The mechanisms of tofogliflozin on body weight reduction were investigated in detail with obese and diabetic animal models. METHODS: Diet-induced obese (DIO) rats and KKAy mice (a mouse model of diabetes with obesity) were fed diets containing tofogliflozin. Body weight, body composition, biochemical parameters and metabolic parameters were evaluated. RESULTS: In DIO rats tofogliflozin was administered for 9 weeks, UGE was induced and body weight gain was attenuated. Body fat mass decreased without significant change in bone mass or lean body mass. Food consumption (FC) increased without change in energy expenditure, and deduced total calorie balance (deduced total calorie balance=FC-UGE-energy expenditure) decreased. Respiratory quotient (RQ) and plasma triglyceride (TG) level decreased, and plasma total ketone body (TKB) level increased. Moreover, plasma leptin level, adipocyte cell size and proportion of CD68-positive cells in mesenteric adipose tissue decreased. In KKAy mice, tofogliflozin was administered for 3 or 5 weeks, plasma glucose level and body weight gain decreased together with a reduction in liver weight and TG content without a reduction in body water content. Combination therapy with tofogliflozin and pioglitazone suppressed pioglitazone-induced body weight gain and reduced glycated hemoglobin level more effectively than monotherapy with either pioglitazone or tofogliflozin alone. CONCLUSION: Body weight reduction with tofogliflozin is mainly due to calorie loss with increased UGE. In addition, tofogliflozin also induces a metabolic shift from carbohydrate oxidation to fatty acid oxidation, which may lead to prevention of fat accumulation and inflammation in adipose tissue and liver. Tofogliflozin may have the potential to prevent obesity, hepatic steatosis and improve insulin resistance as well as hyperglycemia.

Tofogliflozin, a novel sodium-glucose co-transporter 2 inhibitor, improves renal and pancreatic function in db/db mice.

BACKGROUND AND PURPOSE: Although inhibition of renal sodium-glucose co-transporter 2 (SGLT2) has a stable glucose-lowering effect in patients with type 2 diabetes, the effect of SGLT2 inhibition on renal dysfunction in type 2 diabetes remains to be determined. To evaluate the renoprotective effect of SGLT2 inhibition more precisely, we compared the effects of tofogliflozin (a specific SGLT2 inhibitor) with those of losartan (an angiotensin II receptor antagonist) on renal function and beta-cell function in db/db mice. EXPERIMENTAL APPROACH: The effects of 8-week tofogliflozin or losartan treatment on renal and beta-cell function were investigated in db/db mice by quantitative image analysis of glomerular size, mesangial matrix expansion and islet beta-cell mass. Blood glucose, glycated Hb and insulin levels, along with urinary albumin and creatinine were measured KEY RESULTS: Tofogliflozin suppressed plasma glucose and glycated Hb and preserved pancreatic beta-cell mass and plasma insulin levels. No improvement of glycaemic conditions or insulin level was observed with losartan treatment. Although the urinary albumin/creatinine ratio of untreated db/db mice gradually increased from baseline, tofogliflozin or losartan treatment prevented this increase (by 50-70%). Tofogliflozin, but not losartan, attenuated glomerular hypertrophy. Neither tofogliflozin nor losartan altered matrix expansion. CONCLUSIONS AND IMPLICATIONS: Long-term inhibition of renal SGLT2 by tofogliflozin not only preserved pancreatic beta-cell function, but also prevented kidney dysfunction in a mouse model of type 2 diabetes. These findings suggest that long-term use of tofogliflozin in patients with type 2 diabetes may prevent progression of diabetic nephropathy.

Laparoscopy-assisted appendectomy through an umbilical port in children.

INTRODUCTION: We report surgical techniques for single-incision laparoscopy-assisted surgery (SILAS) in the treatment of pediatric acute appendicitis. METHODS: We performed SILAS in 15 cases of acute appendicitis between January and September of 2009. SILAS is a surgical method that involves making the incision at the umbilicus, inserting a wound retractor XS, suspending the abdominal wall with a hook, and appendectomy with the same procedures as conventional appendectomy. RESULTS: SILAS appendectomy was performed in all 15 cases with the exception of one case where one 3-mm port was added. Compared to open appendectomy, blood loss was significantly lower and postoperative hospitalization time was shorter, although there was no significant decrease in operative time, or postoperative fasting time. No postoperative complications, such as wound infection, intestinal obstruction, intra-abdominal abscess, or bleeding, were encountered. CONCLUSION: SILAS was safely performed and is superior to open appendectomy with regard to cosmetic outcome.

Melanophore lineage and clonal organization of the epidermis in Xenopus embryos as revealed by expression of a biogenic marker, GFP.

Melanophore lineage during embryogenesis of Xenopus laevis was traced using the overexpression of a biogenic marker, green fluorescent protein (GFP). Two different approaches were applied after injection of GFP mRNA (hence a marker construct) into each blastomere at the 16-cell stage. In in vivo experiments, the embryos injected with a marker construct were grown until stage 45, in which melanophores were distributed over the whole body and were good enough for checking GFP expression at their migratory destination. In in vitro experiments, neural tubes of the embryos injected with a marker construct were isolated and cultured at stage 21 to examine by virtue of GFP expression how neural crest cells differentiate into melanophores. The results obtained from both in vivo and in vitro experiments indicated the following: 1) selected animal blastomeres vastly contribute to the development of melanophores, whereas other animal blastomeres do so slightly at a limited pace; and 2) vegetal blastomeres never contribute to melanophores in normal development, whereas certain vegetal blastomeres have a potential to give rise to melanophores in vitro. The analyses using GFP also disclosed that the dorsal and ventral epidermis derive from the restricted animal blastomeres in the normal development. Since the dorso-ventrality of the epidermis has been inseparably coupled with integumental pigmentation, the clonal organization of the epidermis observed in the present study is discussed in the light of pigment pattern formation attributed by melanophores.

Further studies on the melanophores of periodic albino mutant of Xenopus laevis.

It is still unknown why dermal melanophores disappear during larval development, and why no or very few epidermal melanophores appear during and after metamorphosis, in Xenopus laevis showing periodic albinism (ap). To elucidate these points, we investigated the occurrence of depigmentation in mutant (ap/ap) melanophores during in vitro proliferation and the incidence of melanophore differentiation from mutant melanoblasts in the skin in vitro. During in vitro proliferation of mutant melanophores, ap-type melanosomes decreased in number gradually and instead the number of premelanosomes increased in the cells, which caused depigmentation at the light microscopic level in the culture. Depigmentation was observed only in mutant melanophores, and not in wild-type (+/+) melanophores. These results suggest that autonomous depigmentation of mutant dermal melanophores is the cause of the disappearance of these cells in vivo. Dopa-positive melanoblasts were demonstrated in both wild-type and mutant skins. However, the melanoblasts of metamorphosed mutant froglets did not differentiate in vitro, while those of wild-type froglets did. These results suggest that mutant melanoblasts in the skin of froglets lose the potency to differentiate into melanophores, and that this causes the lack of mutant melanophores in the froglets. The site of action of the ap gene is also discussed.

N-CAM and N-cadherin are specifically expressed in xanthophores, but not in the other types of pigment cells, melanophores, and iridiphores.

Little is known about cell-cell communication in pigment cells, whereas a number of signalling molecules have been implicated to control their migration, differentiation, and proliferation. We set out to investigate the expression of cell adhesion molecules (CAMs) in the three different types of pigment cells in poikilotherms, Oryzias latipes and Xenopus laevis. In the present experiments, the expression of N-CAM and N-cadherin in the pigment cells in vitro was examined by immunocytochemistry. Melanophores and xanthophores were isolated and cultured from scales or skins, while iridophores were harvested from skins or peritoneum. The results showed that N-CAM and N-cadherin were specifically expressed in xanthophores, but not in melanophores or iridophores in both O. latipes and X. laevis. N-CAM and N-cadherin basically colocalized in the restricted regions of xanthophores, although the N-caderin-expressed region was broader than the N-CAM-expressed region in the same cell. The incidence of N-cadherin expression was higher than that of N-CAM expression. N-CAM and N-cadherin were expressed at the tip or the base of dendrites, or at the edge between dendrites in dendritic xanthophores. N-CAM and N-cadherin usually localized in small and narrow regions of xanthophores. This distribution pattern was essentially similar in xanthophores with round morphology, which exhibited spot, band, or semicircular immunoreactive regions on the peripheral edge of the cells. The difference in the distribution of pigment granules within the cells, culture period, fixatives, or immunofluorescent markers used in the experiments did not alter the immunostaining pattern.

A ventrally localized inhibitor of melanization in Xenopus laevis skin.

Melanophores normally differentiate in dorsal but not in ventral skin of Xenopus laevis. We have sought factors which might regulate this differentiation pattern, and we have obtained a putative melanization inhibiting factor (MIF) from ventral but not from dorsal skin. Preliminary studies reveal that MIF is destroyed by heat or trypsin treatment, indicating its protein composition, and has a molecular weight in the range of 300 kDa. The effects of MIF on the differentiation of neural crest derivatives to melanophores were examined in vitro in the presence of tyrosine and fetal calf serum (FCS). Tyrosine enhances melanophore differentiation in vitro at concentrations equivalent to those estimated in adult Xenopus blood plasma (20 microM). FCS also stimulates melanization, by way of materials other than the tyrosine contained in FCS. MIF strongly inhibits outgrowth and melanization of neural crest cells from neural tube explants. MIF also inhibits the differentiation of melanoblasts contained in cultured explants of ventral skin. Inhibition of melanization or melanophore differentiation by MIF occurs even in the presence of L-tyrosine and/or FCS. We suggest that MIF plays an important role in the establishment of dorso-ventral pigment patterns in amphibia.

Proliferation in vitro of melanophores from Xenopus laevis.

Melanophores of wild-type and periodic albino mutants of Xenopus laevis were successfully cultured in vitro. They proliferated in the presence of alpha-melanocyte-stimulating hormone (alpha-MSH or cyclic adenosine monophosphate (cAMP) at a doubling time of 8-10 days. These proliferating melanophores retained their phenotypes, ability to synthesize melanin, and melanin-dispersing response to MSH stimulation. Neither depigmentation nor selective cell death of periodic albino melanophores was observed for at least 4 months during the cultivation.

Mode coupling in thin-film chirped gratings.

Mode coupling in thin-film chirped gratings is discussed. TE-TM-mode coupling is shown to occur for inclined incident light. The wavelength resolution of a chirped-grating demultiplexer is described in terms of mode coupling.

Cytoskeletal architecture of dermal chromatophores of the freshwater teleost Oryzias latipes.

Cytoskeletal construction of dermal chromatophores of Oryzias latipes was studied by immunofluorescence microscopy. A microtubule system was most prominent in melanophores where a large number of microtubules emanated from the center of the cell. Xanthophores had an arrangement basically similar to that of melanophores, though the radial pattern became more irregular in the peripheral region where intersecting wavy microtubules were quite frequent. Oval-shaped leucophores exhibited the least-developed microtubule system, where the limited number of microtubules formed a loose basket-like architecture. Intermediate filaments were ubiquitously present in all types of chromatophores and were found to be vimentin-immunoreactive. Examination of doubly-labeled cells indicated that vimentin filaments had similar distribution patterns with microtubules. Orderly arranged bundles of actin filaments were found only in xanthophores, while in melanophores and xanthophores, actin expression was diffuse without displaying a conspicuous filamentous organization. Colchicine treatment induced depolymerization of microtubules and retraction of dendrites in varying degrees in cells in culture and in situ. Melanophores in culture are very sensitive to the treatment while xanthophores appeared to be more resistant in respect to the maintenance of cell morphology.