Objective: To analyze the clinical spectrum of skin conditions in neonates at Hamdard university hospital. Study Design: Descriptive (Observational) cross sectional study. Methods: This study was conducted from January 2008 to December 2009. All neonates seen at Hamdard university hospital during this period were examined. Neonates with skin conditions with in 28 days of birth were registered on a predesigned questioner by the house officer these cases were confirmed by the pediatric consultant, followed by detail physical systemic examination and skin examination. Dermatologist was involved in the diagnosis of difficult cases. Results: Total numbers of new born seen during the year 2008-2009 were 1660, there were 65% males and 35% females, 1360 (81.92%) were above 2.5 Kg at birth, 18.08% were below 2.5 Kg. Numbers of neonates with skin lesions were 577 (34.75%). Neonates with skin infections were 25.12%, 15.59% had with nappy rash and 15.59 % had erythema toxicum neonatrum. Neonates with milia were 60 (10.39%) and with erythema were 27 (4.67%). Conclusion: Clinical spectrums of neonatal skin are different in this study as compared to other regional and international studies. StreszczenieCel: Analiza kliniczna spektrum chorób skóry u noworodków w szpitalu Uniiwersyteckim Hamdard. Projekt badania: Opisowy (obserwacyjny) przekrój badania. Metody: Badanie zostało przeprowadzone w okresie od stycznia 2008 do grudnia 2009 roku. W tym okresie zbadano wszystkie noworodki widziane w szpitalu uniwersyteckim Hamdard. Noworodki z chorobami skóry w 28 dni od urodzenia były zarejestrowane na gotowych kwestionariuszach przez lekarza rezydenta, następnie te przypadki zostały potwierdzone przez konsultanta dziecięcego, po szczegółowym systemowym badaniu fizykalnym i badaniu skóry. Dermatolog był zaangażowany w diagnostyce trudnych przypadków. Wyniki: Całkowita liczba noworodków obserwowana w latach 2008 -2009 wynosiła 1660, w tym 65% płci męskiej i 35% płci żeńskiej, 1360 dzieci (81,92%) było powyżej 2,5 kg po urodzeniu, 18,08% było poniżej 2,5 kg. Liczba noworodków z zmianami skórnymi wynosiła 577 (34,75%). Noworodków z zakażeniami skóry było 25,12%, 15,59% miało pieluszkowe zapalenie skóry a u 15,59% stwierdzono toksyczny rumień noworodków. Noworodków z prosakami było 60 (10,39%) a z rumieniem 27 (4,67%). Konkluzja: Kliniczne spektrum skóry noworodków w tym badaniu różni się w porównaniu do innych badań regionalnych i międzynarodowych.
Human pluripotent embryonic stem cells (hESCs) have great promise for research into human developmental biology, development of cell therapies for the treatment of diseases, toxicology, and drug discovery. Traditionally, undifferentiated hESCs are maintained on mouse embryonic fibroblasts (MEFs), which impede the clinical applications of hESCs. Here we have examined the long-term stability of the Japanese hESC line (KhES-1) in feeder-free culture. KhES-1 cells were cultured with MEF conditioned medium (CM) and different doses of basic fibroblast growth factor (bFGF) in six-well-plates of which the surface was coated with Matrigel. KhES-1 cells were maintained for at least 40 passages. In this culture system, the cells maintained stable proliferation rates and steadily expressed Oct-4, Nanog, and alkaline phosphatase. In addition, KhES-1 cells maintained without direct feeder contact formed embryonic bodies with expression of markers from the three germ layers. Here we demonstrated that Japanese human embryonic stem cells KhES-1 were cultured long term in a feeder-free method, while retaining pluripotency in vitro.
Axons in the peripheral nervous system have the ability to repair themselves after damage, whereas axons in the central nervous system are unable to do so. A common and important characteristic of damage to the spinal cord, brain, and peripheral nerves is the disruption of axonal regrowth. Interestingly, intrinsic growth factors play a significant role in the axonal regeneration of injured nerves. Various factors such as proteomic profile, microtubule stability, ribosomal location, and signalling pathways mark a line between the central and peripheral axons’ capacity for self-renewal. Unfortunately, glial scar development, myelin-associated inhibitor molecules, lack of neurotrophic factors, and inflammatory reactions are among the factors that restrict axonal regeneration. Molecular pathways such as cAMP, MAPK, JAK/STAT, ATF3/CREB, BMP/SMAD, AKT/mTORC1/p70S6K, PI3K/AKT, GSK-3β/CLASP, BDNF/Trk, Ras/ERK, integrin/FAK, RhoA/ROCK/LIMK, and POSTN/integrin are activated after nerve injury and are considered significant players in axonal regeneration. In addition to the aforementioned pathways, growth factors, microRNAs, and astrocytes are also commendable participants in regeneration. In this review, we discuss the detailed mechanism of each pathway along with key players that can be potentially valuable targets to help achieve quick axonal healing. We also identify the prospective targets that could help close knowledge gaps in the molecular pathways underlying regeneration and shed light on the creation of more powerful strategies to encourage axonal regeneration after nervous system injury.
In the context of fulfillment of maqās. id al-Sharī'ah,
The use of this novel method adds a new dimension to the presentation of scientific work at surgical and medical conferences and as part of journals and textbooks by permitting users to view scientific data and techniques on mobile devices as videos or as three dimensional environments at their own leisure.
Abstract-The survivable logical topology mapping (SLTM) problem in an IP-over-WDM optical network is to map each link (u, v) in the logical topology (at the IP layer) into a lightpath between the nodes u and v in the physical topology (at the optical layer) such that failure of a physical link does not cause the logical topology to become disconnected. It is assumed that both the physical and logical topologies are 2-edge connected. For this problem Kurant and Thiran [12] presented an algorithmic framework called SMART that involves successively contracting circuits in the logical topology and mapping the logical links in the circuits into edge disjoint lightpaths in the physical topology. In a recent work [21] we presented a dual framework involving cutsets and showed that both these frameworks possess the same algorithmic structure. Algorithms CIRCUIT-SMART, CUTSET-SMART, CUTSET-SMART-SIMPLIFIED and INCIDENCE-SMART were also presented in [21]. Effectiveness of both these frameworks as well as their robustness in providing survivability against multiple failures depends on the lengths of the cutset cover and circuit cover sequences on which they are based. To improve their effectiveness and robustness, in this paper we first introduce the concept of generalized cutset cover and generalized circuit cover sequences. We present an algorithm to get a generalized cutset (circuit) cover sequence from any given cutset (circuit) cover sequence. We then present GEN-CUTSET-SMART and GEN-CUTSET-SMART-SIMPLIFIED algorithms that remove some of the shortcomings of the dual framework of [21]. We prove that there is a one-to-one correspondence between the set of generalized circuit cover sequences and the set of generalized cutset cover sequences. We then show that for each execution of GEN-CIRCUIT-SMART there exists an execution of GEN-CUTSET-SMART-SIMPLIFIED such that the groups of edges that they map into edge disjoint lightpaths are exactly the same. In other words, the distinction between the primal and dual methods disappears when they use generalized sequences. Preliminary simulation results confirm our expectation that GEN-CUTSET-SMART-SIMPLIFIED will perform better than CIRCUIT-SMART and CUTSET-SMART-SIMPLIFIED (when started with a circuit or a cutset sequence) in terms of number of additional protection edges to be added.
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